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multiverse
31-12-2009, 12:44 PM
Hello All,

Lyme disease is a hidden epidemic. For some reason, official authorities have greatly limited information or provided mis-information about this disease, which is now widespread in the U.S. and in Europe (and perhaps elsewhere). So few medical doctors are trained or informed about it. And many of those who know something about it, don't dare to say anything because of the possible (or probable) consequences on their career. I urge all of you to become informed.

Lyme disease is not easily diagnosed or treated. There are many false negative tests, as the most common test prescribed for it is totally useless. in addition, the disease itself has a host of diverse symptoms which mimic other diseases. So many people with Lyme in the States are treated for diseases that they don't have (to name a few, cardiac disorders, auto-immune disorders, psychiatric disorders, rheumatism, arthritis.) And when they cannot find Lyme, patients are often mis-treated in other ways, through denial of treatment, or by being characterized as delusional.

Here is a link to a trailer for the film "Under Our Skin," a feature length film speaking of the Lyme epidemic and the untold suffering associated with it: http://underourskin.com/watch.html

Here is a short video about Lyme which presents the work of the Turn the Corner Foundation which was organized to raise awareness about the disease: http://www.youtube.com/watch?v=XnRrdtusWdw. The Foundation's Web site is: http://turnthecorner.org/index.htmHere's a link to a symptoms checklist put together by Dr. Burrascano, the doctor who founded the Foundation: http://www.lymedisease.org/resources/handouts1.html. You will see from this list that the symptoms are quite varied, and can mimic many other diseases.

Here is the reference for a very well documented book that gives a lot of background information: "Amazon.com: Healing Lyme: Natural Healing And Prevention of Lyme Borreliosis And Its Coinfections (9780970869630): Stephen Harrod Buhner: Books@@AMEPARAM@@http://ecx.images-amazon.com/images/I/51L%2BmErxbBL.@@AMEPARAM@@51L%2BmErxbBL" by Stephen Harrod Buhner (Raven Press, 2005). Please note that he is not a 'fanatic' about the natural approach, but actually goes thoroughly over a number of the conventional and natural approaches possible.

Another site (http://www.fibroandfatigue.com/lymedisease.php?utm_source=adwords&utm_medium=ppc&utm_sponsored=lyme_content&utm_campaign=lyme) (http://www.fibroandfatigue.com/lymedisease.php?utm_source=adwords&utm_medium=ppc&utm_sponsored=lyme_content&utm_campaign=lyme) has this interesting information:
Because the symptoms are so variable, most patients are usually not considered for testing or treatment. If testing is done, however, standard tests will miss over 90% of cases of chronic Lyme disease. The standard tests include an immunoassay test of IgG and IgM antibodies and a Western blot for confirmation. The problem with these tests is that they are designed to detect acute Lyme disease and are very poor at detecting chronic Lyme disease. In addition, doctors (infectious disease, internists, family practice, etc.) most often use the Center for Disease Control (CDC) criteria to define a positive test. This criterion was never meant to be used for diagnosis, but rather for epidemiological surveillance (tracking data).Dr. John D. Bleiweiss was a doctor who worked to inform people about Lyme disease. The state of New Jersey went after his license for his "rogue" views about the disease. He committed suicide shortly thereafter in 1995. Here is a detailed article by him: http://74.125.95.132/search?q=cache:akOUf3SI__8J:cassia.org/essay.htm+hepatitis+as+related+to+Lyme+disease&hl=en&ct=clnk&cd=1&gl=us&ie=UTF-8

And here is an interesting book that theorizes about the disease's origins: [URL="http://www.amazon.com/Lab-257-Disturbing-Governments-Laboratory/dp/006078184X/ref=sr_1_1?ie=UTF8&s=books&qid=1262261866&sr=1-1"]Lab 257: The Disturbing Story of the Government\'s Secret Germ Laboratory. The Amazon description of the book says, Based on declassified government documents, in-depth interviews, and access to Plum Island itself, this is an eye-opening, suspenseful account of a federal government germ laboratory gone terribly wrong. For the first time, Lab 257 takes you deep inside this secret world and presents startling revelations on virus outbreaks, biological meltdowns, infected workers, the periodic flushing of contaminated raw sewage into area waters, and the insidious connections between Plum Island, Lyme disease, and the deadly West Nile virus.
This information needs to get out and remain available!

multiverse
21-02-2010, 12:56 PM
This article outlines how Lyme disease can be mis-diagnosed as Attention Deficit Disorder:
http://www.samento.com.ec/sciencelib/4lyme/howlymediseas.html

hoverfly
21-02-2010, 08:39 PM
There is a cover-up going on with Lyme.

I wanted my Dr to test for it, but he said :
1) it was very unlikely I'd have it, as it is very rare, and that
2) I'd not been in any area's of high risk.

Well.

1) Wrong, it is not rare.

2) Apart from the fact I live in a rural area, I've also been to the scottish highlands on dozens of occasions, since the sixties. Thing was, he never even asked me if I'd travelled anywhere at all. He just assumed - via his crystal ball.

:)

multiverse
22-02-2010, 11:01 PM
There is a cover-up going on with Lyme.
:)

Yes, there is a huge cover up! I'm amazed that a disease even as apparently rare as Morgellons is being talked about in conspiracy circles, but Lyme disease is talked about so little, even though it has been around for at least 30 years. Speaking about reducing population, Lyme is a very "convenient" disease because it mimics so many other diseases and, can be dormant in your body, can produce false negatives, can damage organs without you knowing it. It is vicious disease.

Most insurance companies don't even cover basic tests or healing. We had an insurance contract that explicitly stated it would not cover Lyme disease!

I spoke with a Lyme specialized doctor who said that 5 out of 6 bites will go unnoticed by victims.

Where we used to live, no matter where you go in nature (even on lawns), you could be sure of coming back with ticks. I even met a woman who went on a walk in another state where she got covered from head to foot with what she thought was dust, and then discovered that they were deer ticks. She is now disabled. So many stories have I heard... I have met so many people who were in terrible conditions, crippled or with other serious effects because of Lyme. And they all suffered terribly from the lack of information - especially among doctors - and lack of proper medical care, often being ridiculed through denial of their condition, etc.

With so many powerful pesticides around, how is this infestation of ticks possible?...

Why do so few people know about Lyme? And why are doctors so much in denial? Are they stupid or fearful or both?

multiverse
22-02-2010, 11:06 PM
I wanted my Dr to test for it, but he said :
1) it was very unlikely I'd have it, as it is very rare, and that
2) I'd not been in any area's of high risk.

Well.

1) Wrong, it is not rare.

2) Apart from the fact I live in a rural area, I've also been to the scottish highlands on dozens of occasions, since the sixties. Thing was, he never even asked me if I'd travelled anywhere at all. He just assumed - via his crystal ball.

:)

A crystal ball would probably be better than your doctor, better, in fact, than most doctors! ;)

In the States, it is difficult though possible to find Lyme-literate doctors who work with insurance. I hope that they exist in Scotland too!

wonderfullife
08-09-2011, 08:09 PM
There is a cover-up going on with Lyme.

I wanted my Dr to test for it, but he said :
1) it was very unlikely I'd have it, as it is very rare, and that
2) I'd not been in any area's of high risk.

Well.

1) Wrong, it is not rare.

2) Apart from the fact I live in a rural area, I've also been to the scottish highlands on dozens of occasions, since the sixties. Thing was, he never even asked me if I'd travelled anywhere at all. He just assumed - via his crystal ball.

:)
There is definatly a cover up with Lyme

wonderfullife
08-09-2011, 08:23 PM
Yes, there is a huge cover up! I'm amazed that a disease even as apparently rare as Morgellons is being talked about in conspiracy circles, but Lyme disease is talked about so little, even though it has been around for at least 30 years. Speaking about reducing population, Lyme is a very "convenient" disease because it mimics so many other diseases and, can be dormant in your body, can produce false negatives, can damage organs without you knowing it. It is vicious disease.

Most insurance companies don't even cover basic tests or healing. We had an insurance contract that explicitly stated it would not cover Lyme disease!

I spoke with a Lyme specialized doctor who said that 5 out of 6 bites will go unnoticed by victims.

Where we used to live, no matter where you go in nature (even on lawns), you could be sure of coming back with ticks. I even met a woman who went on a walk in another state where she got covered from head to foot with what she thought was dust, and then discovered that they were deer ticks. She is now disabled. So many stories have I heard... I have met so many people who were in terrible conditions, crippled or with other serious effects because of Lyme. And they all suffered terribly from the lack of information - especially among doctors - and lack of proper medical care, often being ridiculed through denial of their condition, etc.

With so many powerful pesticides around, how is this infestation of ticks possible?...

Why do so few people know about Lyme? And why are doctors so much in denial? Are they stupid or fearful or both?

+1
Doctors it's all about money and polotics

wonderfullife
08-09-2011, 08:26 PM
Perhaps the biggest ongoing medical scandal of the past hundred years is the fact that it has been known since 1911 that Multiple Sclerosis is caused by a bacterium, and that the medical establishment covered this up, in order to make money selling symptom relievers to MS patients. Since 1911, overwhelmingly much medical research has been conducted where living Borrelia bacteria were found in the brains of people who were diagnosed with MS.

Time and time again. By at least a dozen medical researchers. In at least ten countries. Since 1911 – the past one hundred years. Several older but also recent autopsy findings linked to in this article found that all deceased MS patients’ brains harbored living Lyme spirochetes. Even when tests, notorious for their large percentage of false negatives were used on living MS patients, staggeringly many tested positive for active Lyme borreliosis.

Then why isn’t this common knowledge? Surely, those thousands of MS experts and MS researchers can’t be all wrong?
Read the rest here
http://www.owndoc.com/lyme/multiple-...of-a-cover-up/

wonderfullife
08-09-2011, 08:27 PM
What have you heard about tickborne Lyme for the last 30 years? That it’s rare, scary, acute, treatable… The government warns about its spread and implores people to go to a doctor upon seeing the telltale bulls-eye rash. What happens when they actually do?

Many have researched the controversial beginnings of Lyme disease, but this article focuses on what happens to victims when they contract it and what they can do now.

Under Our Skin is a documentary that lends a voice to the many who in fact suffer from chronic Lyme and are victims of a greater abomination.
Why do conventional doctors tell them it’s in their head? Why won’t they quickly test for it? Treat it? Acknowledge it? Why do medical boards shut down doctors who can treat and cure Lyme?

Lyme’s Disease is NOT RARE – Bigger Than AIDS

In the late 70s, a Lyme, Connecticut mom reported a mysterious new disease sweeping the town, leaving its people with debilitating, chronic symptoms. In 1981, Dr. Willy Burgdorfer discovered the Lyme bacteria, called Borrelia burgdorferi.

The bacteria spirochetes closely resemble syphilis in their make up. While a carrier tick is feeding, its backwash enters the host and transmits Lyme. The corkscrew spirochetes wreak havoc, drilling into any healthy cells and tissue. They create painful, crippling neurological and immunological damage.

In the beginning, doctors only knew that it resembled syphilis but remained unaware of its wide spread, how to proceed, and the political, medical clash that awaited them.

In recent years, the CDC has reported over 35,000 new Lyme cases annually but admit that since it is so overlooked the actual number may be 12 times higher, up to 420,000 cases each year.

Think of how much more likely it is to contract Lyme than the media-touted West Nile virus which is only reported at around 1,300 cases annually. If the actual number of Lyme cases is even just a modest amount above the CDC’s 35,000, then Lyme is far more prevalent than AIDS, reported at 39,000 cases annually.

Since 1982, the number of cases continues to climb and spike prompting media reports and health officials to label it epidemic as early as 1989. Reported cases have tripled since 1992. Every summer we hear the same cautionary reports. Yet doctors constantly tell their patients “You don’t have Lyme” or “Lyme only happens in such-and-such state, not here.”
Lyme is a national health crisis in every state and has traveled the globe!
Since this infectious disease is viewed with eyes that won’t see and hands that won’t treat, the miniscule 35,000 reported cases are unquestionably a mere fraction of people sick with Lyme.

Patients often look normal and are told they have M.S., Lou Gehrig’s, psychological disorders, Parkinson’s, ADHD but not Lyme. Therefore, many walk around with Lyme and have no clue why they are so ill, why treatments don’t work and are left to wonder. Many are left to die.

Without Early Eradication Lyme is Chronic, Expensive, Does Not Leave Easily

Lyme patients often state that they’ve seen an average of 30 doctors, spent over $100,000 in medical care and waited up to 15 years for a Lyme diagnosis. Why??

Lyme disease antibodies can be detected early with a blood test. If caught early it can be treated with an inexpensive bottle of antibiotics. But that is rarely the case. Patients are told it’s not Lyme, it won’t be tested for, it’s something else and so the struggle begins…

When the patient remains ill, why, it couldn’t possibly be chronic Lyme because doctors view it as acute and are not allowed to believe chronic Lyme exists. If “acute” Lyme isn’t cured with two weeks of antibiotics, which it won’t be if the bacteria has taken hold due to waiting, then the patient is told it must be something else and years of sickness, pain, and ineffective treatments ensue.

Talk to someone who’s been through this battle. They will most likely tell you they were dismissed, referred to psychiatrists and multiple specialists. Lyme can attack any area of the body and manifest endless symptoms.
Lyme patients have seen specialists for chronic pain, arthritis, Chrohn’s, iritis, organ failure, brain and neurological problems, dyslexia, insomnia… you name it. All for one disease that could have been treated early. But no one will believe them and after seeing so many specialists they are often labeled crazy, hypochondriacs, attention loving, and depressed.

The spirochetes can cleverly avoid the antibiotics and hide from the immune system. It’s frightening to think that specialists often prescribe immune suppressive drugs – the most counterproductive plan for Lyme patients.
The CDC now hints at chronic Lyme with sarcastic quote marks and insists that it be called Post-Treatment Lyme Disease Syndrome (PTLDS). They openly admit that the first round of conventional treatment might not bring a cure and that the patient is in for a long ride of pain and sometimes years of antibiotics, the only recognized conventional treatment.

They LIE and state that there is no credible scientific evidence that PTLDS is caused by persistent infection, that it must be residual damage, that the Lyme is gone. They also make a big point in telling people to avoid their own research on the internet, not to believe the inaccurate information out there, just keep seeing the doctor who left them untreated for so long.

The CDC says before PTLDS treatment takes place, confirm the diagnosis – fat chance that will happen.

So how did that fiasco begin?
http://healthfreedoms.org/2011/07/01...r-up-rages-on/

wonderfullife
08-09-2011, 08:29 PM
In 1980, the government started allowing patents on living organisms like pathogens. Perfect timing for scientists to make a mad dash for parts of newly-discovered Lyme and keep the information locked to protect future profits.

These so called experts research it with federal funds, then start private firms and patents. They write guidelines for insurance companies and HMOs so that the disease doesn’t exist (yet) or require coverage. Not only do Lyme victims spend hundreds of thousands for medical treatment, but they can’t be covered for Lyme!

The Biggest Blow In The Lyme Cover Up

The Infectious Diseases Society of America (IDSA), made up of a board of doctors, created within themselves an authority to write the rule book on all things Lyme. It is the absolute bane of both the Lyme community and conscientious doctors everywhere.

They are the ones who decided that there is no chronic Lyme, that it’s easy to treat and cure, and will be cured within two weeks of oral antibiotics or else the patient has another infirmity. Doctors must follow their diagnosis and treatment guidelines or face punishment from state medical boards. Patients’ proof of cure never sways the boards – doctors broke the rules.

Out of the 400 references listed in the back of the guidelines, over half of them are directed at articles that they and their teams wrote. They have closed the door on outside contrary research.

These are the very guidelines insurance companies consult to deny medical treatment coverage. The majority of complaints that lead to doctors’ suspensions come from insurance companies, not patients or other physicians. The insurance companies wish to rid doctors who cost them the most.

The trio of insurance companies, Lyme guidelines, and Big Pharma restrict consumer choice in medical care and extort these patients.

While the IDSA acknowledges post-Lyme syndrome, they audaciously attribute it to the “aches and pains of daily living” and that poor treatment results are due to prior traumatic stress. Are they really that dumb?

No, but they are cold blooded and know exactly the nature of the disease and its destruction.

They should know…after all, they have a lot invested in it…
Busted On The Money Trail!

Connecticut Attorney General Richard Blumenthal investigated the ISDA panel members for possible violation of antitrust laws and conflicts of interest.

Of the 14 panel authors of the first edition guidelines: 6 of them or their universities held patents on Lyme or its co-infections, 4 received funding from Lyme or co-infection test kit manufacturers, 4 were paid by insurance companies to write Lyme policy guidelines or consult in Lyme legal cases, and 9 received money from Lyme disease vaccine manufacturers. Some of the authors were involved in more than one conflict of interest.

So why are guideline authorities taking money from companies who have a direct interest in specific outcomes? When will doctors speak up?
So How Does This Cover Up Saga Continue?

The media keeps trumpeting the lies. CBS News recently published a story called “Lyme Disease Lies – And Truths.” Each segment features a FACT OR FICTION tidbit which is really a confusing mash up rife with deception. They pull their information from the IDSA and Dr. John Halperin who wrote a book better used for toilet paper called Lyme Disease: An Evidence-based Approach.
The article calls the following liars: people who claim to have “chronic” Lyme disease, those who believe they still have Lyme because they test positive for antibodies after treatment, those who believe their brain fog results from Lyme, the Lyme “advocacy groups” that claim anyone actually died from it, anyone who claims this syphilis like disease is spread sexually, and those that believe lengthier care is needed.

Dr. Halperin states that Lyme is benign, easy to treat, no one has died from it, are rarely hospitalized, and brain infection from Lyme is rare.

Doctors like Leo Galland are stepping out with more truth. His article on Huffington Post discloses more about chronic Lyme infection. At the bottom of his article, you will see that the majority of the 500 comments are Lyme victims sharing their nightmare stories.

Organizations that pretended to protect public health with no commercial interests (CDC, NIH, Universities) partner with Big Pharma and are not in the business of seeing anyone healed. Maybe generations from now when there is enough of an outcry, when many have lived ill and died, some drug company will try to be the hero of the day and come up with a poisonous drug to treat Lyme.

Even that scenario is highly unlikely as chronic Lyme is not allowed to exist. But when it does there will be a vaccine waiting for you.

So tragically in the meantime, Lyme victims serve as a host for the parasitical medical establishment, lining the coffers until they are bled completely dry. The real ticks (the poli-ticks) are still here.

Watch Under Our Skin for more mind blowing information. Find out about the doctor who discovered an actual link between the Lyme spirochetes and disorders like dementia, Alzeimer’s, M.S. and more. One alternative health practitioner has not seen one M.S., ALS or Parkinson’s patient in the last five years who did not test positive for Borrelia burgdorferi.

You will also see proof that Lyme inflicted mothers experience multiple miscarriages and their babies are riddled with the disease. Babies who survive often develop late stage neurological damage during childhood and adolescence. All events that the IDSA swear have never happened. They insist that Lyme cannot be spread to the unborn child.

You will witness the families grieving over their dead loved ones. Lyme Disease is listed on their death certificates.

You will hear from doctors who were bullied, investigated, and ousted for attempting to actually treat Lyme, usually with intravenous and lengthier antibiotics. After all, isn’t that how other infectious diseases are conventionally treated – Tuberculosis, HIV, Hepatitis?
Conscientious doctors have to treat Lyme secretly if they want to help their patients without losing their license. They have to tell their patients, “Don’t mention Lyme.” How’s that for a cover up?
So What Now? What If I Have Lyme?

Chances are, you know someone who is manifesting the aforementioned symptoms and is battling the never ending circle of finding proper diagnosis and treatment. They may or may not remember a tick bite. Since the truth about Lyme is so stifled it is more than likely spread through blood transfusions (as with Babesiosis) and shared between couples (as shown in Under Our Skin).

They most likely have been diagnosed with one of the mysterious “incurables” like MS, ALS, or even early Parkinson’s and Alzheimer’s. The latter two are increasingly diagnosed in younger patients.

Or perhaps they were dismissed as crazy and bear the misery of not knowing that they actually suffer from Lyme. Regardless, they suffer and believe they must wait until research catches up to them before they die.
http://healthfreedoms.org/2011/07/01...-chronic-lyme/

wonderfullife
08-09-2011, 08:31 PM
The Infectious Diseases Society of America wrote guidelines on tickborne diseases that included Lyme, Human Granulocytic Anaplasmosis, and Babesiosis. HFA reported the rise of Babesiosis, more threatening in its lack of early symptoms and undetected presence in blood supplies. So anyone suffering from tickborne infection is going to have the same run around as Lyme victims. Those with the malaria-like Babesiosis parasite can also have Lyme and vice versa.

The political-medical battle over Lyme (and Babesiosis) was left to the dogs from the beginning. Many have struggled and found their own way, with alternative doctors and unconventional methods. The CDC would like you to believe that such unfortunates stumble on “goat’s blood” and false promises of stem cell help, but we know better than that.

Unfortunately, Under Our Skin only covered doctors who were using aggressive antibiotic treatment for progressive Lyme. Even some of those doctors had their licenses revoked or were compelled to close their practice. Constant use of antibiotics are harsh and leave people with more health problems, possible resistance and Candida yeast overgrowth.

Prevention is ideal but obviously not fail-proof.

Good Naturopathic doctors have an affinity for detecting and treating bacterial and parasitical infections. This is why the absolute most important action we can take is protecting their rights to help their clients. It is no mistake that many states are introducing bills to criminalize alternative health practitioners. We need their knowledge and expertise more than ever…The FDA is always at work trying to snuff out the following talked about Lyme supplements.

Oregano and colloidal silver have helped people with many aggressive infections such as Lyme, AIDS, and Tuberculosis. They are powerful bacteria and virus fighters and when used properly do not harm healthy cells unlike standard antibiotics.

MMS is an intense bacteria and malaria destroyer. It has been a life saver for many in the Lyme community. The more clever bacteria types cannot use the host to evade MMS which destroys thick bacterial walls. Careful MMS use encourages rigorous toxin removal. Many online Lyme support groups prefer treatments like Rife technology and MMS for successful healing.

MMS and Lyme Disease-

Follow these links to learn more about how MMS can be used to treat Lyme disease without intense anti-biotic treatment. Heal your body naturally for optimum health!
http://healthfreedoms.org/2011/07/01...ses-treatment/

wonderfullife
08-09-2011, 08:32 PM
Jesse Ventura Conspiracy Theory - Plum Island Part 2 of 4 - YouTube

wonderfullife
08-09-2011, 08:33 PM
The most common tick-borne disease in humans is Lyme borreliosis. Extensive field and laboratory tests have revealed that the Borrelia bacterium is present in a larger proportion of ticks than has been shown by earlier studies. Another finding is that migratory birds play an important role in the spreading of ticks and pathogenic agents borne by ticks.

Ticks are to be found in most parts of the world, and more than 900 species have been identified so far. The geographic distribution of these many tick species varies and the most prevalent species in Norway is the forest tick (Ixodes ricinus), which can be the bearer of a number of bacteria and viruses that can infect animals and humans and cause disease.

In recent years, there has been increasing focus on ticks and the diseases a tick bite can cause and there are also indications that ticks are occurring in new areas of the country. This has resulted in an increase in the number of disease cases, both as regards Lyme borreliosis (LB) and other illnesses such as tick-borne encephalitis (TBE).

As part of her doctoral research at The Norwegian School of Veterinary Science, Vivian Kjelland has carried out extensive field and laboratory studies with a view to increasing our knowledge in this field. She has examined the occurrence of Borrelia burgdorferi sensu lato (s.l.) in ticks and which genotypes of the bacterium occur in ticks in Norway. Her results show that a larger proportion of the ticks were infected, compared to the findings of earlier Norwegian and Scandinavian studies.
http://www.news-medical.net/news/201...e-disease.aspx

wonderfullife
08-09-2011, 08:39 PM
Celebrities With Lyme Disease - YouTube

wonderfullife
08-09-2011, 08:46 PM
When future historians examine the numerous events that have contributed to the rapid emergence of knowledge related to infectious diseases during the latter portion of the 20th century, it is probable that research contributions related to infections caused by Bartonella species will be considered of unique medical importance. Although predated by a substantial body of important observations, two manuscripts1,2 published in 1990 in the same issue of the New England Journal of Medicine set the stage for a scientific revolution in our understanding of Bartonella infections. Relman and colleagues used polymerase chain reaction (PCR) to amplify bacterial DNA from lesions of AIDS patients with bacillary angiomatosis.1 When compared with known eubacterial sequences, the uncultured organisms were most closely related to Rochalimaea quintana, the cause of Trench Fever. Independently, Slater and colleagues described the isolation of a fastidious gram-negative organism in blood cultures from immunocompromised and non-immunocompromised febrile patients.2 The organisms described in these two manuscripts were subsequently characterized as B. quintana or a newly defined species B. henselae. During the ensuing nine years, research efforts have begun to elucidate the importance of Bartonella species as veterinary and human pathogens.

In 1993, Brenner and colleagues3 provided evidence to justify reclassification of the four species in the genus Rochalimaea. Previously designated Rochalimaea species were united with the genus Bartonella, and named Bartonella quintana, Bartonella vinsonii, Bartonella henselae, and Bartonella elizabethae. This reclassification removed the family Bartonellaceae from the order Rickettsiales, and resulted in the transfer of these organisms from the family Rickettsiaceae to the family Bartonellaceae. In 1995, Birtles and colleagues4 proposed the unification of the genus Grahamella with the genus Bartonella, resulting in the addition of five Bartonella species: B. talpae, B. peromysci, B. grahamii, B. taylorii, and B. doshiae. Historically, Grahamella species have been characterized as arthropod-transmitted hemotropic gram-negative bacteria of small mammals, fish, and birds, which are of no known pathogenic consequence for larger mammals. The role of rodents as reservoir hosts for Bartonella species is an important area of current investigation. In effect, these reclassifications eliminated the previous genera, Rochalimaea and Grahamella.

In 1992, Schwartzman5 summarized the rapidly expanding clinical spectrum of human illness caused by infections due to Bartonella organisms. In more recent years, Bartonella species have become associated with several distinct clinical syndromes in people: bacillary (pertaining to bacilli or rodlike forms) angiomatosis,6–8 bacillary peliosis (extravasation of blood) hepatis,7,8 relapsing fever with bacteremia,2,9 cat scratch disease (CSD),10–12 endocarditis,13– 15 granulomatous hepatosplenic syndrome,16 retinitis and swelling of the optic nerve,17 osteolytic lesions,18,19 and granulomatous pneumonia, which we reported in a chronically-ill renal transplant patient.20 A role for B. henselae in the pathogenesis of AIDS encephalopathy has also been proposed.21

In 1993, Bartonella infection was associated with human endocarditis for the first time. Within a year, B. quintana, B. elizabethae and B. henselae were shown to cause endocarditis in people, providing one of several examples that illustrate the rapid recognition of new clinical entities associated with human Bartonella infections.13–15 As a result of reviewing these reports, we isolated and characterized a novel Bartonella subspecies from a dog with endocarditis.22,23 Subsequently, we have obtained serologic evidence to support tick transmission of B. vinsonii subsp. berkhoffii to dogs. We have also identified 7 additional cases of endocarditis and a case of granulomatous lymphadenitis associated with B. vinsonii infection in dogs. The medical importance of members of the genus Bartonella as canine pathogens or the role of dogs as a reservoir for human infection awaits additional study.

Bacillary angiomatosis, also called epithelioid angiomatosis, is a vascular proliferative disease of the skin that is characterized by multiple, blood-filled, cystic tumors.6,7 When visceral parenchymal organs are involved, the condition is referred to as bacillary peliosis hepatis, splenic peliosis or systemic bacillary angiomatosis. These conditions, now recognized to be infectious manifestations of B. henselae or B. quintana, have been more frequently documented in immunocompromised individuals, particularly AIDS patients, but have also been reported in immunocompetent individuals. Prior to the AIDS epidemic, bacillary angiomatosis had been reported in association with tuberculosis or advanced cancer, presumably a reflection of co- existing Bartonella infection. In a study from the Greater San Francisco Bay Region of Northern California, B. henselae was isolated from the blood of 7 cats belonging to 4 patients with bacillary angiomatosis.24 An important observation in this study, which has been extended by findings from our laboratory, is that B. henselae bacteremia can persist in naturally- infected cats for periods of at least 21 months.25 Experimentally, we were able to transmit B. henselae via intravenous or intramuscular inoculation of blood, but not via intramuscular inoculation of urine sediment.26 These results strongly suggest that cats should be screened for B. henselae infection prior to use as a blood donor. Although experimental studies following World War I indicated that human urine could successfully transmit B. quintana to people, and anecdotal reports indicate exposure to cat urine may have caused CSD in people, our results fail to support transmission of B. henselae through urine. Considering that current studies have identified 25 to 40% of healthy cats as asymptomatic carriers of B. henselae, the potential of human exposure to infected cat urine in litter boxes could be substantial.

Persistent or relapsing fever, accompanied by malaise, anorexia, and weight loss has been documented frequently in immunocompromised individuals with Bartonella infections.2,7,20 Acute febrile illness with bacteremia, bacillary angiomatosis, bacillary splenitis and other chronic disease manifestations associated with Bartonella infections are being recognized with increasing frequency in immunocompetent people.9,26 Persistent B. henselae bacteremia, of approximately 3 months duration, was identified in an immunocompetent man, who was potentially infected by tick exposure.27 This report suggests that immunocompetent people can experience prolonged illness with persistent bacteremia. Recurrent bacillary angiomatosis due to presumed therapeutically refractory B. quintana infection has been reported in an AIDS patient.28

For nearly a century regional lymphadenopathy has been associated with animal contact, particularly cat scratches.5,29 Over the years, numerous microorganisms have been implicated as the cause of CSD. In 1983, small, argyrophilic (easily impregnated with silver), gram-negative, pleomorphic bacteria were seen within blood vessel walls and macrophages in lymph nodes of patients with CSD.30 In 1988, a bacteria,31 later designated Afipia felis,32 was cultured from lymph nodes of CSD patients. In the same year, Cockerell and colleagues proposed a possible association between epithelioid angiomatosis and CSD in a letter to Lancet.33 In 1992, Regnery and colleagues at the Centers for Disease Control,10 identified seroreactivity to B. henselae antigens in 88% of 41 patients with suspected CSD compared to 3% of controls. Similarly, a case-controlled Connecticut study of CSD patients and their cats34 identified a strong association with cats 12 months of age or younger, a history of a scratch or bite, contact with fleas, and seroreactivity to B. henselae antigen. Additional support that B. henselae is the predominant cause of CSD was provided when DNA was amplified from lymph node samples of 21 of 25 (84%) patients with suspected CSD, using a polymerase chain reaction assay.12 A similar study from Sweden identified B. henselae DNA, but failed to identify A. felis DNA, in a large number of patients with suspected CSD.35 We have cultured Bartonella species from 17 of 19 cats owned by 14 patients with CSD.25 In summary, recent studies indicate that B. henselae is the predominant, but not the sole cause of CSD. In 1995, Clarridge et al. isolated a novel Bartonella species,36 which was named B. clarridgeiae,37 from a cat belonging to a patient infected with HIV from whom B. henselae was isolated. Our studies have implicated B. clarridgeiae as a cause of inoculation papules, fever and regional lymphadenopathy (CSD) in 3 people. Based upon PCR- RFLP analysis of the 16S and the 16S-23S rRNA genes, approximately 10% of the isolates obtained in our laboratory from cats are B. clarridgeiae.

Historically, atypical manifestations of CSD have included tonsillitis, encephalitis, cerebral arthritis, transverse myelitis, granulomatous hepatitis and/or splenitis, osteolysis, pneumonia, pleural effusion, and thrombocytopenic purpura. Previously, Bartonella infection would not have been considered a likely differential diagnosis by the physician in patients lacking a history of lymphadenopathy or animal contact. As evidenced by reports in the past four years, the spectrum of human disease associated with the genus Bartonella is likely to expand, requiring periodic reassessment as new information becomes available.

Whether members of the genus Bartonella are pathogenic for cats or contribute to previously described instances of argyrophilic bacteria in lymph nodes of cats with persistent lymphadenopathy38 or to peliosis hepatis39 remains to be determined. Although B. henselae bacteremia can be documented in 25 to 41% of healthy cats,24,25 we have observed self-limiting febrile illness of 48 to 72 hours duration, mild to moderate transient anemia, and transient neurologic dysfunction in cats experimentally infected with B. henselae by blood transfusion.26 Self-limiting fever also occurred in 4 B. henselae bacteremic cats from the same household following minor surgical procedures. Due to the high percentage of chronically bacteremic healthy cats in the United States, establishing a cause and effect relationship between disease manifestations and bacteremia in cats will require epidemiologic analysis.

Bartonella henselae and B. bacilliformis can be found within erythrocytes, whereas B. quintana maintains an epicellular location on the erythrocyte.40 Cell lysis, using a lysis centrifugation technique, greatly facilitates bacterial isolation from blood. Although organisms within the genus Bartonella are fastidious and slow-growing, they can be cultured successfully with agar plates containing 5% defibrinated rabbit or sheep blood, that are maintained at 35oC in a high humidity chamber with a 5% CO2 concentration. In our experience, bacterial colonies may not be visible until 10 to 56 days after inoculation of the agar plate. Because members of the order Rickettsiales are cultivable only in their host cells or living tissues, cultivation of Bartonella species on bacteriologic media, in conjunction with DNA divergence studies, provided additional justification for removal of members of the genus Bartonella from the order Rickettsiales. Bartonella are small, curved, gram-negative rods. In tissues, the organisms stain positively with silver stains such as the Warthin-Starry stain.

The diagnosis of Bartonella infection should be confirmed by culturing the organism from blood or tissues such as lymph node or heart valve or by amplifying DNA from tissues using PCR. Seroconversion, detected by IFA or ELISA techniques, can be documented in people with acute disease and in cats following experimental infection. The kinetics of the serologic response to B. henselae antigens in chronically-infected experimental cats is highly variable in degree and duration.26 A seroepidemiologic survey, incorporating 577 samples from throughout North America identified an overall prevalence of 28%, with prevalence rates ranging from a low of 4–7% in the Midwest and great plains region to 60% in the southeast.41 High seroprevalence rates correlate with warm, humid climates conducive for the environmental maintenance of cat fleas,41,42 which have been shown to be capable of transmitting B. henselae from cat to cat.43 A seroepidemiologic study of 592 cats in Baltimore, MD identified an overall seroprevalence rate of 14.7%, with a much higher prevalence in feral cats (44.4%) as compared to pet cats donated to the City Municipal Animal Shelter (12.2%).44 Although providing useful epidemiologic data, serologic test results may be of limited clinical utility for several reasons. We have been unable to detect B. henselae-specific antibodies in some bacteremic cats and have been unable to culture Bartonella from some cats in which antibodies are detectable. Negative blood cultures obtained from cats seroreactive to B. henselae antigen may reflect low level bacteremia or the timing of the blood culture, since experimentally-infected cats experience a relapsing bacteremia. Numerous naturally-infected cats are persistently bacteremic, generally in conjunction with low antibody titers.25 In our experience, high antibody titers generally correlate with positive blood cultures. The extent of serologic cross reactivity to Bartonella species requires additional clarification.45 In unpublished studies, we have demonstrated co-infection with B. henselae and B. clarridgeiae in cats.

Because of disparate results among studies and an overall lack of microbiologic data in clinical therapeutic trails, numerous issues related to treatment of Bartonella infection remain controversial. In contrast to the apparent lack of response to antimicrobial treatment in human CSD patients,46,47 bacillary angiomatosis, parenchymal bacillary peliosis, and acute Bartonella bacteremia appear to respond to antimicrobial treatment, even in immunocompromised individuals.48 Doxycycline, erythromycin and rifampin are recommended antibiotics,49 but clinical improvement has been reported following the use of penicillin, gentamicin, ceftriaxone, ciprofloxacin, and azithromycin. Treatment for 2 weeks in immunocompetent individuals and 6 weeks in immunocompromised people is generally recommended. Relapses, associated with bacteremia, have been reported in immunocompromised people despite treatment for 6 weeks. Antimicrobial efficacy has not been established for any antibiotic for eliminating B. henselae bacteremia in cats. Results from our laboratory and others indicate incomplete treatment responses in cats treated for 2 or 4 weeks with doxycycline or enrofloxacin.50,51 In contrast to other reports,50,51 cats experimentally-infected with B. henselae by blood transfusion do not develop protective immunity following homologous or heterologous challenge with B. clarridgeiae. These differences in experimental results are most likely due to alterations in virulence, induced during in vitro culture of the organism.

Based upon recent advances in our knowledge of the zoonotic potential of members of the genus Bartonella, the designations cat scratch disease and cat scratch fever may be most appropriate when considering human disease manifestations from a historical perspective. Because cat scratch disease generally denotes a self-limiting illness characterized by fever and lymphadenopathy and because the recognized spectrum of human disease manifestations associated with Bartonella infections (which may not include fever or lymphadenopathy) has expanded considerably in recent years, it is becoming obvious that the designation CSD lacks clinical, microbiologic and zoonotic utility. Although cats are a major reservoir for B. henselae and potentially B. clarridgeiae, some patients deny the possibility of a cat scratch or bite wound, or indicate no contact with cats. Transmission from environmental sources or other animal hosts is probable and the more inclusive term bartonellosis may facilitate enhanced future understanding of diseases caused by members of the genus Bartonellaceae.

Although recent research findings have substantially improved our understanding of the clinical, microbiologic and zoonotic aspects of diseases caused by Bartonella species, the exact mode of transmission, the relative role of various insect vectors such as fleas and ticks, the identification of potential reservoir hosts, and the spectrum of animal and human illnesses caused by these organisms remains largely undetermined. For example, although it is well established that the human body louse transmits B. quintana, the reservoir and mode of transmission that results in bacillary angiomatosis in the United States has not been established. The pathogenic potential of these organisms appears to be of considerable importance in dogs as well as immunocompromised and immunocompetent people.

I would like to acknowledge contributions by Dorsey Kordick, Brandee Pappalardo and Barbara Hegarty for the generation of data from my laboratory related to Bartonella infection in cats and dogs, and the Bayer Corporation, SmithKline Beecham Animal Health, Pfizer Animal Health, Intervet Inc., Heska Corporation, the Triangle Cat Fanciers, and the American Veterinary Medical Foundation for funding our work. I would also like to gratefully acknowledge the collaboration of Dr. Ken Wilson, The Veterans Affairs Medical Center and Division of Infectious Diseases, Duke University Medical Center, Drs. Don Brenner and Rus Regnery at the Centers for Disease Control and Dr. Ted Hadfield at the Armed Forces Institute of Pathology.

wonderfullife
08-09-2011, 08:48 PM
Subject: FW: Lyme/unexplained aggression
Permission was given to cross post this.
We recently had a very strange event that I think we should share around the animal rescue community:

Young (~2 years) male, a Lab mix, came into our program with a "questionable" background. He may have been aggressive toward some children, maybe not. We kept him for a good long while --- months of fostering in our premier foster home, with no problem -- and placed him carefully, with a single mid-age man who absolutely adored him. We also, as we do with all our dogs, tested him for Lyme. He had it; we treated it; case closed -- we thought.

Everything went very well after adoption -- he was the star of his obedience classes, a frequent alumni visitor to our clinics - for over a year. And truly adored by his adopter.

Then, over a year after placement, Mojo became suddenly, erratically, and seriously aggressive: literally attacked visitors to the home, people at the vet's waiting room, etc. Terrifying. Very sudden. Totally inexplicable. He was returned to us with genuine heartbreak from a very loving adopter.
Mojo then went to our regular vet and was a totally different dog: bared teeth and growling to anyone who approached his kennel, lunging at other dogs when being walked, etc. We figured that whatever was happening with him, he had become implacable and started a TDC (Tough Decisions Committee - something we "convene" and that is open to anyone with an interest in the dog when we think that euthanasia might be an option).

However, someone at the vet's office said that perhaps we should test him for Lyme. Huh???????? They had had a regular client of theirs come in recently with similar, out of the blue aggression, and it turned out that was the problem - puzzled them, but seemed to be the case. Okay -- hey, we'll try anything -- so we had him tested. He was high positive! Fine, we started treatment while we continued to figure out what to do with him via the TDC.

Almost immediately, however, once the antibiotics were begun, the Mojo we knew came back!! He was himself again -- bouncy, happy, a bit neurotic, but not at *all* aggressive! The staff at the vet's was amazed, but all confirmed this change.

We didn't believe it; and the veterinarians didn't believe it .... BUT a thorough search of the internet turned up a number of studies and anectodal observations indicating that in some dogs (and in some humans!!) the primary symptom of their Lyme Disease can be sudden, irrational and serious aggression.

Well, we've known for a while to check the thyroid levels of dogs that show aggression that just "doesn't fit". Now we have added testing for Lyme as well. And we have --- results not yet in -- another dog that we placed over a year ago who has been returned because of out-of-the-blue aggression ... and he has also tested high positive for Lyme! We've started treatment and will be monitoring his response.

So --- plug this in to your protocols. It's worth checking out. I spent the day today with Mojo ... and he truly is just the same dog we placed over a year ago. (We've let his original adopter know -- because he vowed that it had to be *something* causing this behavior. But he cannot take Mojo back because his roommate, one of the people attacked, won't even consider it. For the record, there were no skin-breaking contacts in any of these attacks, but plenty of fear and we consider them as serious as if they were full-fledged bites.)

We actually have additional insight into this because one of our volunteers (human) has had Lyme Disease. Took many months for her to be diagnosed, and once she was, she learned that it's a VERY nasty bug that really remains around permanently, waiting for a chance to "crop up" again. When we place Mojo again (and our TDC unanimously agrees that we should do this), we're going to explain the background, these amazing events, and require that the adopters have him tested every six months, whether or not he's showing symptoms. We have no idea whether that will work or be sufficient - we're rather flying blind in this -- but it seems a rational approach.

I'll post again if we learn more from the second dog (also a Lab mix). But based on what we know now, it is a real possibility: Lyme *can*, in a few rare cases, cause aggression, aggression that can be reversed.

wonderfullife
08-09-2011, 08:51 PM
It is now realized that lyme disease can mimic the following conditions: Aamyotrophic Lateral Sclerosis, Parkinson’s disease, multiple sclerosis, Bell’s Palsy, reflex sympathetic dystrophy, neuritis, psychiatric illnesses such as schizophrenia, chronic fatigue, heart failure, angina, irregular heart rhythms, fibromyalgia, dermatitis, autoimmune diseases such as scleroderma and lupus, eye inflammatory reactions, sudden deafness, SIDS, ADD and hyperactivity, Autism, chronic pain and many other conditions.

Lyme Disease is now thought to be the fastest growing infectious disease in the world. There are believed to be at least 200,000 new cases each year in the U.S. and some experts think that as many as one in every 15 Americans is currently infected (20 million persons). Many people who have lyme disease do not know they are infected. Lyme Disease is the fastest growing epidemic in the world. LD is grossly underreported so there may be far more than the 200,000 cases reported annually in the U.S. Dr.Harvey and Salvato estimate that 1 billion persons in the world may be infected with LD. LD is thought to be a contributing factor in 50 % of patients who have chronic illness.

There is compelling evidence that Lyme disease can be spread by sexual and congenital transfer. One physician has cared for 5000 children with Lyme Disease.. 240 of these children were born with the disease. Dr. Charles Ray Jones, the leading pediatric specialist on Lyme Disease, has found 12 breast fed children who have developed Lyme Disease. Miscarriage, premature births, stillborn, birth defects, and transplacental infection of the fetus have all been reported. Studies at the Univ. of Vienna have found Borrelia burgdorferi (the spirochete that causes Lyme Disease) in urine and breast milk of mothers with lyme disease.
Read the full article here:
http://www.newswithviews.com/Howenstine/james26.htm

http://www.littleangelsonlinestore.c...infant-death-2

wonderfullife
08-09-2011, 08:52 PM
Lyme Disease is a multi-system disease which can affect virtually every tissue and every organ of the human body. It is a disease which can be mild to some, and devastating to others. It can cripple and disable, or fog your mind. It can affect men, woman, and children, and even your family dog. (1-5,7-19) You may test negative for the disease, and still have it, or test positive and be symptom free. Some will get symptoms within days of a tick bite, while others may have it for years before they are even diagnosed. Some Lyme patients are told they have fibromyalgia, chronic fatigue syndrome, MS, or some other disease of unknown origin. (See abstracts of the 1996 International Lyme Conference) There are some studies which strongly support that the infection can be transmitted from mother to the unborn fetus, and may even cause still birth and has been implicated in some SIDs deaths. (MacDonald 20,45,52,53)

Why is Lyme disease such a mystery? Why does it mimic so many other disease? Why is it so difficult to detect? The reasons come from the microbiology of the bacteria that causes Lyme Disease.

Lyme disease is caused by a spiral shaped bacterium known as a spirochete. Diseases that are caused by spirochetes are notorious for being relapsing in nature, difficult to detect, and great imitators of other diseases. Syphilis, Tick-Borne Relapsing Fever, and Leptospirosis are other examples of spirochetal diseases. Lyme disease is caused by a bacteria called Borrelia burgdorferi, named after the man who isolated it from a Deer Tick in 1981, Dr. Willy Burgdorfer. The following is a tutorial to help explain away the mysteries of this bacteria, and why it causes so much controversy between patients and the medical community. (1)
The Structure of the Lyme Bacteria

The structure of the Lyme spirochete is unlike any other bacteria that has ever been studied before. It is one of the largest of the spirochetes (0.25 microns x 50 microns) It is as long, as a fine human hair is thick. Borrelia burgdorferi is a highly motile bacteria, it can swim extremely efficiently through both blood and tissue because of internal propulsion. It is propelled by an internal arrangement of flagella, bundled together, that runs the length of the bacteria from tip to tip. Like other Borrelia bacteria Borrelia burgdorferi has a three layer cell wall which helps determine the spiral shape of the bacteria. What makes this bacteria different from other species, is that it also has a clear gel-like coat of glyco-proteins which surround the bacteria. This extra layer is sometimes called the Slime Layer or S-layer. (See diagram 1) (45,46,59)

This means: This extra layer of glyco-proteins may act like a stealthy coat of armor that protects and hides the bacteria from the immune system. The human immune system uses proteins that are on the surface of the bacteria as markers, and sends attacking antibodies and killer T-cells to those markers, called outer surface protein antigens (OSP antigens). This nearly invisible layer is rarely seen in washed cultures, but can be seen regularly in tissue biopsies.(46)

The Lyme bacteria is different from other bacteria in its arrangement of DNA. Most bacteria have distinct chromosomes that are found floating around inside the cytoplasm. When the bacteria starts to divide and split in two, the chromosomes divide and the new copies of the chromosomes enter the new cell. The arrangement of DNA within Borrelia burgdorferi is radically different. It is arranged along the inside of the inner membrane. It looks something like a net embedded just underneath the skin of the bacteria. (46)

This means: We really don't understand the mechanisms of how Bb regulates its genetic material during its division.
Another unique feature to Borrelia burgdorferi are Blebs. This bacteria replicates specific genes, and inserts them into its own cell wall, and then pinches off that part of its cell membrane, and sends the bleb into the host. Why it does this we don't know. But we do know that these blebs can irritate our immune system. Dr. Claude Garon of Rocky Mountain Laboratories has shown that there is a precise mechanism that regulates the ratio of the different types of blebs that are shed. (46) In other bacteria the appearance of blebs often means the bacteria can share genetic information between themselves. We don't know if this is possible with Borrelia species. There have been reports of a granular form of Borrelia, which can grow to full size spirochetes, and reproduce. These granules are so small that they can be filtered and separated from live adult spirochetes by means of a micro-pore filter. (Stealth Pathogens Lida Mattman Ph.D. 66)

The division time of Borrelia burgdorferi is very long. Most other pathogens such as Streptococcus, or Staphylococcus, only take 20 minutes to double, the doubling time of Borrelia burgdorferi is usually estimated to be 12-24 hours. Since most antibiotics are cell wall agent inhibitors, they can only kill bacteria when the bacteria begins to divide and form new cell wall.(35,59-62)

This means: Since most antibiotics can only kill bacteria when they are dividing, a slow doubling time means less lethal exposure to antibiotics. Most bacteria are killed in 10-14 days of antibiotic. To get the same amount of lethal exposure during new cell wall formation of a Lyme spirochete, the antibiotic would have to be present 24 hours a day for 1 year and six months! Note: Antibiotics kill bacteria by binding to the bacteria's ribosomes, and interrupting the formation of cell wall proteins.
Like other spirochetes, such as those that cause Syphilis, the Lyme spirochete can remain in the human body for years in a non-metabolic state. It is essentially in suspended animation, and since it does not metabolize in this state, antibiotics are not absorbed or effective. When the conditions are right, those bacteria that survive, can seed back into the blood stream and initiate a relapse. (59-62,70)

This means: Just because a person is symptom free for long lengths of time doesn't mean they aren't infected. It may be a matter of time. Whereas viral infections often impart a lifelong immunity, Lyme, like other bacterial infections, does not retain active immunity for long periods of time. People are often reinfected with Lyme. (96)

How does the Lyme bacteria travel from the bloodstream to other tissues? While we have known for a long time that the Lyme spirochete can show up in the brain, eyes, joints, skin, spleen, liver, GI tract, bladder, and other organs, we didn't understand the mechanism by which it could travel through capillaries and cell membranes. (Abstract 644) Then Dr. Mark Klempner presented at the 1996 LDF International Lyme Conference an interesting paper that gave us part of the answer.
Read more here
http://www.lymeneteurope.org/info/th...f-lyme-disease

wonderfullife
08-09-2011, 08:54 PM
The patient is a college graduate with Lyme encephalopathy (LE). While stopped at a traffic light, she described her thought processes as having a “fog-like” sluggishness. When the light changes, she knows the change from red to green has significance, but at that moment cannot recall that green means go and red means stop.



This is one of many examples of cognitive impairments associated with Lyme disease. Although some cognitive symptoms are indirectly a result of other neurological or emotional impairments, others are a direct result of dysfunction of the cerebral cortex where cognitive processing occurs. Laboratory tests such as SPECT scans, MRI’s, PET scans, and psychological testing have demonstrated physiological and anatomical findings associated with dysfunction of the cerebral cortex in patients with Lyme and tick-borne diseases. The examination of human and animal brains have further supported these findings.



The cognitive impairments from Lyme disease are very different than we see in Alzheimer’s disease. Lyme disease is predominately a disease of the white matter, while Alzheimer’s is predominately a disease of the gray matter. Memory association occurs in the white matter, while memory is stored in the gray matter. White matter dysfunction is a difficulty with slowness of recall, and incorrect associations. In contrast, gray matter dysfunction is a loss of the information which has previously been stored. For example, and Alzheimer’s patient may not recall the word “pen”, while an LE patient may have a slowness of recall or retrieval of a closely related word. Some of the symptoms I will describe are also found in encephalopathies associated with other illnesses, such as chronic fatigue syndrome, lupus stroke, AIDS, or other diseases which affect the brain. Although no single sign or symptom may be diagnostic of Lyme disease in a mental status exam, we instead look for a cluster and a pattern of signs and symptoms that are commonly associated with Lyme disease.

Everyone with LE has their own unique profile of symptoms. The assessment of these signs and symptoms is one facet of the total clinical assessment of Lyme disease. There are many ways of categorizing cognitive functioning. Let’s begin with a simple model of perception, encoding these perceptions into memory, processing what we perceive, imagery, and finally organizing and planning a response.

Simple mental functions such as flexing the index finger of the right hand, correlates with a relatively simple brain circuitry. More complex functions such as flying an airplane requires the action of a more integrated neural circuitry. The difference between these two actions is like the difference between playing middle C on a piano vs. a symphony playing an entire concert.



Attention Span

Many Lyme disease patients have acquired attention impairments which were not present before the onset of the disease. There may be difficulty sustaining attention, increased distractibility when frustrated, and a greater difficulty prioritizing which perceptions are deserving of a higher allocation of attention.

If we compare attention span to the lens of a camera, we need the flexibility to constantly shift the allocation of attention dependency upon the current life situation. For example, we shift back and forth between a wide angle and a zoom lens focus to increase or decrease acuity of attention depending on the needs of the current situation. A loss of this flexibility results in some combination of a loss of acuity (hypoacusis), and/or excessive acuity to the wrong environmental perceptions (hyperacusis). Hyperacuity can be auditory (hearing), visual, tactile (touch), and olfactory (smell).

Auditory hyperacusis is the most common. Sounds seem louder and more annoying. Sometimes there is selective auditory hyperacusis to specific types of sounds. Visual hyperacusis may be in response to bright lights or certain types of artificial lighting. Tactile hyperacusis may be in response to tight fitting or scratchy clothing, vibrations, temperature and merely being touched may be painful. Some patients prefer to wear loose fitting sweat suits and are frustrated that being touched can be painful. Olfactory hyperacusis may result in an excessive reactivity to certain smells, such as perfumes, soaps, petroleum products, etc.



Memory

Memory is the storage and retrieval of information for later use. There are several different memory deficits associated with LE. Memory is broken down into several functions – working memory, memory encoding, memory storage and memory retrieval.
Working memory is a component of executive functioning. An example of working memory is the ability to spell the word “world” backwards. Sometimes there are impairments of working memory as it pertains to a working spatial memory, i.e. forgetting where doors are located or where a car is parked.

Encoding is the placement of a memory into storage. We cannot retrieve a memory that was not encoded correctly into memory in the first place. One patient described being upset that someone had eaten yogurt in her kitchen during the night. Her activity during the night was not encoded into memory.

Short term (recent) memory is the ability to remember information for relatively brief periods of time. In contrast, long term memory is information from years in the past (or remote). In LE, there is first a loss of short term memory followed by a loss of long term memory very late in the illness. Patients may have slowness of recall with different types of explicit (or factual) information, such as words, numbers, names, faces or geographical/spatial cues. Not as common, there may also be slowness of recall if implicit information, such as tying shoes, or doing other procedural memory tasks.

Errors in memory retrieval include errors with letter and/or number sequences. This can include letter reversals, reversing the sequence of letters in words, spelling errors, number reversals, or word substitution errors (inserting the opposite, closely related or wrong words in a sentence.



Processing
Processing is the creation of associations which allow us to interpret complex information and to respond in an adaptive manner. Some LE patients say they feel like they acquired dyslexia or other learning disabilities, which were not present previously. Examples of processing functions that may be impaired in the presence of LE include the following:

Reading comprehension: The ability to understand what is being read.

Auditory comprehension: The ability to understand spoken language.


Sound localization: The ability to localize the source of a sound.


Visual spatial perception: Impairments result in spatial perceptual distortions. One example is microscopia, in which things seem smaller than they really are. One patient lost depth perception, and had several accidents when the car in front of her stopped. A problem associated with visual spatial processing is optic ataxia, in which there is difficulty targeting movements through space. For example, there may be a tendency to bump into doorways, difficulty driving and parking a car in tight spaces, and targeting errors when placing and reaching for objects. One patient with optic ataxia, was stopped by a policeman while driving two miles to my office because he kept swerving across the center line. Before Lyme disease he could consistently shoot 13 to 14 out of 15 free throws from the basketball foul line. Now he averages 3 of 15, and misses some shots be several feet.

Transposition of laterality: The ability to rotate something 180 degrees in your mind. For example, the ability to copy, rather than mirror, the movements of an aerobics instructor facing you.

Left-right orientation: The ability to immediately perceive the difference between left and right. Although this is a part of congenital Gertsmann’s syndrome or angular gyrus syndrome, acquired left-right confusion is the result of an encephalopathic process.

Calculation ability: The ability to perform mathematical calculations without using fingers or calculators. Many LE patients describe an increased error rate with their checkbook.

Fluency of speech: The ability of speech to flow smoothly. This function is dependent upon adequate speed of word retrieval.

Stuttering: The tendency to stutter when speech is begun with certain sounds.

Slurred speech: A slurring of words, which can give the appearance of intoxication.

Fluency of written language: The ability to express thoughts into writing.

Handwriting: The ability to write words and sentences clearly.

Imagery
Imagery is a uniquely human trait. It is the ability to create what never was within our minds. When functioning properly, it is a component of human creativity, but when impaired, it can result in psychosis. Imagery functions that can be affected by LE include:

Capacity for visual imagery: The ability to picture something, such as a map, in our head.

Intrusive images: Images that suddenly appear which may be aggressive, horrific, sexual or otherwise.

Hypnagogic hallucinations: The continuation of a dream, even after being fully awake.

Vivid nightmares: A tendency towards nightmares of a vivid Technicolor nature.

Illusions: Auditory, visual, tactile and/or olfactory perceptions which are distorted or misperceived.

Hallucinations: Hearing, seeing, feeling and/or smelling something that is not present. In LE, sometimes this takes the form of hearing music or a radio station in the background. Unlike schizophrenic hallucinations, these are accompanied by a clear sensorium, and the patient is aware hallucinations are present.

Depersonalization: A loss of a sense of physical existence.

Derealization: A loss of a sense that the environment is real.

Organizing and Planning
Organizing and planning a response is the most complex mental function, and is dependent upon all the functions already described. These functions, along with attention span and working memory, are referred to as executive functioning. Organizing and planning functions that can be
affected by LE include:

Concentration: The ability to focus thought and maintain mental tracking while performing problem solving tasks.

“Brain fog”: Described by many LE patients. Although difficult to describe in objective, scientific terms: it is best described as a slowness, weakness, and inaccuracy of thought processes. Prioritizing, organizing, and implementing multiple tasks with effective time management.

Simultasking: The ability to concentrate and be effective while performing multiple simultaneous tasks.

Initiative: The ability to initiate spontaneous thoughts, ideas and actions rather than being apathetic or merely responding to environmental cues.

Abstract reasoning: The capacity for complex problem solving.

Obsessive thoughts: May interfere with productive thought.

Racing thoughts: May interfere with productive thought.


An assessment of each of these areas of functioning is a critical component in the clinical assessment of LE. The cognitive assessment is only a part of the assessment of LE. Other components include the psychiatric assessment, the neurological assessment, a review of somatic symptoms, epidemiological considerations and laboratory testing when indicated. I have gradually developed a structured cognitive assessment which focuses upon the areas mentioned after examining many patients with late stage neuropsychiatric Lyme disease.
http://www.johndrullelymefund.org/ly...tive_impai.htm

wonderfullife
08-09-2011, 08:55 PM
I, Dana, became interested in the link between Lyme Disease (LD) and Hypothyroidism after my own young son contracted Lyme Disease in the late summer of 2005. Below is my son’s story—a child who was healthy and did not exhibit any signs of Hypothyroidism until AFTER he contracted Lyme Disease.

A few weeks before school began in 2005, my youngest son became ill with what I thought was a virus. He had a fever, sore throat, headache, and a stiff neck. I checked the lymph nodes behind his neck and ears and found them enlarged. I basically treated his symptoms the rest of the weekend with Motrin, and kept a watchful eye on him.

The following Monday, I had him see our family practitioner, who ran tests for Strep and Mononucleosis. Because the tests were negative, a viral illness was diagnosed. She stated it would need to run it’s course, and if he wasn’t better in a week, bring him back in.

Trusting the doctor, I took him home and continued to treat his symptoms. My son’s sore neck and throat got better, but other symptoms persisted–his fever continued and his lymph nodes were still swollen. Additionally, his eyes were bloodshot and he had no appetite. A second trip to the Doctor found a low White Cell Count, and we were instructed to come back in a month to recheck it. She also reiterated that he is probably just fighting a virus.

That weekend my older son noticed his brother had a weird red rash on his back, 2 weeks after his flu-like symptoms began. The numerous areas of rash were very faint, round and very large. There was some central clearing in each one. A third visit to the doctor concluded with a diagnosis of Lyme Disease. I was actually thankful to finally have a diagnosis. She stated a Lyme test would be run, but because the rash is so distinctive, she was going to treat him for Lyme Disease right away with Amoxicillin for 2 weeks.
Because I research anything that interests me, I got on my computer and started my investigation on “Lyme Disease”. Almost immediately I found out that the typical Lyme Rash, called “Erythema Migrans”, is conclusive for Lyme Disease. Even if the Lyme test comes back negative, treatment is necessary. However, by the time my son was treated, the “Borrelia Burgdorferi” (LD) infection had already disseminated or spread throughout his body and brain. That was why he had multiple bullseye rashes on his body.

Because the doctor did not suspect LD early on, I learned that my son already had progressed to Stage 2 or Early Disseminated Lyme Disease. The treatment for disseminated LD needed to be longer than 3 weeks on Amoxicillin! I called my Doctor and asked if she would please prescribe a longer course of antibiotics. She said that she would prescribe one more week and that would be enough to take care of the infection. So, my son was “allowed” to be on Amoxicillin for 4 weeks.

I also asked the Doctor if she thought that he might be better off on Doxycycline, instead of Amoxicillin, since literature states that Doxycycline is a better choice, especially if there is a chance of co-infections. She explained that because my son was only 10 years old, Doxycycline can discolor any permanent teeth that have not yet erupted. It was suggested that I call my dentist and ask his opinion. I did call my son’s dentist and he concurred with the Doctor about teeth discoloration. So, I reluctantly, decided to stick with the Amoxicillin.

However, because my son was showing signs of cognitive dysfunction, including short term memory loss and word recall problems (he is an A student), I was concerned that 4 weeks of antibiotics would not get rid of the LD infection. Luckily, through further research online, I found there was a “Pediatric Lyme Specialist” on the East Coast who might be able to help my son. After calling his office, his nurse explained that he really should be on antibiotics longer than a month, because my son was showing brain involvement. She asked me to send her all of my son’s records and recent blood work. By the way, my son’s Lyme test did come back positive for Lyme Disease.

My son was now in good hands. This wonderful, compassionate Doctor prescribed an additional 3 month course of Amoxicillin, which meant he was treated a total of 4 months on Antibiotics. He also suggested I buy a good Probiotic for the Yeast overgrowth that occurs during antibiotic treatment. Gradually, my son recovered his normal mental function and his other symptoms resolved during the antibiotic treatment. However, I was watchful for any return of symptoms, since my research show that these nasty bacterial “Borrelia Burgdorferi” Spirochetes are resistant to antibiotics because they do not have a cell wall. They are able to invade any and all organs or tissue in the body and cause destruction, slowly.

My son did recover, to a certain extent. However, to this day I do not know if the Amoxicillin was completely successful. What I do know is that because my son was not treated the first few weeks he was sick with LD, it was enough time for the “b. Burgdorferi” Spirochetes to invade his organs and brain.

THE PROGRESSION OF MY SON INTO HYPOTHYROID

About a year later, I noticed my son was more fatigued and getting headaches again, daily, as well as being moody and an easily aroused temper. He was also hungry all the time and gaining weight. Because I was diagnosed with Hypothyroidism in 2004, I was aware of Low Thyroid symptoms. Also, we have a family history of Thyroid problems. My Grandmother, my now deceased Father, my younger sister, and my Maternal Aunt have all have been diagnosed with Hypothyroidism. So, when I started to see symptoms of this in my son, I decided to monitor his temperature. Sure enough, his temperature was low throughout the day, never getting above 97.9. I set up an appointment with our local family practitioner, and when the results came back, he dismissed had Low Thyroid. My son’s TSH was 1.78 and his FT3 was almost mid-range. But, his FT4 was very, very low.

I knew, though, from my own experience and research that he was in fact Low Thyroid. But, I decided to wait it out a little longer to see if this might be temporary. It wasn’t. Unfortunately, I personally did not have a good Thyroid Doctor, and after much soul searching, I decided the best thing for my son would be to start him on a “trial” of Armour. By this time I had already been “self” treating myself with Armour, because I did not have the support from my own Endochronologist. I discussed with my son what all this entailed and he was willing to try it.

I started him on 1/4 grain of Armour and he did well. I waited out each increase for at least a few weeks and slowly he started to feel better. He started to lose the excess weight and his headaches lessoned. During this time, I continued to search for a better Thyroid Doctor. I slowly increased his Armour until we got to 3/4 grains. I did not want to increase any further until I had his Thyroid labs done, so I kept him on 3/4 grains for over a month. I luckily found a good Doctor an hour away from us and set up an appointment. Even though I knew in my heart that I was doing the “right” thing in self-treating my son, I was a little nervous on that first appointment.

However, after discussing my son’s symptoms and explaining his improvement, our new Doctor concurred that he probably did have a Thyroid problem. He agreed to run thyroid tests to see how his numbers were compared to the last Thyroid panel. He also greed to start prescribing Armour for my son. I asked the new Doctor to check his FT3 and FT4 along with TSH. He was fine with that. Well, my son’s lab results indicated an improvement in his FT3, but his FT4 was still too low. So, the Doctor agreed that I could raise my son to 1 grain Armour. My son is continuing to improve on 1 grain Armour and I will hold this dose for 6 weeks. I suspect we are almost there in his treatment with Armour and I am reassured that my son will continue to improve.

STRONG LINK BETWEEN MY SON’S LYME DISEASE and THYROID DISEASE
Now you have read my own son’s story of his Lyme Disease and his subsequent Hypothyroid diagnosis. And my goal here is not only for you to be aware of Lyme Disease, but to highlight that there is a strong link between LD infection and later developing Thyroid Disease, Auto-immune Dysfunction and/or Adrenal Dysfunction.

John D. Bleiweiss, M.D., a Lyme Disease specialist, states, “Increasingly, I am encountering thyroid disease in LD. A local endocrinologist has remarked to me privately that the incidence of thyroid involvement in LD may be greater than expected from the normal population.” He goes on to say, “In many of these patients, the thyroid dysfunction was seen to originate in the pituitary or hypothalmus. Remaining alert to the possibility of thyroid disease is essential because there can be considerable clinical overlap with LD. Subacute thyroiditis is the most prevalent thyroid phenomenon I see in LD. Hypoadrenalism can uncommonly develop: www.lymenet.de/lymcheck.html#essay

Dr. James Howenstine, a Lyme Disease expert, states, “Profound dysfunction of the hypothalamus, pituitary, adrenal, thyroid glands and gonads is very common in mycoplasmal, fungal, and anerobic bacterial infections. http://www.rumormillnews.com/cgi-bin...cgi?read=51356 He goes on to say, “There is considerable evidence that many patients with Chronic Fatigue Syndrome, Fibromyalgia, and Lyme disease have an infectious disease. Lyme disease needs to be considered in every patient with a chronic illness.”

Many of those who have Low Thyroid or Low Adrenal function have also been diagnosed with either Fibromyalgia or Chronic Fatigue Syndrome, which to me are “catch all” diagnoses that Doctors have used in order to “label” us with a disease they don’t understand.

There is considerable evidence that these diseases are actually caused by either a bacteria or virus. And, because of these infections, our bodies’ immune systems’ are weakened. That theory, in turn, pre-disposes us to developing various autoimmune disease as well as Thyroid and Adrenal disorders. My own son was perfectly healthy until he was bitten by a Lyme infected tick. This, I truly believe, set the stage for his own Thyroid to fail.

It is true that Thryoid disease in my own family is rampant. Many of us have developed Low Thyroid and Adrenal Disorders. I, personally, was diagnosed with Low Thyroid in 2004. I suspect that I have suffered from Low Thyroid most of my adult life. I too have some suspicion that I could have been infected with LD during my early years and will soon be testing for it. http://centralfloridaresearch.com/lab/ It could very well be that I was bitten by a tick during one of those summers I spent in Northern Wisconsin. Certainly Wisconsin is an epidemic state according to the CDC. www.cdc.gov/ncidod/dvbid/lyme/riskmap.htm The Lyme Bacteria, “”Borrelia Burgdorferi”, has now been found in mosquitos, biting flies, fleas, and various other vectors www.wildernetwork.org/faq004.html It can be transmitted in utero and by breast milk. So it can be impossible to know for sure who is really “safe” from this insidious and very destructive infection. There is evidence that “b. Burgdorferi” bacteria could even be transmitted, sexually. www.anapsid.org/lyme/std.html We all know that the “b. Burgdorferi” cousin, Syphilis, can be spread through sexual contact.

“Transmission of the disease has been clearly documented after bites by fleas, mites, mosquitos and ticks. There is compelling evidence that Lyme disease (LD) can be spread by sexual and congenital transfer.” http://www.samento.com.ec/sciencelib...endhowens.html

“The Sacramento, California blood bank thinks that LD can be spread by blood transfusions. The CDC (Center of Disease Control) in Atlanta, Georgia states that their data indicates that Bb can survive the blood processing techniques used for transfusions in the US.” http://www.samento.com.ec/sciencelib...endhowens.html

“Biology professor, Lida Mattman, author of Cell Wall Deficient Forms: Stealth Pathogens, has been able to recover live spirochetes of Bb from mosquitos, fleas, mites, semen, urine, blood, and spinal fluid.” www.digitalnaturopath.com/cond/C351537.html#H2

BELOW ARE MORE FACTS ABOUT LYME DISEASE

LD is most often transmitted by a tick bite. Only 20-30% of those infected ever recall a tick bite. The more common tick vectors are the Deer Tick and the Lone Star Tick. However, other ticks can also transmit the LD bacteria. http://www.canlyme.com/ticks.html Ticks prefer to live wooded areas, fields, yards and even near the ocean. Even if you are not a nature lover and prefer to stay in your house, you are not safe from LD tick bites. Your own pets, cats or dogs, can bring these ticks into your household. Because some of these ticks are as small as a pin-head when in there nymphal stage, it can be virtually impossible to know if you were bitten. They have a two year life cycle and are most active April through October. However, depending on where you live, you are not even safe in the winter months. Every state in the US has cases of Lyme Disease. But, the most endemic areas include Northeastern states, Pacific Northwestern states and the Great Lake states. LD is found in many other countries as well and include many different “strains” of the LD bacteria. The following countries have reported cases of LD: Scandinavia, Central Europe, Southern Europe, Western Europe, Russia, Japan, China and Australia.

And, many, many cases of LD go unreported or misdiagnosed. According to the following website: www.emedicine.com/derm/topic536.htm , “Epidemiologic data suggest that the actual incidence of Lyme disease could be as much as 10 times higher than the CDC data indicate. This probably is a result of a restrictive case definition from the CDC, inevitable misdiagnosis, and the fact that physicians tend to underreport reportable diseases of all kinds.”
The President of a Lyme Testing Facility, Dr. Nick Harris, goes on to say, “Lyme disease, in fact, might be the most insidious — and least understood — infectious disease of our day. “If it weren’t for AIDS,” says Nick Harris, Ph.D., President of IgeneX, Inc., a research and testing laboratory in Palo Alto, California, “Lyme would be the number one infectious disease in the United States and Western Europe.” www.mercola.com/2001/jul/25/lyme_disease.htm

Lyme Disease is now thought to be the fastest growing infectious disease in the world. There are believed to be at least 200,000 new cases each year in the US and some experts think that as many as one in every 15 Americans is currently infected (20 million persons). www.digitalnaturopath.com/cond/C351537.html#H2
Read more here:
http://www.stopthethyroidmadness.com/lyme-disease/

wonderfullife
08-09-2011, 09:00 PM
n the late 1970’s, I treated a depressed patient who appeared to have more than just depression. Her weight increased from 120 to 360 pounds, she was suicidal, had papille­dema, arthritis, cognitive impairments, and anxiety. This patient became disabled, went bankrupt, and had marital problems. Like many whose symptoms could not be explained, she was re­ferred to a psychiatrist. However, I was never comfortable labeling her condition as just an­other depression. At the time, I did not consider her illness could be connected to other diagnostic entities, such as neuroborreliosis, erythema migrans disease, erythema chronicum migrans, Bannwoth’s syndrome, Garin-Bujadoux syndrome, Montauk knee, or an ar­thritis outbreak in Connecticut With time, the connec­tion between Borrelia burgdorferi infections and men­tal illnesses such as depression became increasingly

apparent.

In my database, depression is the most common psychiatric syndrome associated with late stage Lyme dis­ease. Although depression is common in any chronic illness, it is more preva­lent with Lyme patients than in most other chronic illnesses. There appears to be multiple causes, including a num­ber of psychological and physical fac­tors.

From a psychological standpoint, many Lyme patients are psychologically overwhelmed by the large multitude of symptoms associated with this disease. Most medical conditions primarily affect only one part of the body, or only one organ system. As a result, patients singularly afflicted can do activities which allow them to take a vacation from their dis­ease. In contrast, multi-system diseases such as Lyme, depression, chronic Lyme disease can penetrate into multiple as­pects of a person’s life. It is difficult to escape for periodic recovery. In many cases, this results in a vi­cious cycle of disappointment, grief; chronic stress, and demoralization.

It should be noted that depression is not only caused by psychological factors. Physical dysfunction can directly cause depression. Endo­crine disorders such as hypothyroidism, which cause depression, are sometimes associated with Lyme disease and further strengthen the link be­tween Lyme disease and depression.

The most complex link is the association between Lyme disease and central nervous system functioning. Lyme encephalopathy results in the dysfunction of a number of different mental func­tions. This in turn results in cognitive, emotional, vegetative, and/or neurological pathology. Although all Lyme disease patients demonstrate many similar symptoms, no two patients present with the exact same symptom profile.

Other mental syndromes associated with late state Lyme disease, such as attention deficit disorder, panic disorder, obsessive-compulsive disorder, etc., may also contribute to the develop­ment of depression. Dysfunction of other specific pathways may more directly cause depression. The link between encephalopathy and depression has been more thoroughly studied in other illnesses, such as stroke. The neura1 injury from a stroke causes neural dysfunction that causes depression. Injury to specific brain regions has different statisti­cal correlation with the development of depression. Once depression or other psychiatric syndromes occur with Lyme disease, treating them effectively improves other Lyme disease symptoms as well and prevents the development of more severe conse­quences, such as suicide.

Suicidal tendencies are common in neurop­sychiatric Lyme patients. There have been a number of completed suicides in Lyme disease patients and one published account of a combined homicide/suicide. Suicide accounts for a significant number of the fatalities associated with Lyme disease. In my database, suicidal tendencies occur in approxi­mately 1/3 of Lyme encephalopathy patients. Homicidal tendencies are less common, and oc­curred in about 15% of these patients. Most of the Lyme patients displaying homicidal tendencies also showed suicidal tendencies. In contrast, the incident of suicidal tendencies is comparatively lower in individuals suffering from other chronic illnesses, such as cancer, cardiac disease, and diabetes.

To better understand the link between Lyme disease and suicide, let’s first look at an overview of suicide. Chronic suicide risk is particularly associ­ated with an inability to appreciate the pleasure of life (anhedonia). People tolerate pain without becoming suicidal, but an inability to appreciate the pleasure of life highly correlates with chronic suicidal risk. Of course, there are many other factors that also contribute to chronic risk. For example, one study demonstrated that 50% of patients with low levels of a serotonin metabolite (5HIAA) in the cerebrospinal fluid committed suicide within two years. Apart from factors which contribute to chronic suicidal risk, there are also factors which trigger an actual attempt, i.e.; a recent loss, acute intoxication, unemployment, recent rejection, or failure. There is much impairment from Lyme disease which increases suicidal risk factors. However, suicidal tendencies associated with Lyme disease follow a somewhat different pattern than is seen in other suicidal patients. In Lyme patients, suicide is difficult to predict. At­tempts are sometimes associated with intrusive, aggressive, horrific images. Some attempts are very determined and serious. Although a few attempts may be planned in advance, most are of an impul­sive nature. Both suicidal and homicidal tendencies can be part of a Jarish-Herxheimer reaction.

I cannot emphasize enough the behavioral significance of the Jarish-Herxheimer reaction. As part of this reaction, I have seen and heard numer­ous patients describe becoming suddenly aggressive without warning. I can appreciate skepticism regarding this statement. How can this be ex­plained? Like many other symptoms seen in Lyme disease, it challenges our medical capabilities. In view of this observation, I advise that antibiotic doses be increased very gradually when suicidal or homicidal tendencies are part of the illness.
http://www.mentalhealthandillness.co...AndSuicide.htm

wonderfullife
08-09-2011, 09:02 PM
Most of us in New England and certainly here in Connecticut have heard of Lyme Disease. It got its name from Lyme, CT as it was first officially identified there. There are certain geographic regions where Lyme Disease is more abundant but according to the International Lyme and Associated Diseases Society (ILADS), the disease is prevalent across the United States and throughout the world. ILADS states that Lyme disease is one of the fastest growing infectious diseases in the nation.

Lyme Disease is transmitted by the bite of a tick that is infected with the Borrelia burgdorferi spirochete. It often begins with a flu-like illness with fever, severe headache, sore throat and joint pain. If left untreated or treated improperly it can cause cardiac problems, meningitis, encephalitis and cranial neuropathies, eyelid droop, facial weakness, numbness or pain, shoulder droop, sensory distortions and other neurological symptoms. Some people experience arthritic symptoms in one or more joints.

What your may not know is that Lyme disease may also cause or worsen brain based cognitive symptoms such as memory, concentration, word finding difficulties, ADHD-like symptoms, learning disabilities, obsessive compulsive disorder, crying spells, rages, depression, bipolar disorder, panic, anxiety disorder and psychoses. When Lyme disease affects the brain it is referred to as Lyme neuroborreliosis or Lyme encephalopathy and the person is usually totally unaware of its presence.

A study by Hajek et al, published in American Journal of Psychiatry (February 2002; 159:297-31) found that one third of psychiatric inpatients showed signs of past infection with the Lyme spirochete. ILADS found that even severe neuropsychiatric symptoms can be reversed or eliminated when antibiotics are added to the indicated psychiatric treatment.

One of my patients had been treated for unremitting depression with no relief from antidepressant medication. His extreme fatigue and lack of motivation due to tiredness had been diagnosed as symptoms of depression – which they are. His ability to concentrate was severely affected and his job performance was suffering. He spent much of his day sleeping which brought no energy. After he sought out a physician who specializes in Lyme disease and was put on an intensive round of antibiotics, the fatigue and all symptoms of depression completely went away and the ineffective antidepressant was discontinued. His symptoms had been misdiagnosed as depression but were actually caused by Lyme disease.

Lyme disease is difficult to diagnose for several important reasons. First, less than 50% of all Lyme patients recall a tick bite. Secondly, Lyme disease often causes a bull’s eye rash which if present requires no further verification before starting treatment. But less that 50% of patients with Lyme disease recall ever having the rash. Thirdly, to add to the difficulty, many of the standard blood tests developed to detect Lyme disease have a high incidence of false negative results. Some of them show negative results even in the presence of the classic bull’s eye rash.
Consider Lyme disease if there are cognitive changes, extreme fatigue, weight changes, intense headaches, fibromyalgia, multiple sclerosis, explosive rages, sudden mood swings, or ‘spider bites’. For children, think about Lyme disease if there are behavioral changes, fatigue, academic problems, learning disabilities, headaches, sore throats, migrating pains. The key here is to notice changes from prior functioning even if the change was gradual.

One of my adolescent patients had developed extreme irritability, fatigue, lack of motivation and poor concentration. His symptoms appeared primarily psychological and behavioral and the change in functioning raised the question of possible drug abuse. His mother sought counseling to help him as his motivation had decreased significantly and his school work started to suffer. After a full psychological assessment was completed his mother followed the recommendation to have her son evaluated for Lyme disease. After months long treatment with antibiotics, all of the symptoms completely resolved. Her son’s mood improved, irritability disappeared, motivation returned, and his ability to concentrate increased to normal levels. The key factor in this situation was the definite and significant change in her son’s functioning. In adolescents this may be a warning of sign of drug use. Or as it was in this case, a sign of Lyme disease.

Find a physician who specializes in diagnosing and treating Lyme disease. Many cases of Lyme disease are being missed by general practitioners without specialized training in Lyme disease. Specialists know which lab tests to use, which labs have the most reliable results, and when and how to treat Lyme disease.

Be sure to treat Lyme disease with appropriate antibiotics for at least two weeks to four weeks after symptoms have resolved. This may include a minimum six week trial of antibiotics. For late stage Lyme disease, this may involve longer term intravenous treatment with antibiotics. There is evidence that treating with antibiotics for too short a time may actually make things worse than if not treated. ILADS has published guidelines for the diagnosis and treatment of Lyme disease. For more information visit www.ILADS.org.

wonderfullife
08-09-2011, 09:04 PM
The link between Lyme neuroborreliosis (LN) and aggression is reviewed from multiple perspectives. Cases are presented and discussed. It appears Lyme disease (LD) and other related tick-borne diseases contribute towards causing human aggression and violence. Greater attention to this area has the potential of reducing crime and saving lives. Narrow and restrictive opinions on the diagnosis and treatment of Lyme disease can contribute to the increased consequences of late stage disease, which includes aggression and violence associated with Lyme disease and other related tick-borne diseases.

Lyme disease (LD) is a multi-systemic disease with a predominance of dermatological, musculoskeletal and neuropsychiatric symptoms. Predominant symptoms are first dermatological, then musculoskeletal, and finally involve the central nervous system (CNS) in late stage disease. These symptoms may be cognitive, psychiatric and other neurological impairments. Late stage LD, with a predominance of cognitive, psychiatric and neurological symptoms has been called many different names throughout history and in different geographical regions. Recently used terms include Neuropsychiatric Lyme disease, Neurolyme, Lyme Encephalopathy and Lyme neuroborreliosis. The causative agent of LD is Borrelia burgdorferi (Bb.), a spirochete, with many similarities to syphilis. Since vectors which transmit Bb. are often infected with other microbes, an infection with Bb. is sometimes complicated by other tick-borne pathogens. Interactive copathogens are more common in more severe and more chronic cases.



Although aggression is a normal human function, dysregulated aggression causes violence, which does not facilitate adaptation and poses a major threat to individual health, social stability and the survival of our species. Pathological aggression and violence are not a result of any one cause. Instead, it is a result of a combination of contributors to violence, which are not adequately compensated by the deterrents to violence. Many of these contributors are unknown and others have described some (1,2,3,4,5). This paper shall focus upon a contributor, which has not been the subject of a large amount of research in the past, the role of infectious diseases, and more specifically tick-borne diseases and LN.
http://actionlyme.50megs.com/neurobo...aggression.htm

wonderfullife
08-09-2011, 09:07 PM
The existence of the Lyme disease epidemic is officially covered up in the UK, its myriad presentations routinely misdiagnosed as everything from "M.E." to MS to hypochondria. This is the first admission by a US government body that the cause is an incapacitating biowar agent:

SAN ANTONIO (AP) -- The $10.6 million Margaret Batts Tobin Laboratory Building will provide a 22,000-square-foot facility to study such diseases as anthrax, tularemia, cholera, lyme disease, desert valley fever and other parasitic and fungal diseases. The Centers for Disease Control and Prevention identified these diseases as potential bioterrorism agents.".

http://www.msnbc.msn.com/id/10039154/

So, for the first time, a US government body admits that Lyme disease is a biological warfare agent. This is the reason that hundreds of thousands of men, women and children around the world have been left to rot with wrong diagnoses, or have had their Lyme disease acknowledged but been told that it is an "easily-treated" disease, given 3 weeks' antibiotics, then told to shove off when their symptoms carried on after that.

In Britain the existence of the epidemic is denied completely, and virtually no effort made to warn or educate the public about the dangers of ticks, which carry the bacteria Borrelia burgdorferi.

The Borrelia genus has been a subject of biowar experimentation at least as far back as WW2, when the infamous Japanese Unit 731, which tortured and experimented on live prisoners, studied it.

The reality is, Lyme disease is for many a chronic, horrendous, incapacitating disease producing crippling fatigue, constant pain, loss of memory, possible paralysis, psychosis, blindness and even death.

It was an ideal biowar agent because it evades detection on routine tests, has an enormous range of different presentations, and can mimic everything from ADHD to multiple sclerosis to carpal tunnel syndrome to rheumatoid arthritis to chronic fatigue syndrome (M.E.) to lupus to schizophrenia. Enemy medical staff would never know what had hit them, nor even that ONE illness had hit their population, rather than an unexplained rise in dozens of known conditions.

Honest doctors and scientists who tried to treat or research Lyme disease according to ethical principles have been viciously persecuted by government-backed organisations in the US, Europe and elsewhere. Many specialists in the US were threatened with loss of their license or had anonymous, false allegations sent to the medical board, which tied them up in mountains of paperwork and legal fees...some were forced out of medicine or even driven to suicide.

Instead, medical disinfo agents, most of whom have a background in military/biowarfare units, such as Dr Allen Steere, Mark Klempner, Philip Baker, Edward McSweegan, David Dennis, Alan Barbour etc were enabled to assume top positions in Lyme research , CDC, NIH etc from where they issued false information , covering up the true seriousness and chronic nature of the disease, and comdemned untold numbers to a living hell.

Please help Lyme patients publicise this scandal, which has caused suffering on a massive scale. Contact me by email if you are interested in helping.

Thank you.

Lisa

Lymerayja
e-mail: [email protected]
Homepage: http://www.lyme-rage.info

http://www.indymedia.org.uk/en/2005/11/328067.html
http://www.rense.com/general69/lyme.htm

wonderfullife
08-09-2011, 09:09 PM
Lyme disease, which is initiated by the bite of a deer tick, is difficult to diagnose, but your dentist may be able to detect this mysterious disease, reports the Academy of General Dentistry (AGD), an organization of general dentists dedicated to continuing dental education. Patients with Lyme disease report pain in their teeth, chewing muscles and jaw joint, which drives them to the dentist.



"Unfortunately, most patients are not diagnosed properly until their Lyme disease is at a later stage, when it is more difficult to treat," says AGD spokesperson Manuel Cordero, DDS. "Diagnosing this disease is very tricky because it can hide itself behind many dental problems, including toothaches and jaw pain."



A study of 120 patients with Lyme disease revealed that about 75 percent of patients reported pain in the chewing muscles, and 72 percent reported temporomandibular joint pain. Burning mouth was reported by 25 percent of these patients, and 70 percent reported a sore throat. About 47 percent of the patients visited up to 10 doctors before being properly diagnosed.



Updated: November 2008

http://www.knowyourteeth.com/infobit...d=334&aid=1348

wonderfullife
08-09-2011, 09:11 PM
The mouth is the most important factor in the breakdown of health; there is no close second. All the antibiotics, and all the holistic approaches to healing, are likely to fail if the mouth has been overlooked.

The mouth is a reservoir of bacterial infections that become entrenched within the structure of teeth and trigger the high number of chronic degenerative diseases now epidemic in America, including Lyme.

Lyme has the ability to embed itself in tooth structure, where it goes undetected and remains unreachable by antibiotics. Each tooth has some three miles of tubules that emanate from the main canal. Bacteria hide out in all that footage. Lyme is a spirochete similar to spirochetes that cause syphilis. Spirochetes by nature burrow into tissue, such as teeth, bones, and soft tissue like the brain. These areas are the toughest to get to, impenetrable by drugs and herbs.

Many dentists do not realize that antibiotics cannot reach bacteria in dead teeth. In the case of endodontic therapy, or root canal, the dead tooth lacks a blood supply to its interior. Antibiotics circulating in the bloodstream have no way penetrate this dead tissue and hence have no effect on the bacteria.

Herbs are a little more effective, because they tend to make the body healthier by raising the immune function. But they can't knock out bacteria.

Energetic Approach Proves Most Effective in Lyme
Andrew Landerman, DDS, of Sebastopol, California, has mastered the use of energetics to get at Lyme. According to Landerman, one must focus on the oral cavity when dealing with Lyme because the oral cavity, in part or whole, blocks the immune functions, especially when incompatible dental materials are used. He has found this is the genesis of much degenerative disease, and it is often overlooked by both physicians and dentists today.

"Energy can pass through hard or soft tissue with no interference, much the same way as sound travels better through more dense structure than it does through air," Landerman says. "The sound of a blue whale can be heard by other whales in the water several hundred miles away. I first started to understand the relationship between Lyme and the oral cavity when I checked all the teeth in the mouth associated to symptoms in the body. As I went through this process, it became obvious that in Lyme, there are certain teeth more prone to show degenerative conditions than other teeth. I began to see a pattern develop. The first molars, top and bottom, are particularly affected. In time, I saw that the pattern also included the two front teeth, top and bottom."

He learned to use percussion, a method of tapping the tooth to send it a tiny shock to see how it responds. All teeth and their extraction sites relate to the different organs through the Chinese medical system of meridians, and they are all connected energetically. "As you go around the mouth," he says, "you see a pattern of low or high voltage in some teeth. No amount of herbs or remedies would get these underperforming or overperforming teeth to change their readings for the better. "

Landerman studied years ago in Germany, where he saw dentists extract affected teeth, and patients improved. But it bothered him that the pulp of the extracted teeth appeared normal. He wondered if those teeth had really needed to come out.

Metal is used in fillings and often under crowns. Metal interferes with the body's energetic network and suppresses or negatively excites the immune system. It doesn't matter if it's gold or nickel - all metal is problematic. "Nickel is probably the worst because it is carcinogenic; it knocks out the immune system," Landerman states. Mercury is about the most active of metals. The higher the temperature, the more it is released, poisoning the system.

One must remove the intrusive dental materials in order to correct the energetic flow of the related organ meridian, to restore proper function of the organ. Without this, degenerative diseases such as Lyme can take root. "It makes sense; you want to go back and correct the cause of the block," says Landerman. "The oral cavity is the seat of most of the energetic blocks in the system."

Landerman understands that teeth respire. "Normally, in a healthy tooth, fluid will go from the inside of the tooth to the outside," he explains. "That is their gatekeeper mechanism, their way to keep bad bacteria out of the tooth. But if a tooth is compromised, the fluid goes the other way - outside in. That is how infections enter the oral cavity, breed virulent pathogens, and can create havoc throughout the body for decades."

He figured he could use respiration to his advantage. "It took me probably 15 to 18 years to come up with homeopathic remedies that would change these teeth back to normal readings," he says. "Then we could save the teeth. If I could cause the homeopathic solution to go into the tooth, the tooth would be partially or wholly healed. Experience has proven the truth of this."

Landerman's patients are fitted with a tray and a custom-made homeopathic remedy. They bathe the affected teeth for an hour a day for as long as prescribed. The remedy transmits the homeopathic solution to the tooth and the tooth responds. If it can, the tooth returns to normal. Homeopathy is able to move fluids into the tooth.

"We need to knock down the Lyme hiding in the miles of tubules and in the bony socket," Landerman says. "I have my patients do this procedure at least once a year. And you do not have to have a Herxheimer reaction to get better. In homeopathy, if you hit the nail on the head, you won't have a Herx."
Focal Infection - Starts in the Mouth and Migrates

Where Lyme and other chronic diseases are concerned, the big enemy is root canals. American dentistry has been slow to recognize the negative impact of this procedure. Elsewhere in medicine, when a part of the body dies, say, a foot turns gangrenous, it is cut off. But in a root canal, dead teeth are left in, filled with a sealant where the nerve was drilled out. These teeth always cause energetic blocks.

George Meinig, DDS, FACD, author of Root Canal Cover Up, questions how standard dentistry can claim that infections seated in the mouth do not affect the body. "Patients who have heart conditions, knee or hip replacements, are told by their physician or dentist that for the remainder of their lives, they must have an antibiotic prescription before and after any dental treatment, including cleaning of their teeth," he wrote. "The reason antibiotics are needed is because it has been proven bacteria that live in the mouth can easily enter the bloodstream and travel to the heart and joints where they frequently cause endocarditis and many other infections."

This is called the focal infection theory. Meinig and Landerman believe that this valuable information was buried years ago by a minority group of autocratic dentists within the American Dental Association (ADA) who just couldn't grasp the concept.

The infectious mechanism was initially documented by Dr. Weston A. Price, chairman of the Research Section of the American Dental Association from 1914 to 1923. Price would extract a tooth that had undergone a root canal and implant it under the skin of a laboratory rabbit. He documented that in almost every case the animal would develop the same disease that the patient did. Price found he could embed small pieces of the root instead of the entire tooth, or pulverize the teeth and inject the powder, and cause the same results. Eventually, he found that he could culture the bacteria from a root-filled tooth and inject the toxins from it into the laboratory animal and reproduce the disease from the toxins alone. Price also found that bacteria present in the roots of the teeth and cementum were also present in the first few millimeters of adjacent bone in the jaw. The sterilization process involved in root canals simply does not work.

History tells us that the ADA wanted to promote root canal therapy as a new service and never moved forward with Price's report. Penicillin was discovered in 1928, the study of viruses soon followed, and antibiotics took center stage. However, the Germans made a big study of focal infections.
http://findarticles.com/p/articles/m.../ai_n32149711/

wonderfullife
08-09-2011, 09:12 PM
Here is a UK Lyme petition

http://www.ipetitions.com/petition/uklymepetition/

wonderfullife
08-09-2011, 09:16 PM
Gulf War Syndrome or Gulf War Illness has been used to describe a collection of chronic signs and symptoms reported by U.S., British, Canadian, Czech, Danish, Saudi, Egyptian, Australian and other Coalition Armed Forces that were deployed to Operation Desert Storm in 1991. Over 100,000 American veterans of Desert Storm /Desert Shield (approximately 15% of deployed U. S. Armed Forces) returned from the Persian Gulf and slowly (6-24 months or more) and presented with a variety of complex signs and symptoms characterized by disabling fatigue, intermittent fevers, night sweats, arthralgia, myalgia, impairments in short-term memory, headaches, skin rashes, intermittent diarrhea, abdominal bloating, chronic bronchitis, photophobia, confusion, transient visual scotomata, irritability and depression and other signs and symptoms that until recently have defied appropriate diagnoses (see publications). These symptoms are not localized to any one organ, and the signs and symptoms and routine laboratory test results are not consistent with a single, specific disease.

Although there is not yet a case definition for Gulf War Illness, the chronic signs and symptoms loosely fit the clinical criteria for Chronic Fatigue Syndrome and/or Fibromyalgia Syndrome. Some patients have additionally what appears to be neurotoxicity and brainstem dysfunction that can result in autonomic, cranial and peripheral nerve demyelination, possibly due to complex chemical exposures. Often these patients have been diagnosed with Multiple Chemical Sensitivity Syndrome (MCS) or Organophosphate-Induced Delayed Neurotoxicity (OPIDN). Chemically exposed patients can be treated by removal of offending chemicals from the patient's environment, depletion of chemicals from the patient's system and treatment of the neurotoxic signs and symptoms caused by chemical exposure(s). A rather large subset (~40%) of GWI patients have transmittible infections, including mycoplasmal and possibly other chronic bacterial infections, that have resulted in the appearance of GWI in immediate family members and civilians in the Gulf region. It is likely that veterans of the Gulf War who are ill with GWI owe their illnesses to a variety of exposures: (a) chemical mixtures, primarily organophosphates, antinerve agents and possibly nerve agents, (b) radiological sources, primarily depleted uranium and possibly fallout from destroyed nuclear reactors, and (c) biological sources, primarily bacteria, viruses and toxins, before, during and after the conflict. Such exposures can result in poorly defined chronic illnesses, but these illnesses can be treated if appropriate diagnoses are forthcoming.

Studies on Gulf War Illnesses: Chronic Infections

Identification of Mycoplasmal Infections in Gulf War Illness Patients and their Family Members:

Scientists at The Institute for Molecular Medicine have found that slightly under one-half of the very sick Gulf War Illness patients in a pilot study with the signs and symptoms of Chronic Fatigue Syndrome or Fibromyalgia Syndrome have chronic invasive infections involving certain uncommon mycoplasmas, such as Mycoplasma fermentans. This has now been confirmed in a large Department of Defense - Department of Veterans' Affairs clinical trial. Staff at The Institute for Molecular Medicine have recommended that these infections can be successfully treated with certain antibiotics, allowing the recovery of patients who have been long-term disabled. Similarly, in ongoing preliminary studies on Chronic Fatigue Syndrome and Fibomyalgia patients, we have found that a subset of patients have mycoplasmal infections that can be successfully treated with antibiotics, allowing patients to recover from their illnesses.

These chronic bacterial infections can spread to immediate family members. In a recent study we found that spouses of veterans with Gulf War Illness and chronic infections, such as M. fermentans, were at high risk for the infection. We also found that the children (aged 2-11 years) of Gulf War veterans with Gulf War Illness and a positive test for mycoplasmal infection (mostly M. fermentans) often were diagnosed with Autistic Spectrum Disorders (ASD). Upon examination of the ASD patients we found that over 80% had the same infection as their veteran parent. The onset of ASD (after the veteran returned from service) and the presence of the same infection suggested transmission of the infection and its involvement in ASD.



Identification of Other Infections in Gulf War Illness Patients:

The Institute for Molecular Medicine has been engaged in examining the blood of Gulf War Illness, Chronic Fatigue Syndrome, and Fibromyalgia patients for chronic infections that could explain their clinical conditions. In preliminary research we have found that some patients have microorganism infections, such as those caused by Brucella species, Y. pestis or other bacteria. This line of investigation is now being actively pursued at the Institute.
http://www.immed.org/illness/gulfwar..._research.html

wonderfullife
08-09-2011, 09:18 PM
We are an online community and a movement of individuals affected by chronic Lyme and associated diseases. We have many titles or labels including patient, family, neighbor, scientist, advocate, doctor, insurer, health policy expert, and legislator. We are here because Lyme and associated diseases are a growing, silent, often ignored, and misunderstood epidemic devastating our lives, our neighborhoods, and our communities. We want to learn about this illness and understand the experiences of those affected. We also have questions, ideas, and insights about this illness that we hope to share.

Through our collective and collaborative discourse on this Lyme disease commons, we give and receive support, educate ourselves, and gain valuable insights leading to innovation and transformation of treatments and lives. As a movement we provide support, foster science, inform and educate, produce legislation, and create health care treatment and policy changes. Our goals are to prevent the illness, find the cure, improve treatments, and assure access to high quality health care for ourselves and our neighbors. Alone we are divisible, at times invisible, but as a community we are invincible.
http://www.tickbytesonline.com/

wonderfullife
08-09-2011, 09:21 PM
http://voicesfromtheshadowsfilm.co.uk/2011/trailer/

wonderfullife
08-09-2011, 09:24 PM
"You might have seen me struggling to finish dead last at the World Championship trials a few weeks ago. It wasn't pretty. Once upon a time, I ran under 44.94 seconds in the 400m at the Olympic Games. That's pretty good, I promise. I am now more than £10,000 in debt, with an immune system ravaged by Epstein-Barr virus (or glandular fever), pride swallowed, confidence shattered and, most importantly, my dreams and goals of the last decade close to being laid out before me in tatters.

It wasn't meant to be like this. I'm in danger of becoming the Nearly Man. Writing this could be a pointless exercise in self-absorption, but I want to highlight the lesser-told story of elite sport: the one that doesn't necessarily end in glory.


I was struggling to run, and none of the team physios could relieve the sensation. I was finding it hard to sleep, waking up almost every 90 minutes, all night long. Two weeks later I was very, very tired, and running times in training that were just embarrassing. A month prior I had been on top of the world, and now I could barely beat the club-level athletes I trained with. I felt as though my athletic ability had been erased overnight. It turns out, it had. I was diagnosed with the Epstein-Barr virus, and a weight lifted from my shoulders as we finally put a name to what was going on. That was quickly replaced by a descent into the reality facing me.

But the route out of Epstein-Barr is complicated and ambiguous. There is no real treatment. The virus can attack the brain - in my case the Hypothalamus, the part that controls your "fight or flight" response - which gives it a psychological potency. That makes onlookers think "it's all in your head".

And now I face the reality. In all likelihood I will be cut from lottery funding at the end of this year, and rightly so. UK Athletics have been wonderful in keeping me on through all the troubles thus far, I am incredibly thankful for that. I have almost no other income; the amount I was receiving in lottery funding was barely enough to live on anyway.

Unless I find some sort of large private sponsorship, I will be forced into retirement less than a year before the biggest event British sport has ever seen. Can I really just be some guy working in a shop somewhere while the London Olympics inspire and improve our country? While my one-time contemporaries achieve greatness?

I really don't want a reasonably fast run, in a preliminary round of a major championship, to be the only highlight in a decade of hardship and discipline which left me with five-figure debt. This is the lesser-told road, the one that ends in a muddy field, not an awe-inspiring land of BBC montages soundtracked by Sigur Ros. For every success, there are many, many more for whom things did not go right. That's the beauty of sport.

You don't embark on a quest for Olympic greatness because it's a guaranteed easy ride. Fingers crossed, I can change the cards I have been dealt."
Read more here: http://niceguidelines.blogspot.com/2...son-of-dr.html

wonderfullife
08-09-2011, 09:25 PM
The FDJ line up for the Tour de France has been announced, and is without the team’s big winter signing Pierrick Fédrigo. The three-time Tour stage winner has had a relatively quiet season to date and has decided not to start the race thanks to poor form, fatigue and a niggling back injury.

"[Team manager] Marc Madiot asked me what I wanted to do, and I told him that I did not want to go,” Fédrigo explained. “I need vacation. I am at the bottom of a hole. I need to rest, need to look after myself, because I’ve not managed to get rid of my back problems.

“Go to the Tour without being 100%, would not do any good at all!”

Fédrigo had raced for Bbox Bouygues Telecom (now Europcar) since 2005, leaving at the end of last year over worries about the team finding a new sponsor. The rider known as the Nose of Marmande has ridden every Tour since 2003, and finished every edition besides that debut. His three stages have all come from breakaways, in 2006, 2009 and last year, when he outsprinted the lead group that included seven-time race winner Lance Armstrong in Pau.

In the absence of Fédrigo FDJ has no obvious leader, although it does include another three-time stage winner in Sandy Casar;; the team’s aim will be to chase stage victories.

Most of the team is experienced at this level, but Gianni Meersman, Arnold Jeannesson and Arthur Vichot will be making their Tour debuts.



Read more: http://www.velonation.com/News/ID/88...#ixzz1WvIQbXWh

He has Lyme

And here if you can read french: http://www.velochrono.fr/actu/2011/f...n-bacterienne/

wonderfullife
08-09-2011, 09:27 PM
This was published back in 1990

Two neurologists have reported that a 20-year-old man suffered a stroke as a result of meningitis brought on by Lyme disease. Eleven similar cases have been documented in Europe, they say.

In a report published yesterday in Stroke, a journal of the American Heart Association, the two neurologists at the Walter Reed Army Medical Center in Washington recommend that victims of inexplicable strokes be tested for Lyme disease.

''This is not the first time stroke has been linked to Lyme disease,'' said Dr. Eugene F. May, who, with Dr. Bahman Jabbari, wrote the report. ''But it is not a widely known syndrome.''

Lyme disease is caused by a tick- transmitted bacteria, called Borrelia burgdorferi. Its early symptoms are a skin rash, headaches and fever, but if untreated the disease can cause arthritis as well as heart and neurological damage. It is rarely fatal.

Link Is Long Suspected

Neurologists say a link between Lyme disease and stroke has long been suspected. ''Everybody has been looking for this for years,'' said Dr. John J. Halperin of the State University of New York at Stony Brook. ''This is probably the best documentation we've had so far.''
http://www.nytimes.com/1990/08/17/us...ar-old-gi.html

wonderfullife
08-09-2011, 09:30 PM
The similarity of clinical and pathological manifestations of syphilis caused by Treponema pallidum [1] and Lyme disease caused by Borrelia burgdorferi [2] is well established. In analogy to Treponema pallidum, Borrelia burgdorferi persists in the brain in chronic Lyme neuroborreliosis [3]. How Borrelia burgdorferi is able to survive in infected tissues for years or decades is not well understood. Ways for long term survival may be through transformation into more resistant atypical forms and through intracellular localization.

As early as 1905 it was suspected that the classical spiral (vegetative) form was not the only one that spirochetes could assume [1,4]. Transformation of various types of spirochetes into cystic forms through end knob, loop, ring-shaped and spherule formation has since been repeatedly reported [5-10]. Agglomeration of spirochetes into colonies [11-14], enclosing numerous cystic forms, has been observed both in vitro and in vivo [12].

Treponema pallidum and Borrelia burgdorferi produce vesicular budding from the membrane, which may become detached. In Borrelia burgdorferi these free vesicular or granular structures contain spirochetal surface proteins and linear and circular DNA [15,16].

Granular disintegration of spirochetes resulting in a chain of fine granules also occurs under adverse conditions [17-22]. Minute granules are liberated from the periplasmic sheath through budding and extrusion, which may multiply and may be transmissible [23-31]. Their presence in syphilitic patients was regarded as confirmatory of the syphilitic nature of the lesions even in the absence of classical spiral forms [26,27,30]. These spore-like minute granules (0.1–0.3 μm in diameter) may pass the 0.2 μm "China" filter (32) and can grow into young spirochetes [6,19,25-38]. The newly formed spirochetes are delicate L or metacyclic forms [25,32,39].

These various atypical forms were suggested to be part of a complex developmental cycle, a form of resistance to adverse conditions, and a source for reproduction under more favorable conditions. Reconversion of cystic Borrelia burgdorferi into the typical spiral form has been demonstrated in vitro and in vivo [8,10,31,40].

The occurrence of pleomorphic forms of Treponema pallidum in the brain in general paresis and their abundance in juvenile paresis is well documented [6,18,26,41,42].

Treponema pallidum may invade virtually all parenchymal and mesenchymal cells, including plasma cells, macrophages, neurons and glial cells [39,40,43]. Atypical and cystic forms of Treponema pallidum have been observed both extra- and intracellularly [30]. It has also been described in other spirochetal infections [e.g. [44-46]].

Only limited data are available on the occurrence of atypical, cystic or granular forms of Borrelia burgdorferi in infected tissues. Their occurrence has been reported in skin lesions [14], in an ex vivo system in tonsil tissue [47] and on silver stained hippocampus section in a patient with concurrent Alzheimer disease (AD) and Lyme neuroborreliosis [48]. Intracellular localization of Borrelia burgdorferi was observed in macrophages and keratinocytes in the skin [14] and in neurons and glial cells in vitro and in vivo [3,49-51].

The goal of the present study was to compare whether atypical and cystic forms of Borrelia burgdorferi spirochetes induced in vitro are similar to those occurring in vivo. Three patients with chronic Lyme neuroborreliosis were used in the study. Immunodetection of reactive microglia and astrocytes was also performed to detect neuroinflammation.
Methods
Cultivation of Borrelia burgdorferi spirochetes in BSK II medium

Borrelia burgdorferi spirochetes strains B31 and ADB1 [3,51-53] were cultivated in BSK II medium [54]. To 500 ml BSK medium (Sigma B 3528) containing 6% rabbit serum (Sigma R-7136) and 7% gelatin (Difco 0143-15-1), 6 mg acetyl muramic acid (Sigma A 3007) and 0.2 g N-acetyl glucosamine (Sigma A8625), Rimactan (Novartis, 420 ul) and Fosfocin (Boehringer Mannheim, 300 ul) were added. The spirochetes were cultivated at 32°C. The pH of BSK II medium was adjusted to pH 7.

To induce atypical spirochete forms 5 ml of cultivated Borrelia burgdorferi spirochetes (5 × 105/ml) were exposed to various harmful conditions. Spirochetes were exposed to strong acidic and basic conditions by adjusting the pH of the BSK II medium to pH2 and pH10 using sterile 1 M HCl or 1 M NaOH. The harmful effect of alcohol was analyzed by adding 1 ml of either 70% or 95% ethanol to 5 ml cultivated spirochetes. Heat shock was produced by cultivating spirochetes at 45°C.

Spirochetes are known to bind Congo red and Thioflavin S [55,56], both of which are widely used to stain amyloid. To analyze whether they may induce atypical Borrelia forms, 1 mg or 5 mg of Congo red, or 1 mg or 5 mg Thioflavin S were directly added to 5 ml of spirochete culture. The same amounts dissolved in 2 ml of 70% alcohol were also used to induce atypical spirochetes. The effect of acridin orange, another fluorochrom which binds to spirochetes, was also analyzed by adding 1 mg or 5 mg acridin orange powder to 5 ml of cultivated spirochetes.

Following 1 hour, 6 hours, and 1 week exposure times, 50 μl samples were taken and put on glass slides, cover-slipped, and then examined by dark field microscopy. Series of 50 μl samples were used to prepare smears for histochemical and immunohistochemical investigation. Additional 500 μl samples were removed and fixed in glutaraldehyde for atomic force microscopy (AFM) analysis. Spirochetes cultivated at 32°C at pH 7 for the same periods of time were used as controls. An exception with respect to the exposure times was induction of osmotic shock by cold H2O. Two ml sterile cold H2O was added to 5 ml cultured spirochetes that had been collected by centrifugation at 1000 rpm for 5 minutes. Here the samples were examined following 1 and 6 hours of exposure.

In order to analyze whether the typical spiral Borrelia form may be resuscitated, at the end of each experiments 200 μl samples were reinoculated in BSK II medium at Ph7 and following one week of culture at room temperature, 30 μl samples were analyzed by dark field microscopy.
Infection of cell cultures with Borrelia burgdorferi

Superior cervical ganglia from 8- to 12-day-old chicken embryos were dissociated as described previously [57]. Briefly, neurons were separated from non-neuronal cells using a density gradient formed with Percoll. The sympathetic neurons were then grown for 3–4 weeks in serum containing medium on a polyornithine substrate pre-coated with heart-conditioned medium [57]. Neurons dissociated from the telencephalon of 21-day-old rat were cultured either on collagen or polylysine substrate in a serum-containing medium [58]. Rat primary astrocytes (106) were prepared as described earlier [59]. Following the characterization of the primary astrocytic cell cultures using anti-GFAP antibody (Dako, Z334) more than 95% of the cells were GFAP reactive (not shown here). The cells were cultured in 2 well chambers (177429 Lab-Tek, Christschurch, New Zealand) or in six well clusters (3506, Costar, Acton, Maryland) in a humidified CO2 (6%) incubator at 37°C.

To infect neurons and astrocytes, Borrelia spirochetes of the virulent strains B31 and ADB1, the latter having been cultured from the brain of a patient with concurrent Lyme neuroborreliosis and AD [3], were employed. Equal volumes of medium for the given primary cells and for spirochetes (BSK II) were used as the culture medium. The final concentration of spirochetes in the infected medium corresponded to 5 × 105/ml. Before exposure to spirochetes, the cells were tested with 4',6-diamidine-2'-phenylindole dihydrochloride (DAPI, 236 276, Boehringer Mannheim, Germany) to exclude Mycoplasma infection. Parallel cultures not infected with spirochetes were always used as controls.

After 1 week exposure, the medium was removed and the cells were rinsed with PBS (2 ml, 2 × 3 minutes). To analyze the morphology of free floating spirochetes, 50 μl samples of culture medium were taken and analyzed by dark field microscopy. Smears were also prepared for histochemical and immunohistochemical analyses.

After 1 week exposure, 200 μl samples from all infected cell cultures were also re-inoculated in BSK II medium and were cultivated at room temperature, Ph 7, for one week. Then 30 μl samples were analyzed by dark field microscopy.
Detection of apoptosis by deoxynucleotidyltransferase (TdT)-mediated dUTP nick end labeling (TUNEL)

Cells in 6 wells chambers were fixed with 4% paraformaldehyde for 10 minutes in room temperature. Following an incubation with proteinase K (20 μg/ml) in TRIS HCL (pH 7.4) for 15 minutes at 37°C the cells were rinsed with 2 ml PBS (2 × 3 minutes). Then cells were treated with a permeabilisation solution containing 0.1% Triton X100, in 0.1% sodium citrate, for 2 minutes on ice followed by a rinse with PBS (2 × 3 minutes).

The cells were incubated with a freshly prepared TUNEL reaction mixture kept on ice containing 45 μl of TUNEL label solution (1767291, Boehringer) containing unlabeled dNTPs and fluorescein isothiocyanate tagged dUTP (FITC-dUTP) and 5 μl of TUNEL enzyme (Terminal deoxynucleotidyl Transferase (TdT) (1767305, Boehringer) for 1 hour and 30 minutes at 37°C in a humidified chamber. For a negative control the TUNEL enzyme was omitted from the TUNEL reaction mixture and 50 μl TUNEL label solution alone was used.
Detection of pleomorphic Borrelia forms in vivo

Brains of three patients with pathologically and serologically confirmed Lyme neuroborreliosis and concurrent AD were analyzed [3]. From the brains of these three patients, aged 74, 78, and 86 years, spirochetes were successfully cultivated in BSK II medium. In two of them (strains ADB1 and ADB2) 16SrRNA gene sequence analysis identified the spirochetes as Borrelia burgdorferi sensu stricto (s. s.).

To detect whether atypical and cystic forms of Borrelia burgdorferi spirochetes are present in the brains of these patients, frozen sections of the hippocampus, frontal, temporal and parietal cortex were analyzed using dark field microscopy, as well as histochemical and immunohistochemical techniques. Before immunostaining the sections were fixed in acetone for 10 minutes at 4°C. Acetone fixed frozen sections which were cut from samples taken from identical brain areas in three control patients without neurological symptoms and without brain lesions were also processed and analyzed in the same fashion.

Paraffin sections (20 μm thick) cut from various cortical samples (from archival material of the Armed Forces Institute of Pathology, USA) of two patients (31 and 52 year old males) with clinically, serologically and pathologically confirmed general paresis, were also analyzed for the presence of Treponema pallidum. The goal was to compare atypical spirochetal forms of Borrelia burgdorferi in Lyme neuroborreliosis with those of Treponema pallidum in general paresis.
Dark field microscopy, histochemical and immunohistochemical analysis of spirochetes

From cultivated Borrelia spirochetes exposed to various harmful conditions, 50 μl samples were used as wet preparation for dark field microscopy analysis. Additional samples (50 μl) were used to prepare smears for the histochemical and immunohistochemical analyses. In order to analyze free floating spirochetes in Borrelia infected cell cultures, 50 μl samples of the co-culture medium were analyzed.

Smears and brain sections were stained with the Warthin-Starry and Bosma-Steiner silver techniques as described for the detection of spirochetes. Spirochetal DNA was detected in smear preparations of cultivated spirochetes exposed to various adverse conditions, in infected cells, and in unfixed frozen brain sections by staining with DAPI (236 276, Boehringer Mannheim, Germany) following instructions of the manufacturer. The same preparations were also used for immunohistochemical analysis. Smears prepared on glass slides from cultivated spirochetes, from medium of infected cells, and from cryostat cut brain sections were fixed in acetone for 10 minutes at 4 °C prior to immunostaining. Infected cells in six wells, where acetone cannot be used, were fixed in 4% paraformaldehyde for 5 minutes. Before immunostaining, frozen brain sections following acetone fixation were incubated in 0.1% amylase for 5 min at 37°C. The following anti-Borrelia burgdorferi antibodies were used: monoclonal anti-OspA (H5332, H3T5, Symbicom, 1:50) and anti-flagellin (G 9724, H605, Symbicom, 1:50), polyclonal B65302R (Biodesign, 1:100) and BB-1017 (1:500) [3] antibodies. The specificity of these mono- and polyclonal antibodies was previously tested by Western blot analysis [3].

For immunostaining, the avidin-biotin-peroxidase technique was used. Following 24, 48 or 72 hours incubation with a primary antibody at 4°C, the sections were incubated with the appropriate secondary antibodies. For the monoclonal antibodies, a biotinylated F(ab) fragment of affinity isolated rabbit anti-mouse immunoglobulin (Dako, E413) was used. The immunoreaction was revealed by diaminobenzidine (DAB) alone, or with nickel-ammonium sulfate as described previously [60]. Frozen sections immunostained in the absence of a primary antibody or with an irrelevant mono- or polyclonal antibody were used as negative controls. Immunostaining was also performed with various anti-Borrelia burgdorferi antibodies using FITC tagged anti-mouse or anti-rabbit secondary antibody depending on the primary antibody used. The green fluorescence of Borrelia burgdorferi spirochetes was analyzed with a Zeiss fluorescent microscope. A monoclonal antibody (Biogenesis 7263-1006 or Chemicon MAB995, dil.1: 200) for the analysis of the presence of bacterial peptidoglycan, a bacterial cell wall component of virtually all Eubacteria, including spirochetes, was also used as previously described in detail [61].

Floating paraffin sections (20 μm thick) of the cerebral cortex of the two patients with general paresis were immunostained with a polyclonal anti-Treponema pallidum antibody (Biodesign, B65210R).
Detection of neuroinflammation

Paraffin sections of the hippocampus, frontal and parietal cortices of the three patients with Lyme neuroborreliosis were also used for the immunohistochemical detection of reactive microglia and astrocytes. Anti-HLA-DR (clone CR3/43, M775, Dako) and anti-CD68 (clone KP1, M814, Dako) monoclonal antibodies were used to visualize microglia and a polyclonal anti-GFAP antibody (Z334, Dako) to detect astrocytes. Paraffin sections of the same cortical areas of a female patient (aged 59 years) without brain lesion were used as controls. In addition, sections of the three patients with Lyme neuroborreliosis were also immunostained with the omission of these primary antibodies.
Atomic force microscopy (AFM) analysis

To 500 μl samples of cultivated Borrelia spirochetes exposed to various harmful conditions 500 μl of 2.5% buffered glutaraldehyde was added. Samples were then stored at 4°C until used for the atomic force microscopy (AFM) analysis. 20–50 μl samples were put on the surface of a Nucleopore® filter of 2 μm hole size and were dried at room temperature in air, as previously described [62]. The filters were fixed on metallic discs or on glass slides using a double face rubber strip, and were imaged with a Bioscope I atomic force microscope (AFM) and a Nanoscope® III atomic force microscope (AFM) equipped with a J-scanner. All the images were taken in the tapping mode at room temperature in air. The scanning rate varied from 0.1 to 5 Hz. Images were obtained in both the constant force mode providing true height, and the amplitude mode, for highlighting sharp contours. The images were processed and the measurements were done using the Nanoscope III image processing software.

The human brains analyzed were from the University Institute of Pathology, Lausanne, Switzerland. The study adhered to the tenets of the Helsinki Declaration. Animal experimentation conformed to the Guide for the Care and Use of Laboratory Animals, formulated by the National Research Council, 1996, and the Swiss law on animal protection.
Results

Figure 1 illustrates the typical morphology and colony-like formation of strains B31 (A-D) and ADB1 (E-H). Panels A and B show the regular coiled morphology and colony-like aggregates of spirochetes (B31 strain) as observed by dark field microscopy analysis. Regularly coiled OspA-immunoreactive spirochetes of the same strain are seen following immunostaining with a monoclonal anti-OspA antibody in panel C. An atomic force microscopy (AFM) image of a regularly coiled fragment of a Borrelia spirochete (strain B31) is visible in panel D. The typical coiled morphology of spirochetes of the ADB1 strain, which were cultivated from the brain of a patient with chronic Lyme neuroborreliosis, is illustrated in panels E and F by dark field microscopy and in panel G by immunohistochemistry using a polyclonal anti-Borrelia burgdorferi antibody (Biodesign, B65302R). The primary anti-Borrelia burgdorferi antibody was revealed with FITC-tagged secondary antibody showing green fluorescence. Panel H illustrates the typical spiral appearance of spirochetes (strain ADB1) by silver impregnation using the Bosma-Steiner microwave technique.

The typical spiral forms of Borrelia spirochetes were converted to atypical and cystic forms when exposed to various unfavorable culture conditions. Atypical and cystic forms were seen at 1 hour exposure. Their numbers increased following 6 hours exposure and was highest at 1 week, where the majority of spirochetes showed atypical morphology. Osmotic shock induced by cold sterile distilled water induced atypical and cyst forms of the majority of spirochetes following 1 and 6 hour exposure. The atypical and cyst forms retained an affinity for silver and were immunoreactive with the various anti-Borrelia burgdorferi antibodies.
http://www.jneuroinflammation.com/content/5/1/40

wonderfullife
08-09-2011, 09:32 PM
Does Borrelia burgdorferi cause an inadequate antibody response by altering B cell activation in the lymph node?
One of the characteristic features of Lyme disease is lymphadenopathy or swollen lymph nodes. It's not too surprising when a lymph node draining a site of infection swells. However when investigators looked at the lymph node draining the inoculation site of Borrelia burgdorferi in mice, they found that the spirochete had somehow altered the course of activation of B cells producing the antibodies that targeted the spirochete.

Before discussing the findings in the paper, a review of how the antibody response evolves in the lymph node is in order. An antibody response to microbial proteins is sparked when antigen from microbes breaching the skin layer flow into the draining lymph node or are carried to the lymph node by dendritic cells. Lymph nodes are where naive B cells, upon recognition of antigen, differentiate into plasma cells, which secrete large amounts of antibody that target the invading microbe. The antibodies which bind most tightly to protein antigens are made with T cell help in germinal centers, which emerge from the rare B cells in the lymph node that produce antibody capable of recognizing the antigen. (I say "rare" here because each B cell in the lymph node produces antibodies with different antigenic specificities to ensure that any microbe that the host may possibly encounter will be recognized by antibodies displayed by at least a few B cells.) Upon binding the antigen and reception of critical signals from T cells, the B cells migrate to areas in the lymph node containing fixed networks of follicular dendritic cells (FDCs), a type of immune cell with long branched processes that extend out from the body of the cell. (FDCs differ from the dendritic cells that bring antigen to the lymph node.) The B cells then start to proliferate wildly, doubling every 6 to 8 hours (faster than B. burgdorferi!). As the B cell numbers surge, they form germinal centers, which can be identified easily by standard histological stains (see image below). The lymph node may even swell, depending on how much the B cells proliferate.
As the B cells multiply in the germinal center, a process called somatic hypermutation, which is promoted by signals received from T cells, causes a large number of mistakes to be made within the segment of DNA encoding the antigen binding portion of the antibody. Consequently, the antibodies displayed by some germinal center B cells are no longer able to bind to the microbial antigen whereas those made by other B cells will bind better. The FDC processes, whose surfaces are loaded with antigen, continuously probe the antibodies expressed by the newly arising B cells. Since the new B cells are programmed to die unless they express antibody able to bind the antigen displayed by the FDCs, only B cells displaying antibody that bind most tightly to the antigen will survive. This process by which B cells expressing the antibodies with the highest affinity for antigen are selected is called affinity maturation. Somatic hypermutation and affinity maturation can only occur in germinal centers. The B cells also undergo class switching, in which the class of antibody expressed by the B cells switches from IgM and IgD, which are expressed by naive B cells, to IgA, IgE, or one of the IgG subclasses. The exact switch that occurs is governed by the cytokines that the B cells are exposed to. Which cytokines are present depends on the nature of the infection. Eventually the B cells expressing high-affinity antibodies of the appropriate class differentiate into antibody-secreting plasma cells, which are released from the lymph node to circulate throughout the body and fight the infection.

So what happens in the lymph nodes during a B. burgdorferi infection? When the investigators inoculated B. burgdorferi into or underneath the skin of mice, the lymph node draining the site swelled considerably, enlarging by more than a factor of 10 by the tenth day of infection.
What the investigators saw when they looked at lymph node sections under the microscope was very different from the textbook description of T-cell dependent B cell activation that I gave above. First of all, live B. burgdorferi was found in the lymph node draining the site of infection in mice. This is unusual since phagocytes would normally greet and destroy any microbe that managed to find its way into the lymph node.
Second, massive proliferation of B cells accounted for lymph node swelling, but the expansion of B cell numbers wasn't occurring in well-defined germinal centers. The authors also noted that T cells were not increasing in number. These observations suggested that T cells, which are required for germinal centers to form, were not fully participating in B-cell activation. The lack of germinal centers suggested that somatic hypermutation and affinity maturation were not occurring.

From their observations, the authors speculated that B. burgdorferi somehow subverted B cell activation in the lymph node so that the end result was a large number of plasma cells secreting antibodies of poor quality. By poor "quality," I assume that the authors meant that the affinity of the antibody for B. burgdorferi proteins was low and that the "wrong" subclasses of IgG antibodies were expressed. The most abundant IgG subclasses being produced in the draining lymph node at its most swollen state were IgG2b and IgG3. Whether other IgG subclasses would be more effective at clearing B. burgdorferi from the host and whether the affinities of the antibodies for B. burgdorferi proteins were poor still need to be determined experimentally. Perhaps a classic T-cell dependent B cell response involving the formation of germinal centers accompanied by somatic hypermutation, affinity maturation, and appropriate class switching would have led to production of "high" quality antibodies. If the authors are correct, they have revealed yet another means by which B. burgdorferi could persist in the host.
http://spirochetesunwound.blogspot.c...eri-cause.html

wonderfullife
08-09-2011, 09:33 PM
The arthritic form of Lyme disease was first reported in the 1970s by Allen Steere, who described the condition in a group of children (and a few adults) residing in and around the town of Lyme, Connecticut. Lyme arthritis can strike when Borrelia burgdorferi introduced into the skin by an Ixodes tick burrows into deeper tissues and ends up in the joints, usually the knee. Swelling results from an inflammatory response to B. burgdorferi residing in the joint. Lyme arthritis is treated with antibiotics, which destroy the bacteria driving inflammation. Unfortunately, arthritic symptoms endure in ~10% of treated patients despite the complete or almost complete eradication of the infection, as determined by negative PCR tests for B. burgdorferi DNA in joint fluid. Such cases are called antibiotic-refractory Lyme arthritis, which can persist for months or sometimes years. In severe cases cartilage and bone erode. Although the pathogenesis of antibiotic-refractory Lyme arthritis could involve persistence of small numbers of B. burgdorferi (or their antigens) in the joints, investigators have been seeking an autoimmune mechanism to explain the prolonged attack on joint tissue by the immune system after the spirochetes have been cleared.

Many autoimmune diseases are linked to variants of HLA (immunity) genes such as those encoding the MHC class II complex. Antibiotic-refractory Lyme arthritis is associated with MHC class II variants that are able to bind to fragments of the B. burgdorferi protein OspA (outer surface protein A) encompassing amino acid residues 165 through 173. Antigen-presenting cells whose MHC class II molecules display OspA165-173 peptides on their surface stimulate T cells that recognize the OspA peptide. How OspA165-173-reactive T cells cause autoimmunity has been an area of intensive research, yet a clear answer has not emerged.

One potential pathway to autoimmunity is molecular mimicry, in which a cross-reactive host protein in the joint continues to stimulate OspA165-173-specific T cells even after the eradication of B. burgdorferi by antibiotics. Although the simplicity of the molecular mimicry model is appealing, exhaustive efforts to find a cross-reactive autoantigen that stimulates OspA165-173-specific T cells have failed. Moreover, levels of OspA165-173-reactive T cells decline soon after initiation of antibiotic therapy despite continuing arthritis following treatment. Thus, chronic arthritis does not seem to involve molecular mimicry driven by a cross reaction between the OspA165-173 epitope and a self-antigen in the joint. It is possible that molecular mimicry involves another B. burgdorferi antigen that is able to bind the MHC class II variants found in genetically susceptible individuals.

Other potential routes to autoimmunity in antibiotic-refractory Lyme arthritis patients emphasize the role of the high levels of key proinflammatory cytokines and chemokines found in their joint fluid, levels even higher than those found in treatment-responsive patients prior to initiation of antibiotic therapy:
In a model known as bystander activation, the immune response to OspA165-173 (or another B. burgdorferi antigen) causes an excessive inflammatory response that activates other T cells that react to autoantigens in the joint.
The immune system is unable to turn off the intense inflammatory response associated with OspA165-173 after the spirochetes are cleared from the joint.

Although much attention has been focused on the role of host genetics, a recent study indicates that the genetics of the pathogen could also influence the course of Lyme arthritis. In the July 2009 issue of Arthritis and Rheumatism, Allen Steere and his collaborators showed that antibiotic-refractory Lyme arthritis is associated with different strains of B. burgdorferi. The strains were typed from joint fluid samples collected before or during antibiotic treatment. Among the methods available to group B. burgdorferi isolates, they used the 16S-23S ribosomal RNA intergenic spacer type (RST), of which there are three. Antibiotic-refractory arthritis was defined as joint swelling lasting for at least 3 months after the start of antibiotic treatment. Antibiotic treatment consisted of 8 weeks of oral antibiotics or up to 4 weeks of antibiotics administered intravenously. Joint fluid from all 17 patients in the study tested positive by PCR for B. burgdorferi DNA prior to or during antibiotic treatment.

The authors found that all 7 Lyme arthritis patients infected with RST1 strains had the antibiotic-refractory form. Joint fluid was obtained after antibiotic treatment from 5 of the 7 patients; all 5 samples tested negative for B. burgdorferi DNA by PCR. In contrast, 2 of 6 and 3 of 4 infected with RST2 and RST3 strains, respectively, were successfully treated with antibiotics (see the table below from the Jones et al. 2009 article). A larger number of samples is needed to demonstrate that the difference observed between RST1 and RST2 strains is statistically significant, but there is a clear trend towards RST1 infections having the greatest association with antibiotic treatment failure and RST3 having the least, with RST2 having an intermediate effect. The duration of arthritis also depended on the infecting RST strain.
How do RST1 strains cause arthritis to persist even after the apparent eradication of the spirochetes by the recommended course of antibiotics? The investigators proposed that RST1 strains provoke a stronger inflammatory response in the joint than RST2 or RST3 strains. Coupled with an immune response to OspA165-173 in genetically susceptible patients, this could cause inflammation to continue at high levels even after elimination of the spirochetes from the joints. RST1 strains may be more likely than the other genotypes to spark intense joint inflammation even in patients who are not genetically prone to antibiotic-refractory arthritis.

In future studies, it would be interesting to see if proinflammatory cytokine levels are related to the RST type that infects the joint. Ultimately, researchers need to identify the B. burgdorferi gene or genes whose variation among the RSTs causes the different treatment outcomes of Lyme arthritis.
http://spirochetesunwound.blogspot.c...me%20arthritis

wonderfullife
08-09-2011, 09:36 PM
Eating Crow with Lyme

At the end of another busy day in the office I leaned back in my chair and propped my weary feet on the corner of my desk, the only flat space not otherwise occupied by charts, forms, and the remnants of lunch. Gary, my office partner, and I were sharing “war stories.” A couple of our patients that day had been particularly challenging. “You know what?” he grinned. “Medicine is a humbling profession!” Oh, how true!

Medicine is humbling in many ways. Not only is the human body infinitely complex and prone to all sorts of pestilence and manifold frailties, it seems like the rules keep changing! Is margarine better for you than butter, or not? For those with diverticulosis, should your diet be free of seeds, nuts, and skins? Or does that extra fiber actually do you good? Should ladies in their menopausal years be on estrogen to prevent osteoporosis ... or ... not? As new information is available, we sometimes have to rethink the old standard recommendations. On more than one occasion I have offered authoritative advice, and later been forced to “eat crow”!
Never has the crow been more difficult to swallow nor had more profound implications for my patients than on the topic of Lyme disease. I used to believe (and most of my fellow family physicians continue to believe) that Lyme disease is hard to get and easy to treat. In fact, I as much as stated this in previous articles I wrote on the subject.1 For years I reassured my patients with tick bites that their chances for contracting Lyme disease were slim. I gave them a list of symptoms to watch for and adopted a “wait and see” approach. For those suffering from Lyme-like symptoms, but with no clear history of tick bite and rash, I rarely did blood work.

But I am now convinced that, at least in my neck of the woods (northeastern Pennsylvania), Lyme is easy to get and hard to treat!

What changed my mind? Personal experience. A family member began to suffer a wide variety of strange symptoms 12 years ago, including facial numbness, slurred speech, problems with balance, abdominal pain, and headache. After a few baseline studies, her physician informed her that she was depressed and offered antidepressants. She told the physician she had read about Lyme disease and requested testing. He refused, stating (as I had to several of my patients) that her lack of history of tick bite and the classic rash disqualified her from any consideration of Lyme disease. But she worked and lived on a farm, had pets in the house, cut her own firewood, and spent much of her day outdoors. Deer (carriers of the primary Lyme disease vector, the blacklegged deer tick) were as plentiful as cows on the farm. The
ingredients were all there ...

She changed doctors and her new physician agreed to order an ELISA antibody screening study for Lyme disease. It was negative, she was reassured, and further workup was deferred. But the symptoms persisted, gradually worsening with time. She developed heart rhythm disturbances, migratory joint and muscle aches, and increasing weakness. The Lyme studies were repeated, this time including the Lyme Western Blot. Again, she failed to meet Centers for Disease Control criteria for Lyme disease. Multiple specialists, including neurologists, rheumatologists, and cardiologists, saw her; no one could figure out what was wrong. I kept thinking, “This seems to fit Lyme disease, but the tests are negative ... Hey, what do I know, these guys are specialists; I’d best keep my mouth shut.” Finally she was seen by a Lyme specialist. He initiated aggressive therapy for what he recognized clinically, and what was shown on repeat testing, to be a raging untreated case of Lyme disease. After years of misery and tens of thousands of dollars in medical costs, she is gradually getting better.

This same scenario has been experienced at the HSLDA headquarters in Northern Virginia. Multiple coworkers are suffering with Lyme disease, but struggling to find adequate treatment in a skeptical and woefully uninformed medical system. The impact on HSLDA cannot be overstated!

How is it that so many competent, caring practitioners are blinded to the truth of this epidemic? The answer is simple, actually. Like me, they followed the rules as established by the powers that be at the Centers for Disease Control, unaware that there was even controversy regarding the diagnosis and treatment of Lyme disease.

In reality, however, a battle rages between the governmental healthcare policymakers in their well-insulated ivory towers and many frontline clinicians, for whom personal experience clashes with the so-called “standard of care.”

The true victims of this war are innocent Americans: hardworking, upright, and honest individuals like my family member and my HSLDA colaborers, suffering mightily with this brutal disease but with precious few viable options for treatment.

In a role outside his usual job as HSLDA chairman, Michael Farris was appointed by the governor of Virginia to head a task force to explore the issue of the Lyme epidemic in Virginia. The goal of the task force is to discover better ways to prevent, diagnose, and treat Lyme. Surrounded by those in the throes of the illness, Mike is a motivated man! As he volunteers his time, energy, and intellect to this monumental project, I hope and pray that his efforts will shine new light into the murky waters of the Lyme controversy. Please join me in those prayers, and if Lyme disease becomes a topic in your state’s legislature, get informed and get involved!
http://www.hslda.org/courtreport/V27N4/V27N408.asp

wonderfullife
08-09-2011, 09:42 PM
Yost testimony - YouTube

wonderfullife
08-09-2011, 09:44 PM
LIVING WITH LYME DISEASE - PART ONE - YouTube

wonderfullife
08-09-2011, 09:45 PM
LIVING WITH LYME DISEASE - PART TWO - YouTube

wonderfullife
08-09-2011, 09:46 PM
LIVING WITH LYME DISEASE - PART THREE - YouTube

wonderfullife
08-09-2011, 09:47 PM
http://www.tv3.ie/videos.php?video=3....65.370&page=1

wonderfullife
08-09-2011, 10:17 PM
What Is Hip Dysplasia?
Learn about this crippling joint disease and holistic approaches to helping your pet live a more comfortable life.
Joan Hustace Walker

Page 1 of 3

Hip dysplasia is a crippling, degenerative joint disease that affects the ball-and-socket joint of an animal's hip. Hip dysplasia is a problem found primarily in dogs, although many practitioners believe that the disease has been underdiagnosed in other species such as cats. The records of the Orthopedic Foundation for Animals (OFA) show that 24.8 percent of Maine coon cats evaluated from 1974 through 1996 were dysplastic.

Among dogs, large- to giant-sized breeds continue to be those most frequently troubled by this disease, with as many as 50 percent of some breeds suffering from hip dysplasia, according to a release from Cornell University. Some breeds with a high rate of hip dysplasia include Bernese mountain dogs, bloodhounds, boxers, rottweilers, and Saint Bernards, but smaller breeds, such as the Welsh corgi and the toy breeds, can develop the disease, too. Hip dysplasia may be underdiagnosed in small-sized dog breeds simply because their minuscule weight and light frames enable them to function without showing symptoms of the disease. The belief is that a lax and disfigured hip may not cause a tiny 10-pound dog, such as a Yorkshire terrier, as much pain as a giant-sized 150-pound dog in which even a mild case of dysplasia can be crippling.

Is My Dog Dysplastic?
Typical symptoms for hip dysplasia include pain, heat, and sometimes swelling in the joint. The dog may be grouchy when touched, wanting to be left alone. The dog may also appear cow-hocked (a condition where the back elbow joints turn in), stand toe-out, and perhaps have some muscle atrophy. (When a dog is in pain, she doesn't want to move the part that hurts, so if a hip is sore, she may not want to use her rear legs. After a few weeks, these muscles become flabby.)

The dog may be uncomfortable after sitting for long (or short) periods of time. Often, a dog with abnormal hips will "puppy sit" (sit on one hip), rather than sit squarely on her haunches (although some adult dogs with normal hips may also "puppy sit"). The dog may have a fever, have trouble moving, or may pace or pant with pain. An indicator that something is wrong may be as subtle as the dog suddenly shying away from you.

Of course, these symptoms can be the same as those displayed for a variety of conditions and/or diseases unrelated to hip dyplasia. For example, if a dog has strained the ligaments and tendons of the hip joint while chasing a squirrel, there may be some pain or heat in the hip region. A dog with hip dysplasia-like symptoms may actually be suffering from arthritis or even Lyme disease. In other words, the symptoms of hip dysplasia are somewhat vague. A clinical diagnosis (made by feeling the hips) is not sufficient to determine whether a dog has hip dysplasia. The only way to definitively determine whether or not a dog is dysplastic is to X-ray the dog's hips.
http://www.dogchannel.com/dog-vet-library/joint/article_1961.aspx

A lot of lyme patients are having huge problems with their joints, hips a lot are having to have hip replacements, knee replacements etc
Lyme or Bb loves magnesium and it lives in our bones depleting our magnesium levels.

wonderfullife
08-09-2011, 10:30 PM
Late disease symptoms occur months to years after onset of infection and is not necessarily preceded by other features of Lyme disease. Symptoms include:

Arthritis

About half of people with Lyme disease will develop arthritis several months after being infected.

The knee is the most commonly affected joint, but other large joints may be involved.

Arthritis often is migratory (first one joint will hurt and get better, then another joint will hurt).

About 10 percent of people with untreated infections will develop chronic arthritis (typically lasting five to eight years) that can cause erosion of cartilage and bone.

http://www.arthritis.org/disease-center.php?disease_id=13&df=effects

wonderfullife
08-09-2011, 11:04 PM
To not treat Lyme disease means....
A 28 year old female came into my office 18 months ago. She complained of acute left hip pain for 3 days and was unable to walk. My previous training told me that it was something called "toxic synovitis," an acute joint inflammation or a hip joint, possibly do to a virus or a rheumatological disorder. She was in severe pain, I prescribed a Medrol dose pack and Vicodin. Her initial labs showed a sed rate of 32 a CRP of 160- which is off the charts, a Lyme C6 peptide index of 0.3, vitamin D reversal, a Lyme WB 41 band on the 13 band test. She took antibiotics for 2 months for presumptive Lyme disease and got better. She stopped the antibiotics and relapsed 4 months later. This time her hip and knee hurt. She had mild neurological signs of peripheral neuropathy.

"Standard" labs were negative for Lyme. Her sed rate was 47 and her CRP 30.
After one week of resuming antibiotics she was better. Her course was complicated by a yeast infection. Her antibiotics were adjusted. After 4 months, a more careful history elicited- some tingling in the hands, some fatigue and some subtle cognitive issues.

At 7 months her CRP was normal at 1.2 and she felt entirely normal; all the symptoms had resolved. New labs showed that her vitamin D dihydroxy 1,25 had climbed to 98. The vitamin D hydroxy 25 was 12. I was a little nervous about the vitamin D and prescribed 2 months of Benicar. The levels quickly corrected 28 and 20 respectively.

After 3 negative Labcorp WB for Lyme, the last two showing no bands, a Lyme WB was sent to IgeneX. This time she was CDC positive and IgeneX positive by IgM criteria. She had positive bands 23,31,34,41 and 58.

We both felt confident that the diagnosis of Lyme disease had been correct all along.
She has been maintained on low doses of maintenance antibiotics and is symptom free.

To not treat Lyme disease means: To not consider Lyme in the differential diagnosis, to omit neurological examinations of my patients, to not order the labs I am familiar with- stop practicing medicine as I know it- just go through the motions to make a living, and still smile? Not worth it. If that what it comes down to I will leave medicine and find something else to do.

More importantly: God knows what would have happened to the patient?
Posted by Lyme report: Montgomery County, MD at 2:12 PM
http://lymemd.blogspot.com/2009/02/why-i-cant-stop-treating-lyme-disease.html

wonderfullife
08-09-2011, 11:19 PM
Eva Sapi's recent research calls into question everything we thought we knew about Lyme "cysts." In fact it destroys the old thinking.

We have heard about cell wall antibiotics, intracellular antibiotics and cyst-busters. Think again.

She investigated the effect of various antibiotics on Lyme spirochetes and round body forms - also know as cystic forms.

Doxycycline worked according to plan. Doxy inhibits protein synthesis - it kills bacteria, including Lyme, by action within the cytoplasm, inhibiting the manufacture of proteins required for the bacteria's survival. Doxy and others are commonly referred to as intracellular antibiotics.

Spirochete loads decreased by about 90% while cyst levels increased by 200% - just as expected.

Then amoxicillin data was presented. Amoxicillin inhibits the formation of bacterial cell walls. Amox and similar drugs should then only be effective in killing spirochetes with an intact cell wall. This is where the results start deviating from the plotted course.

Amoxicillin killed 90% of spirochete forms - OK, but -- it also killed 68% of the cystic forms! Amoxicillin and other cell wall drugs are not cyst busters - only specific anti-parasite drugs kill cysts - or so we thought.

Well lets think again for a second: what are cysts? Are they balled up forms of spirochetes with a different kind of membrane - or blebs (also described) expressed through the spirochete membrane? Maybe the former retain much of the cell wall from the original spirochete - maybe that is why amoxicillin works here.

This would seem to clear up a nagging question raised by others. Are cysts and L-forms really the same thing? These results show that cysts cannot represent a version of L-forms or spheroplasts which result when gram negatives shed their cell walls. If this were the case a cell wall drug would be ineffective. Cysts and L-forms are distinct and different forms. (There may be a hole in this reasoning. I will explain later).

OK So we have learned something new: cell wall antibiotics can also kill some cyst forms which are not L-forms.

Let's look at some more data. Tigecyline is a not a cyst drug either. Wrong. Tigecycline kills 90% of spirochetes, good so far, but it also kills 90% of cysts! Tigecycline is an intracellular antibiotic similar to doxycycline! Another fly in the ointment.

OK. Cysts with their lower metabolic rate, still need ribosomal proteins to survive, just not at the levels of intact spirochetes. Tigecyline is a more powerful drug, higher levels are delivered into the cytoplasm of the cysts. This makes sense. Cyst forms are still essentially a pleomorphic version of Lyme bacteria with somewhat different features. In this scenario, cysts could be L-forms. But we have already shown that this is not true because amoxicillin can kill them. Right?

Amoxil is a cell wall drug. I thought so. Kersten, (antimicrobial agents and chemotherapy, May 1995, p. 1127-1133) states that Beta-lactam antibiotics, which include amox, penicillin and Rocephin, have been shown to cause a specific loss of total intracellular RNA in the absence of cell wall hydrolysis. In other words, amoxil could possibly work in part as an intracellular agent. If this is right cyst forms of Lyme could still be L-forms. So perhaps we have not shown that L-forms and cyst forms are different after all.

The question remains unanswered.

Let's get to the Cyst-busters. It takes antiparasitic drugs, so we thought, to kill the cysts. Cyst-busters, anti-parasite drugs, kill parasites (and Lyme cysts) not bacteria. The so called cyst-busters were heretofore used in combination or cycled with other antibiotics. Previous thinking was that typical antibiotics would kill spirochetes and/or L-forms and that cyst busters would disrupt only the cystic forms.

Cyst-busters do not kill intact spirochetes - so we are told. Very wrong this time.

I cannot cover the whole Sapi study. The most exciting finding is that Tindamax (tinidazole) - our premier Cyst-buster, is the most effective drug overall. This "cyst-buster" kills 90% of cysts and spirochetes: by far the best drug. We don't know it's effect on L-forms, but we can guess. Tindamax probably works by an intracellular mechanism. If this is true it should be equally effective against L-forms.

It gets even better. Tindamax is the only drug which does a great job on biofilm colonies as well!
(not to be discussed now). More on biofilms later.

Tindamax passes the blood brain barrier and penetrates well into most tissues. It has been effective in my patients with neurocognitive deficits - neuroborreliosis.

Recently I tried it on another sort of patient. This patient has had intractable Lyme arthritis of his knees. This young athlete had been extensively treated with IV Rocephin followed by a year of typical oral antibiotics. Knee effusions have persisted - until I prescribed Tindamax. Now, after two months, the fluid in his knees has evaporated. His knees are dry and painless for the first time in over one year.

This raises the question: should Tindamax be used as mono-therapy? Well, I cannot endorse blanket use at this time. Tindamax has a black box warning. It has been associated with cancer in some laboratory animals. Perhaps there are more compelling reasons to use Tindamax, but this will have to wait for another post.

My nagging question:

Why does penicillin kill Lyme? It shouldn't. Lyme is a gram negative bacteria. While certain Beta-lactam antibiotics can kill gram negative bacteria, penicillin cannot. Penicillin is only active against gram positive bacteria.

Maybe this other mechanism alluded to above, the alternative intracellular RNA mechanism is significant and explains why penicillin kills Lyme spirochetes. Maybe not.

We need to continually reevaluate things which we have assumed to be true, because many of them are not.
Posted by Lyme report: Montgomery County, MD at 6:31 PM
http://lymemd.blogspot.com/2011/07/everything-you-thought-you-knew-about.html

wonderfullife
08-09-2011, 11:41 PM
Introduction

Many people in the United Kingdom with M.E. who are now being tested privately are finding they are infected with bacteria from the Borrelia Burgdorferi species that cause Borreliosis or Lyme disease. It wouldn't be surprising if a very significant percentage of those currently with a diagnosis of M.E. are actually infected with Borrelia or similar bacteria. An e-mail group poll showed that 80% of those with a diagnosis of Borreliosis or Lyme disease had a previous diagnosis of M.E.
Borreloisis & Lyme Disease

Borrelia is the name of a group of bacteria, of which there are many species, over 300 I believe, some of which are pathogenic. Borreliosis is the name of the disease caused by infection with these bacteria. Lyme disease has a narrower definition and can only be caused by 3 strains of Borrelia so it can exclude many people with long term illness caused by the bacteria. The terminology used to define infections caused by Borrelia are not clearly defined. Lyme disease and Borreliosis are often wrongly used interchangeably in the literature and sometimes the terms Lyme Borreliosis and Neuroborreliosis are used. Although the term Borreliosis would be far more appropriate, it is seldom used in the UK which is why I often refer to the term Borreliosis/Lyme.

Lyme disease was first recognised in the USA in 1975, when an outbreak occurred in Lyme, Connecticut, USA. The Borrelia bacteria were only discovered in 1982 which is one of the reasons why many people, including doctors, don’t know much about it.

Some people who have Borreliosis/Lyme have co-infections with other tick-borne pathogens such as babesia, erlichia or bartonella, and these cause illness too. Babesia are malarial-like protozoa which infect red blood cells, while the others are bacteria.

More about Borrelia

Borrelia bacteria are very large spirochaetes with a long thin spiral type shape and are similar to those causing syphilis. They can exist in several different forms including a dormant cyst, a motile spirochete and intracellular cell wall deficient forms. The spirochaete is able to change to a different form when a threat occurs (e.g. from the immune system or antibiotics) making it very difficult to eradicate. Borrelia can rapidly invade every type of tissue and every system in the body causing havoc in the host. Many symptoms are caused by Borrelia as it causes the immune system to produce cytokines (chemical messengers that help to regulate the immune response) and it produces many biotoxins, mainly neurotoxins, which are attracted to many areas of the body such as the central nervous system, peripheral nerves, muscles, joints, lungs, etc.

A main source of Borrelia infection is by a tick bite from an infected tick. Just one bite is all you need from an infected tick - this is only the size of a pinhead and may go unnoticed by the victim. If you read the literature on Lyme disease, it often refers to the American Deer Tick as being the source of infection, but in the UK the main vector is the Sheep Tick. Its small creatures like mice and birds which are natural reservoirs for the infections in the UK and it is they who provide the first meal for the newly hatched baby ticks. However, any animal could have ticks which carry Borrelia, including pets. Migrating birds can carry all sorts of bugs and infected ticks from other countries such as Africa.

It is not just ticks that can transmit the infection. Any biting insect such as mosquitoes and fleas are now believed to be able to carry and transmit Borrelia too. It is possible that Borrelia bacteria can sometimes be transmitted from mother to baby via the placenta, in breast milk, between sexual partners, and also by blood transfusions, though this is not yet widely accepted and more evidence is required. Borrelia has been isolated in human body fluids such as semen, tears and urine, unpasteurized cow’s milk and even found in African dust.

There are 3 strains of Borrelia defined as causing Lyme disease, but there are also other strains which are pathogenic. In the USA it is Borrelia burgdorferi sensu stricto which causes Lyme disease, while in the UK and Europe it is B. burgdorferi ss, B. garinii or B. afzelii. B garinii is thought to cause more neurological symptoms than B. burgdorferi ss and B. afzelii is thought to cause more coetaneous symptoms.

Ticks in the UK are infected with Borrelia

Many UK doctors don't know that you can get infected with Borrelia from ticks in the UK. The Natural History Museum tested many of its UK specimen ticks (PCR testing) and found between 8 and 97% were infected depending on the species of the tick. Some of the specimens were 100 years old. Another study from Swansea showed 30% of ticks in woods in South Wales were infected with Borrelia and 7% with a co-infection erlichosis. It can only take one tiny tick bite from an infected tick for a human to become infected – a bite that goes totally unnoticed more often than not.

Symptoms

Some people get a bull’s eye rash after a tick bite, which is a classic symptom of Lyme disease, but not everyone does. The symptoms of Borreliosis/Lyme can be the same as M.E., e.g. painful joints and muscles, ‘brainfog’, memory problems, headaches, Flu-like, neurological symptoms, stiff neck, numbness, tingling, extreme fatigue, sleep problems, neurally mediated hypotension, noise or light sensitivity and many more. Like M.E., there is a vast array of symptoms, but not everyone gets all of them. Borreliosis/Lyme can also mimic other diseases such as Fibromyalgia Syndrome, Multiple Sclerosis, Lupus and Motor Neurone Disease.

Some people get symptoms of Borreliosis/Lyme within a few days or weeks of a tick bite, but for some it is much longer, even years. The symptoms can be cyclical and they are often worse in women around the time of menstruation. As with M.E. some of the symptoms may vary from one day to the next in an unpredictable fashion. Some people get the illness more mildly or more severely than others. If it is left untreated some people may go on to develop long term or life-long severe debilitating illness. Some people can go into remission after a period of time, only for the disease to recur at a later stage – this is because the bacteria can change into a dormant cyst form and then change back again into the spirochaete form when the time is right, for example when the person is stressed or immunosuppressed.

The literature about Lyme disease often refers to early stage disease and late stage disease (often called late Lyme). The early stage symptoms may have fewer symptoms such as Flu-like, malaise, headaches, joint and muscle pain and/or fatigue and with or without a bull’s eye rash. This rash is called localized erythema migrans and may occur a few days before the other symptoms. Its not very clear cut though and some people may get many more symptoms early on including neurological ones. The spirochaete has been shown to enter the central nervous system within 12 hours of entering the blood stream. If the illness is left untreated it can progress and become a chronic multisystem disease within a few weeks or months. Some people, however, may just develop the symptoms of this late stage without having or recognising an early stage. For example, some may only have mild early stage symptoms and just think it’s a cold or a bout of Flu, without realising what it really is. All too often the early stage, which is so much easier to treat, goes unrecognised and untreated, as some people do not get a rash or do not notice the tick bite. In fact even if a tick bite is reported to a doctor in the UK, the doctor may well not realise its importance. Some people may go into remission after the early stage, even if it is left untreated, and maybe just forget about it. The illness, however, can recur in its chronic late form weeks, months or maybe even years later. It’s the late stage of the disease that all too often goes undiagnosed in the UK as standard NHS tests are usually negative by this time and it’s often the symptoms of this chronic stage that can be misdiagnosed as M.E.

Its quite possible that those who are chronically infected with Borreliosis/Lyme also have collateral conditions which may give additional symptoms.


• Evidence has shown that the hypothalamic-pituitary link is malfunctioning causing pituitary suppression. Pituitary and endocrine abnormalities could be quite common.

• It is possible that the cellular hormone receptors may be blocked. For example thyroid receptors could be blocked resulting in symptoms of subclinical hypothyroidism. This implies that blood testing may not pick up the hypothyroidism as there will be more thyroid hormone in the blood and less in the cells due to the receptor blockade.

• Magnesium deficiency is also often present which can give rise to several symptoms.

• Deficiency in vitamin B12 could also be present.

Diagnosis & Testing

In the early 1990s the United States Center for Disease Control and Prevention (CDC) set up a definition of Borreliosis/Lyme for an epidemiological study into this disease.

These narrow rigid criteria have been followed throughout the world ever since. More recently the CDC revised these guidelines, which now clearly state that these criteria are NOT intended for diagnostic purposes and that patients must be primarily diagnosed by clinical symptoms. Despite this, the new advice seems to have gone unheeded resulting in many cases going undiagnosed, especially late/chronic ones.

The original outdated guidelines are still rigidly adhered to in the UK. Most UK doctors, including Infectious Diseases specialists, are UNAWARE that:-

• The illness can be spread by factors other than ticks. This is not indicated in the new guidelines as it is not widely accepted yet.

• Ticks in the UK can carry and transmit Borrelia.

• Different strains of Borrelia which are defined as causing Lyme disease can give different disease expressions. One of the common strains in the UK, B. garinii, tends to cause more neurological symptoms, while another common strain found in the UK, B. afzelii, tends to cause more coetaneous symptoms, when compared with B. burgdorferi ss which tends to cause more arthritic symptoms. Although this is mentioned briefly in the CDC guidelines, much of the literature about Lyme disease refers to symptoms caused by B. burgdorferi ss which is commonly found in the USA.

• There are more strains of Borrelia that can cause illness than those defined to cause Lyme disease.

• The illness should be diagnosed by clinical evidence rather than by tests alone since these are not reliable enough.

• If a bull’s eye rash occurs, treatment should start immediately without testing, as tests may be negative in the very early stages.

• An active infection can exist when there is a negative serology test.

• There can still be an active infection when symptoms persist or recur after antibiotic treatment.


Most NHS doctors do not understand the pathophysiology of Borreliosis/Lyme and seem unaware of its extremely diverse symptoms. The illness is fairly new in the medical world and so is poorly described in medical textbooks.

In some Eastern European countries where it is endemic, they diagnose borreliosis/Lyme by symptoms but in the UK doctors won't normally do that, in fact most wouldn't even know what to look for. NHS doctors in the UK rely on highly unreliable two-tier antibody tests to diagnose Borreliosis/Lyme. First they do the Elisa test and if that is negative the patient is deemed not to be infected – end of story. If the patient is fortunate enough to get a positive Elisa test a Western Blot test is then carried out – this is just as unreliable as the first test and excludes even more infected patients! Some people may be positive for the Western Blot but not the Elisa, but they would never be tested. Apparently the UK Western Blot tests don’t test for every strain of Borrelia, even all those pathogenic strains found in the UK let alone those contracted overseas, but many doctors, even Infectious Diseases specialists, don't realise this. The UK tests may pick up some cases but would miss many many more – maybe more than 90% are missed. There are many people who have been found negative with NHS tests and positive by other private testing.

The above indicates that there could be many misdiagnosed cases of Borreliosis/Lyme in the UK, especially chronic ones. All too often people with chronic active infection are fobbed off as having post-Lyme disease or M.E.

Antibody tests for Borreliosis/Lyme are highly unreliable for a number of reasons some of the main ones being:-

• Borrelia infections cause malfunctioning of the immune system. Co-infections only add to this.

• The infection can go into cyst form which reduces the immune response.

• The infection can go into intracellular cell wall deficient form which cannot be detected by antibodies as there is no cell wall.

• The antibodies are in immune complexes, and so cannot be detected by the test.

• The spirochetes can be encapsulated in host tissue (lymphocytic cell walls) and thus hide from the immune system. I’ve seen them described as wolves in sheep’s clothing.

• The spirochetes are deep in the host tissue, especially tissue with a very poor blood supply.

• Recent infection - before the immune response has taken hold.

• The disease is in the late stage. Those who are chronically infected very often have negative antibody tests.

• Recent treatment with various drugs including antibiotics and anti-inflammatories.

• Factors which cause immunosuppression.

• Lab techniques.

• The lab does not test for the strain. The UK Western Blot does not test for every pathological strain, even all those found in the UK let alone those found abroad.


The only decent tests you can do at the moment are private. These are costly and include:-

• The Bowen Research & Training Institute Inc. test in the USA. This is an antigen test, i.e. they actually look for the Borrelia rather than antibodies to it and they also test for co-infections at no extra cost.

• IGeneX, Inc. tests in the USA. IgeneX do a Western Blot test that may sometimes give a false negative as it looks for antibodies but it is far better than the UK Western Blot and may sometimes help convince doctors that you have Borreliosis/Lyme, though not all will believe it. They also do PCR tests.

• There is also private blood microscopy to test for Borrelia-type bacteria done in the UK. I think there is a considerable waiting list for this.

• Someone in the UK is trying to set up PCR tests (looking for DNA fragments of Borrelia) and cultures - these will be a while yet - private again I'm afraid. It is very very difficult to culture Borrelia, which is why it isn't detected by NHS bacterial culture tests.

• There is also the Acarus vet's lab in the UK which can test humans for babesia, a co-infection, as some pets are diagnosed with this.


Testing is important so you know what infections you’ve got, so you can at least begin to get doctors to believe you have a treatable disease. However, if tests are negative the illness should not be ruled out if you have the symptoms. The CDC state that “there is no reliable test for Lyme disease at this time”.

Information on Borreliosis/Lyme

Details of tests and information on Borreliosis/Lyme can be found on the links/files on the EuroLyme and the Infections groups for patients and professionals.
Other useful sources of information on Borreliosis/Lyme are Lyme Disease Network which is actually recommended to UK doctors, and International Lyme And Associated Dieases Society for health professionals.

Treatments

Details of possible treatments are all in the files of Eurolyme. “Diagnostic Hints and Treatment Guidelines for Lyme and Other Tick Borne Illnesses” by Dr J Burrascano is a good starting point. There are various antibiotic treatments for Borreliosis/Lyme, what suits one may not suit another. The illness is much easier to treat in the early stages, the longer a person has had the illness the harder it is to treat. It may not be completely curable in long term chronic cases, but there are a growing number of people much much improved after treatment with long courses of antibiotics. Some people are lucky and can get their GPs to prescribe the antibiotics, but many have problems and have to pay privately. All too often, especially when prescribed by NHS doctors including infectious disease specialists, the antibiotics are given for too short a time or too low a dose to eradicate the bacteria fully. Some people who have babesiosis as a co-infection (similar to malaria) need an expensive antimalarial drug costing approximately £700 a month for several months and the NHS are refusing treatment on the grounds of cost. A consultant was willing to prescribe drugs privately to one person with Lyme disease, but not on the NHS.

At the moment there are a few of us on Samento (TAO free cats claw), an immune modulating herb, including myself. Apparently some of us are doing well on Samento, and some are not, but its early days yet. Some people need to take the herb for quite a long time before symptoms start to improve. More information on Samento can be found on www.samento.com.ec (also has some information on Borreliosis/Lyme) or www.samento-faq.eu.kz.

The Marshall Protocol is fairly new, so it’s early days yet, but it has potential. For this protocol benicar, known as Olmesartan or Olmetec in the UK, is given in high doses to suppress inflammation which allows antibiotics to work better and be given in lower doses. Some people with M.E. are being helped by this and again some are not. There was an article on ImmuneSupport.com not so long ago. Some are getting benicar on the NHS some are not, it depends on the doctor. “Lyme disease (Borreliosis). A Plague of Ignorance Regarding the Ignorance of a Plague” by Scott Taylor which can be found in the Eurolyme files also covers this protocol.
http://www.mesupport.co.uk/index.php?page=borreliosis-lyme-m-e

wonderfullife
08-09-2011, 11:53 PM
http://www.whatdotheyknow.com/request/babesia_statistics_for_the_uk_2

302bluefog
09-09-2011, 12:24 AM
Hey, I forgot where the other thread went. Can you please post the name of the exact blood test and/or all the test I need to have done? Thank you.

wonderfullife
09-09-2011, 12:38 AM
Hey, I forgot where the other thread went. Can you please post the name of the exact blood test and/or all the test I need to have done? Thank you.

The other thread is here :http://forum.davidicke.com/showthread.php?t=170626

The test is the Elisa test not sure if any good. Then the western Blot You may find that a lot of people have a number of tests before they get a positive. As the Lyme works in a six week cycle.

This guy seems to be a Lyme Literate Doc in the USA :http://www.blogger.com/profile/11035327980787631502

Or maybe he can point you in the right direction if you are in the USA.

Uk Breakspears is a good place to go to be tested privatly.

Good website for anyone in the UK http://www.bada-uk.org/

It seems a lot of people are actually going to vets to get tested and there is one place in UK that does animals as well as humans.
Our animal friends get treated better than us humans.

wonderfullife
09-09-2011, 12:40 AM
Hey, I forgot where the other thread went. Can you please post the name of the exact blood test and/or all the test I need to have done? Thank you.

Bluefog,
How are you doing?
I had some oxygen yesterday no depth and I will say it really helped.
Peace
WL:)

wonderfullife
09-09-2011, 12:59 AM
Some say don't waste your money with the ELISA test
This eems better:http://www.lymedisease.org/lyme101/lyme_disease/lyme_diagnosis.html

or here :LABS with good Lyme Tests
IGeneX www.igenex.com 800-832-3200
Stony Brook www.path.sunysb.edu/labs/ticklab/ticklab…
631-444-3824
MDL www.mdlab.com 877-269-0090

302bluefog
09-09-2011, 03:14 AM
Some say don't waste your money with the ELISA test
This eems better:http://www.lymedisease.org/lyme101/lyme_disease/lyme_diagnosis.html

or here :LABS with good Lyme Tests
IGeneX www.igenex.com 800-832-3200
Stony Brook www.path.sunysb.edu/labs/ticklab/ticklab…
631-444-3824
MDL www.mdlab.com 877-269-0090

Ok, Thank you...Im about to read this..

http://arthritis.webmd.com/lyme-disease-test

^I found this when I googled "ELISA test"

.

razorbill
09-09-2011, 10:47 AM
Thanks for all the info, WFL!

I lost one close and one distant family member to ALS, what a horrible disease!
I was unaware of the lyme connection until now, but will pay more attention to it from now on.


The article about root canal treatments is absolutely spot on, but very few people know about this.

The book The Cure for All Diseases by Hulda Regehr Clark doesn't just point out the problem but also offers solutions (detox, diet, zapping) - applicable to lyme disease as well as any other parasite related condition.



The mouth is a reservoir of bacterial infections that become entrenched within the structure of teeth and trigger the high number of chronic degenerative diseases now epidemic in America, including Lyme.

Lyme has the ability to embed itself in tooth structure, where it goes undetected and remains unreachable by antibiotics. Each tooth has some three miles of tubules that emanate from the main canal. Bacteria hide out in all that footage. Lyme is a spirochete similar to spirochetes that cause syphilis. Spirochetes by nature burrow into tissue, such as teeth, bones, and soft tissue like the brain. These areas are the toughest to get to, impenetrable by drugs and herbs.

Many dentists do not realize that antibiotics cannot reach bacteria in dead teeth. In the case of endodontic therapy, or root canal, the dead tooth lacks a blood supply to its interior. Antibiotics circulating in the bloodstream have no way penetrate this dead tissue and hence have no effect on the bacteria.

Herbs are a little more effective, because they tend to make the body healthier by raising the immune function. But they can't knock out bacteria.

Energetic Approach Proves Most Effective in Lyme
Andrew Landerman, DDS, of Sebastopol, California, has mastered the use of energetics to get at Lyme. According to Landerman, one must focus on the oral cavity when dealing with Lyme because the oral cavity, in part or whole, blocks the immune functions, especially when incompatible dental materials are used. He has found this is the genesis of much degenerative disease, and it is often overlooked by both physicians and dentists today.

"Energy can pass through hard or soft tissue with no interference, much the same way as sound travels better through more dense structure than it does through air," Landerman says. "The sound of a blue whale can be heard by other whales in the water several hundred miles away. I first started to understand the relationship between Lyme and the oral cavity when I checked all the teeth in the mouth associated to symptoms in the body. As I went through this process, it became obvious that in Lyme, there are certain teeth more prone to show degenerative conditions than other teeth. I began to see a pattern develop. The first molars, top and bottom, are particularly affected. In time, I saw that the pattern also included the two front teeth, top and bottom."

He learned to use percussion, a method of tapping the tooth to send it a tiny shock to see how it responds. All teeth and their extraction sites relate to the different organs through the Chinese medical system of meridians, and they are all connected energetically. "As you go around the mouth," he says, "you see a pattern of low or high voltage in some teeth. No amount of herbs or remedies would get these underperforming or overperforming teeth to change their readings for the better. "

Landerman studied years ago in Germany, where he saw dentists extract affected teeth, and patients improved. But it bothered him that the pulp of the extracted teeth appeared normal. He wondered if those teeth had really needed to come out.

Metal is used in fillings and often under crowns. Metal interferes with the body's energetic network and suppresses or negatively excites the immune system. It doesn't matter if it's gold or nickel - all metal is problematic. "Nickel is probably the worst because it is carcinogenic; it knocks out the immune system," Landerman states. Mercury is about the most active of metals. The higher the temperature, the more it is released, poisoning the system.

One must remove the intrusive dental materials in order to correct the energetic flow of the related organ meridian, to restore proper function of the organ. Without this, degenerative diseases such as Lyme can take root. "It makes sense; you want to go back and correct the cause of the block," says Landerman. "The oral cavity is the seat of most of the energetic blocks in the system."

Landerman understands that teeth respire. "Normally, in a healthy tooth, fluid will go from the inside of the tooth to the outside," he explains. "That is their gatekeeper mechanism, their way to keep bad bacteria out of the tooth. But if a tooth is compromised, the fluid goes the other way - outside in. That is how infections enter the oral cavity, breed virulent pathogens, and can create havoc throughout the body for decades."

He figured he could use respiration to his advantage. "It took me probably 15 to 18 years to come up with homeopathic remedies that would change these teeth back to normal readings," he says. "Then we could save the teeth. If I could cause the homeopathic solution to go into the tooth, the tooth would be partially or wholly healed. Experience has proven the truth of this."

Landerman's patients are fitted with a tray and a custom-made homeopathic remedy. They bathe the affected teeth for an hour a day for as long as prescribed. The remedy transmits the homeopathic solution to the tooth and the tooth responds. If it can, the tooth returns to normal. Homeopathy is able to move fluids into the tooth.

"We need to knock down the Lyme hiding in the miles of tubules and in the bony socket," Landerman says. "I have my patients do this procedure at least once a year. And you do not have to have a Herxheimer reaction to get better. In homeopathy, if you hit the nail on the head, you won't have a Herx."
Focal Infection - Starts in the Mouth and Migrates

Where Lyme and other chronic diseases are concerned, the big enemy is root canals. American dentistry has been slow to recognize the negative impact of this procedure. Elsewhere in medicine, when a part of the body dies, say, a foot turns gangrenous, it is cut off. But in a root canal, dead teeth are left in, filled with a sealant where the nerve was drilled out. These teeth always cause energetic blocks.

George Meinig, DDS, FACD, author of Root Canal Cover Up, questions how standard dentistry can claim that infections seated in the mouth do not affect the body. "Patients who have heart conditions, knee or hip replacements, are told by their physician or dentist that for the remainder of their lives, they must have an antibiotic prescription before and after any dental treatment, including cleaning of their teeth," he wrote. "The reason antibiotics are needed is because it has been proven bacteria that live in the mouth can easily enter the bloodstream and travel to the heart and joints where they frequently cause endocarditis and many other infections."

This is called the focal infection theory. Meinig and Landerman believe that this valuable information was buried years ago by a minority group of autocratic dentists within the American Dental Association (ADA) who just couldn't grasp the concept.

The infectious mechanism was initially documented by Dr. Weston A. Price, chairman of the Research Section of the American Dental Association from 1914 to 1923. Price would extract a tooth that had undergone a root canal and implant it under the skin of a laboratory rabbit. He documented that in almost every case the animal would develop the same disease that the patient did. Price found he could embed small pieces of the root instead of the entire tooth, or pulverize the teeth and inject the powder, and cause the same results. Eventually, he found that he could culture the bacteria from a root-filled tooth and inject the toxins from it into the laboratory animal and reproduce the disease from the toxins alone. Price also found that bacteria present in the roots of the teeth and cementum were also present in the first few millimeters of adjacent bone in the jaw. The sterilization process involved in root canals simply does not work.

History tells us that the ADA wanted to promote root canal therapy as a new service and never moved forward with Price's report. Penicillin was discovered in 1928, the study of viruses soon followed, and antibiotics took center stage. However, the Germans made a big study of focal infections.
http://findarticles.com/p/articles/m.../ai_n32149711/

motleyhoo
10-09-2011, 08:17 AM
What a "coincidence" that Lyme disease first appeared near Plum Island precisely after they began experimenting with ticks by injecting them with viruses and bacteria to see how easily they could transmit them to their hosts. Lyme is man-made and that's why it's covered up.

.

biba
10-09-2011, 12:28 PM
Here is a UK Lyme petition

http://www.ipetitions.com/petition/uklymepetition/

Hi 'wonderfullife'. :)

I've only been able to 'skim' read this great thread, as I'm pushed for time today.
I live in an area that has deer, so, a Lyme disease area. But there isn't too much attention paid to it's dangers - I guess that might put the tourists off.:rolleyes:
Anyway, to my point, I signed the petition and here's part of the email they sent me....

------- FORWARD THIS TO YOUR FRIENDS -------
Hi,

I wanted to draw your attention to this important petition that I recently signed:

"UK Lyme Petition"
http://www.ipetitions.com/petition/uklymepetition/?utm_medium=email&utm_source=system&utm_campaign=Send%2Bto%2BFriend

I really think this is an important cause, and I'd like to encourage you to add your signature, too. It's free and takes just a few seconds of your time.

Thanks!
------------------------------

..... I've been cross posting this on Forums and Facebook, so hopefully, more people will become aware of Lyme Disease.

octopus
10-09-2011, 12:40 PM
What a "coincidence" that Lyme disease first appeared near Plum Island precisely after they began experimenting with ticks by injecting them with viruses and bacteria to see how easily they could transmit them to their hosts. Lyme is man-made and that's why it's covered up.

.

Interesting article here about the CIA's six-legged soldiers:

http://pakistancyberforce.blogspot.com/2011/08/cias-six-legged-soldiers-spread-dengue.html

wonderfullife
10-09-2011, 08:35 PM
Allow me a tiny I Told You So. In February, I wrote a story for SELF Magazine about the rising incidence of diseases other than Lyme that are caused by tick bites. (And told you about it here, of course.) The story highlighted one particular tick-borne parasite, Babesia, and a serious problem with the infection it causes, babesiosis: that it was moving into the blood supply. We dug through FDA transcripts and CDC field reports in order to reveal that federal health authorities were very concerned about this prospect, and that more than 100 babesiosis infections caused by transfusions had already occurred — not just in the few states where the tick species carrying Babesia are found, but throughout the United States because blood products are shipped nationwide.

Ours was the first reporting we could find about babesiosis in the blood supply, and it didn’t get the attention it should have, probably because women’s magazines tend to be dismissed as not-serious — even though SELF’s health and medical reporting has won prizes and been turned into books. But based on research released this morning, our story at SELF wasn’t hyping the problem. If anything, we understated it.

OK, enough infomercial. Here’s the news: In a paper released ahead-of-print by the Annals of Internal Medicine, researchers from the Centers for Disease Control and Prevention, Rhode Island and New York State report that 159 cases of babesiosis were caused by transfusions in the past 30 years and “the risk may be increasing.” Twenty-seven of the patients died.

Here are the details of their analysis. Between 1979 and 2009:

•There were 159 known cases of babesiosis caused by transfusions (and 3 more caused by a related organism, for 162 total)
•Infected donors were tracked down for 136 of those cases
•30 of the cases were caused by 12 donors, because donated blood is split into multiple products
•All but 4 of the cases were linked to receiving red blood cells (the remaining 4 involved platelets)
•77 percent of the cases occurred in the last 10 years, suggesting the risk is increasing
•Cases occurred in all 4 seasons of the year, though tick bites are seasonal
•Cases occurred in 19 states, but 87 percent of them were in the 7 states where Babesia is considered to be endemic — which the authors say may represent higher risk, or perhaps just greater awareness.
To the right, you can see a breakdown of 141 of the cases they analyzed, broken down by year of diagnosis and also by state where the case was discovered. (They are looking at 141, not 162, because they did not analyze multiple cases from the same donor.) You can see that the trend line is rising — and also where transfusion cases were found outside of the seven endemic states in the Northeast and upper Midwest.

The researchers say:

The 162 transfusion-associated cases we enumerated undoubtedly represent a fraction of those that occurred. The extent to which cases were not detected, investigated, or reported (to the CDC, to other public health authorities, or in publications) is unknown, both in general and with respect to periods, regions, and various case characteristics and outcomes. As underscored by the incidental diagnosis of Babesia infection, even severe cases in babesiosis-endemic regions can be missed or misdiagnosed, not just cases that are asymptomatic or mild or that occur in other U.S. regions. Even if a case is diagnosed, a transfusion investigation might not be considered, conducted, completed, or conclusive… Our findings underscore the year-round vulnerability of the U.S. blood supply—especially, but not only, in and near babesiosis-endemic areas.

Why is this happening?

Some details first about the organism: Babesia microti (and the related B. duncani) are parasites that take up residence in red blood cells. One prominent researcher, not part of this paper, has called it “America’s malaria” – and like malaria, it causes flu-like chills and fever, and so is often ignored or misdiagnosed. But, also like malaria, it can cause anemia, organ failure and death.

Exactly how much babesiosis is there in the US? That’s hard to say. Public health authorities have perceived the risk growing for several years, but it was only this past January that the illness became a reportable disease — meaning that, if a physician diagnoses it in a patient, he or she is supposed to pass news of the case up the hierarchy to a state health department, who pass it on to the CDC.

Since the parasite travels in red blood cells, you can see how it might be a transfusion risk. But just how much of a risk it poses, and what to do about it, has been sparking sharp debate for a number of years. (Here are the minutes from an FDA meeting in 2008, and an FDA summary of the issue from 2010.) The American Association of Blood Banks declared babesiosis in blood a top priority back in 2009.

At the moment, potential donors get asked: “Have you ever had babesiosis?” But most people don’t know the illness exists, and because it can be asymptomatic, people can be infected and not know it.

Moreover, babesiosis isn’t something you can diagnose by looking at a blood donor. If someone is infected and experiencing symptoms, those symptoms are likely to be nonspecific — so what might indicate babesiosis might also indicate flu, or a cold, or a number of viral illnesses. But if you ruled out blood donors on the possibility they might have a cold, you’d quickly cut the US blood supply to unsustainable levels.

The problem might be solved if there were a test that could detect Babesia in a blood sample. Right now, there is not. To authorize a test, the FDA needs for a company to bring one forward. Yet so far, babesiosis is not so widespread that it would guarantee enough sales to justify a test’s R&D costs, and thus no pharmaceutical company has volunteered to develop one. In a companion editorial to the paper released today, Dr. David Leiby of the American Red Cross’s Holland Laboratory says this must change:

What is not acceptable, however, is the status quo. With reports of 162 transfusion-associated cases of babesiosis probably representing only a fraction of actual cases and a potential causal or contributory role for babesiosis in the deaths of B. microti–infected blood recipients, the time to act is now.

http://www.wired.com/wiredscience/2011/09/ticks-blood-supply/

I wonder how much is in the UK blood supply or even worldwide.

wonderfullife
10-09-2011, 08:38 PM
Hi 'wonderfullife'. :)

I've only been able to 'skim' read this great thread, as I'm pushed for time today.
I live in an area that has deer, so, a Lyme disease area. But there isn't too much attention paid to it's dangers - I guess that might put the tourists off.:rolleyes:
Anyway, to my point, I signed the petition and here's part of the email they sent me....

------- FORWARD THIS TO YOUR FRIENDS -------
Hi,

I wanted to draw your attention to this important petition that I recently signed:

"UK Lyme Petition"
http://www.ipetitions.com/petition/uklymepetition/?utm_medium=email&utm_source=system&utm_campaign=Send%2Bto%2BFriend

I really think this is an important cause, and I'd like to encourage you to add your signature, too. It's free and takes just a few seconds of your time.

Thanks!
------------------------------

..... I've been cross posting this on Forums and Facebook, so hopefully, more people will become aware of Lyme Disease.

Thank you for cross posting the petition.
I would say that your area probably does have lyme it's not just the deer spreading it also birds, mice, squirrals, dogs, cats the list goes on.

wonderfullife
10-09-2011, 08:38 PM
What a "coincidence" that Lyme disease first appeared near Plum Island precisely after they began experimenting with ticks by injecting them with viruses and bacteria to see how easily they could transmit them to their hosts. Lyme is man-made and that's why it's covered up.

.

+1

wonderfullife
10-09-2011, 08:43 PM
Thanks for all the info, WFL!

I lost one close and one distant family member to ALS, what a horrible disease!
I was unaware of the lyme connection until now, but will pay more attention to it from now on.


The article about root canal treatments is absolutely spot on, but very few people know about this.

The book The Cure for All Diseases by Hulda Regehr Clark doesn't just point out the problem but also offers solutions (detox, diet, zapping) - applicable to lyme disease as well as any other parasite related condition.

Thanks for the book recommendation.
Lyme is a great mimic and can lie dormant for 10,20 or even 30 years.
I am sorry to hear about your close ones.
My father and mother and brother and myself all nearly died from Lyme.
I was adopted so there is no connection via genes or DNA.I am sure a lot more have suffered that we were unaware about.
Our animals greatly suffered back then no one suggested LYME.

wonderfullife
10-09-2011, 09:11 PM
Interesting article here about the CIA's six-legged soldiers:

http://pakistancyberforce.blogspot.com/2011/08/cias-six-legged-soldiers-spread-dengue.html

Very intresting article thanks for posting

wonderfullife
10-09-2011, 09:14 PM
Ecologists worldwide are challenged to contribute solutions to urgent
and pressing environmental problems by forecasting how populations,
communities, and ecosystems will respond to global change. Rising to
this challenge requires organizing ecological information derived from
diverse sources and formally assimilating data with models of ecological
processes. The study of infectious disease has depended on strategies
for integrating patterns of observed disease incidence with mechanistic
process models since John Snow first mapped cholera cases around a
London water pump in 1854. Still, zoonotic and vector-borne diseases
increasingly affect human populations, and methods used to successfully
characterize directly transmitted diseases are often insufficient. We
use four case studies to demonstrate that advances in disease
forecasting require better understanding of zoonotic host and vector
populations, as well of the dynamics that facilitate pathogen
amplification and diseas e spillover into humans. In each case study,
this goal is complicated by limited data, spatiotemporal variability in
pathogen transmission and impact, and often, insufficient biological
understanding. We present a conceptual framework for data-model fusion
in infectious disease research that addresses these fundamental
challenges using a hierarchical state-space structure to (1) integrate
multiple data sources and spatial scales to inform latent parameters,
(2) partition uncertainty in process and observation models, and (3)
explicitly build upon existing ecological and epidemiological
understanding. Given the constraints inherent in the study of infectious
disease and the urgent need for progress, fusion of data and expertise
via this type of conceptual framework should prove an indispensable tool.

Data-model fusion to better understand emerging pathogens and improve
infectious disease forecasting.

LaDeau SL, Glass GE, Hobbs NT, Latimer A, Ostfeld RS

Ecol Appl 2011 07; 21 (5): 1443-60

wonderfullife
10-09-2011, 09:16 PM
This is the first installment of a two-part account of a recent forum on tick-borne illnesses in Sag Harbor. Part two will be published Wednesday.

Bitten by a tick as a child during a summer stay in Bridgehampton, Ally Hilfiger began experiencing full-blown flu-like symptoms and joint pain by age seven. Over the next 11 years, she was diagnosed by different doctors with diseases ranging from arthritis to fibromyalgia and multiple sclerosis.

“I spent a lot of my life in what is called the Lyme Fog,” Ms. Hilfiger told an audience of 100 people attending a forum on Lyme and other tick-borne diseases in Sag Harbor last Friday. “Nothing helped with the pain or the disorientation.”

At age 19, she saw a psychologist in Connecticut who said “this sounds like Lyme.” Earlier blood tests for Lyme, she recalled, had been “marginal or inconclusive.” With this diagnosis, however, “which included a co-infection” with babesiosis, she embarked upon a seven-year regime of antibiotics and IV drips.

She has been symptom-free for the past year. “I believe I went through this so I can stand before you and spread this message,” she said. “You must be an advocate for this disease. You must also know that tests can be wrong and doctors can make mistakes. You know your body and when things aren’t right you need to trust your instincts.”

The forum, “Lyme Disease in the Hamptons — What You Need to Know,” was presented by Time For Lyme, Inc. on August 19 at Bay Street Theater. Four panelists provided detailed information on the disease, including updates on the latest research, common misconceptions, prevention strategies and a personal story of mis-diagnosis.

Time for Lyme is a non-profit organization based in Greenwich, Connecticut, the mission of which is to fund and promote outreach for Lyme and other tick-borne diseases. According to co-founder Diane Blanchard, the group is dedicated to increasing awareness of the diseases through education and prevention programs.

The purpose of Friday’s program, Ms. Blanchard told the audience, was “to introduce you to some very important resources right here in your own community.”

The panelists included George P. Dempsey, M.D., a family practioner in East Hampton who has been studying Lyme among his East End patients since 2000; Darin G. Wiggins, M.D., chairman of the Department of Emergency Medicine, Southampton Hospital; Benjamin J. Luft, M.D., an academic physician, researcher and chairman of the Department of Medicine at Stony Brook State University, who is involved in research on the disease; and Ms. Hilfiger, the Time for Lyme spokesperson who told of her long struggle with the disease. The panel was moderated by Dr. Luft.

“My goal is to make Lyme disease manageable for those who live out here,” said Dr. Dempsey. While Lyme was first diagnosed in 1975 in Lyme, Connecticut, Dr. Dempsey said that records show that a Dr. John Walker wrote about Lyme-like symptoms on an island off the coast of Scotland in 1764. And Pliny the Elder, who lived between 23-79 A.D., wrote “Ticks: the foulest and nastiest creatures that be.”

CO-INFECTIONS COMMON

There are now some 10 tick-borne diseases that have been identified and at least 32 percent of infected ticks carry more than one pathogen, making co-infections like Ms. Hilfiger’s very common, Dr. Dempsey said. Spring is the most active time for nymphs and is the time, he said, “when we see the most disease.” Nymphs tend to be down low, in leaf mulch and other warm, moist areas. Adult ticks, on the other hand, are capable of jumping and are often found in high grass or on animal trails. “They have a highly developed sense of smell and wait for an animal, such as a deer, to come by and then jump on it.” In general, ticks do not like dry environments, windy settings, beaches, rocks and pebbles, which is a good list of landscaping “do’s” that will help minimize the tick population on a property.

Through his highly graphic slides, Dr. Dempsey sought to reassure the audience that “not every insect bite is a tick bite and not every tick bite carries disease.”

A tick bite rash usually doesn’t hurt, it is not that itchy, the area tends to be warm and the bite site gets progressively larger. “If the rash lasts more than two or three days and is larger than a silver dollar, then it could be a tick,” he said. While the bull’s eye rash is believed to be the hallmark of Lyme, Dr. Dempsey was quick to point out with slides that there is a wide range of rash-like manifestations.
http://northshoresun.timesreview.com/2011/09/17177/experts-give-tips-on-dealing-with-tick-borne-illness/

wonderfullife
10-09-2011, 09:22 PM
Following a Tick Bite: Double Infections by Tick-Borne Encephalitis Virus and the Spirochete Borrelia and Other Potential Multiple Infections.

Bröker M.


Source

Novartis Vaccines and Diagnostics GmbH, Marbury, Germany.


Abstract

In Central Europe and large parts of Asia, tick-borne-encephalitis (TBE) and Lyme borreliosis caused by the spirochetal bacterium of the genus Borrelia are among the most common diseases transmitted by the bite of a tick. When in regions with overlapping TBE virus and Borrelia endemicity, a tick bite causes the victim to become ill, it is important that appropriate serological and other laboratory investigations form part of the differential diagnosis. Account must always be taken of the fact that a tick bite may be followed by a double infection with the TBE virus and Borrelia. For this reason, a comprehensive diagnostic work-up aimed at detecting co-infection by both pathogens, even when the tick bite occurs in an endemic region for both pathogens but the initial clinical symptoms suggest an infection with only one of the two pathogens. The present article discusses a number of published cases of a co-infection with TBE virus and Borrelia and other potential multiple infections.

© 2011 Blackwell Verlag GmbH.


PMID: 21848518 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/21848518

wonderfullife
11-09-2011, 12:03 AM
ScienceDaily (Sep. 9, 2011) — A new commentary published online in The FASEB Journal argues that patients should be diligent and demand proof of safety and benefit before beginning any treatment regimen for chronic pain, as some treatments have very little scientific evidence that they actually alleviate the conditions for which they are prescribed. In the article, Phillip J. Baker, Ph.D., Executive Director of the American Lyme Disease Foundation, dispels myths surrounding chronic Lyme disease, using it as an example of why patients should ensure that diagnostic and treatment tools are approved by the Food and Drug Administration and not just recommended by other patients and physicians."Despite repeated warnings by the Centers for Disease Control and Prevention and the Food and Drug Administration, the diagnosis of chronic Lyme disease often is based on the false results of non-standard test procedures, not approved by the FDA," said Baker. "This is inexcusable since 46 FDA-approved tests are available and used routinely by various state public health laboratories. A false diagnosis can result in patients being placed on prolonged antibiotic therapy or some other unproven and potentially harmful remedy."

Baker also says that before agreeing to undergo any treatment regimen for chronic pain, patients should ask their physician to provide results from published, placebo-controlled studies proving that the proposed remedy is both beneficial and safe. Testimonials by previously treated patients -- regardless of the number -- are not sufficient proof of benefit and safety. Unapproved and undocumented treatments are usually not covered by health insurance and therefore result in a huge financial burden to the patient. Chronic Lyme disease must be considered as part of a broad-based, multidisciplinary effort to understand the cause and treatment of chronic pain in general as outlined by the Institute of Medicine's report, "Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research."

"When doctors don't know what's causing a patient to experience chronic pain, desperation can set in," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "That desperation, however, is no excuse for pushing the boundaries of the Hippocratic Oath by diagnosing a patient with a poorly defined health condition, like chronic Lyme disease, for which the only remedies are unproven and may only cause more harm."
http://www.sciencedaily.com/releases/2011/09/110908145337.htm

wonderfullife
11-09-2011, 12:09 AM
http://www.coasttocoastam.com/show/2011/09/14


This will be on the 14th September 2011

wonderfullife
11-09-2011, 01:20 PM
Dr Harold Smith's testimony - YouTube

wonderfullife
11-09-2011, 02:50 PM
http://www.tickedoffandfedup.com/Lida_Video.html

This lady did a lot of work on the Lyme disease she claimed M.S is like Lyme she has unfortunatly died now but video is worth a watch.

wonderfullife
11-09-2011, 02:57 PM
Lida Mattman at the Autoimmunity Research Foundation's Chicago Conference - YouTube

Her second to last presentation. She worked on Lyme well into her 90's until her death.

wonderfullife
11-09-2011, 03:03 PM
-forms have been shown to occur among many species of bacteria and are suspected to be involved in persistent infections. Since their discovery in 1935, numerous studies characterizing L-form morphology, growth, and pathogenic potential have been conducted. However, the molecular mechanisms underlying the formation and survival of L-forms remain unknown. Using unstable L-form colonies of Escherichia coli as a model, we performed genome-wide transcriptome analysis and screened a deletion mutant library to study the molecular mechanisms involved in formation and survival of L-forms. Microarray analysis of L-form versus classical colonies revealed many up-regulated genes of unknown function as well as multiple over-expressed stress pathways shared in common with persister cells and biofilms. Mutant screens identified three groups of mutants which displayed varying degrees of defects in L-form colony formation. Group 1 mutants, which showed the strongest defect in L-form colony formation, belonged to pathways involved in cell envelope stress, DNA repair, iron homeostasis, outer membrane biogenesis, and drug efflux/ABC transporters. Four (Group 1) mutants, rcsB, a positive response regulator of colanic acid capsule synthesis, ruvA, a recombinational junction binding protein, fur, a ferric uptake regulator and smpA a small membrane lipoprotein were selected for complementation. Complementation of the mutants using a high-copy overexpression vector failed, while utilization of a low-copy inducible vector successfully restored L-form formation. This work represents the first systematic genetic evaluation of genes and pathways involved in the formation and survival of unstable L-form bacteria. Our findings provide new insights into the molecular mechanisms underlying L-form formation and survival and have implications for understanding the emergence of antibiotic resistance, bacterial persistence and latent infections and designing novel drugs and vaccines.

Citation: Glover WA, Yang Y, Zhang Y (2009) Insights into the Molecular Basis of L-Form Formation and Survival in Escherichia coli. PLoS ONE 4(10): e7316. doi:10.1371/journal.pone.0007316
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007316

wonderfullife
11-09-2011, 03:27 PM
One Woman’s Journey Through Lyme
by Sue Massie (N.D. Candidate)

Mysterious Symptoms for Years
At 42, with six lovely children and a wonderful husband, I thought my life was over! I was very ill with migraines, slurred speech, difficulty swallowing, atrophy in my muscles, excruciating pain throughout my body, memory loss, light and noise sensitivity, etc. These are just a few of the symptoms I suffered from on and off over the years, and they were progressively getting worse.

Paralyzed From The Neck Down
I eventually became paralyzed from the neck down, and developed an ALS-like condition.My husband was also very ill with debilitating symptoms including “buggy” eyes, migraine headaches, rib pain, radiating jaw pain, chest compression, fatigue and a racing heart (intermittent). We spent years trying a number of neurologists, cardiologists (including Yale), and all kinds of specialists, only to be given a new diagnosis with each visit. These included TIAs, Grave’s disease, possible MS, and even stress. Finally a Lyme-literate neighbor suggested my husband might have Lyme disease. I thought it was a ridiculous idea because my dad was supposedly the first case diagnosed back in 1980 in Monmouth County, New Jersey, and he was just fine (or so I thought). Our neighbor handed me the list of symptoms, and my husband had just about every one of them! I asked for her doctor’s name and we saw him immediately. He diagnosed my husband with Lyme disease and treated him with long-term antibiotic therapy. Six months after his diagnosis, I was also tested and diagnosed, and I started treatment as well. Five out of six of our children have now been diagnosed with Lyme disease* and had to be put on a special educational program to help them with their studies. (Lyme can often affect children and contribute to ADD, ADHD, memory problems, dyslexia, anger outbursts, fatigue, etc.)

102 ALS Patients Tested Positive For Lyme - In Treatment

I have talked with over 8,000 people with Lyme. 102 of these cases are ALS-diagnosed patients who were properly tested for Lyme and came uppositive. I feel that people who are diagnosed with ALS/Lou Gehrig's disease, Multiple Sclerosis, Alzheimer’s, Lupus, Fibromyalgia, Chronic Fatigue and many other neurological and degenerative diseases, could actually have Lyme disease. To date, there is no definitive, 100% positive test for Lyme disease. However, patients should request (from a Lyme-literate doctor) to have a PCR test (to determine genetic material of Borrelia) or a Western Blot blood test (antibody assay) done by Igenex Labs in California (www.igenex.com). Most doctors are following the diagnostic protocol of doing a Lyme titre or ELISA test, which are not accurate. If a patient who has Lyme disease actually tests positive using the Lyme titre or ELISA test, their doctor would then order a Western Blot blood test. According to the Center for Disease Control, a patient must have a minimum of five bands (specific numbers and bands are how they read these tests), in order to be labeled positive for Lyme by Western Blot. Another important consideration is that Lyme antibodies must be present for a positive result, and if the patient has been taking steroids, Advil, Motrin, or other anti-inflammatories or antibiotics, this could cause a false-negative result. For this reason, patients should be clear of all OTC’s and prescription medications for a minimum of six weeks before testing, but even this cannot guarantee an accurate result.

My Lab Results Would Have Been Considered Negative
After testing, I only had one band - number 41, which is the “flagellin” (or tail) of the spirochete, specific for Borrelia bacteria (Lyme), so I would have been told that I was negative. Quite often, patients have to be diagnosed by symptoms alone. I know that most people reading this story probably know of someone who has been to various doctors, and is suffering without an adequate diagnosis, and people just label them as being a hypochondriac, etc.

Initial Signs Often Missed
Lyme disease is not necessarily associated with a “bull's eye rash and sore knees.” Less than 20% of patients ever see the tick, and less than 30% get the classic bull's eye rash. Tucking your pants in your shoes or wearing white so you can see ticks does not provide full protection. I was the only one in my family that saw a tick on the back of my hand, and only my one son had a rash (not a bull's eye, but more like impetigo all over his body). Co-infections are also a big part of Lyme, meaning not only do the tiny ticks infect you with Borrelia bacteria, but there is also possible infection with Babesia, Ehrlichia, Bartonella, mycoplasma, and the conditions of Epstein-Barr and HHV-6 (human herpes-6) viruses.

Dedicated To Helping Others
I have talked with thousands all over the U.S., including Hawaii and Alaska, Great Britain, Germany, Australia and even Japan. I am now a Certified Natural Health Professional. My health has improved about 95% and I have been off antibiotics for 2 years (after being on a multitude of them for 3 1/2 years). It has been a long journey for me, but now I am dedicated to helping others heal from Lyme.
http://www.springboard4health.com/notebook/health_lyme_disease.html

wonderfullife
11-09-2011, 04:34 PM
MY STORY

By Tom Grier, M.S.

In 1978 something strange happened to me that I now believe was the harbinger of more ill fortunes to come. In the winter of 1978, I was training for a marathon foot race.

It was being held early in the summer, so I had to train all winter by running on a small sixteenth-mile indoor track.

The running track was deep in the bowels of an old campus building that was built in the late 1800s. It had dim lighting and a funny smell, and was always heated to about 85 degrees.

I was constantly being asked by the track coach to relocate so that the track and field team could train. When Spring approached, I was only too glad to run in the mud and grime of the local woods.

I enjoyed splashing through puddles and traversing streams, celebrating the joy of being young. In an average week, I would run more than 60 miles.

I ran two marathons that summer, and continued to run in the woods through the changing leaves, right up until the snow became impassable.

During this time, I was taking graduate school courses in immulogy and microbiology at the medical school in Duluth.

It was while I was in the microbiology lab that I saw the first of many personal medical conundrums which would follow.

I pricked my finger and placed a drop of my blood on a slide. I did a routine blood smear which allowed me to do a white blood cell count and a differential ratio of the various cell types. I was shocked when I found I had 7% eosinophils. A normal count would be 1%.

In a patient with extreme allergies 3-4 % would be normal, but 7% was quite high. I had an instructor repeat the smear, and she found it to be even higher.

There were some discussions of a rare fatal blood disorder, perhaps a parasitic disease, but we all opted for the more conservative explanation of allergies.

Even though I hadn't had so much as a sniffle or sneeze all year, we all concluded that my spring time allergies were kicking in. We also ignored the fact that my neutrophil count was down, and my overall WBC count was low.

A week later I got shingles on one side of my body. Why? I was in the best shape of my life.

I only had a mild fever and a mild case of shingles, but why did I get an outbreak of herpes zoster at age 24? Normally, shingles is a condition elderly people get when their immune systems are compromised.

About this time I also had a case of nonspecific urethritis; a burning sensation when I urinated. I was treated with two weeks of tetracycline and it went away, and so did my Shingles.

I really gave very little thought to these events, and it was only years later that I would learn of a disease called Human Granulocytic Ehrlichiosis (HGE), which I now believe I had contracted from a tick bite I received during all the training I was doing in the woods.

What I didn't know then was that I probably had a second tick-borne disease that would not even be isolated for another three years - Lyme Disease!

I had always been able to function on just a few hours sleep, but by 1980 I was sleeping a lot, and when I was awake I was tired, depressed, fatigued, and constantly distracted.

It seemed I could not get myself to concentrate on any one project for long. I had transferred graduate schools, to the University of Washington.

There, I lived in a cabin in the woods where I had to chop my own wood for heat. The cool, humid weather was perfect for ticks, and I was bitten many times.

In 1980, tick-borne diseases in America were an anomaly, so I never gave a thought that I could have ever contracted anything serious from a tick bite.

Even if I did, the symptoms would certainly manifest themselves within a few days of the bite, so tick-borne diseases never entered my thinking.

I spent a summer camping all through Europe, and once again the concern of tick bites never entered my thinking.

The doctoral program in Geriatrics I had enrolled in was unexpectedly moved from the College of Biological Sciences to the College of Sociology.

I quit school and went to work, with the idea I would go back to graduate school the following fall.

I eventually found myself in the pharmaceutical business as a salesman.

During the next decade, thoughts of school faded as I continued to suffer from unexplained depression and fatigue.

I started to gain weight, and had what felt like a continual hangover that lasted from the time I awoke until I slept. When I did sleep, it was a tortured sleep where I would toss and turn and tear at my covers. I despised warmth and craved cold. My bed in the morning would look like a war zone.

Needless to say, my personal relationships were suffering. It was now 1984.

I had moved back to Duluth, Minnesota, and I continued to experience an ever increasing array of symptoms. I now regularly had sharp shooting pains in my chest that felt like ice picks.

I had heart palpitations; my es were sensitive to bright lights; I had manic mood swings, where I would be awake all night reading or playing piano. This was usually followed by weeks of wanting to do nothing but stay in bed.

Yet, all through these years I always had one faculty I could depend upon, and that was my brain. If I read something I knew it. I remembered it, and I could quote it almost word for word.

During one of my manic episodes, it was nothing to read an entire book or two in a single afternoon. I was a walking encyclopedia of knowledge, but I was still unable to pick up on what was wrong with me.

Then, around Thanksgiving of 1990, I had an episode I could not ignore. By this time I was severely obese. I was tired all of the time, and I now had to put all my efforts into my job just to keep up. I was the top salesman in the country, and yet I could not find the time to answer my own mail.

I was using all my weekends and all of my vacation time to just to keep up. I kept thinking that I was going through a bad patch and things would go back to normal.

I would lose some weight and things would be fine. I'd catch up on work and start to enjoy my prosperity.

As a top salesman, I was now being sent all over the country to sales conventions to help promote our drugs, and to give training seminars to fellow salesmen.

I was even asked if I wanted to become a trainer. A few years earlier this would have been a wonderful perk and a great honor, but now it was torture.

I went to New Orleans, Las Vegas, Orlando, New York, Colorado Springs, Philadelphia, Cleveland, and Chicago. Each and every time it was torture. I wanted to get through the day as quickly as possible, so I could go to bed and sleep.

I skipped cocktail parties; I skipped awards banquets; I even skipped important dinners with company executives - all so that I could just get those extra few hours of sleep I would need to get me through the next day.

At national sales conferences, while three thousand of my fellow employees were at dinner and seminars, I would sneak back to my hotel room and sleep.

Still, I was considered the top salesman in the region overall, and top in the country for our two newest products. I felt like a complete fraud.

While returning from a regional sales conference, I got lost and confused while changing planes in the Chicago Airport. I was sitting at the wrong gate for an hour, waiting for my plane to be called. Everything around me looked strange.

The people sounded like cackling geese. Everyone looked like they were in fast motion, like someone had sped up the projector. Every time I turned, I was dizzy and disoriented. I was sweating, and completely lost.

I had to get to a completely different end of the terminal. Because of the metal in my suspenders, when I went through the metal detectors I set them off.

Here was a sweating, nervous, completely disoriented man trying desperately to get to his connecting flight, talking what was must have sounded like gibberish to the security guards, about a flight that had left more than an hour earlier.

I was finally personally escorted to a sales agent, and had to spend the next several hours trying to collect my wits.

The following week, I had bouts of disorientation that would come and go. My heart palpitations were getting worse.

That summer, I thought a camping trip in the Wisconsin Dells would give me some rest and perspective. I returned to work even worse than before and farther behind. By the time Thanksgiving arrived in 1990, I was only going through the motions of working at all.

I now had severe joint pain in my ankles; I had an unmistakable pressure building up in my head; I was getting lost driving to places that I had been to hundreds of times.

I went to the doctor many times, and each time it was some vague "...lets wait and see?" kind of attitude.

I was now sleeping almost 18 hours a day, and sweating so profusely that I often soaked through my sheets and into the mattress.

During this time, I was the head of our local Pharmaceutical Salesman Association, and I had to debate a panel of doctors on the topic of what benefit pharmaceutical salesmen served the medical community. It was a hostile debate on the doctor's turf.

I wasn't worried though, because I slept up to about an hour before, debated for two hours, and went home and slept another 12 hours straight. The few hours that I spent awake were now like hazy dreams to me. Sleep was my only refuge. I now cared about nothing else.

In March of 1991, I was diagnosed with chronic atrial fibrillation. This was the first solid diagnosis I had received in the past year.

My doctor investigated low blood sugar, high blood sugar, Wolf-Parkinson-White Syndrome, Sick Sinus Syndrome, Menier's Syndrome, Sinus Infection, anxiety panic attacks, viral encephalitis, meningitis and finally, Multiple Sclerosis.

By April of 1991, I now had a constant severe pressure in my head. When I turned my head, the pressure would migrate from the top of my head to the back of my head.

My vision was now reduced to a circle directly in front of my eyes, and my peripheral vision was just a blurry swirling mess of lights and images.

When I would move my head, there was a disturbing gurgle as I heard bubbles move around inside my head.

I found myself for hours in a trance like state almost catatonic, and severe body jerks would awaken me. These jerks were so severe that I had to catch myself to keep from falling.

Then, one day I did fall. Everything was a blurry mess. was in the middle of the street floundering in front of oncoming traffic.

I checked myself in at the local hospital where I was being worked up for Multiple Sclerosis.

While I was in the hospital, my family doctor went on vacation and the neurologist on duty took over my MS work up. As she walked into my room for the very first time, she picked up my chart and immediately asked what the results of my Lyme tests were?

I told her in slurred speech that no one had ever mentioned Lyme disease. She said, "Well, we'll complete the MS work up, but it will all come back negative."

Negative? Why? "Because you have classic late stage Lyme."

Even before I had a scheduled spinal tap and MRI, she had ordered IV Rocephin.

What was it she saw in my chart that in but a few minutes she could diagnose Lyme Disease? Had not others read my chart and investigated my case for nearly a year?

Where a team of specialists could only reluctantly come up with MS after nearly a year of tests, this neurologist was confident in five minutes that I had Lyme disease?

I felt relieved that I had a treatable disease, but I was angry that it was not recognized earlier! Had I not given my doctors everything they needed to make the diagnosis?

Did I not patiently submit to tens of thousands of dollars of tests? Did my doctors not have every marvel of medical science at their beckon call?

Did I not agree to go to half a dozen different specialist so that they could work as a team to diagnose me? What had I done wrong that allowed them to miss a simple diagnosis of Lyme disease?

The answer was evident when my family doctor came back three days later and visited me at my bedside in the hospital. The first thing he said almost apologetically was "Who'd of ever thought it would be a Zebra Disease like Lyme?".

A Zebra Disease! Meaning it was as unlikely to find a Zebra in the local woods as it would be to find Lyme disease.

After all, you don't look for malaria in Alaska, and apparently my doctor didn't look for Lyme in Minnesota!

Yet, by 1991, hadn't Lyme become an established local pathogen? Surely a newly discovered tick-borne disease would cause doctors to learn all they could about this disease.

This was my assumption, but it would be almost a year later when certain pieces of this puzzle would start to fit together.

I was too sick to do anything now except concentrate on getting better.

I was told in a matter-of-fact manner that all Lyme was easily treated in 21 days, and that I would soon be back to work. Twenty one days later, I was sicker than before treatment.

Every muscle in my body twitched and pulsated, and the pressure in my head was far worse. I could only sit up in bed for a few minutes before the pressure got worse, and I would pass out.

I was hallucinating both visually and auditory. I heard phones ring when there were none. I saw shadows twist into menacing shapes. I heard voices talking.

At night, I saw flashing lights fill my vision, and my ears were constantly buzzing with static and ringing.

I felt for the first time that I may be truly going mad. I had to sleep with headphones on, playing classical music to drown out the noise in my own head.

To make matters worse, my Neurologist who had been so sure about Lyme disease, now seemed completely unsure.

She wanted to stop my antibiotic treatment because I wasn't "cured" yet. In fact, in many ways I was worse.

"What about herxheimer reactions?", I said. "Those only last a few days", she replied.

I had to fight for treatment every single week. My heart was worse; my brain was shot; my mind was a hopeless jumble of uncontrolled thoughts - images and sounds that haunted me.

It was as if several minds had been merged into one, and there was no way to sort the images.

During this time, I lost my disability status and was now without a job, living on my savings.

It seemed that my whole life was out of control, yet doctors had no empathy because, despite it all, my verbal skills were quite good.

The skill by which I earned a living was now my enemy. Every word I articulated expressed a cogent, coherent, lucid individual.

I thought that, by clearly expressing my symptoms in a rational manner, I would give doctors some scientific insight to this disease. I was wrong!

I learned something that, in all of the years I had called on doctors as a salesmen, I had failed to observe.

Most doctors have almost no scientific curiosities about new diseases, and always want the short story, one paragraph or less.

How do Iiagnose it? How do I treat it? Anything that isn't black and white in medicine is dangerous territory, as far as the doctor is concerned.

I was alive, I could walk, I could talk. "So", the doctors asked, " What's the problem?"

Doctors I had called on for ten years were now distancing themselves from me, because I was a threat to their paradigm of thinking about Lyme. I was pointing out things about Lyme disease that they had never known. I had read several hundred journal articles, and I thought sharing this knowledge would be met with open arms.

I soon realized that I was a threat to doctors because where they had made one mistake, they had probably made hundreds.

Ignorance was not only bliss; it was safer. The maxim of the new medical community was:

Unknown conditions were medical-legal time bombs best left to other doctors to defuse. My journey had brought me to an unsavory conclusion.

Some of the same people I went to school with - the same people I taught as a graduate student - were playing it safe.

They were in essence cowards, unwilling to risk a shred of security to advance their knowledge of a disease that was threatening the lives of their patients.

There was safety in numbers, and until their peers were treating Lyme dease aggressively, they were not about to be the lone maverick.

When hundreds of Lyme patients in a community all started complaining of the same persisting symptoms post-antibiotic treatment, eventually the lower ranks of doctors started reporting this to the infectious disease specialists.

The infectious disease specialists responded by saying persistent symptoms were post-Lyme Syndrome, or psychosomatic disorder. The family practitioners were placated.

If the Infectious disease doctors weren't worried, why should they do anything different?

Then, more Lyme patients came forward, and the infectious disease experts were placed in an adversarial position.

They had ignored the dozens of studies and case histories showing culture positive patients post-treatment.

They are now in a position of either admitting they are wrong, and chronic relapsing seronegative Lyme Disease really does exist, or they can talk in vague generalities, always falling back on the old dogma:

All infected patients are antibody positive.

This is the medical loop hole that allows them to pass on treang complicated patients, and skirt all controversy. " We tested them; they were negative; end of story. Go away!"

But ask yourselves this:

Currently, there is a 4.2 million-dollar NIH study to investigate the cause of Chronic Relapsing Lyme Disease.

Much of this study's conclusion will be dependent upon using antibody serologies for determining diagnosis and relapse.

If there is even one single study or accepted case history that proves a seronegative patient can still be culture positive for Borrelia burgdorferi, then isn't the entire basis of using any antibody serologies flawed?

If the study is flawed in the beginning, the entire conclusion will be baseless.

This is exactly how we got off on the wrong foot in the beginning. We depended upon serologies to indicate the endpoint and cure.

We didn't know better then, but we should certainly know better now! So what's going on? Is it denial? A cover-up? Ignorance? Arrogance? The inability for egos to yield to the truth?

"There are none so blind, as those who will not see." I think it is a combination of all of these things.

What keeps me devoted to bringing Lyme Disease research to the attention of doctors isn't just the daily reminder of my own symptoms, but something that occurred to an acquaintance of mine.

At the same time I was tentatively diagnosed with MS, I was told about a pharmacist I used to call on who was diagnosed with what I was told was myasthenia gravis. It was a year later when I learned it wasn't MG he was diagnosed with, but MS. I promptly went over to see him at his house, and I was shocked at what I had seen.

What once was a strapping 250-pound outdoors man was now a shriveled 100 pound invalid. He couldn't walk; he could only use one arm; saliva dripped from his mouth and his speech was almost indiscernible.

I did a symptom check list, only to find that he had several tick bites, a history of rashes, and over half of the Lyme symptoms on Burrascano's symptom checklist.

Since his doctor, a man I had known for more than ten years, was clearly not informed about Lyme Disease, the family asked him to consult with a Lyme specialist - a young family practice doctor that was barely out of her residency.

The elder physician went to the patient's house, and at the families request took several blood and urine samples, as well as cerebrospinal fluid, which were all to be sent to Mayo clinic, Igenix labs, and Marshfield Clinic for analysis.

In the meantime, the patient was placed on 500 mg. amoxicillin three times a day. He immediately burst into fever and sweats, and had difficulty swallowing.

Although the family doctor was informed that this was a favorable and predictable Herxheimer reaction, the medication was stopped. While waiting for the results of the tests, the patient died of respiratory collapse.

When the results never came, I went to the clinic lab director; a person I knew for years from working with her on the John Bear Grease Dog Sled Race. Renee' told me that all t samples were destroyed the same day they were collected.

The doctor told her "...we don't send tests out of house." This meant that there was never any intention to find the truth about the patient's true condition.

What the physician didn't know was that the family had kept several of the urine samples in the freezer.

Upon learning what the doctor had done, they authorized the Lyme specialist to send a sample in for analysis. It was determined there were particles of Borrelia burgdorferi in the urine.

The particles were at such a high concentration that it was one of the highest positives ever seen.

The remaining samples are still frozen, but the family has no interest in pursuing malpractice or medical negligence against a family friend.

To me, it was a premeditated act on the physician's part to cover up the fact that he had misdiagnosed a treatable disease.

Perhaps he felt it was a waste of time to even do the tests, but he indicated to the family that the samples would be drawn and sent to the various labs as requested.

Yet, within minutes of returning to his clinic, he had the lab manager destroy all of the samples!

It now became apparent to me that, not only did most doctors not know much about Lyme disease, they didn't want to know!

Many other things also became apparent to me, but the biggest revelation, was that doctors were unwilling or unable to say: "I was wrong, I made a mistake."

Either it was their egos unable to humble themselves, or it was a fear of medical malpractice that could end their career.

In either case, they were ignorant of Lyme disease and had put too much faith in tests, and not enough faith in their patients.

Since then, I have seen and heard many tragic Lyme disease stories - some of them ending in wheel chairs, and still others in death.

The line in the sand that now divides the Lyme-aware from those who treat Lyme like a strep throat, is now so deep it is a chasm that I fear has become too large to build a bridge across.

I am now convinced that it will take a public statement by the AMA and NIH to overcome the fear that doctors have for treating Lyme disease aggressively.

There will have to be a national paradigm shift for doctors to feel safe in treating chronic relapsing Lyme disease without the fear that their own peers are questioning what they are doing.

We must also legislate to eliminate third party provider's influence, such as HMO groups that pay a bonus to groups of physicians for holding down medical costs.

This makes the doctors police their own peers in order to receive large bonuses.

We need to eliminate insurance companies from being able to influence physician treatment decisions.

Even now, Blue Cross of Minnesota is challenging a law which states that only the doctor, and not the insurance provider, can decide on the length of treatment.

Their challenge is:

The patient is seronegative, and therefore cannot have an active infection, so they won't pay for IV Rocephin.

Yet they are willing to pay for less expensive oral antibiotics.

Is it really a belief she is not actively infected, or is it actually a cost containment policy? All patients want is access to treatment!

The argument that antibiotics are overused and cause super infections is also flawed logic. [b]It was underuse of antibiotics that caused antibiotic resistant forms of tuberculosis to evolve.

The director of the CDC during the sixties was recently quoted in Discover Magazine as saying:

"We didn't know we had a slow dividing bacteria that could hide in the body and sequester itself away from antibiotic treatment. If we knew then what we know now, we would have blasted tuberculosis with whatever it took to eradicate the infection off the surface of the earth.

If we ever see those conditions again we will be ready!" Will we?

Post edited by: Canuck, at: 02/18/2009 10:06

i broke up tom's really long, long paragraphs, bolded/emphasized things in his wonderful, detailed personal story so NEURO LYME folks like me could read and comprehend it all.

i worked directly with tom on another project his LYME ON THE BRAIN series of articles found in lyme facts of breaking things up for us NEURO lyme folks.

bettyg, group leader, iowa activist, llmd coordinator
http://www.mdjunction.com/forums/lyme-disease-support-forums/studies-research/374434-tom-griers-lyme-ms-story

wonderfullife
11-09-2011, 04:53 PM
Three Main Categories of Lyme Disease Tests:

1. Indirect Tests (serum antibody tests):

ELISA; Western Blot; IFA; Borreliacidal Antibody Assay (Gunderson test);T-cell Activation Test

2. Direct detection tests:

PCR (DNA amplification); Lyme Urine Antigen Test (LUAT); Antigen Capture Test; culturing of skin, blood, CSF, urine, or tissue; immune complex / antigen-antibody test

3. Tissue Biopsy and Staining:

Silver Stain; Gold Stain; Fluorescent Tagged Monoclonal Antibody Stains; Acrodine Orange; Gram Stain; Muramidase; etc.

There is a great deal of confusion and controversy surrounding Lyme disease testing. The first problem is that most of the manufacturers of these tests want you to believe that their tests are the best. At every medical convention, I listen to sales pitch after sales pitch from sales people making their product sound infallible. Often the terminology is confusing and the customer frequently misinterprets what is really being said.

For example, a salesman may say the rate of false positive or false negative is less than one percent. This sounds like the test is more than 99% accurate. In reality, what it is saying is if you have 1000 test samples from the same known laboratory sample, then in less than ten samples will there be a result that differs significantly from the other 990.

In any of this, did you hear the words: "percent reliability" or "percent accuracy" in diagnosing Lyme disease in humans? No! People often mistake "false positive rate" for accuracy. The truth is that no Lyme disease test to date is close to 100% accurate, because each test has its own particular set of shortcomings. So, while the first problem with Lyme disease tests is in the way they are promoted, the second problem is the way the tests are primed to recognize laboratory strains of Bb, rather than wild types. Third, the Lyme spirochete can hide in the human body, and fool the immune system into thinking it isn't there. So, no antibodies are produced, resulting in negative tests. Stealth technology isn't new, it evolved millions of years ago by the first bacteria that evaded its host's defenses.

Immune Responses

The first antibody our body makes in response to a foreign invader is usually immunoglobulin type M, abbreviated as IgM. This large antibody takes two to four weeks to be made in quantities large enough to be consistently measured. It is at its peak of production four weeks after exposure to an antigen. The IgM antibody will only stay in circulation for about six months, and then levels are usually too low to detect. If infection persists, this antibody may also persist. In general, a Lyme patient who consistently has detectable IgM levels is usually chronically ill, but its absence is not a reliable indicator of cure.

The second antibody we make after the IgM is the IgG antibody. This antibody takes four to eight weeks to form, and is gone in less than twelve months. It peaks at about six weeks. This antibody crosses the placenta, so an infected mother can pass this antibody to her child. An IgG antibody titer in a newborn does not have to mean active infection. It does mean the mother has had exposure, and the child must be carefully monitored for signs of the disease.

Because of the difference in the two antibodies, two separate tests are available to test for their presence. Therefore, a physician must specify whether or not a patient should have an IgM or IgG Western Blot, or an IgM or IgG ELISA test.

IgM:

This is the earliest of the antibodies to appear in response to an infection. It is produced in quantity. It is six times larger than the IgG antibody. Because of its size, this immunoglobulin does not cross the placenta. Since it cannot enter the fetus from the mother, any newborn that starts to make IgM antibodies against Lyme disease must be infected. However, a fetus exposed to Borrelia burgdorferi early in the pregnancy may never make an antibody response to the Lyme bacteria because the baby's immune system doesn't recognize it as foreign.

IgG:

This antibody remains the longest and is the foot soldier of the immune system. It attacks viruses, bacteria, yeast, toxins, and transplants. The IgG antibody can kill bacteria indirectly by tagging or marking the foreign invaders for destruction by the killer cells (T-cells, macrophage). Or, it can kill the bacteria directly by evoking compliment, a series of enzymes and proteins that will dissolve the intruder.

Note: It was once thought that plasma cells could produce antibodies that could conform to any shape necessary to attack foreign intruders. If this were true, we would have almost unlimited immunity. It is now thought that each person has a finite collection of specialized lymphocytes that are able to create a finite number of antibodies. Each antibody shape is predetermined, and can be produced by only one type of lymphocyte. When the body is invaded by a foreign antigen, it will stimulate one of these cells, and only that cell will begin to clone itself. This process takes several weeks. If we lack the right cell type to do the job, we are left with a gap in our immunity. This might account for why some Lyme patients with certain tissue types have greater morbidity, while others have relatively mild symptoms.

Dr. Alan Steere, M.D., observed that Lyme arthritis patients with tissue type HLA-DR2 and HLA-DR4 had more severe arthritis and chronic disease. Other tissue types have been associated with an increased incidence of multiple sclerosis and other neurological diseases. It might be that different patient tissue types might account for a difference in patient's symptoms to a greater degree than different strains of the bacteria.

It is known that this bacteria has an affinity for specific tissues. If you have a specific lack of immunity, this may cause the disease to manifest differently in those tissues. For example, let's say hypothetically that your heart is infected with Borrelia burgdorferi bacteria. Perhaps most people make an antibody that suppresses attachment of Bb to certain fibers in the heart. If you lack that antibody, the infection may continue more aggressively and manifest differently - for instance, causing an enlargement of the muscle fibers or destruction of the conduction pathways.

Instead of lacking a specific antibody, perhaps some individuals make a different kind of antibody, an antibody that not only attacks the bacteria - but may attack the heart as well! It is well known and documented that some patients produce auto-antibodies, which are antibodies that our own body produces that attack our own tissues. This is the basis of autoimmune disease. In some Lyme disease patients, an auto-antibody against cardiolipin has been clearly established in Lyme patients with Lyme carditis.

Perhaps, in addition to other Lyme tests, we should also be tissue typing patients and searching for auto-antibodies? Tissue typing requires a small blood sample, and costs about $200.

Western Blot

The Western Blot essentially makes a map of the different antibodies the immune system produces to the bacteria. The map separates the antibodies by the weight of their respective antigens and are reported in units called kilo daltons or kDa. For example, a Western Blot may report bands at 22, 23, 25, 31, 34, 39, and 41 kDa. Each of these bands represents an antibody response to a specific protein found on the spirochete. The 41 band indicates an antibody to the flagella 41 kDa protein and is nonspecific. The 31 kDa band represents the OSPA protein and is specific for just a few species of Borrelia, as is the 34 band OSPB, and 23 kDa OSPC.

In 1994, the Association of State and Territorial Public Health Laboratory Directors, under a CDC grant, decided that there should be consistency between labs reporting Lyme disease Western Blots, and that a specific reporting criteria should be established. The consensus committe, chaired by Dr. Michael Osterholm, Ph.D., MN, set nationwide standards for Western Blot reporting. This sounds good, but one could argue they made a bad situation worse. Prior to the hearing, virtually every lab had accepted bands 22, 23, 25, 31, and 34 kDa as specific and significant, and reported them as positive for exposure to Borrelia burgdorferi. Not only are these bands specific for Borrelia species, but they represent all of the major outer surface proteins being used to develop the Lyme vaccines. The committee, without any clear reasoning, disqualified those bands as even being reportable.

After the consensus meeting, those bands were no longer acceptable. The result was that what had been a fair-to-good test for detecting Lyme disease had now become poor, arguably useless. Many scientists have questioned these new reporting criteria, and several wrote letters of protest to both the committee and to laboratory journals. Many labs stopped reporting the actual bands and instead, simply reported the test as positive or negative, thus preventing any further interpretations. (90)

How badly did the Lab Directors bootstrap this test? The following is an analysis of the new guidelines presented as an abstract and lecture at the 1995 Rheumatology Conference in Texas, chaired by Dr. Alan Steere, MD. (1995 Rheumatology Symposia Abstract #1254, Dr. Paul Fawcett, et al.)

This was a study designed to test the recently proposed changes to Western Blot interpretation by the Second National Conference on Serological Testing for Lyme Disease, sponsored by the CDC. The committee proposed limiting the bands that could be reported in a Western Blot for diagnosis of Lyme disease. Out of a possible 25 bands, 10 specific bands were selected as being reportable. An lgG Western Blot must have five or more of these bands: 18, 21,28, 30, 39, 41,,45, 58, 66 and 93 kDa. An lgM Western Blot must have two or more of the following three bands: 23, 39, 41.

Conspicuously absent are the most important bands, 22, 23, 25, 31, and 34, which include OSPA, OSP-B and OSP-C antigens - the three most widely accepted and recognized Bb antigens. These antigens were the antigens chosen for human vaccine trials. This abstract showed that, under the old criteria, all of 66 pediatric patients with a history of a tick bite and bull's-eye rash who were symptomatic were accepted as positive under the old Western Blot interpretation.

Under the newly proposed criteria, only 20 were now considered positive. (The number of false positives under both criteria was zero percent.) That means 46 children who were all symptomatic would probably be denied treatment! That's a success rate of only 31%.

*Note: A misconception about Western Blots is that they have as many false positives as false negatives. This is not true. False positives based on species specific bands are rare.

The conclusion of the researchers was: "the proposed Western Blot reporting criteria are grossly inadequate, because it excluded 69% of the infected children."

Elisa Test

The Enzyme-Linked Immunosorbant Serum Assay is the simplest, least expensive, easiest to perform, and most common Lyme test ordered. It is a test based on detecting the antibodies that our bodies make in response to being exposed to Borrelia burgdorferi (Bb). It is a preferred test by laboratories, not because it is more accurate than other Lyme tests, but because it is automated. Many different patient samples can be performed by a single machine simultaneously. This allows for a faster turnover, less costs, and theoretically, standardized test results that are consistent from lab to lab.

We are told by manufacturers, health departments and clinics that the Lyme ELISA tests are good, useful tests, but in two blinded studies that tested laboratories for accuracy, they failed miserably. Lorie Bakken, MS/MPH, showed in her studies that there was not only inaccuracy and inconsistency between competing laboratories, but also between identical triple samples sent to the same lab. In other words, identical samples often resulted in different results! In the first study, forty-five labs correctly identified the samples only 55% of the time.

In the latest study by the College of American Pathologists, 516 labs were tested. The overall result was terrible! There were almost equal numbers of false positives as false negatives. Overall, the labs were 55% inaccurate. The labs could only give a correct result 45% of the time. You are actually better off to flip a coin!

The basis of the ELISA test is that it can be primed to be very specific for particular antibodies. This is done by taking a laboratory sample of the Lyme bacteria and breaking the sample down into fragments. These fragments, or antigens, are then embedded on the side of a reagent vessel like a test tube. Then the patient's serum is added, and any free (non-complexed) antibodies specific for the test strain will then bind to the antigens, which are linked to special enzymes that will change color when antibodies are present. The sample is continually diluted until the reaction no longer occurs and no color change can be detected. The sample is then reported as a dilution ratio, such as one part serum to 256 parts water, or 1:256.

The ELISA test sounds simple and straight forward, but it has a couple of major flaws. Borrelia species are some of the most polymorphic bacteria known to exist. In other words, most Borrelia species can significantly change its surface proteins enough during cell division as to evade our immune system, and may differ from laboratory strains enough to result in negative tests, even if antiBb antibodies are present! In Europe, this problem is intensified because they have recognized three species of Borrelia that cause Lyme disease, and so they have available three separate ELISA tests. The questions in America are: 1) Have we recognized all the strains and species of Borrelia that cause Lyme disease symptoms, and 2) are we incorporating them into our tests? The answer is no. Convenience and expedience has chosen that we don't prime our ELISA tests withwild strains, but use a laboratory strain.

When a lab reports that their ELISA test has had high specificity and high sensitivity, it is usually interpreted by doctors as being a more accurate test, but the doctors don't know what the lab is actually measuring. One of the hidden problems of serologic Lyme tests is the fact that the tests must be primed with a source of bacteria to create the reactions with the patient's antibodies. To do this, virtually all labs rely on a laboratory strain of Bb known as strain B-31.Taking purified antigens from strain B-31 and injecting them into mice, they then can extract a monoclonal antibody to each antigen, or a polyvalent antibody soup. This antibody is concentrated and purified, and then added to the ELISA test to test the efficacy and performance of the test. Unlike the wild strains, B-31 grows well in culture, and this makes it a perfect choice as a consistent and inexpensive source of Bb. But the affinity the mouse monoclonal antibody has to B-31 antigen is quite different from the affinity the patients' antibodies have to the same antigen. This means the test may register as negative because the test cannot detect the slightly different antibody profile that a wild strain of Bb can produce. In other words, the labs are really comparing apples to oranges! This is why, when the American College of Pathologists used human sera to test the accuracy of 516 different laboratories ELISA tests nation wide, the overall accuracy was only 45%.

In the quest for specificity, most ELISA tests have become so specific that the test may fail to detect antibodies from related strains of Borrelia. This would include different genospecies that cause Lyme disease, as well as different Borrelia species that cause Tickborne Relapsing Fever. Would a cross reaction to the Borrelia species that cause Tick-borne Relapsing Fever be so bad?

The real Achilles' Heal of an ELISA Test is that it can only detect free antibody. It cannot detect any antibody that has become complexed with antigen.

The ELISA test depends on the active, free antibodies to attach to the free antigens that have been embedded on the walls of the test tube. If the antibodies in the serum being tested are already attached to antigens, then the enzyme reaction cannot take place. If we think of antibodies as sort of keys that fit into locks, and that on the surface of the bacteria are specific locks we now call antigens, you can see that once a key is inserted into a lock, the key is no longer available to open any other locks.

What makes this test so misleading is that many doctors accept high readings as an indication that the patient must really be sick. This logic is exactly backwards. If a patient is really infected with lots of bacteria, that means they have a lot of bacterial antigens floating around in the blood that are complexing free antibodies. So, as free antigen increases, free antibody decreases. Since the ELISA test detects only free antibody, a negative test might actually indicate a more serious infection. Many times, I have seen totally asymptotic patients with ELISA titers over 1000 be treated as though they were on death's doorstep simply because they had a high titer, while patients with borderline titers who are practically disabled are ignored, because a low titer is perceived as meaning less infected! These conclusions are erroneous and actually opposite to the truth, which is that a high titer means greater natural immunity.

This phenomena can actually be observed by using vaccines. If a patient has been vaccinated for a disease like tetanus, they will carry a high titer of free antibodies. If you try to measure those antibodies an hour after a booster shot is given, they will test negative. This is because the injected tetanus antigen complexes all available free antibody before the body can make more, so the measurable free antibody level drops.

The nature of all antibody is to seek out the proper antigen. The level of free antibody available is variable and often inadequate for the amount of antigen available. As antigen increases (i.e. The bacteria are dividing faster than the immune system can handle), free antibody drops.

What a high ELISA test may be a better indicator of is what level of immunity is the patient capable of mounting against this infection? A high titer is the same thing as saying the patient has a high natural immunity, and a low can mean that the patient may be overwhelmed by infection.

In one year-long study by Dr. Sam Donta, MD, done on chronic Lyme patients, the initial ELISA tests proved to be more than 66+% inaccurate (1996 LDF Conference lecture). Other researchers have also found the ELISA tests to be inaccurate. Using a 45-panel diagnostic testing protocol from the NIH for testing the efficacy of the ELISA and Western Blot, researchers found the accuracy of the Lyme ELISA varied from about 5075%, and were routinely inconsistent. The CDC's ELISA test did no better on average than any other ELISA. It is the CDC ELISA test which is used for surveillance of emerging Lyme disease in the United States, yet the test was correct only about two out every three tests. Too often, a single negative ELISA test can prevent a sick patient from getting treatment, even despite having serious symptoms!

In my opinion, the ELISA test is worthless as a diagnostic tool in Lyme disease. It is inconsistent and inaccurate, and should be discontinued as a tool to diagnose Lyme. If the NIH and CDC truly believe, as they've stated, that the diagnosis of Lyme disease is to be made on the basis of symptoms, then these tests should be temporarily banned until each manufacturer can prove efficacy using human serum.

wonderfullife
11-09-2011, 05:18 PM
Lyme Disease is a multi-system disease which can affect virtually every tissue and every organ of the human body. It is a disease which can be mild to some, and devastating to others. It can cripple and disable, or fog your mind. It can affect men, woman, and children, and even your family dog. (1-5,7-19) You may test negative for the disease, and still have it, or test positive and be symptom free. Some will get symptoms within days of a tick bite, while others may have it for years before they are even diagnosed. Some Lyme patients are told they have fibromyalgia, chronic fatigue syndrome, MS, or some other disease of unknown origin. (See abstracts of the 1996 International Lyme Conference) There are some studies which strongly support that the infection can be transmitted from mother to the unborn fetus, and may even cause still birth and has been implicated in some SIDs deaths. (MacDonald 20,45,52,53)

Why is Lyme disease such a mystery? Why does it mimic so many other disease? Why is it so difficult to detect? The reasons come from the microbiology of the bacteria that causes Lyme Disease.

Lyme disease is caused by a spiral shaped bacterium known as a spirochete. Diseases that are caused by spirochetes are notorious for being relapsing in nature, difficult to detect, and great imitators of other diseases. Syphilis, Tick-Borne Relapsing Fever, and Leptospirosis are other examples of spirochetal diseases. Lyme disease is caused by a bacteria called Borrelia burgdorferi, named after the man who isolated it from a Deer Tick in 1981, Dr. Willy Burgdorfer. The following is a tutorial to help explain away the mysteries of this bacteria, and why it causes so much controversy between patients and the medical community. (1)

The Structure of the Lyme Bacteria

The structure of the Lyme spirochete is unlike any other bacteria that has ever been studied before. It is one of the largest of the spirochetes (0.25 microns x 50 microns) It is as long, as a fine human hair is thick. Borrelia burgdorferi is a highly motile bacteria, it can swim extremely efficiently through both blood and tissue because of internal propulsion. It is propelled by an internal arrangement of flagella, bundled together, that runs the length of the bacteria from tip to tip. Like other Borrelia bacteria Borrelia burgdorferi has a three layer cell wall which helps determine the spiral shape of the bacteria. What makes this bacteria different from other species, is that it also has a clear gel-like coat of glyco-proteins which surround the bacteria. This extra layer is sometimes called the Slime Layer or S-layer. (See diagram 1) (45,46,59)

This means: This extra layer of glyco-proteins may act like a stealthy coat of armor that protects and hides the bacteria from the immune system. The human immune system uses proteins that are on the surface of the bacteria as markers, and sends attacking antibodies and killer T-cells to those markers, called outer surface protein antigens (OSP antigens). This nearly invisible layer is rarely seen in washed cultures, but can be seen regularly in tissue biopsies.(46)

The Lyme bacteria is different from other bacteria in its arrangement of DNA. Most bacteria have distinct chromosomes that are found floating around inside the cytoplasm. When the bacteria starts to divide and split in two, the chromosomes divide and the new copies of the chromosomes enter the new cell. The arrangement of DNA within Borrelia burgdorferi is radically different. It is arranged along the inside of the inner membrane. It looks something like a net embedded just underneath the skin of the bacteria. (46)

This means: We really don't understand the mechanisms of how Bb regulates its genetic material during its division.

Another unique feature to Borrelia burgdorferi are Blebs. This bacteria replicates specific genes, and inserts them into its own cell wall, and then pinches off that part of its cell membrane, and sends the bleb into the host. Why it does this we don't know. But we do know that these blebs can irritate our immune system. Dr. Claude Garon of Rocky Mountain Laboratories has shown that there is a precise mechanism that regulates the ratio of the different types of blebs that are shed. (46) In other bacteria the appearance of blebs often means the bacteria can share genetic information between themselves. We don't know if this is possible with Borrelia species. There have been reports of a granular form of Borrelia, which can grow to full size spirochetes, and reproduce. These granules are so small that they can be filtered and separated from live adult spirochetes by means of a micro-pore filter. (Stealth Pathogens Lida Mattman Ph.D. 66)

The division time of Borrelia burgdorferi is very long. Most other pathogens such as Streptococcus, or Staphylococcus, only take 20 minutes to double, the doubling time of Borrelia burgdorferi is usually estimated to be 12-24 hours. Since most antibiotics are cell wall agent inhibitors, they can only kill bacteria when the bacteria begins to divide and form new cell wall.(35,59-62)

This means: Since most antibiotics can only kill bacteria when they are dividing, a slow doubling time means less lethal exposure to antibiotics. Most bacteria are killed in 10-14 days of antibiotic. To get the same amount of lethal exposure during new cell wall formation of a Lyme spirochete, the antibiotic would have to be present 24 hours a day for 1 year and six months! Note: Antibiotics kill bacteria by binding to the bacteria's ribosomes, and interrupting the formation of cell wall proteins.

Like other spirochetes, such as those that cause Syphilis, the Lyme spirochete can remain in the human body for years in a non-metabolic state. It is essentially in suspended animation, and since it does not metabolize in this state, antibiotics are not absorbed or effective. When the conditions are right, those bacteria that survive, can seed back into the blood stream and initiate a relapse. (59-62,70)

This means: Just because a person is symptom free for long lengths of time doesn't mean they aren't infected. It may be a matter of time. Whereas viral infections often impart a lifelong immunity, Lyme, like other bacterial infections, does not retain active immunity for long periods of time. People are often reinfected with Lyme. (96)

How does the Lyme bacteria travel from the bloodstream to other tissues? While we have known for a long time that the Lyme spirochete can show up in the brain, eyes, joints, skin, spleen, liver, GI tract, bladder, and other organs, we didn't understand the mechanism by which it could travel through capillaries and cell membranes. (Abstract 644) Then Dr. Mark Klempner presented at the 1996 LDF International Lyme Conference an interesting paper that gave us part of the answer.

Many researchers have observed that the Lyme spirochete attaches to the human cells' tip first. It then wiggles and squirms until it enters the cell. What Dr. Klempner showed was that when the spirochete attached to the human host cell, it caused that cell to release digestive enzymes that would dissolve the cell, and allow the spirochete to go wherever it pleases. This is very economical to the bacteria to use our own cell's enzymes against us, because it does not need to carry the genes and enzymes around when it travels. Dr. Klempner also showed that the spirochete could enter cells such as the human fibroblast cell (The skin cell that makes scar tissue.) and hide. Here the pathogen was protected from the immune system, and could thrive without assault. More importantly, when these Bb-fibroblast cultures were incubated with 10 x the MIC for IV Rocephin, two thirds of the cultures still yielded live spirochetes after two weeks, and in later experiments for more than 30 days. If we can't kill it in a test tube at these high concentrations in four weeks, how can we hope to kill it in the human body? (22,48,79,80,)

This means: The infection can enter the tissue that is optimal for its survival, and it may evade the immune system and antibiotics by hiding inside certain types of cells.

Another interesting observation about this bacteria is how it interacts with our body's immune system; Dr. David Dorward of Rocky Mountain Labs made a video tape of how Borrelia burgdorferi acts when surrounded by B-cells. (The type of white blood cell that makes antibody.) The spirochete attached tip first, entered the B lymphocyte, multiplied and ruptured the cell. It repeated this process for three days until the B-cells were able to come to an equilibrium. A matter of concern was that some of the spirochetes were able to strip away part of the B-cell's membrane, and wear it like a cloak. (Dorward, Hulinska 1994 LDF Conference Vancouver BC)

This means: If this spirochete is evolved enough to attack our B-lymphocytes, then it may also be evolved in other ways that we do not yet understand. It is for certain that its ability to kill B-lymphocytes evolved as part of a defense mechanism to evade its own destruction. The observation that it can use the B-cell's own membrane as camouflage indicates that it may be able to go undetected by our immune system. The way our immune system is supposed to work is that it recognizes foreign invaders as being different from self, and attacks the infection.

Unfortunately, the immune system sometimes attacks our own cells. This is called autoimmune disease. If a foreign invader has a chemical structure similar to our own tissue antigens, our bodies sometimes make antibodies against our own tissues. In people with Lyme disease scientists have discovered auto-antibodies against our own tissues including nerve cells (axons), cardiolipid, myelin (also seen in MS), myelin basic protein (also seen in MS), and neurons (brain cells) (23,28,38-40,43,45,56,57,60,88)

When the immune system finds a foreign invader, it tags that invader in a number of ways. A cell called the macrophage can engulf the bacteria, and then communicate to other immune cells the exact description of the bacteria. Another cell might mark the cell with antibody which attracts killer T-cells. Some types of T-cells communicate to other cells what to attack, and regulate the immune assault. But sometimes the body can produce a type of antibody that doesn't attack or help. A blocking antibody will attach and coat the intruder, but it won't fix compliment, and it shields the bacteria from further immune recognition. In Lyme we have seen quantities of IgG4 blocking antibody such as is seen in some parasitic infections. (Tom Schwann RML 92 LDF Conference) *Note: Compliment is a term used for a series of 18 + digestive proteins that are only activated by signals from our immune system, such as compliment fixing antibodies.

In order for the immune system to make an attacking antibody, the immune system must first find an antigen which it can attack. Unfortunately, as seen by freeze fracture electron microscope, photographs of the Lyme bacteria show that most of the antigens are on the inside of the inner membrane, and not on the outside. (60) This makes the bacteria less visible to the immune system and more difficult to attack. The most intriguing fact about Borrelia spirochetes is their well documented ability to change the shape of their surface antigens when they are attacked by the human immune system. When this occurs, it takes several weeks for the immune system to produce new antibodies. During this time the infection continues to divide and hide. (1,47,63,66)

It appears that Borrelia are able to change their surface antigens many times, and can do it quickly. In one study by Dr. Andrew Pachner MD, he infected mice with a single strain of Borrelia burgdorferi. After several weeks, he was able to isolate two slightly different forms of the bacteria. The bacteria from the bloodstream was attacked and killed by the mouse's immune sera, but the bacteria isolated from the mouse's brain was unaffected by the immune sera. The bacteria isolated from the mouse's brain had a new set of surface antigens. It appears that contact with the CNS caused the bacteria to change its appearance. Since the brain is isolated from the immune system and is an immune privileged site, the bacteria became its own separate strain. (47,97)

This means: Infections of the bloodstream may be different from the infections that are sequestered in the brain. While we continue to have active immunity in the bloodstream, the brain has no immune defenses except for circulating antibodies. So, if those circulating antibodies are ineffective to attack the bacteria in the brain, then the brain is left without any defenses, and the infection goes unabated.

Over 100 references, abstracts and diagrams are inserted into the text to support the statements in this chapter.

Another peculiar observation of these bacteria is seen inside the bacteria. When the genetic control mechanisms of this bacteria are inhibited with antibiotics known as DNA Gyrase Inhibitors (ciprofloxin) the bacteria start to produce bacterio-phage. A phage is a virus that specifically attacks bacteria. In this case there are two distinct forms. This means the Lyme bacteria at one time were attacked by viruses. It was able to suppress them, but the DNA to make the phage is still incorporated within the DNA of the bacteria. Perhaps activation of this phage could one day be beneficial to treating chronic Lyme patients? (JTBD 94)

What happens when the infection gets to the brain? In the case of Lyme disease, every animal model to date shows that the Lyme spirochete can go from the site of the bite to the brain in just a few days. (41,60, abstract 644) While we know these bacteria can break down individual cell membranes and capillaries, its entrance into the brain is too pronounced for such a localized effect. When the Lyme bacteria enters the human body, we react by producing several immune regulatory substances known as cytokines and lymphokines. Several of these act in concert to break down the blood brain barrier. (E.g. Il-6, Tumor Necrosis Factor-alpha, Il-1, Transforming Growth Factor-beta etc.) In addition to affecting the blood brain barrier, these cytokines can make us feel ill, and give us fevers. (54,60,) (JID 1996:173, Jan)

Since the brain has no immune system, it prevents infection by limiting what can enter the brain. The capillary bed that surrounds the brain is so tight that not even white blood cells are allowed to enter. Many drugs can't enter either, making treatment of the brain especially hard. For the first ten days of a Lyme infection, the blood brain barrier is virtually nonexistent. This not only allows the Lyme bacteria to get in, but also immune cells that can cause inflammation of the brain. (41) *Note: The breakdown of Bb was shown to occur by tagging WBCs, albumin, and other substances known not to cross the BBB with radioactive Iodine. The CSF was tested, and then the animals were infected with Bb. Then the CSF was tested everyday for several weeks. The result: No cross over of Iodine in the control group, 100% crossover in the infected group for 10 days. The infection had the same result as injecting the radioactive iodine directly into the brain. (60)

When the human brain becomes inflamed, cells called macrophages respond by releasing a neuro-toxin called quinolinic acid. This toxin is also elevated in Parkinson's Disease, MS, ALS, and is responsible for the dementia that occurs in AIDS patients. What quinolinic acid does is stimulate neurons to repeatedly depolarize. This eventually causes the neurons to demyelinate and die. People with elevated quinolinic acid have short-term memory problems. (27,29-37,40-42,74,75, 82-84,87-90)

This means: If we think of all of our brain cells like telephone lines, we can visualize the problem. If all of the lines coming in are busy, we can't learn anything. If all of the lines going out are busy, we can't recall any memories. Our thinking process becomes impaired.

A second impairment to clear thinking that Lymies experience is the restriction of proper circulation within the blood vessels inside the brain. Using an instrument called the Single Photon Emission Computer Tomography scanner (SPECT scans), we are able to visualize the blood flow throughout the human brain in 3-D detail. What was seen in the brains of chronic neurological Lyme patients was an abnormal "swiss-cheese" pattern of blood flow. The cortical, or thinking region of the brain, was being deprived of good circulation; the occipital (eyesight) regions had an increase flow. This could help explain why most Lyme patients complain of poor concentration and overly sensitive eyes. (91)

Lyme Tests

There's a Lyme test, so what's the problem? There are several Lyme tests, but most of them are dependent on the body's ability to make antibody against this bacteria. As we have seen, this may be a problem. There is the S-layer protecting the bacteria; the surface antigens are not readily exposed; there may be a blocking antibody; the bacteria might be inside a human cell; the bacteria might be down regulating the immune system through cytokines; the bacteria might have altered its antigenic appearance to fool the immune system; the bacteria might be cloaked in B-cell membrane; the bacteria might be hiding in joints, tendons, white blood cells, skin cells or the brain. Remember, if even just one spirochete survives, it could cause a relapse. Then there is another problem - the tests that detect antibody can only detect free uncomplexed antibody. (23,25,55,70)

When an antibody is formed, it is meant to latch on to something and never let go until it is destroyed. Like a lock and key, antibodies fit their associated antigens. Once the antibody attaches to the antigen it is no longer is a detectable antibody, because it has now become an antibody-antigen complex. This complex is not measurable using today's commercially available tests. Also, as the amount of antigen increases, the amount of antibody can decrease, because the antigen will trap out the available antibody and sequester it. So, a person who has a bad infection but is making a limited amount of antibody can be overwhelmed by antigen, thus making antibody detectable only if you can detect the complex.

This means: People who have the worst infections may have the lowest antibody titers, and test negative. Note: It takes four weeks from the tick bite to test positive.

There are two main categories of Lyme tests. The most common and least specific is the Enzyme Linked Immune Sera Assay or ELISA, the other is an Immuno Blot or Western Blot. The Western Blot essentially makes a map of the different antibodies we make to the bacteria. The map separates the antibodies by size and weight, and is reported in units called kilo daltons or kDa. For example, a Western Blot may report bands at 22, 25, 31, 34, 39, and 41 kDa. Each of these bands represents an antibody response to a specific protein found on the spirochete. The 41 band indicates an antibody to the flagella protein, and is non-specific. The 31-kDa band represents the OSP-A protein and is specific for Borrelia, as is the 34 band OSP-B and 25 kDa OSP-C.

In 1994, the NIH decided that there should be consistency between labs reporting Lyme Disease Western Blots, and that a specific reporting criteria should be established. This sounds good, but one could argue they made a bad situation worse. The consensus committee decided to set the standards for a positive test based on the number of bands that appear. Whereas every lab prior to the hearing had accepted bands 25, 31, and 34 as specific and significant, the NIH, without any clear reasoning, disqualified those bands from being reportable. The result was that what had been a fair good test had now become poor or even useless. (90)

How badly did the NIH bootstrap this test? The following is an analysis of the new guidelines presented as an abstract and lecture at the 1995 Rheumatology Conference in Texas. (1995 Rheumatology Symposia Abstract # 1254 Dr. Paul Fawcett et al.)

This was a study designed to test the recently proposed changes to Western Blot Interpretation. At the Second National Conference on Serological Testing for Lyme Disease, sponsored by the NIH, the committee proposed limiting the bands that could be reported in a Western Blot for diagnosis of Lyme Disease. An IgG Western Blot must have five or more of these bands: 18, 23,28, 30, 39, 41, 45, 58, 66, and 93 kDa. An IgM Western Blot must have two or more bands of the following three bands: 23, 39, 41. Conspicuously absent are the most important bands, 22, 25, 31 and 34, which include OSP-A, OSP-B and OSP-C antigens - the three most widely accepted and recognized antigens. These antigens are so immuno-reactive that they were the antigens chosen for human vaccine trials. Yet they are not considered important enough to include in the diagnostic criteria. Why?

This abstract showed that, under the old criteria, all of 66 pediatric patients with a history of a tick bite and Bull's Eye rash who were symptomatic were accepted as positive under the old Western Blot interpretation. Under the newly proposed criteria, only 20 were now considered positive. That means 46 children who were all symptomatic would probably be denied treatment! That's a success rate of only 31 %. The number of false positives under both criteria was ZERO %. * Note: A misconception about Western Blots is that they have as many false positives as false negatives. This is not true. False positives are rare. The conclusion of the researchers was: "the proposed Western Blot Reporting Criteria are grossly inadequate, because it excluded 69% of the infected children."

We are told by manufacturers, health departments, and clinics that the Lyme ELISA tests are good and that they are useful, but in two blinded studies that tested laboratories accuracy, they failed miserably. In the latest study, 516 labs were tested. The overall result: 55% inaccurate! You are actually better off to flip a coin! (98, 99)

Repeatedly, there have been patients who are seronegative for antibodies, yet culture positive. Despite this, our medical community is dependent on these tests and relies upon them as though they were 100 % accurate. No matter how bad the tests are, as long as we have them doctors will use them. This is why doctor Samual Donta, M.D., called for a complete ban of the Lyme ELISA test at the 1996 LDF Lyme Conference. He found that, in some cases, Lyme ELISAs were more than 75 % inaccurate, yet it was relied upon as though it were the last word - and all too often it is.

The worst problem for chronic Lyme patients is that, after they are treated with antibiotics, they are told they are cured even if they have a recurrence of symptoms. There is a persistent dogma in medicine that 28 days of IV antibiotics cures all Lyme Disease. In fact, the ongoing six-year-old Nantucket Island Lyme Treatment Study showed IV antibiotics to have the highest relapse rate in late Lyme disease! This was because doctors put too much faith in IV antibiotics as being so powerful, that they did not follow up IV's with oral antibiotics. The key to treating late Lyme appears to be the length of antibiotic treatment, not the method. If IV's are followed up by six months or more of oral antibiotics, the relapse rate dropped to 13%. (Dr. Leslie Fein MD, MPH, Magnarelli MD, MPH 96 LDF Conference)

I have included in the references several published studies, case histories and abstracts that deal with culture positive patients who had been previously treated aggressively with antibiotics, often including intravenous antibiotics. Most of these cases are patients who are seronegative for any Lyme antibodies, yet are culture positive. If we are repeatedly culturing this bacteria out of patients who have been treated and who are negative by all other tests, we need to rethink our understanding of this disease! We need to treat symptoms, not tests; we need to recognize that, while Lyme is a treatable disease, in some cases it appears to be incurable. I would not like to be the doctor who under treats this disease, now knowing that relapses are potentially more dangerous than treating until the symptoms are gone. (4,6,42,49,67,68,70-96) (Lawrence C, Lipton RB, Lowy FD, and Coyle PK. Seronegative Chronic Relapsing Neuroborreliosis. European Neurology. 1995; 35(2): 113-117)

Too often, I have seen the word cured used in Lyme Disease Studies, only to find that the researchers have redefined the word cure to mean seronegative. Seronegativity is not synonymous with cure. The numerous culture positive cases in recent years should have negated that kind of logic years ago, and yet, in 1997, researchers are still publishing studies that use antibodies and PCR as the end point for cure. It's time to ask the patients one simple question: How are you feeling?

So, let's say hypothetically you are bitten by an infected tick, you get a rash, you get sick, and you have a positive test. So you get 2-4 weeks of antibiotics and you get better, but then you get sick again. No problem! You go back to your doctor, and he says, "Well, we'd better give you another Lyme test" - and its negative. Why? Even though you have an active infection, the antibiotics cleared that infection from your blood stream. That is where your immune system is. The rest of the pathogens are hiding from the immune system inside your joints, your tendons, and your brain. Only now you don't have antibiotics to fight the infection, or any antibodies!

In a study by Dr. Musher, M.D., he looked at incompletely treated Tertiary Syphilis patients, and compared them to those Tertiary Syphilis patients who never got antibiotics. He found that the incompletely treated group went into dementia faster.

Why? Because they had no natural immunity left. Their ability to make sufficient antibody was diminished, because the antibiotics eliminated the stimulus from the blood stream, but the infection was still hidden in the brain! (35,61,62,65,74,83)

Conclusion: Lyme is an extremely complex disease that can cause long term chronic infections. Patients can be seronegative, yet culture positive (even after aggressive antibiotic therapy). The infection enters the brain early in the infection (within days). The sequestered bacteria within the CNS can be so different from the initial infection that serum antibodies are ineffective. Incomplete antibiotic treatment of Lyme Encephalitis can harm the patient.

Addendum 1:

The Final Note: Recently, there have been some very large educational institutions that have maintained a strong position on Lyme disease being easily detected and treated, with a high degree of success. Let me site two such examples:

First, several state health departments, including the Minnesota State Department of Health, have received mailings from Yale University pertaining to Lyme Disease. (Reference: The Yale Medicine Special Report by Marc Wortman, 1996 Yale Medicine Magazine pp.1-15, May 15th, 1996) This report was sent to several health departments throughout the United States who had received a CDC grant to initiate a patient education program on Lyme disease.

In the table of contents,Yale describes themselves as being the "Lyme Dream Team". The "dream team" then goes on to recommend what to do, "If you are bitten by a Deer Tick....".(Excerpts from page 11, Yale Medicine, May 15th, 1996)

If you suspect the tick was attached for at least 36 hours, observe the site of the bite for development of the characteristic skin rash, erythema chronica migrans, (sic) usually a circular red patch, or expanding "bull's eye", that appears between three days and one month after the bite. Not all rashes at the site of the bite are due to Lyme disease. Allergic reactions to tick saliva are common. Preventative antibiotic treatment is not necessary, is costly, and may cause side effects.
If symptoms of later-stage Lyme disease develop - arthritic swelling of a joint, most often the knee, or facial nerve palsy - have a test done. If the test is positive, have a more precise test done. Only if this test proves positive should a course of antibiotic therapy begin. Expect some symptoms to linger up to three months. No further antibiotic treatment is necessary.

Once the Minnesota State Health Department became aware of this passage, the reprint was pulled from their educational literature sent to Health Department Lyme Education Trainers. (A program developed from a CDC grant.) The advice in this excerpt is in direct conflict with the Minnesota Guidelines for the Treatment of Lyme Disease. More importantly, in my opinion, it is bad advice that is potentially dangerous to patients!

The passage inferrs that, if you have a tick attached for 35 hours, you couldn't get Lyme. If you do have a tick bite and a rash, there is no need to seek treatment - don't go to the doctor unless you have late symptoms. The symptoms the Yale medical "Dream Team" deems as important enough to go to the doctor are a severely swollen knee, or Bell's Palsy. Even if you have these symptoms, but your ELISA Lyme test is negative, you can't have Lyme and should not seek treatment. If the ELISA is positive, you need to have a second confirmatory Western Blot Lyme test. If this test is negative, you can't have Lyme disease!

Let's review this medical advice:You are bitten by a deer tick, it is attached for 35 hours, you get a rash at the site of the bite, you develop late stage symptoms, you have a positive ELISA Lyme test, but you shouldn't pursue treatment if a second test is negative!! Apparently, antibiotic therapy is more dangerous than having late stage disease!

If your doctor wants to take on the medical/legal risk of not treating a positive tick-bite rash, symptoms, and a positive test, then he is a very brave soul. In my opinion he would be at risk of malpractice and could be held accountable for any irreparable harm that occurs due to refusal to treat late stage Lyme symptoms with antibiotics.

This article by Yale is an example of two erroneous prevailing attitudes within the medical community about Lyme disease. First, don't treat seronegative Lyme disease (even apparently in presence of a rash, and late state symptoms, post tick bite), the test are accurate. Second, once you treat with antibiotics, even despite the persistence of symptoms, the patient is cured. The trouble with relying on these two absolutes in Lyme disease is that they are quickly dismissed by any case of seronegative Lyme, or a single patient that is culture positive post-antibiotic treatment.

I would not want my reputation and credential dependent upon such a flimsy foundation. If one example of seronegative Lyme exists, or culture positive Lyme post treatment, it refutes everything these institutions have insisted is true. (See two such references, Lawrence & Masters.)

Why do these erroneous beliefs persist? Let me site my second example of large educational institutions disseminating information to doctors that supports these beliefs. The American College of Physicians and Surgeons offers a teaching seminar to doctors on how to diagnose and treat Lyme disease. Included is a VHS video tape that has several vignettes of doctors dealing with patients with potential Lyme disease. In every case, there is either a dependence on Lyme testing - or, once the patient has been treated, they are no longer capable of sustaining infection.

In my opinion, the absence of information about the accuracy of Lyme testing, the incidence of sero-negative Lyme, and the possibility of relapse post treatment, indicated to me that the tape is designed to give doctors a method of dumping Lyme patients. In no case presented is sustained treatment advocated, suggested, or advised. If symptoms persist, the patient has either post-Lyme Syndrome, or needs further testing, including a psychological work up, to find some other cause for the patient's symptoms.

In my opinion, the advice on the ACP video is based on two wrong conclusions: First, that serological Lyme tests are accurate. Second, that active infection cannot persist post-antibiotic treatment - therefore treating relapses with further antibiotics is unnecessary. (Unless supported by further serum antibody testing.) In every case that is presented, the doctor is given an opportunity to give up on his patient before considering sustained antibiotics to treat the persisting symptoms. It is a wonder that any of the patients are diagnosed at all, considering the apparent lack of recognition of even the most common Lyme disease symptoms.

Nowhere on the tape do I hear doctors asking about common and frequent symptoms of Lyme disease, such as: stiff, crunchy neck, visual complaints, heart palpitations, muscle twitches (especially in the face), fatigue, depression, urinary frequency, and memory problems. The only symptoms the educators seemed concerned about was a history of a deer tick bite, a bull's eye rash, and swollen joints. How can you make a clinical diagnosis if you don't know the most basic of symptoms? The truth is, there is no effort made to make a clinical diagnosis, except by an erythema rash. What is distressing about using the rash as diagnosis is that, in the Vanderhoof study of over 1000 chronic Lyme patients, it took on average 5.3 doctors to diagnose Lyme even in the presence of a bull's eye rash. This same study showed that a delay in treatment of more than a few months led to a much higher incidence of relapse, or chronic symptoms.

The key to dumping a Lyme patient is how to write the patient's chart to support a non-Lyme diagnosis. In no instance is the patient ever asked how they are feeling, nor is the patient's response to antibiotics ever to be considered as the end point of treatment. Once again, the clinical picture is ignored in favor of either serology, or a blind belief that all Lyme patients are cured with a few weeks of treatment. But I as you what brought the patient to the doctor? Symptoms! So, if the cure does not alleviate the symptoms, what good has the short course of antibiotics done? I can understand why treatment is discontinued in patients who feel cured, but when they are still sick it seems unconscionable. In fact, I find that the very same doctors who advocate short term treatment in Lyme disease, rarely seem to follow the same protocol when they or a family member gets sick.

I once had a discussion with an Internal Medicine Specialist, whom I've known for ten years, about the length of treatment for his Lyme patients. He was very vocal about how most Lyme is really Ehrlichiosis, and that all Lyme patients get two weeks of doxycycline, period - no exceptions. Except one. When I met him at an airport that summer, I came to learn his son had been bitten by a tick that spring. As a precaution, he kept his son on amoxicillin for three months, even though he had no symptoms or rash! Yet his late stage Lyme patients still receive two weeks of doxycycline.

Apparently the treatment for the proverbial goose is different than for the gander! It is always difficult to refute large educational institutions, and any individual doctor who tries may be jeopardizing his career. An equally difficult battle is getting doctors who have adopted these false tenets as absolutes to change their minds. It is a difficult thing for a doctor to admit that his or her paradigm of diagnosis and treatment is flawed and possibly harmful. The revelation that perhaps hundreds of patients should have received extended therapy could be an unsettling realization for many doctors.

The first hurdle is having to go against large teaching institutions who have the full support of the NIH, CDC, or AMA.Then, there is the second issue of having to confront previous patients.What does a doctor say to a patient who really had a treatable illness instead of MS? Any new change in diagnosis and treatment is a scary proposition for most doctors if it means confronting failures. Few want to be the vanguard force in leading that crusade, but the ones who do support their patients are heroes.

While large institutions continue to disseminate their opinions and view points to millions, it is a much smaller audience that the opposition can address. Right now, doctors have to win their battles one patient at a time, and in doing so they face persecution and criticism.

Treating Lyme patient is not a profitable endeavor. Lyme patients take too much time, require lots of counseling and education, and often continue to return with symptoms despite aggressive treatment. The physician who treats Lyme disease aggressively enters into a controversial area of medicine. It is simply easier to avoid Lyme patients than treat them, because, in treating them, they have to go against all the major medical institutions who have declared only their treatment protocols are acceptable. But let's look at the real area of interest that large institutions have in not treating Lyme disease - profit!

No profit in treating Lyme patients - treatment is a low yield return. Today's clinics thrive on high profit, low overhead procedures. It is much more profitable and less risky to do a fifteen minute $600 EMG test for carpal tunnel syndrome than it is to encourage Lyme patients to spend an hour in an exam. The net reward per time spent is too small. Low overhead, low risk, high dollar return is why hospitals focus on programs to combat smoking, weight loss, drug rehabilitation, repetitive strain disorders, depression, birthing centers, diabetes education, etc. How often do you see hospitals seeking out quadriplegics, MS patients, ALS, and other chronic disabling diseases? Many of these programs have to be government subsidized before they are profitable enough for institutions to take them on.

Every major medical research facility in the last few years has been focused on two areas of research: vaccines and tests. While only 15,000 patients a year are reported as having Lyme disease (CDC figures), hundreds of thousands are tested. By one institution's own figures, they give 100 tests for every case they treat. Amazingly, Olmstead County in Minnesota has yet to report a single case of Lyme disease to the CDC. This means they have made their money by testing, not treating. (Most tests are unnecessary, because Lyme disease, according to the NIH, is a clinical diagnosis made on the basis of symptoms.) Perhaps millions of people will be vaccinated with the new vaccines. So, whoever owns that concession stands to make a fortune.

Addendum 2:

It used to be a dogma that you either publish or perish, but now it's apply for patents or perish. The last four major announcements of "new Lyme tests" were released as press releases before a single study was published in any peer review journal as to the real effectiveness of the tests. Institutions now compete with each other for patents on tests. The real money is to own the test that is going to be the new standard in medicine. This is why they publicize the slightest advancement even before they publish. They want the business before they are forced to compare their product to the competition. None of these institutions want to tell you how bad their test is they only want to tell you how much better it is than the competition's.

Let me give you an example: the University of Minnesota tried to develop a new PCR test for early Lyme detection. The PCR test is only as good as the primers1 you use, and, if you won the patent with bad primers, you are stuck. You either buy the rights to use someone else's primers, or you use what you have. So, what do you do if you have lousy test results? You don't compare them to the competition, but rather with an easier standard. In this case, the University didn't compare their test to other PCR tests, but instead compared it to culturing. The abstract stated that patients with tick bite and bull's-eye rash were only successfully cultured 4% of the time, but the PCR was 18% positive therefore, the PCR test was four times more useful than culturing. The trouble with this comparison is that most labs can get 80% culture success, thus the researchers are setting arbitrary standards to make the test look good. This PCR test is actually four times less accurate than culturing, if the culturing is done by a competent lab.

What nobody seems to question is that the bull's-eye rash indicates 100% of the test subjects were infected, and that this PCR test only detected 18 out of every 100 tested! But no one wanted to summarize the conclusion that their test was poor, and worse than the competition. The newspaper headline read "New Lyme Test More Accurate in Early Lyme." More accurate than what??? It's all in how you express your conclusion. This study, of course, was never published, because peer review journals would have rejected it. Instead, an abstract was presented at a rheumatology conference, and a press release issued on what the press called ".a new and better Lyme test."

The trouble is that it's all hype, yet many doctors will read the headline and think that this is a better test just because it is new. The fact is that most new tests aren't better, they just represent new patents, and have better press. Recently, the Minneapolis Tribune published a press release from the U of MN on a new, FDA approved PCR test for Lyme that used synovial fluid from an enlarged knee. In the article, it gave the cost of the test, where to send it, and the labs telephone number for people to make arrangements for sending in samples. What the article implied was this was the best and newest Lyme test available. What the article failed to do was compare it to any other test, or to emphasize that most press releases of this type are less than altruistic. The patients have become secondary in the business of Lyme disease. The patients are tested, vaccinated, and sent out the door in a rush to maintain rapid turnover. Complicated patients that require treatment slows this process down, and decreases profits.

The days of doctors going on house calls are a thing of the past. It's not the doctor's fault, though. Monthly administrative meetings within most large clinics look at profit and loss statements just as though medicine were any other business. Administrators address issues of income and expenses, just like any other corporation. If patents on tests are profitable, that's what you do. If house calls aren't, then that's what you stop. The formula is maximum amount of money per hour versus least expenses per hour, with the least possible risk. The net result is: tests are profitable, vaccines are profitable, and treating Lyme patients is not profitable.

So, how do you justify not treating? You create treatment protocols that fit the needs of the clinic and not the patient. Then, you put the entire weight of the institution behind these protocols, and intimidate everyone who disagrees. Let's put these protocols to the test. If one sero-negative, culture-positive patient exits post-antibiotic treatment, their protocols crumble. It is interesting that, while most published studies supporting Lyme as a relapsing disease of active infection are either position papers, opinion/editorial pieces, or are based on that institution's own Lyme serology tests! When an institution uses its own serology tests as an endpoint for cure, the fox is definitely watching the hen house.

Serology cannot determine cure. EVER! Yet it is still being done! The American College of Physicians and Surgeons has recently published a newsletter, "The ACP Initiative on Lyme Disease, Vol. 1, Issue 1". Which sites a recently published paper that uses serology as an end point for cure, and has a short period of a few months as a follow up. At no time were the patients symptoms assessed as the basis of successful treatment. Instead, serologies were used as the determinant (Reference: Cetriaxone (IV Rocephin), compared with doxycycline for the treatment of Lyme disease. Dattwyler RJ, Luft BJ, Kunkel MJ, Finkel MF, Wormser GP, Rush TJ, Grunwaldt, et al New England J. of Med. 3373(5):289:294 July 31 1997.) The conclusion of this paper was that a short course of doxycycline (the least expensive drug known for treating Lyme disease) is as effective as a short course of "costly" IV Rocephin.

It is quite a bone to throw to the health insurance industry by saying all Lyme patient can now be treated a short period of time with the least expensive drug, but is it true? Let's examine this article and premise: At the 1993 LDF Conference, a study was presented by Dr. Daniel Cameron, MD. In his study of more than 40 nursing home patients, he found that the relapse rate for IV Rocephin for four weeks was 25%, but the relapse rate for doxycycline was 87%. The difference in this study was that the follow up was 13 months not three months.

In a six year, ongoing study using the population of Nantucket Island, there was an interesting statistic that occurred involving the use of IV Rocephin. Since the entire population of 5000+ on the island went to only four doctors, it was easy to do long term followups on patients who were treated for Lyme disease. What was found was IV Rocephin had the highest rate of relapse, unless followed up for several moths with oral antibiotics. This was because the short duration of four weeks of treatment was inadequate to prevent relapse. This was why 57% of these patients had documentable relapses.

So, any current study that compares short-term doxycycline success with IV Rocephin is comparing two inadequate treatments to each other. Yet, the conclusion does not talk about total effectiveness it simply states the two drugs are equally effective (or ineffective). By not doing long filially to determine overall relapse rate, the New England Journal study makes doxycycline look good.

The key to the Nantucket Island study, spotting the high incidence of relapse, was in the length of the followup. The longer the followup, the higher the relapse rate. Some have said that this high relapse rate may be due to reinfection, but subsequent animal models have shown this to be otherwise.

At the 1997 LDF conference, a study was presented using naïve beagles as subjects. In this study, three groups of six beagles were studied. One group of six was infected; using infected ticks, and treated with four weeks of amoxicillin. Another group was infected and treated with a double dose of doxycycline for four weeks.

The third group was the control. In the doxycycline treated group, at three months post-treatment, it appeared that 100% were cured. But, at two years at autopsy, five of the six (5/6) beagles were shown to have active infection, or complete relapse. The key to uncovering the high incidence of relapse was a long, two-year followup period. The current study cited by the ACP totally ignored this experience showing the necessity of long followup periods, and the fallibility of antibody serologies used as end points to treatment, or as a measure of affecting a cure.

A more basic study showing the inadequacy of doxycycline goes back to 1989, in an abstract from Austria. Here, the researcher incubated a live culture of Borrelia burgdorferi with doxycycline for two weeks. The culture appeared to be dead, as both motility and reproduction had ceased. The culture did not have the appearance, however, of the amoxicillin treated culture, which was filled with Lysed cells. So, using micropore filters, the researcher filtered doxycycline treated cultures, and separated the intact Borrelia from the supernatant. He then washed them, and placed the filtrate back into fresh culture media. Over two thirds of the cultures reactivated, becoming motile and beginning to reproduce. It appeared that doxycycline immobilized the bacteria by interrupting protein syntheses and metabolism. This pushed the cells into a non-metabolic state. Since the doubling rate is often used as a means of determining if the cells are alive, it was assumed that the cultures were dead, when they were in fact just dormant.

The most recent New England Journal study is deeply flawed, yet it will have an immediate impact on the use of IV Rocephin. The design of this study has ignored previous studies that show a long-term followup is needed. It ignores the fact that the use of antibody serology cannot be used as the endpoint for treatment, or for determining cure. It does not use adequate methods to document the presence of live bacteria. The study does not use the patient's symptoms as a basis of cure. So, I ask, who has something to gain from this kind of study?

It seems very coincidental that, in the past, paid medical advisors on Lyme disease for the insurance industry produce study after study showing that, in the short term, doxycycline is as effective as other more expensive drugs. Once again, the basis of this study is a dependence on serologies, and short-term treatments leading to total cure. There are dozens of studies, case histories and abstracts, which document sero-negative.

Lyme, and culture positive Lyme post-treatment. Yet, these studies are being ignored. Today, major health institutions have backed themselves into a corner, and are using their influences, economic resources, and authority to make their view point the only viewpoint.

But do these physicians that disseminate this anti-Lyme point of view really believe what they are promoting, or are they just defending a position they have taken because they don't what to admit they have taken a position which may prove to be wrong? The answer is in the fact that most of these researchers have chosen to completely ignore studies documenting active infection post-treatment, or sero-negative Lyme disease. Instead, they only accept their own studies, using their own antibody tests as endpoints for cure.

1. A PCR primer is a short piece of specific DNA that primes the test to only amplify any matching DNA.

2. Naive means uninfected animals.

wonderfullife
11-09-2011, 07:50 PM
Bonnie Bassler: The secret, social lives of bacteria - YouTube

Bacteria talk to each other.

wonderfullife
11-09-2011, 08:47 PM
Cerebrospinal fluid findings in adults with acute Lyme neuroborreliosis.

Djukic M, Schmidt-Samoa C, Lange P, Spreer A, Neubieser K, Eiffert H,
Nau R, Schmidt H

J Neurol 2011 09 6

Presence of BB-specific antibodies in the cerebrospinal fluid (CSF) with
evidence of their intrathecal production in conjunction with the white
cell count in the CSF and typical clinical symptoms is the traditional
diagnostic gold standard of Lyme neuroborreliosis (LNB). Few data are
available on the CSF lactate concentration in European adults with the
diagnosis of acute LNB. The objective of the study was to investigate
the CSF changes during acute LNB. Routine CSF parameters [leukocyte
count, protein, lactate and albumin concentrations, CSF/serum quotients
of albumin (Q(Alb)), IgG, IgA and IgM, and oligoclonal IgG bands] and
the Borrelia burgdorferi (BB)-specific antibody index were
retrospectively studied in relation to the clinical presentation in
patients diagnosed with acute LNB.

A total of 118 patients with LNB were categorized into the following
groups according to their symptoms at presentation;
group 1: polyradiculoneuritis (Bannwarth's syndrome),
group 2: isolat ed facial palsy and
group 3: predominantly meningitic course of the disease.
In addition to the CSF of patients with acute LNB, CSF of 19 patients
with viral meningitis (VM) and 3 with neurolues (NL) were analyzed.
There were 97 patients classified with definite LNB, and 21 as probable
LNB. Neck stiffness and fever were reported by 15.3% of patients. Most
of these patients were younger than 50 years. Polyradiculoneuritis was
frequently found in patients older than 50 years. Lymphopleocytosis was
found in all patients. Only 5 patients had a CSF lactate ≥3.5 mmol/l,
and the mean CSF lactate level was not elevated (2.1 ± 0.6 mmol/l). The
patients with definite LNB had significantly higher lactate levels than
patients with probable LNB. Elevated lactate levels were accompanied by
fever and headache. In the Reiber nomograms, intrathecal immunoglobulin
synthesis was found for IgM in 70.2% followed by IgG in 19.5%.
Isoelectric focussing detected an intrathecal IgG synthesi s in 83
patients (70.3%). Elevated BB AIs in the CSF were found in 97 patients
(82.2%). Patients with VM showed lower CSF protein concentration and
CSF/serum quotients of albumin than LNB patients. In acute LNB, all
patients had elevated cerebrospinal fluid (CSF) leukocyte counts. In
contrast to infections by other bacteria, CSF lactate was lower than 3.5
mmol/l in all but 5 patients. The CSF findings did not differ between
polyradiculoneuritis, facial palsy, and meningitis. The CSF in LNB
patients strongly differed from CSF in VM patients with respect to
protein concentration and the CSF/serum albumin quotient.

wonderfullife
11-09-2011, 08:59 PM
...Lyme Disease is one hell of a battle, the battle to get a diagnosis, a battle to fight the disease, a battle to get your insurance to pay for your treatment, a battle to get the medical establishment to recognize and treat this disease as a very serious disease that it is….stories like mine are repeated over and over….
1984 two of my children were diagnosed with Lyme Disease….seven-year old son woke up one morning unable to walk…I am a victim of Lyme Disease…victim of a medical establishment that is reluctant to test or treat these diseases…..excruciating….pain…it became a myriad of symptoms affecting one part of my body one day….learned that it is a multi-system disease….I saw over 20 doctors, speicalists, …. I endured test after test…MRI’s, catscans, EKG’s, EGG’s….I was poked, prodded, analyzed, I began to feel …. I was everything but dissected….tests revealed absolutely nothing….told… need psychological help…if you were sick as I was he would not be sitting behind his desk at work…top hospitals, over five top hospitals….to no avail…no diagnosis….prescription of choice seemed to be antidepressants….went to Mayo Clinic…twice…two weeks…that too, revealed nothing…went home believing that I was going home to die…a retired …nurse … Lyme Disease….had every symptom of Lyme Disease….how did they not know that I had Lyme Disease? …. Was told had Fibromyalgia…. Mayo Clinic states that Lyme is…over-diagnosed….Lyme Disease is one hell of a battle, the battle to get a diagnosis, a battle to fight the disease, a battle to get your insurance to pay for your treatment, a battle to get the medical establishment to recognize and treat this disease as a very serious disease that it is….stories like mine are repeated over and over….
Read and watch more here:
http://lyme-aware.org/news/lydias-blog/952-pennsylvania-public-lyme-hearing-2011.html

wonderfullife
11-09-2011, 09:23 PM
New Borrelia Culture Test - Faster & More Accurate
September 5, 2011 Joe Burrascano, Jr., MD has announced a new lab test available for Lyme doctors to use in determining if Lyme is present. There is no need to wait for antibodies to form since this is a culture-based test. This should provide much faster and more accurate detection, and allow Lyme patients to receive treatment as soon as possible. Please read below for Dr. Burrascano's description of the new test:
In my work as a consultant, I have been working with a private lab located near Philadelphia, Advanced Laboratories, Inc. They wanted to develop a unique and high value test, and, with my interest in Lyme, I naturally encouraged them to work on a better Lyme Disease test.

As a result of some very intensive work on the part of a group of some very brilliant scientists, they have succeeded in developing a reliable and rapid blood culture for Borrelia! See the attached press release.

They actually have rolled out two separate panels- a basic one and an advanced one. In the basic panel, the blood sample is cultured and the positives are identified by histology and growth characteristics, and confirmed by fluorescent immunostaining. Positive reports will include a picture of the Bb growing in that very culture. The advanced panel will do this, but will also do PCR using well characterized and published DNA primer sets, and then all positive PCRs will be confirmed by DNA sequencing.

Remarkably, turn-around time can be as brief as ten days for the basic test, and seven to ten more days for the advanced panel.

This test is being rolled out gradually, with no big public announcements yet. That is why I am e-mailing you, so you can be among the first to be able to order this testing, before the lab gets swamped. Apparently you have to contact the lab to have test kits sent to you. The blood must be sent out the same day it is collected, and the lab provides a prepaid return FedEx mailer. As the lab is not yet accepting specimens over weekends, please do not collect blood on Fridays.

The bad news- New York being New York, this culture will not be available to NY State practitioners for several months. The States of California and Florida may have a delayed availability- I am not sure, so please contact the lab to get this info. However, all other states are OK.

I have no idea on pricing or on insurance issues- again, you will have to contact them for this info. The lab plans to have a booth at the conferences at LDA and at ILADS, so hopefully their presence will allow all to field questions.

The next step in their research is also equally exciting and ground breaking, but I am not at liberty to say yet what is being planned.

I will be travelling over the rest of this week, so I am afraid that I may not be able to answer any calls or e-mails until I get back, so if I do not respond to any contact efforts, please be patient.

As many of you recall, I learned the basics of true, clinical Lyme over 25 years ago thanks to Bb culturing that was available to me by Dr. Alan MacDonald. The new methods being used by this Pennsylvania lab go far beyond what MacDonald was able to do, so I am very excited to not only share this news with you, but I also cannot wait to see how it will change how we practice.

I also predict that Bb will be found in a lot of people, from mildly to severely ill, and that will redefine the role of the immunologist in Lyme to find out why some people recover and why others do not. Strain info as provided by the DNA sequencing data will be equally fascinating to follow.

So, enjoy the good news, and PLEASE, if you are going to begin culturing your patients, keep good records of your results. Data collection and tabulation has never been as important as it is now, with a quantum advance in testing technology.

Best wishes, from Dr. B................................!

http://www.researchednutritionals.com/information.cfm?id=255

wonderfullife
11-09-2011, 11:26 PM
ELIZABETH Wood was 37 years old in July 1985 when she was bitten by a tick while visiting her parents’ home along the Red River north of Emerson.

She recalls having difficulty removing the insect, which fastened itself on one of her legs. A few weeks later, she got a rash.
Today, the combination of a tick bite and a rash within 30 days would alert most, if not all, family doctors to the likelihood of Lyme disease. Caught early, it’s easy to treat with antibiotics.

But a quarter-century ago, little was known about Lyme disease in Manitoba. Health officials didn’t believe it was endemic to the province. In fact, the first doctorreported case in Manitoba did not occur until 1999, and the first confirmed case — using a strict federal Health Department definition — wasn’t registered until 2006.

Wood, who now chairs a Manitoba Lyme disease advocacy group, was told by a doctor at a Winnipeg clinic 26 years ago that she had poison ivy. She thought she knew a thing or two about poison ivy and didn’t buy it.

She later developed severe flulike symptoms that doctors now link to Lyme disease: head and muscle aches, joint pain, fatigue.
"It was like a nightmare, was what it was," Wood said in a recent interview at her Emerson home.

And it still is. More than a quarter-century after that tick bite, Wood’s condition has not greatly improved. She and her husband have spent thousands of dollars of their own money travelling to the United States for diagnosis and treatment for herself and their daughter, whom they believe also has Lyme disease.

Wood is not alone. An untold number of Manitobans with chronic Lyme disease symptoms — including a former deputy minister of health — have gone looking for answers outside the province when doctors here failed to help them.

Ernie Murakami, a former British Columbia doctor who was pressured to stop practising medicine by the B.C. College of Physicians and Surgeons because of his focus on and treatment of Lyme disease patients, said the disease is misunderstood. He says the medical profession is in denial about what he calls a "major epidemic."

"It’s criminal what’s happening in Canada," he said in an interview from Hope, B.C., where he was once chief of staff at the Fraser Canyon Hospital.

"People are having to go across the border (to the U.S.) at tremendous expense to get treatment."

The B.C.-based Canadian Lyme Disease Foundation believes there are thousands of cases such as Wood’s in Canada. Many of those patients are confined to wheelchairs, debilitated by the disease’s symptoms and unable to work.

Jim Wilson, the group’s president, said the blood tests used to detect the disease in Canada are faulty, catching only a fraction of the true cases. That is challenged by infectious disease experts who claim the two-part lab test used here is the gold standard for detecting Lyme disease.

The same experts are also suspicious and dismissive of certain for-profit U.S. labs that are only too ready to return a positive Lyme disease result from ill people who have been unable to find a satisfactory diagnosis for the chronic symptoms that ail them.

Over the past few months, the Free Press has interviewed dozens of Lyme disease advocates, sufferers, experts and government officials. Some of those we contacted asked not to be named because of privacy concerns or the stigma attached to the disease and its advocates. That’s because some in the medical profession consider advocates to be kooks.



AFTER her unsuccessful medical visit shortly after her tick bite a quarter-century ago, Wood did not go to a doctor for about three more years.

By that time her arms and shoulders were so sore, she often had an arm in a sling. In 1988, she went to a clinic on Pembina Highway, where a doctor gave her a cortisone shot, which she said crashed her immune system. A few weeks later, she wound up in the Grace Hospital.

It was the first of several trips to the hospital emergency room. The doctors, unable to diagnose her condition, suggested the pain was all in her head. They suggested she go to a psychiatrist.

In 1989, she gave birth to her daughter, Lizzie. She had spent much of the pregnancy in bed. "It got to the point where I couldn’t brush my own hair. I was so weak," she said.

A chair had to be placed in the tub so she could take a shower.

Around that time, her sister told her about a sign warning of deer ticks and Lyme disease near Pinawa.

She started doing her own research on the disease and asked to be tested for it in Winnipeg. She was told the results were "borderline positive." Doctors ruled it out, she said, because they thought it did not occur in Manitoba.

Since then, she’s said she’s been positively diagnosed for the disease in Ontario and New Jersey.

Her health has also deteriorated: She lost her right kidney, she lost most of the sight in her right eye and surgeons removed a chunk of her colon.

With a lot of effort, she has convinced Manitoba doctors to give her periodic intravenous and oral antibiotics and is now seeing a rural GP who has put her on a cocktail of drugs.

She is far from cured. She still has aches and pains and gets tired easily. But she said without the antibiotics she would not be mobile. She would not be able to function.

"I wouldn’t be alive."

In her Lyme disease advocacy work, she said she’s come across three people in Canada — friends of hers — who have given up hope of ever getting better. They’ve committed suicide. One was a young woman from British Columbia.

"I spoke to her that morning, and she killed herself in the afternoon," Wood said, her voice catching.

ERNIE Murakami has travelled the country advocating for better diagnosis and more aggressive treatment of Lyme disease. At age 80, he seems to have more energy than men decades younger.

Until three years ago, he was a practising physician in British Columbia and taught medical students. He had developed a specialty for treating Lyme disease patients, but he agreed to give up his licence three years ago after an investigation by the province’s college of physicians, which labelled him a Lyme disease "zealot." He estimates he’s treated 3,000 Lyme disease patients.

"If you don’t go along with the (medical) establishment, you’re examined and cross-examined and harassed," he said in an interview.

Fighting the college took a toll on his health, he said, so he gave up treating patients and now simply refers Lyme disease sufferers to doctors and naturopaths (who are allowed in B.C. to prescribe antibiotics) who will treat them.

Murakami thinks Canadian infectious-disease doctors are failing to take Lyme disease seriously and the country’s tests for the disease are too narrow. While just a handful of cases is officially diagnosed in Manitoba each year, across the border in Minnesota the state reports 1,000 or more cases annually.

He also takes issue with infectious-disease doctors who are loath to prescribe more than three or four weeks of antibiotics for patients, claiming long-term Lyme disease sufferers require ongoing treatment with antibiotics.

Murakami has travelled to Manitoba a halfdozen times in recent years to meet Health Department officials. He’s tried to convince officials here of research, he says, that shows Lyme bacteria can remain in the body for long periods of time and multiply — an assertion most infectious-disease experts reject.

He and some local advocates are hoping to convince the province to pass a law that will prevent the Manitoba College of Physicians and Surgeons from harassing doctors who prescribe long-term antibiotics to patients with so-called chronic Lyme disease. Such laws already exist in a halfdozen U.S. states, where the Lyme disease lobby is powerful. But such statutes horrify infectiousdisease doctors and medical officials on both sides of the border. They see it as politicians usurping medical decision-making that rightly belongs to physicians.

DR. Allan Ronald, one of Canada’s foremost infectious-disease doctors, calls Lyme disease "an emerging illness in Manitoba," like West Nile virus was 10 years ago.

About three years ago, he was part of a committee pulled together by Manitoba Health to diagnose and document Lyme and other tickborne diseases.

"In Manitoba, we can only prove the diagnosis on acute (early-stage) Lyme disease in somewhere between 15 and 25 patients a year," Ronald said.

In a recent telephone interview from his cottage, he called chronic Lyme disease a "very controversial, difficult issue."

In the last few years, he said he’s agreed to see more than 30 Manitoba patients who claimed to have chronic or long-term Lyme disease. About half of them were diagnosed by physicians in the United States who prescribed long-term treatment with antibiotics. The same patients wanted Ronald to prescribe those drugs here.

Ronald had them submit a blood sample to test for Lyme disease. Not one of the patients tested positive for the disease, he said.

"In my opinion, they need care," he said of the patients. "It’s not that they don’t need care, but they need care for a better diagnosis."

Dr. Frank Plummer, scientific director general of the National Microbiology Laboratory in Winnipeg, said all stages of Lyme disease are treatable with three or four weeks of antibiotics.

"In the very late stages, some of the symptoms can persist after treatment, but the disease is still cured."

Plummer said there is no scientific evidence that Lyme disease can persist in the body for decades, as some chronic Lyme sufferers and the Canadian Lyme Disease Foundation claim.

Those who claim to have chronic Lyme disease may in fact have some form of chronic fatigue syndrome or fibromyalgia, he said. "They’re treatable symptomatically. They don’t respond to antibiotics."

Likewise, Ronald said it is possible the patients he saw suffered from a "post-infectious disease fatigue syndrome."

Ronald, celebrated for his work with HIV/AIDS care and prevention in Africa, warned that there are doctors "who will call everything chronic Lyme disease." And that makes life difficult for those who stand by the dictates of scientific research.

He said studies have shown no difference in outcomes for chronic Lyme disease sufferers who have been given either long-term antibiotics or a placebo. In one study, a New York state lab sent blood samples from healthy people to a California laboratory known for issuing positive Lyme disease results. Two-thirds came back positive, Ronald said.

But Ronald admits that there is a lot that scientists don’t know about Lyme disease. And he noted that two of his own patients have claimed to have had incredible results from taking antibiotics.

"They’ve gone from being chronic invalids to being well. And you can’t deny people’s subjective experience."





THERE are whispers that the Manitoba College of Physicians and Surgeons, like the B.C. college, have leaned on doctors who have treated considerable numbers of Lyme disease patients. Two Winnipeg doctors, according to one source, stopped taking new Lyme patients last year.

Dr. Bill Pope, the college’s registrar, said he is prohibited by law from disclosing any complaints or investigations that do not result in the discipline of a physician.

Meanwhile, a rural Manitoba doctor who did not want his name revealed said he now has four chronic Lyme disease patients taking extended periods of antibiotics. The treatments include daily intravenous antibiotics for three months and oral antibiotics for six months. He said he learned of the treatment regime from a Minnesota doctor. "Patients are definitely feeling better, although I must tell you I can’t give any long-term prognosis... because I’ve just started that type of treatment lately," the doctor said.

Most infectious disease experts believe such long-term use of antibiotics is unwarranted and may be harmful.

"It’s certainly not the standard accepted treatment," said Plummer. "That’s way more aggressive therapy than is recommended by expert bodies."



DR. Joel Kettner, Manitoba’s chief public health officer, said the province is still figuring out how prevalent Lyme disease is within its borders — and how to diagnose it more accurately. "We’re very interested to know how big a problem this is, and we’re doing quite a bit to try to find out and to try to be open-minded about how big a problem this is."

He said it "could be a misconception" that Manitoba physicians are generally only willing to treat Lyme disease in its initial stage.

"We’re seeing evidence of more recognition, more testing, more reports of diagnosis and more positive test results."

At the urging of disease advocates, Manitoba has stepped up its public-awareness efforts on Lyme and the blacklegged ticks that can carry it.

The province is also hosting a scientific symposium on Lyme disease next spring in Winnipeg.

Researchers from across North America are expected to make presentations at the event. The province is also planning a separate forum for members of the public to talk about their experiences and concerns with the disease, Kettner said.


http://www.winnipegfreepress.com/arts-and-life/life/health/Manitobans-wage-war-with-Lyme-disease-skeptical-doctors-129586928.html

wonderfullife
11-09-2011, 11:34 PM
Health Centres of America

Insurance Reimbursement and Lyme Disease
Lyme Disease and Insurance Reimbursement


This document is to address the concerns presented by insurance companies and their lack of reimbursement coverage for the treatment of Lyme disease. The first and most difficult task however, is to get the medical director for the insurance company to “READ and REVIEW” this documentation and references. The arguments against reimbursement by most insurance companies fall within two major areas:

First is: Diagnosis is not within standard guidelines.

Lyme diagnosis is not within standard of care
There is not such thing as Lyme disease (in this area)
Lyme testing used are not FDA approved or CDC approved i.e. Bowen, MDL, etc.
There is no clinical evidence of Lyme disease with this patient (based on being ill informed and lack of understanding of the stages and symptoms of Lyme disease).
Second is: Treatment is not medically necessary because of one of the two following reasons: 1) Not adequate data supporting diagnosis and/or 2) the treatment is not within the standard of care for Lyme disease

Treatment with IV’s for Lyme disease is not within standard of care
Length of treatment is not standard of care
Antibiotic used is not standard of care
Supplements are not within standard of care
Third and most significant: The insurance company does not want to pay for the treatment of Lyme disease and the medical directors/review board of the insurance company serves to implement that position. The hurdle once again is to get a fair hearing. There are several levels of confronting the insurance company once they have rejected the initial claim. The first step however, is to make sure that the patient’s insurance policy does provide coverage for claims. It is best to have some indication at the beginning of treatment. Remember that even though the insurance company may say they will cover treatment, they always state they reserve the right to review the claim before reimbursement. Make sure the patient understands that coverage is always within the limits of the individual policy and they coverage is always what is “usual and customary.”

Responses to arguments

First Response: responding to requests for more information and patient notes following billing to the insurance company. Second Response: responding to the first rejection letter. Send Letter of Medical Necessity with copies of test results and summary of clinical data.
Third Response: After the patient or physician has received a second letter of rejection send a more detailed response about diagnosis (clinical); lab results that support Lyme disease and secondary conditions and copies of the patients chart and possible detailed information about Lyme disease, diagnosis and treatment. This letter must address “not medically necessary” and “standard of care” and present a detailed description of clinical data to support the diagnosis.
Fourth Response: When a third letter of rejection is sent to the patient or physician, the patient must request a face to face hearing with the insurance company. The insurance company must grant this request. At this time, someone from the physicians office must provide material to support the diagnosis and treatment of Lyme disease and may even have to be on the phone with the insurance company giving supportive information about diagnosis and treatment. This can be the patient’s physician, nurse or someone in the office who understands the diagnosis and treatment of Lyme disease. They key is to be sufficiently armed with refutable information. In the end however, there is no guarantee that the insurance company will respond by reimbursement of treatment. We have found however, that most of the time the insurance company will respond in a positive manner at this point.
Facts to be considered are:

Currently, there are two approaches to the diagnosis and treatment of Lyme disease. Two sets of diagnostic and treatment guidelines, reflecting the different approaches, are available in peer review literature. Thus, two community standards of practice exist.: both diagnosis and treatment of Lyme disease recognized by most state boards. When considering whether standard of care is within guidelines of medical practice the insurance company must understand there are two standards of care. The two standards of care are: 1) traditional – Lyme disease is rare, and if a person does have Lyme disease 2-4 weeks with oral antibiotics for early Lyme disease will solve the problem. Most of the time Lyme disease is not recognized unless there is a EM (bulls eye rash) on the patient. 2) Growing standard that Lyme disease is widespread and treatment should be a minimum of 4-6 weeks of oral antibiotics for early Lymes and IV antibiotics for late stages of Lyme with treatment lasting 4-6 weeks followed by oral treatment of up to 1 year. The primary difference being that with the second frame of reference, physicians believe that Lyme disease should be treated aggressively and for a long period of time. This is especially true for late stage Lyme disease.

Most physicians and insurance companies are not up to date on the diagnosis and treatment of Lyme disease. Their judgment is based on archaic information, misinformation and an unwillingness to update Lyme disease.

Most states have committees or boards who are looking at the diagnosis and treatment of Lyme disease. Their focus is on accurate reporting, better testing and standards of treatment for Lyme disease.

Must consider what stage of Lyme disease the patient is in that is being treated. Late stage of Lyme disease or chronic Lyme disease is treated with IV Infusion treatment. Definitions by the CDC and FDA regarding Lyme disease, diagnosis and treatment.

Problems with current Lyme disease testing Definitions

Medical Necessity – Increasingly across the US , in insurance cases, the term “medical necessity” is being interpreted by the courts as the standard of community care for the illness involved. There are two legally accepted approaches to diagnosis and care of Lyme disease. In cases of recurrent or long-term chronic Lyme disease, treated with IV antibiotics, insurers have been quick to shield themselves behind the standard enabling them to reject or restrict a claim for reimbursement of treatment. Therefore, “medically necessity” by most insurance companies is the traditional definition.

The growing definition of “medical necessity” accepted is that Lyme disease is best diagnosed clinically by a physician who is understands Lyme disease. That testing for Lyme disease is not necessary for diagnosis but encouraged as supportive documentation. Increasingly many state medical boards and the legal system, is recognizing that Lyme disease is on the increase, that the definition of Lyme disease is much broader than previously considered by “traditional standards”, more research must be done, more accurate Lyme disease testing developed, and better treatment methods for Lyme disease patients. There is growing support by the legal system that insurance companies reimburse for the chronic treatment of Lyme disease.

The “key” then, in this latter definition of “medical necessity” is to diagnose Lyme disease “clinically” based on an accurate and detailed medical history that is well documented. Lyme testing is an important validation but when current testing does not support Lyme disease, the clinical evaluation by the physician takes precedence over the blood test.

CDC Definition of Lyme disease – in 1996 the CDC recommends that to properly diagnose Lyme disease you must 1) identification by a physician of EM (rash) in the early stage, or a major system involvement with positive serology; 2) recognition by evaluating physicians of characteristic clinical sign, a history of exposure in an area endemic for Lyme-transmitting ticks, and the use of laboratory tests as an adjunct to diagnosis. The CDC further states that on the Western Blot there must be 5 of 10 bands for IgG and 2 of 3 for IgM. It is important to note that this 1996 definition of Lyme disease, excludes bands for OspA and OspB, the 31kDa and 34kDa bands, respectively, which are very specific in Lyme disease. The ELISA is the second test the CDC recommends for Lyme disease.

Problems with the CDC definition are:

Most tick bites do not produce an EM (rash) Lyme disease is spreading rapidly throughout the US thereby conflicting with the CDC statement that a tick caring Lyme disease is limited to and area they define as endemic for Lyme-transmitting disease.

Both the ELISA and Western Blot measure the immune system’s response to the Lyme spirochete – that is – looking for the immune systems reaction within the blood for antibodies. The believe that is there are no antibodies there is no Lyme disease. What these tests cannot pick up, is that spirochetes have a slow growth rate, can remain dormant for a lengthy period of time, and can invade cellular walls and therefore do not produce an immune system response of antibodies. Therefore there is a high rate of false negative is produced on these tests.

There is a problem of standardization of these tests among labs. FDA Definitions: In 1997 t he FDA says that physicians should use blood testing “only to support a clinical diagnosis”. This is extremely important for insurance companies to understand and especially when insurance companies take the position that the only way to diagnose Lyme disease is with a positive Western Blot or ELISA test. The FDA goes on to say that the results of Lyme tests (WB and ELISA primarily) “may be easily misinterpreted.” Bb is difficult to detect by most laboratory methods in use today, and a little known fact is that there isn’t currently a test approved by the FDA for Lyme Disease.

The Diagnosis of Lyme Disease - Must be made Clinically by a qualified physician.




Diagnosis of Lyme Disease from John’s Hopkins Medical School
The diagnosis of Lyme disease is clinical, and the diagnostician must consider many types of evidence. The history is very important to the diagnosis of the disease (e.g., opportunity for tick exposure? live or work in endemic area? recent tick bites?). The temporality and pattern of the development of symptoms is critical to the diagnosis.

Diagnosis of Lyme Disease by Joseph Burrascano Jr., M.D.

Lyme is diagnosed clinically, as no currently available test, no matter the source or type, is definitive in ruling in or ruling out infection with these pathogens, or whether these infections are responsible for the patient's symptoms. The entire clinical picture must be taken into account, including a search for concurrent conditions and alternate diagnoses, and other reasons for some of the presenting complaints. Often, much of the diagnostic process in late, disseminated Lyme involves ruling out other illnesses and defining the extent of damage that might require separate evaluation and treatment.

>b>Diagnosis of Lyme Disease by Brian A. Fallon, MD; Columbia University

The criteria for diagnosing Lyme disease vary depending upon the purpose. For surveillance studies (3), the diagnosis requires a history of exposure in an endemic area and either: (1) a physician-diagnosed erythema chronicum migrans rash, or, (2) serologic evidence of exposure to Borrelia burgdorferi and one of the following: (a) arthritic symptoms-recurrent brief attacks of joint swelling or joint pain; (b) neurologic symptoms-such as lymphocytic meningitis, cranial neuritis, radiculoneuropathy, and/or encephalomyelitis; or (c) cardiac conduction defects-second or third degree AV block.

This definition, while useful for research purposes, is unduly restrictive because about one-third of patients do not recall a rash and because current serologic testing is generally considered inadequate, producing false negatives and false positives (5). Thus, the diagnosis of Lyme disease at this point remains clinical not serologic.

Because Lyme borreliosis is multisystemic, the differential diagnosis has to be broad, including viral infections, aseptic meningitis, disseminated gonococcal infection, rheumatoid arthritis, late stage syphilis, multiple sclerosis, Guillian-Barre, AIDS, systemic lupus, subacute bacterial endocarditis, thyroiditis, Reiter's syndrome, fibromyaligia, chronic fatigue syndrome, and psychiatric disorders. If treated early, the disease may be limited to an asymptomatic rash or only a few days to a week of flu-like symptoms. In its later stages, patients may have multisystemic disease, leading to an inability to work for months to years. The simplest tasks may become insurmountable.

Report by the FDA in October 1997

The Western blot is a supplemental test only; it is NOT a confirmatory test. No confirmatory serological test exists at this time

Do not make the diagnosis of Lyme disease based on the results of serological lab tests. The diagnosis must be based on a high index of clinical suspicion before laboratory testing.

Do not use seiological tests for Lyme disease for screening asymptomatic patients. The diagnosis must be made clinically. Serological tests for B. burgdorferi are only an aid to establish the diagnosis in the presence of strong clinical suspicion. (The most definitive diagnostic procedure is biopsy and isolation of the organism in culture, which frequently yields the spirochete, but is often not practical.

Definitions of Testing for Lyme disease: In the February 15 issue of the American Journal of Medicine, Mark S. Klempner, M.D., of NEMC and his scientific collaborators in New York , Connecticut and Washington , D.C. , report their findings about the reliability of two Lyme disease tests: an IgG Western blot blood test and the Lyme urine antigen test, or LUAT. The IgG Western blot is a licensed test used to screen blood samples for antibodies to the Lyme bacterium, Borrelia burgdorferi. The LUAT detects proteins derived from the bacterium in urine samples. Although the LUAT has not been approved by the Food and Drug Administration as a valid diagnostic test for Lyme disease, it is widely used, and the NIAID Lyme Disease Advisory Panel asked that it be further evaluated.

Serologic testing is thus not very helpful in a patient with classic erythema migrans, who will be treated for Lyme disease regardless of the serologic test result. The specificity of serologic testing is approximately 90-95% for all stages of the disease. John’s Hopkins University Medical School



Primary Tests for Lyme Disease and validation of results:
The ELISA Lyme test is unreliable, and misses 35% of culture proven Lyme (only 65% sensitivity!) and is unacceptable as the first step of a two step screening protocol. (By definition a screening test should have 95% sensitivity.)

Of patients with acute culture proven Lyme disease, 20-30% remain seronegative on serial Western Blot sampling. Antibody titers also appear to decline over time; thus, the IgG Western Blot is even less sensitive in detecting chronic Lyme infection yet the IgM Western Blot may work. For "epidemiological purposes" the CDC eliminated from the Western Blot analysis the reading of bands 31 and 34. These bands are so specific to Borrelia burgdorferi that they have been chosen for vaccine development. However, for patients not vaccinated for Lyme, a positive 31 or 34 band is highly indicative of Borrelia burgdorferi exposure.

When used as a part of a diagnostic evaluation for Lyme disease, the Western Blot Lyme test should be performed by a laboratory that reads and reports on all 16 bands as part of their routine comprehensive analysis.

Laboratories (such as SmithKline) that use FDA approved kits (for instance, Mardex's Marblot) are restricted from reporting all of the bands, as they must abide by the rules of the manufacturer. These rules are set up in accordance with the CDCs surveillance criteria. and increase the risk of false negative results. These kits may be OK for surveillance purposes, but offer too scanty of an analysis to be useful in patient management.

PCR assay testing and detection of pieces of the spirochete through antigen assays both give stronger indication of the presence of the Lyme pathogen; but currently these tests don’t conclusively prove that live Bb spirochete are present and causing active illness. PCR tests are now available, and although they are very specific, sensitivity remains poor, possibly less than 30%. This is because Bb causes a deep tissue infection and is only transiently found in body humors. Therefore, just as in routine blood culturing, multiple specimens must be collected to increase yield; a negative result does not rule out infection, but a positive one is significant.

Bowen "Rapid Identification of Borrelia burgdorferi" (RIBb). The Bb antigen is identified by the presence of fluorescing structures upon microscopy. At Bowen Research & Training Institute, Inc., located in Palm Harbor , Florida , ongoing research is being conducted using the Bowen Q-RIBb (Quantitative Rapid Identification of Borrelia burgdorferi) test developed by Dr. JoAnne Whitaker. Originally a CLIA approved lab until April of 2003, the institute, lacking in vital grant funding, changed its status from that of a clinical lab to a research facility under the State of Florida Health Department. Since its inception, the main focus at the institute has been the development of an accurate test for the Borrelia burgdorferi (Bb) antigen, the causative agent of Lyme disease. The Bowen Q-RIBb test just recently received its preliminary US Patent approval. Although the Bowen Q-RiBb Test is not presently approved by the FDA for Lyme disease; an application for FDA approval is now pending.

General Statements from John’s Hopkins about Diagnosis of Lymes Disease.

“Within weeks to months of becoming infected, early disseminated Lyme disease may occur (formerly termed stage 2). Approximately 4-10% of patients in the U.S. develop cardiac manifestations, including conduction defects (e.g., atrioventricular block, complete heart block, bundle branch block, fascicular block), tachyarrhythmias (e.g., atrial due to pericarditis, uncommonly ventricular as an escape rhythm), myopericarditis, and mild myocardial dysfunction. Involvement of the central or peripheral nervous systems may occur in up to 10 to 20% of cases, may be manifested by headache, fatigue, stiff neck, and malaise, and includes such diagnoses as Lyme meningitis, neuroborreliosis, cranial neuropathies (especially facial nerve palsy, which can be bilateral), peripheral neuropathy, radiculitis, myelopathy, or brachial plexopathy. Lyme disease may also involve the eye (e.g., follicular conjunctivitis, keratitis, and rarely uveitis or vitritis). Musculoskeletal manifestations of Lyme disease are very common. During early infection, migratory arthralgias and pain in bursae, tendon, muscle, or bone occur in the majority of patients. Weeks to months later, frank arthritis, most commonly mono- or oligoarticular and involving large joints (most commonly knees, but also shoulders, ankles, elbows, and other sites), may develop. Lyme arthritis is one manifestation of persistent or late Lyme disease (previously termed state 3).

In the United States , approximately 60% of untreated patients will develop intermittent episodes of joint pain and swelling, months to years after the infecting tick bite. The most common presentation is a single involved knee but can involve both knees and be migatory, but both large and small joints may be affected, and usually only one or two joints at a time. Over time, the frequency and severity of attacks can decline, and, on average, the proportion of patients with recurrent attacks declines by 10-20% annually. Approximately 10% of untreated patients may develop chronic arthritis, defined as one year or more of continuous joint inflammation.

http://www.healthcentersofamerica.com/information.cfm?id=115

wonderfullife
11-09-2011, 11:43 PM
Autoimmune and Neurodegenerative Disease - YouTube

wonderfullife
11-09-2011, 11:47 PM
ILADS WELCOMES PHYSICIAN RECOVERING FROM ALS
DOCTOR'S CASE SUPPORTS THEORY LYME DISEASE MAY BE THE CAUSE OF ALS
Bethesda MD September 2, 2004 - The International Lyme and Associated Diseases Society (ILADS) strengthened its impressive membership today with the addition of Dr. Dave Martz of Colorado Springs, who joined ILADS 15 months after being diagnosed with Amyotrophic Lateral Sclerosis (ALS). In April of 2003, Dr. Martz began suffering weakness and pain in his muscles. Dr. Martz soon lost much of his mobility. His condition worsened forcing him to retire from the medical practice he loves.

After six frustrating months with hope fading, Dr. Martz discovered the work of Dr. Gregory Bach of Colmar, Pennsylvania. Dr. Bach, who is a member of ILADS, suggested a link between ALS and Lyme disease. IGeneX Reference Laboratory of Palo Alto then confirmed Lyme bacteria in Dr. Martz. Dr. Martz then sought out a local ILADS physician who started Lyme disease treatment based on the recommendations of Dr. Bach. The results were dramatic.

"Before I found Lyme "literate" professionals, I could only function at a level of about 20 percent," says Dr. Martz. "But now that I'm in expert hands, I am up to 75 percent of full function and I hope to return to work soon as a physician, helping others with Chronic Lyme Disease." An internist, and Past President of the Colorado Medical Society, he is committed to giving others opportunities that have been given to him.

The Centers for Disease Controls says that Lyme disease may be under-reported by as much as ten-fold. This means as many as a quarter of a million Americans may contract Lyme disease each year, yet most of them are unaware of it. ILADS will hold its annual meeting in October of this year in Rye, New York.

ILADS president, Dr. Steven Phillips, says, "Dr. Martz is an example of the many physicians and medical experts we encourage to join ILADS so we can continue to raise awareness and make vital advances in the world-wide fight against Lyme disease."

For more information about Lyme disease go to www.ilads.org CONTACT :
Barbara Buchman (301) 263-1080
Christi O'Connor (415) 883-2491
http://www.canlyme.com/martz.html

wonderfullife
11-09-2011, 11:50 PM
Dr. David Martz is kind of a rock star in the Lyme world. You may have read about him in Pam Weintraub’s Cure Unknown, and seen footage of him in the documentary Under Our Skin.

His story is riveting. After a lifetime of good health and a successful career as a physician practicing internal medicine-hematology-oncology for 30 years, in 2003, Martz suddenly started experiencing strange symptoms. First deep fatigue, then profound muscle aches and body-wide pain. Soon he was too weak to get out of bed. As his condition rapidly deteriorated, his physicians gave him a devastating diagnosis: ALS (aka Lou Gehrig’s Disease). They said nothing could stem his physical decline and he would likely be dead within two years.

But events went in a different direction. As his health spiraled downward, Martz connected with a Lyme specialist who prescribed hard-hitting, long-term antibiotics. The gamble paid off. By the end of 2004, Martz was a new man. In fact, the doctor who had diagnosed him so definitively with ALS, now pronounced that condition completely gone.

Martz devoted the next two and a half years to a project that gave extended antibiotics to about 90 ALS patients, and demonstrated objective improvements in 15% of them. He has also treated more than 800 chronic Lyme patients, with good response and minimal side effects. That work is currently being written up for publication.

Martz is moving into a new phase of life now, having recently been named president-elect of the International Lyme and Associated Diseases Society. His term will start in 2011.

Martz will be the keynote speaker at CALDA’s annual patient conference, “Getting Healthy Again in 2010,” on April 24. The event will be held at the Dougherty Station Community Center, 17011 Bollinger Canyon Road, San Ramon, CA. For registration information, click here.

http://www.lymedisease.org/news/touchedbylyme/372.html

wonderfullife
12-09-2011, 06:09 PM
Cochez C, Ducoffre G, Vandenvelde C, Luyasu V, Heyman P

Ticks Tick Borne Dis 2011 09; 2 (3): 156-9

Human granulocytic anaplasmosis (HGA) is a tick-borne rickettsial
infection of neutrophils caused by Anaplasma phagocytophilum. Although
the pathogen was known as a veterinary agent as early as 1932, the link
with human disease was first established in 1990. In the past decennium,
the involvement of HGA as an important and frequent cause of fever with
a history of tick bite was increasingly recognized in many regions of
Europe. This paper presents a 10-year A. phagocytophilum
serosurveillance (2000-2009), wherein 1672 serum samples were tested and
418 were found positive. A total of 111 patients had a history of tick
bite, fever, and at least a 4-fold rise in titre and are thus considered
to be confirmed cases.
These findings suggest that Belgium is a hot spot for HGA infections.

wonderfullife
12-09-2011, 06:11 PM
Balátová P, Kurzová Z, Hulínská D

Epidemiol Mikrobiol Imunol 2011 06; 60 (2): 74-6

The subject of this study is serological screening of blood and CSF
(cerebrospinal fluid) samples for the presence of borrelial and
ehrlichial antibodies. A total of 165 patients suspected to be at risk
of Lyme disease were tested. Indirect immunofluorescence and enzyme
immunoassay were used as diagnostic methods. Ehrlichial antibodies were
detected in 36 (21.8%) patients. Borrelial antibodies were found in 70
samples (42.4%). The widening range of tick-borne diseases brings about
the need for more data on these zoonoses.

wonderfullife
12-09-2011, 06:46 PM
In Lies We Trust: The CIA, Hollywood and Bioterrorism-Full Length Documentary - YouTube

wonderfullife
13-09-2011, 07:46 PM
Eva Špitalská,1
Ivan Literák,2
Elena Kocianová,1 and
Veronika Taragel'ová3
1Institute of Virology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
2Faculty of Veterinary Hygiene and Ecology, University of Veterinary and Pharmaceutical Sciences, Brno, Czech Republic.
3Institute of Zoology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Address correspondence to:
Veronika Taragel'ová
Institute of Zoology
Slovak Academy of Sciences
Dúbravská cesta 9
841 04 Bratislava
Slovak Republic
E-mail: [email protected]
Abstract

Wild birds are known to be a reservoir of infectious disease agents and disseminatory hosts of ticks. The purpose of this work was to obtain information about the occurrence of rickettsial, anaplasmal, and borrelial infections in some ticks that parasitize wild birds in the Czech Republic. A total of 549 subadult ticks of three species Ixodes arboricola (75.0%), Ixodes ricinus (23.1%), and Haemaphysalis concinna (1.8%) were collected from 20 species of birds (Passeriformes). Rickettsiae were detected in 44.0% larvae and 24.5% nymphs of I. arboricola collected from Parus major, Poecile palustris, and Sitta europaea. Rickettsiae-positive I. ricinus larvae (13.7%) were collected from P. major, Cyanistes caeruleus, and S. europaea, and 2.6% of nymphs from Erithacus rubecula and Prunella modularis. Comparison of sequences of a gltA gene fragment with data available in GenBank identified Rickettsia helvetica, a spotted fever rickettsia associated with human infections, and other Rickettsia spp. Anaplasma phagocytophilum was found only in two I. ricinus nymphs collected from E. rubecula and P. major. Infections with Borrelia burgdorferi sensu lato were recorded in 1.3% larvae of I. arboricola acquired from P. palustris and P. major and in 11.8% larvae and 25.0% nymphs of I. ricinus collected from P. major, P. palustris, C. caeruleus, Acrocephalus schoenobaenus, Turdus merula, Carpodacus erythrinus, Sylvia atricapilla, P. modularis, and Phylloscopus collybita. Reverse-line blot hybridization showed infections with Borrelia garinii and Borrelia valaisiana and mixed infections with these two genospecies. This is the first record of a high rate of rickettsial infection in I. arboricola subadult ticks acquired from birds in the Czech Republic and in central Europe. Our study suggests that I. arboricola, P. major, and P. palustris play important roles in circulating rickettsiae.

http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0210

wonderfullife
13-09-2011, 07:47 PM
Timea Kiss,1
Daniel Cadar,1
Alexandra Florina Krupaci,1
Armela Bordeanu,1
Gheorghe Florinel Brudaşcă,2
Andrei Daniel Mihalca,3
Viorica Mircean,3
Lucia Gliga,1
Mirabela Oana Dumitrache,3 and
Marina Spînu1
1Department of Infectious Diseases, Faculty of Veterinary Medicine, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, Cluj, Romania.
2Department of Game and Wildlife Diseases, Faculty of Veterinary Medicine, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, Cluj, Romania.
3Department of Parasitology, Faculty of Veterinary Medicine, University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca, Cluj, Romania.
Address correspondence to:
Timea Kiss
Department of Infectious Diseases
Faculty of Veterinary Medicine
University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca
Mănăştur Street, No. 3-5
Cluj-Napoca 400372
Romania
E-mail: [email protected]
Abstract

Lyme disease is a perfect model of the complex relationship between host, vector, and the vector-borne bacteria. Both dogs and horses in Romania are exposed to infection. The aim of the present study was to assess the seroreactivity against Borrelia burgdorferi sensu lato in dogs and horses from different regions of Romania. 276 samples from dogs and 260 samples from horses located in different regions of Romania were analyzed by ELISA and IFA, respectively. The effect of several factors potentially affecting seroreactivity (location, age, gender, occupation, and vector exposition risk) was evaluated using Fisher's exact test (R 2.12.0). The overall prevalence of anti-Borrelia antibodies was 6.52% (18/276) in dogs, with a significantly higher positivity (46.15%, 6/13, p=0.0005) recorded in a midcountry region. Seroreactivity was correlated with occupation, with working dogs being more exposed. The results may indicate that Lyme borreliosis foci are restricted to small areas, but further studies on Borrelia prevalence in tick populations are needed to confirm this hypothesis. In horses, a global seroprevalence of 11.92% (31/260) was observed. No correlations were found between positive results and age, sex, county, or occupation. This is the first serological survey on antibodies to B. burgdorferi sensu lato in Romanian dogs and horses.

http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0254

wonderfullife
13-09-2011, 07:49 PM
Diana Lupulovic,1
Miguel A. Martín-Acebes,2
Sava Lazic,1
Julio Alonso-Padilla,2
Ana-Belén Blázquez,2
Estela Escribano-Romero,2
Tamas Petrovic,1 and
Juan-Carlos Saiz2
1Scientific Veterinary Institute “Novi Sad,” Novi Sad, Serbia.
2Departamento de Biotecnología, Instituto Nacional de Investigaciones Agrarias, Madrid, Spain.
Address correspondence to:
Juan-Carlos Saiz
Departamento de Biotecnología
Instituto Nacional de Investigaciones Agrarias
Ctra Coruña Km. 7.5
28040 Madrid
Spain
E-mail: [email protected]
Abstract

West Nile virus (WNV), the most widely distributed flavivirus worldwide, has lately reemerged in Europe, causing worrisome outbreaks in humans and horses. Serological analysis by enzyme-linked immunoassay and plaque reduction neutralization test showed for the first time in Serbia that 12% of 349 horses presented specific neutralizing WNV antibodies, which in one case also cross-neutralized Usutu virus (USUV). This is the first time that anti-USUV high neutralizing antibody titers are reported in horses. All these data indicate that WNV and USUV are circulating in the region and advise on the convenience of implementing surveillance programs.

http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0249

wonderfullife
13-09-2011, 07:51 PM
NaturalNews) Lyme disease is the fastest-growing infectious disease in the United States, with as many as 400,000 new cases per year. The Centers for Disease Control (CDC) and the Infectious Diseases Society of America (IDSA), however, deny the existence of chronic Lyme (a disabling disease which results when treatments aren't immediately given following a tick bite), which afflicts many. Most people with chronic Lyme disease don't recall having ever been bitten by a tick. They might learn they have the disease after symptoms manifest, but at that point, treatment is complicated.

Tests for diagnosing Lyme disease are inadequate, for many reasons. For instance, Lyme disease suppresses the body's antibody production, resulting in false negative tests, while antigen tests miss blood samples containing proteins from borrelia burgdorferi, one of the principal organisms implicated in Lyme. What's more: because the CDC and IDSA refuse to recognize it, most doctors aren't taught about chronic Lyme disease and how to treat it.

However, numerous case studies prove that chronic Lyme exists and can often be effectively treated naturally. Doctors, scientists and Lyme advocates have presented these case studies to the IDSA and US Congress, yet the studies are always dismissed. This has prevented doctors and the public from learning about chronic Lyme disease and from policy and funding for research and treatments from being developed.

Because of this, thousands of people are improperly treated or unaware that they have the disease. Doctors, who know about the devastating effects of chronic Lyme disease and understand how to treat it, are persecuted by the medical establishment and have their licenses revoked for putting patients on long-term treatment regimens. More information on the politics of Lyme disease and why this happens can be found in the award-winning 2009 documentary, Under Our Skin: The Untold Story of Lyme Disease, and in Pamela Weintraub's book, Cure Unknown:.

Chronic Lyme is a debilitating, disabling disease that affects every organ and system of the body. It mimics a variety of diseases such as fibromyalgia, rheumatoid arthritis and Chronic Fatigue Syndrome and, in the most severe cases, Parkinson's, ALS or multiple sclerosis. The International Lyme and Associated Diseases Society (ILADS), which recognizes that chronic Lyme exists and establishes effective guidelines for its treatment, estimates that most chronic Lyme disease sufferers experience a level of disability equivalent to that of a person who has suffered from a recent heart attack. A Lyme disease symptom list can be found at: http://www.lymenet.org/BurrGuide200...

Effective treatment protocols are complicated and usually involve years of treatment, along with remedies to heal the organs, tissues and other parts of the body affected by Lyme. Treatment is difficult, partly because borrelia burgdorferi isn't the only organism implicated in the disease. The malarial-like parasite, babesia, along with bartonella, ehrlichia and many others comprise the matrix of infections that is chronic Lyme disease and that has disabled many hundreds of thousands of people in the United States and abroad.

Anyone suffering from undiagnosed symptoms or any of the above-mentioned diseases may have Lyme. Diagnosis can be confirmed by a "Lyme-literate" doctor, who diagnoses the disease based on symptoms and response to treatments, along with unconventional methods of testing. Recommendations for Lyme-literate doctors can be found at: www.ilads.org. Most doctors in conventional medicine don't know how to recognize or adequately treat the disease, so a recommendation from ILADS or a reputable online Lyme disease support group such as LymeNet.org can enable sufferers to find hope and healing from the disease.

References:

Burrascano, Joseph J., MD. Advanced Topics in Lyme Disease: Diagnostic Hints and Treatment Guidelines For Lyme and Other Tick-Borne Illnesses. Sixteenth edition: 2008.

Weintraub, Pamela. Cure Unknown: Inside the Lyme Epidemic. New York: St. Martin's Press, 2008, 2009.

http://www.chroniclymedisease.com/
http://www.townsendletter.com/Jan20...
http://ilads.org
http://www.underourskin.com


Learn more: http://www.naturalnews.com/033557_Lyme_disease_holistic_treatments.html#ixzz1 XrNc0Knj

wonderfullife
13-09-2011, 07:55 PM
Abstract

Background: A comparison of patients with erythema migrans due to Borrelia garinii versus Borrelia burgdorferi has not been reported.

Patients and Methods: One hundred nineteen patients from New York State with erythema migrans caused by B. burgdorferi were compared with 116 patients from Slovenia with erythema migrans due to B. garinii infection.

Results: Patients with B. garinii infection were older, more often reported a tick bite, and developed larger lesions (median largest diameter: 18 and 14 cm, respectively; p=0.01) that more often had central clearing (61.2% compared with 35.3%; p<0.0001). Patients infected with B. burgdorferi, however, more often had systemic symptoms (68.9% vs. 37.1%; p<0.0001), including fatigue (p<0.0001), arthralgia (p=0.0003), myalgia (p<0.0001), headache (p=0.0008), fever and/or chills (p<0.0001), and stiff neck (p<0.0001), and more often had abnormal physical findings (57.1% compared with 11.2%; p<0.0001), such as fever (p=0.0002) or regional lymphadenopathy (p<0.0001). There was a trend for more patients with B. burgdorferi infection to have multiple erythema migrans skin lesions (13.4% compared with 5.2%; p=0.051), and among patients with multiple erythema migrans the number of lesions was greater in B. burgdorferi-infected patients (median: 5.5 compared with 2.0; p=0.006).

Conclusions: The results of the present study indicate that in patients with erythema migrans the clinical features vary according to whether infection is caused by B. garinii or B. burgdorferi.

http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0230

wonderfullife
13-09-2011, 07:57 PM
Lyme disease is a perfect model of the complex relationship between host, vector, and the vector-borne bacteria. Both dogs and horses in Romania are exposed to infection. The aim of the present study was to assess the seroreactivity against Borrelia burgdorferi sensu lato in dogs and horses from different regions of Romania. 276 samples from dogs and 260 samples from horses located in different regions of Romania were analyzed by ELISA and IFA, respectively. The effect of several factors potentially affecting seroreactivity (location, age, gender, occupation, and vector exposition risk) was evaluated using Fisher's exact test (R 2.12.0). The overall prevalence of anti-Borrelia antibodies was 6.52% (18/276) in dogs, with a significantly higher positivity (46.15%, 6/13, p=0.0005) recorded in a midcountry region. Seroreactivity was correlated with occupation, with working dogs being more exposed. The results may indicate that Lyme borreliosis foci are restricted to small areas, but further studies on Borrelia prevalence in tick populations are needed to confirm this hypothesis. In horses, a global seroprevalence of 11.92% (31/260) was observed. No correlations were found between positive results and age, sex, county, or occupation. This is the first serological survey on antibodies to B. burgdorferi sensu lato in Romanian dogs and horses.

http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0254

tschingu
14-09-2011, 10:35 AM
Tests for diagnosing Lyme disease are inadequate, for many reasons. For instance, Lyme disease suppresses the body's antibody production, resulting in false negative tests, while antigen tests miss blood samples containing proteins from borrelia burgdorferi, one of the principal organisms implicated in Lyme. What's more: because the CDC and IDSA refuse to recognize it, most doctors aren't taught about chronic Lyme disease and how to treat it.

I agree that all of the commonly used mainstream-doctor-tests are inadequate, but there are good alternatives as well.
I can personally recommend the BCA, the Lyme Center in Augsburg, Germany for professional diagnosing and advanced laboray testing.
Though this is quiet expensive ~600 euro.
However another, cheaper alternative for a quality test is a live blood analysis through a dark field microscope.

Links:
Lyme Center Augsburg
http://www.b-c-a.de/
and a list of dutch doctors offering live blood analysis
http://www.momo-development.com/08%20praktijkgedeelte/4-netwerk/lymetest.htm

elpressiedente
14-09-2011, 10:46 AM
if any one wishes to try a totally new device for the elimination of Lyme in the human body send me a private message

I live in Australia

wonderfullife
15-09-2011, 07:44 PM
When Tammy Farmer gave birth to her son, Logan, her life changed dramatically, but not in the usual way.

Without knowing it, Farmer was a carrier of Lyme disease, and it wasn’t until she went through the physical stress of childbirth that she began to experience symptoms like excruciating pain and cognitive impairment. Because the tick-borne bacterium that cause Lyme disease can pass through the placenta, Logan was infected before he was born.

As Farmer left the hospital with her newborn, she began the battle of her life, not only fighting for her and her son’s health, but also for other victims of Lyme disease by volunteering for Kansas Lyme Fighters Inc.

Lyme disease can cause a wide array of health challenges that range from gastrointestinal to neurological to musculoskeletal, making it easy to misdiagnose. In fact, the Centers for Disease Control and Prevention estimates that the 328,128 cases of Lyme disease that were confirmed between 1990 and 2008 represent only 10 percent of the actual cases of Lyme disease, according to the Lyme Disease Association. In fact, Farmer was misdiagnosed for seven years with baffled doctors telling her she had everything from multiple sclerosis to lupus.

At times, she was so devastated by the illness that she couldn’t function. “At my lowest moments, I was in bed, incapacitated, because it hurt so badly. It hurt just to have someone walking on the carpet outside my bedroom,” Farmer said.

Farmer and Logan were finally diagnosed three years ago and started aggressive antibiotic treatment. While she still has bad days, she’s beginning to recover. And she’s using her newfound health to help others who suffer from tick-borne illnesses through a nonprofit group she helped to found, Kansas Lyme Fighters. Her volunteer work has been so transformative in the lives of people who battle Lyme disease that the organization nominated Farmer for the United Way Roger Hill Volunteer Center’s 2010 Wallace Galluzzi Outstanding Volunteer award.

In addition to helping raise awareness of tick-borne illnesses, Farmer runs support groups and works as an advocate. But mostly, she comes alongside those who are sick and offers them support and encouragement.

“Tammy’s strength is building community,” said Peggy Blumhagen, president of Kansas Lyme Fighters. “She has opened her home to multiple people who were suffering and created an environment of acceptance, comfort and love. Tammy rarely shares how she feels except when it helps to encourage people who are about to give up on their life. When they realize how much she is suffering also, they gain courage and strength to keep trying to get well.”

Farmer shrugs off the praise. “After something so devastating has affected my family’s life, I couldn’t help but help others,” she says. “I was sick for years before it was figured out, and that’s not uncommon at all. It happens to people all the time, and their lives are as devastated as mine was. Or worse. I had family to support me, but I know a lot of people who don’t.

“When you go through something like this, you narrow down what is important in your life. People are important, and that’s what makes life go around. Making them feel better, even for just a moment.”

For information or to volunteer for Kansas Lyme Fighters, see kansaslymefighters.org.
http://www2.ljworld.com/news/2011/sep/11/firsthand-family-experience-lyme-disease-inspires-/

wonderfullife
15-09-2011, 07:54 PM
Here are the pictures of Lyme rash old pics:
http://ticktalkireland.org/faq.html#lymerash

Now compare them with the new pics that the CDC are using just to confuse even more people:
http://www.cdc.gov/lyme/signs_symptoms/index.html

What are they playing at?

wonderfullife
15-09-2011, 08:01 PM
Johnson ST, Cable RG, Leiby DA

Transfusion 2011 09 12

BACKGROUND: Human babesiosis in the United States is primarily
attributable to infection with the intraerythrocytic protozoan parasite,
Babesia microti. Transfusion-transmitted Babesia (TTB) is a mounting
blood safety concern; approximately 100 US cases of TTB have been
reported since 1980. In response, market withdrawal (MW) and/or lookback
(LB) has been advocated for cellular components derived from
Babesia-positive blood donors.

STUDY DESIGN AND METHODS: Immunofluorescence assay (IFA) and selective
polymerase chain reaction (PCR) testing of Connecticut donors was
conducted from 1999 through 2005. MW/LB was initiated following
established procedures on cellular components derived from IFA and/or
PCR-positive donors. Recipients of these associated components were
offered IFA and PCR testing for B. microti.

RESULTS: A total of 208 seropositive donors were identified, with 474
donations and 656 cellular components subject to MW/LB. Sixty-three
recipients were tested for B. microti; eight (12.7%) were IFA and/or PCR
positive. A significantly higher proportion of B. microti-positive
recipients were identified by LB in 1999 to 2000 (5 of 15, 33.3%) than
after implementation of seropositive donor deferral in 2001 (3 of 48,
6.3%). Significant differences in positive LBs were also found when
comparing index (50% positive) to previous donations (7.3% positive),
and when comparing demonstrably parasitemic to nonparasitemic donors,
33.3 and 2.9%, respectively.

CONCLUSIONS: Recipients of components from B. microti-positive donors
were infected via transfusion, with index donations from parasitemic
donors posing the greatest transmission risk. This report of B. microti
transmission detected through LB, coupled with ongoing TTB cases,
indicates that interventions are needed to reduce transmission of B.
microti to US blood recipients

wonderfullife
15-09-2011, 08:03 PM
Mansueto P, Vitale G, Cascio A, Seidita A, Pepe I, Carroccio A, di
Rosa S, Rini GB, Cillari E, Walker DH

Clin. Dev. Immunol. 2011 09; 2012 : 967852

Human rickettsial diseases comprise a variety of clinical entities
caused by microorganisms belonging to the genera Rickettsia, Orientia,
Ehrlichia, and Anaplasma. These microorganisms are characterized by a
strictly intracellular location which has, for long, impaired their
detailed study. In this paper, the critical steps taken by these
microorganisms to play their pathogenic roles are discussed in detail on
the basis of recent advances in our understanding of molecular
Rickettsia-host interactions, preferential target cells, virulence
mechanisms, three-dimensional structures of bacteria effector proteins,
upstream signalling pathways and signal transduction systems, and
modulation of gene expression. The roles of innate and adaptive immune
responses are discussed, and potential new targets for therapies to
block host-pathogen interactions and pathogen virulence mechanisms are
considered.

wonderfullife
16-09-2011, 01:15 AM
YouTube - Broadcast Yourself.

creation
16-09-2011, 03:49 PM
I have Lyme disease and live in the UK, it ruined my life and i got no help from the doctors here. And the most worrying thing is i don't even know where i picked it up from. I think lots of people are going to become sick in the UK and they won't have a clue what to do.

bush doctor
16-09-2011, 04:41 PM
Has anybody tried cs for lyme dieses.

A few testimonials here:

http://www.colloidsforlife.com/silver_Lyme_Disease.html

wonderfullife
20-09-2011, 06:28 PM
I have Lyme disease and live in the UK, it ruined my life and i got no help from the doctors here. And the most worrying thing is i don't even know where i picked it up from. I think lots of people are going to become sick in the UK and they won't have a clue what to do.

That's the trouble with Lyme is knowing how one picks it up. It could even be passed through the womb and breastmilk. It can be sexually transmitted or a blood transfusion. Sometimes we do not know we have been bitten. Mosquitos, nits, fleas, bed bugs, horse flys, sand flys can pass it on. as well as ticks.
Lyme is a big conspiracy and it is going to be covered up even more if we allow it.
In my mind it all makes perfect sense why every one is getting so sick now and that there are no cures for illness's cancer is on the rise autoimmune disease is on the rise mental health problems on the rise you are right a lot of people are going to get sicker or disabled if any one wanted to know how tptb would wipe out 80% of the population we need not look much further than our own back yards.

wonderfullife
20-09-2011, 06:33 PM
Has anybody tried cs for lyme dieses.

A few testimonials here:

http://www.colloidsforlife.com/silver_Lyme_Disease.html

Yes I have tried CS and I will say it did make a diffrence i swear by CS at the moment I am trying MMS and oxygen therapy which is making a huge difference in me and my Lyme symptoms I am on week 9 of MMS and as Lyme has a six week cycle I would like to see what i am like in another 3 weeks cos then I will be in 2nd 6 week cycle. I still use CS for first aid in the home and heartburn.
Thanks for the link:)

wonderfullife
20-09-2011, 06:34 PM
New Haven, Conn. — Yale School of Public Health researchers in collaboration with Russian scientists have discovered a new tick-borne bacterium that might be causing disease in the United States and elsewhere. Their findings appear in the journal Emerging Infectious Diseases.

This new disease is caused by a spirochete bacterium called Borrelia miyamotoi, which is distantly related to Borrelia burgdorferi, the bacterium that causes Lyme disease. Yale professor of epidemiology Durland Fish and colleagues found this new spirochete, previously known only from ticks in Japan, in deer ticks in Connecticut in 2001, but did not know if it caused disease in humans.

The bacteria have since been found in all tick species that transmit Lyme disease throughout the United States and Europe. By collaborating with a medical team studying tick-borne diseases in Russia, Yale researchers were able to compare disease symptoms in patients infected by the new spirochete in Russia with those having Lyme disease in the United States.

The new disease is characterized by high fever, which relapses without treatment and may be confused with Lyme disease. There are currently no diagnostic tests available, but Yale researchers have recently received a grant from the National Institutes of Health (NIH) to develop a diagnostic test procedure to look for cases of this new disease in the United States.

"This is the first time we will have a chance to identify a new tick-borne disease in the United States based upon evidence that the agent occurs in ticks," said Fish, co-author of the paper and co-investigator on the NIH grant along with Peter Krause, a senior research scientist in the Division of Epidemiology of Microbial Diseases.

They report finding B. miyamotoi in about 2 percent of the deer ticks in the Northeast and Upper Midwest and have been conducting experiments with mice in the laboratory that become infected when fed upon by deer ticks. Because bites from deer ticks cause more than 25,000 cases of Lyme disease each year, according to the CDC, the Yale team is gearing up to determine if there is any illness that is caused by B. miyamotoi infection in the United States.

(Photo: Geoffrey Attardo, School of Public Health)

Contact: Michael Greenwood, Tel: 203-737-5151 , Email: [email protected]


http://insciences.org/article.php?article_id=10347

wonderfullife
20-09-2011, 06:37 PM
Ticks are divided taxonomically into two main families - the soft ticks (Argasidae) and the hard ticks (Ixodidae). The soft ticks have an oval or pear-shaped outline, with the anterior body region broadly rounded and the mouthparts on the anterior ventral surface (except for larval argasids). The hard ticks are flattened dorsoventrally in the unfed state and the mouthparts clearly project anteriorly (as in larval argasids). A sclerotized dorsal plate (scutum) is present in all stages and is often ornate. Only hard ticks of the genus Ixodes transmit Borrelia burgdorferi sensu lato (s.l.). The relapsing-fever Borrelia spp. are transmitted by soft ticks, However, some relapsing fever-like borrelia, such as B. myamotoi, are now known to be transmitted by the hard tick vectors of B. burgdorferi (s.l.).

A large number of hard tick species have been identified as carriers of the genospecies of B. burgdorferi that cause LB. However the presence of the spirochaete in ticks does not necessarily mean that they are capable of transmitting it to new hosts. (B. burgdorferi has also been identified in mosquitoes and deer flies, but these are not thought to be important in the transmission of the spirochaete to humans). Four Ixodes species are recognised as important vectors of LB world-wide : these are Ixodes persulcatus and I. ricinus in the Old World, and I. pacificus and I. scapularis (dammini) in the New World.
I. ricinus, a prostriate tick (Family Ixodidae, Subfamily Ixodinae), is the commonest tick in Northern Europe and is an important vector of both livestock and human diseases (see Table ). It acquired a new significance when in 1983 it was identified as a vector of the newly described spirochaete, B. burgdorferi (Burgdorfer et al. 1983. Acta Tropica 40:79-83).




Detailed ecological studies on I. ricinus have been carried out in Europe for the last 80 years or so, with increasing emphasis on the microclimate and diapause phenomena. The close relative of I. ricinus, I. persulcatus, has been the subject of intense study as an important vector of tick-borne encephalitis in Eastern Europe and temperate Asia. Soon after the implication of I. ricinus as a vector of LB, I. persulcatus was also established as a vector, which effectively extended the range of this disease right across Asia. The main difference in transmission biology between I. ricinus and I. persulcatus is that whereas both nymphal and adult female I. ricinusare implicated as vectors of LB disease, only adult female I. persulcatus are significant vectors because the immature stages rarely bite humans (Korenberg et al Emerg Infect Dis 7:459-62).

The details presented on this website concern I. ricinus unless otherwise stated.
Wild animal hosts of I. ricinus include small mammals, birds, reptiles and deer
http://meduni09.edis.at/eucalb/cms/index.php?option=com_content&task=view&id=51&Itemid=85

wonderfullife
20-09-2011, 06:43 PM
Yale School of Public Health researchers in collaboration with Russian scientists have discovered a new tick-borne disease that they believe may occur in the United States.

This new disease is caused by spirochete bacteria called Borrelia miyamotoi, which is distantly related to Borrelia burgdorferi, the spirochete that causes Lyme disease. Previously known only from ticks in Japan, Professor Durland Fish and colleagues found this new spirochete in deer ticks in Connecticut in 2001, but did not know if it caused disease in humans.

The bacteria have since been found in all ticks species that transmit Lyme disease throughout the United States and Europe. By collaborating with a medical team studying tick-borne diseases in Russia, Yale researchers were able to compare symptoms of patients infected by the new spirochete in Russia with patients having Lyme disease in the United States.
This is the first time we will have a chance to identify a new tick-borne disease in the United States based upon evidence that the agent occurs in ticks,” said Fish, Ph.D., co-author of the paper and co-investigator on the NIH grant along with Peter Krause, M.D., a senior research scientist, in the Division of Epidemiology of Microbial Diseases.


They report finding B. miyamotoi in about 2 percent of the deer ticks in the Northeast and Upper Midwest and have been conducting experiments with mice in the laboratory that become infected when fed upon by deer ticks. Because bites from deer ticks cause more than 25,000 cases of Lyme disease each year according to the CDC, the Yale team is gearing up to determine if there is any illness that is caused by B. miyamotoi infection in the United States.

The article appears in the journal Emerging Infectious Diseases.
http://publichealth.yale.edu/news/news/2011/ticks.aspx

wonderfullife
20-09-2011, 06:45 PM
A new tick-borne disease that may be stealthily infecting some Americans has been discovered by Yale researchers working with Russian scientists.

The disease is caused by a spirochete bacterium called Borrelia miyamotoi, which is distantly related to Borrelia burgdorferi, the spirochete that causes Lyme disease.

B. miyamotoi has been found — albeit relatively rarely — in the same deer tick species that transmit Lyme, and the Yale researchers estimate that perhaps 3,000 Americans a year pick it up from tick bites, compared with about 25,000 who get Lyme disease.

But there is no diagnostic test for it in this country, so it is not yet known whether it has actually made any Americans sick.

The same short course of antibiotics that normally cures Lyme also seems to cure it.

In Russia, where a team in the Siberian city of Yekaterinburg developed a test that can distinguish miyamotoi from other tick-borne spirochetes, it caused higher fevers than Lyme disease typically does. In about 10 percent of cases, the fevers repeatedly disappear and return after a week or two.

The study by the two teams is to be published soon in the journal Emerging Infectious Diseases. Since the disease was only recently discovered, it is unknown whether it does serious long-term damage, as untreated Lyme disease can.

The Yale medical school researchers — Durland Fish, an entomologist, and Dr. Peter J. Krause, an epidemiologist — have recently won a grant from the National Institutes of Health to study the symptoms and develop a rapid diagnostic kit.

Dr. Fish found B. miyamotoi in American ticks 10 years ago, but was repeatedly refused a study grant until the Russians proved it caused illness. “It’s been like pulling teeth,” he said. “Go ask the N.I.H. why.”

The discovery will no doubt add to the controversy surrounding Lyme disease. While most Lyme victims are cured by a two-week course of antibiotics, some have symptoms that go on for years and believe they have persistent infections that the antibiotics did not reach.

Most medical authorities, including the Centers for Disease Control and Prevention and the Infectious Disease Society of America, take the position that “chronic Lyme disease” does not exist and that those victims either have other illnesses or are hypochondriacs. They oppose the solution demanded by some self-proclaimed victims: long-term intravenous antibiotics.

Dr. Krause said it was unlikely that the new spirochete could be responsible for chronic Lyme, because the symptoms do not match: Most of those who think they have chronic Lyme complain of fatigue and joint pain, not repeated fevers.

But he said doctors might consider the new infection, especially in patients who think they have been bitten by ticks, come up negative on Lyme tests and have recurrent episodes of fever.

B. miyamotoi does not appear to cause the “bull’s-eye rash” that helps doctors diagnose Lyme disease, the Russian team found.

“People shouldn’t panic,” Dr. Krause said. “And they also should not jump to the conclusion that we’ve found the cause of chronic Lyme disease. It’s not highly likely, but it’s possible. We just don’t know.”

The miyamotoi spirochete was discovered in Japan in 1995. It was at first believed to be limited to those islands.

In 2001, Dr. Fish found it in about 2 percent of the deer ticks in the Northeast and Upper Midwest and proved that mice could pick it up from tick bites.








A version of this article appeared in print on September 20, 2011, on page D6 of the New York edition with the headline: New Tick-Borne Disease Is Discovered.
http://www.nytimes.com/2011/09/20/health/20tick.html?_r=1

wonderfullife
20-09-2011, 06:47 PM
To better define areas of human Lyme disease risk, we compared US surveillance data with published data on the seroprevalence of Borrelia burgdorferi antibodies among domestic dogs. Canine seroprevalence >5% was a sensitive but nonspecific marker of human risk, whereas seroprevalence <1% was associated with minimal risk for human infection. Lyme disease is caused by Borrelia burgdorferi and transmitted in North America by Ixodes spp. ticks. Routine surveillance for human illness indicates that risk for infection within the United States is highly localized. Residents of 10 states accounted for >93% of the ≈248,000 cases reported to the Centers for Disease Control and Prevention (CDC) during 1992–2006. Annual county-level incidence ranged from 0 to >1,000 cases per 100,000 population. Accurate information about risk is necessary for targeting and motivating Lyme disease prevention efforts. In addition, health care providers require knowledge of local disease risk to properly interpret clinical and laboratory findings. Although risk often can be inferred from surveillance data, reporting practices are subject to bias. Independent measures of disease risk are therefore valuable for validating surveillance findings.

Like humans, domestic dogs are susceptible to opportunistic infection with B. burgdorferi. These infections are often subclinical and pose no risk for direct transmission to humans. Nevertheless, they elicit a robust antibody response. Given the greater proclivity of dogs for tick exposure, canine seroprevalence has been proposed as a sensitive and independent measure of human Lyme disease risk. We compared US national surveillance data on Lyme disease with recently published data on B. burgdorferi antibody seroprevalence in dogs to determine the degree of concordance between these 2 measures of Lyme disease risk and to assess the potential for canine seroprevalence to predict areas of Lyme disease emergence among humans.

http://www.vetscite.org/publish/items/006836/index.html

wonderfullife
20-09-2011, 06:50 PM
St Albans woman’s mysterious illness attributed to ticks.
WHEN a St Albans farmer’s wife discovered she was suffering from a debilitating disease spread by ticks, it wasn’t the two GPs she saw who established the condition. Nor was it the chest specialist, the heart surgeon, neurologist or even an ear, nose and throat specialist she subsequently saw.

It was a close family friend who, upset at seeing Val Barr barely able to walk, had the nous to trawl through internet sites until the myriad symptoms came to just one conclusion - Lyme disease.

Her assumption was confirmed when Val, 55, had further tests and was finally diagnosed by a doctor specialising in that field at the Breakspear Medical Group’s private clinic in Hemel Hempstead – two months after falling ill.

A grateful Val, of Dane End Farm, St Albans, who was extremely fit, active and healthy before being infected, credited her friend: “She saved my life.”

She now wants to warn others to be on the alert if they, too, suspect they have been bitten by a tick to seek immediate treatment.

In April 2010 Val attended a point-to-point course at a hunt in Northaw.

She said: “Through the day I starting getting a headache and feeling nauseous. As the day went on that got progressively worse. I woke up with severe chest pains as well and severe flu-like symptoms.”

A doctor sent Val to Luton and Dunstable Hospital to investigate whether she had possibly had a heart attack, or a blood clot.

Despite extensive tests the hospital couldn’t pinpoint what was wrong and sent her home.

Val said that her symptoms included severe, crushing headaches and low blood pressure. The back of her hands and top of her feet felt as if someone was digging them with needles, because her nervous system was affected.

She saw a chest specialist who investigated her lung function.

Val said: “It was like tunnel vision. His conclusion was that I should go to a physiotherapist to be taught how to breathe because I was hyperventilating.”

There are 76 possible symptoms of Lyme disease, of which Val had 55. Val asked the chest specialist whether she might have the disease but he dismissed her fears.

Val added: “I felt quite upset and patronised.”

Undeterred, her friend stepped in again, contacted a Lyme disease support organisation and was told about Breakspear.

There, Val was finally diagnosed and immediately put on antibiotics.

More than one year on, she takes a whopping 32 pills a day; a combination of antibiotics and medication to support her immune system. She said: “I’m feeling a lot better, not back to normal but my energy levels are returning.”

The keen horsewoman warned that people can be bitten anywhere as the ticks themselves do not just live in “hotspots”.

Fellow sufferers at Breakspear, including one from Harpenden, told Val they had been bitten while gardening.

Val said: “It is totally debilitating. It stops your life dead in its tracks. Be aware. If you see a tick, take it off immediately.”
http://www.hertsad.co.uk/news/st_albans_woman_s_mysterious_illness_attributed_to _ticks_1_1025066

wonderfullife
20-09-2011, 07:04 PM
Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease.

Nadelman RB, Pavia CS, Magnarelli LA, Wormser GP.


Source

Department of Medicine, New York Medical College, Valhalia.


Abstract

PURPOSE:

Borrelia burgdorferi, the etiologic agent of Lyme disease, has rarely been successfully cultured from blood. We report on seven patients from Westchester County, New York, with B. burgdorferi bacteremia diagnosed between April 1987 and August 1987.

PATIENTS AND METHODS:

One hundred thirty-two attempts to isolate spirochetes were made on blood specimens obtained from 104 patients. Twenty-two of these specimens were obtained from nine patients who had recently been bitten by Ixodes ticks but who were asymptomatic. Heparinized blood or serum specimens (0.2 to 0.4 mL) were inoculated onto 6 mL of modified Barbour-Stoenner-Kelly medium. Lyme serology was performed by enzyme-linked immunosorbent polyvalent, IgM, and IgG assays, fluorescent immunoassay, and microhemagglutination.

RESULTS:

Four of the seven patients had erythema migrans, two had facial nerve palsy, and one had a flu-like syndrome without rash. These patients represented 21% (four of 19) of all patients with the characteristic skin lesion who had blood cultures for B. burgdorferi, and 40% (two of five) of all those with facial nerve palsy. Serologic testing was frequently nonreactive; two patients had no detectable antibody on multiple sera by five different assays. All patients improved with antibiotic treatment, and had negative subsequent blood cultures, but five of seven had persistent complaints after completion of therapy.

CONCLUSION:

Culturing blood for B. burgdorferi may be useful in confirming the diagnosis of Lyme disease in selected patients. Use of spirochete blood cultures may facilitate a better understanding of the pathogenesis and natural history of Lyme disease.


PMID: 2294761 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/2294761

wonderfullife
20-09-2011, 07:14 PM
The infection, if untreated, commonly persists for months to years despite the occurrence of host antibody and cellular responses; this observation indicates effective evasion of the immune response. Lyme disease may be disabling (particularly in its chronic form), and thus there is a need for effective therapeutic and prophylactic treatment. [0010] Certain5. burgdorferi genes and proteins have been patented, including Outer Surface Protein D (OspD) (U.S. Pat. No. 5,246,844; issued Sep. 21, 1993). OspD has not proven to be a useful protein for diagnosis or immunoprotection. Other proteins, including OspA and OspC, have been considered as vaccine candidates for Lyme disease, including a recombinant OspA vaccine currently in human clinical trials. Other vaccines are in use or undergoing testing in veterinary applications, including vaccination of dogs. However, animal studies indicate that OspA vaccination may not be effective against all strains of Lyme disease Borreliae. OspA is also not useful for immunodiagnosis, due to weak antibody responses to OspA in Lyme disease patients.
http://www.google.co.uk/patents/about?id=m8HnAAAAEBAJ&output=text

wonderfullife
20-09-2011, 07:21 PM
In 2009, 10 329 cases of Lyme borreliosis were reported in Poland, more
about 20% than in the last year and more about 25% higher
incidence--27.1 per 100 000, and above two times more than the median
incidence in 2003-2007. The highest incidence 114.0 per 100 000 was
registered in podlaski voivodeship. Of total Lyme borreliosis cases 2
504 were hospitalized.

wonderfullife
20-09-2011, 07:27 PM
Abstract
Lyme disease is a multisystem infectious disease, endemic in parts of Europe, including the West of Ireland. Neurological manifestions (neuroborreliosis) are variable. Presenting neurological syndromes include meningitis, cranial neuropathies, myeloradiculitis and mononeuritis multiplex. A lack of specificity in serological diagnosis may add to diagnostic confusion. We reviewed thirty cases of acute Lyme disease in the West of Ireland and found neurological syndromes in 15 (50%), with painful radiculopathy (12 patients; 80%) and cranial neuropathy (7 patients;46%) occurring frequently. Neuroborreliosis needs to be considered in the differential diagnosis of these neurological syndromes in the appropriate clinical context.


Introduction
Lyme disease is a multisystem infectious disease caused by the Borrelia spirochaete genus. The predominant species in North America is Borrelia burgdorferi sensu stricto, and in Europe the predominant species are B. afzelli and B. garinii. Deer and other mammals are the intermediate hosts1. Lyme disease is the most frequently reported arthropod–borne infection of the nervous system in Europe and the USA1. Erythema migrans (EM) is regarded as the most common clinical marker of infection and is estimated to occur in 60-80% of patients1. Neurological manifestations of Lyme disease (neuroborreliosis; NB) comprise an array of both central and peripheral neurological syndromes, mimicking a variety of common disorders2. Typical neurological presenting syndromes include include meningitis, cranial neuropathies (with a predilection for the facial nerve), myeloradiculitis and mononeuritis multiplex3,4. Difficulties in the diagnosis and management of patients with Lyme NB may be compounded by a lack of specificity and sensitivity of serological tests in active disease5.

Seroprevalence studies report the Republic of Ireland as having one of the highest rates of Lyme disease in Europe6. Lyme disease is considered endemic in the West of Ireland7,8. However, few studies have explored the clinical presentation and natural history of Lyme NB in Ireland9-11. We therefore undertook a retrospective analysis of the clinical characteristics of Lyme NB in the West of Ireland. We conducted a retrospective review of the clinical presentation of patients with serologically confirmed Lyme disease diagnosed over a five-year period at a single referral centre in the West of Ireland. We identified the proportion of patients presenting with NB, we define the neurological syndromes at presentation, and report the clinical outcomes.


Methods
The study population included those patients who had serological testing consistent with Lyme disease, based on referrals to the Department of Medical Microbiology, University Hospital Galway. The study period extended from January 1999 to August 2004. During that period, approximately 2100 sera were tested using the screening ELISA. A two-tier diagnostic process was utilized in accordance with international standards12, comprising an initial screening enzyme-linked immunosorbant assay (ELISA) for anti Borrelia antibodies. In those patients who had positive screening ELISA tests, antibody positivity was confirmed by a positive IgG and/or IgM immunoblot assay at the Lyme Borreliosis Unit, Southampton, UK. We identified 42 samples over the sixty-six month study period with serology consistent with Lyme disease.

After obtaining Ethics Committee approval and written informed consent from the referring physician, we then obtained clinical data for 32 patients. Data was collected by chart review and included demographic characteristics, potential exposure to tick bite, clinical presentation and results of imaging and cerebrospinal fluid analysis. Patients were included in the study in whom there was a clear temporal relationship between the onset of a clinical syndrome known to be associated with Lyme disease, (such as EM) and serological testing. Exclusion criteria were equivocal serological results or positive tests that were deemed to represent convalescence serology. Two patients were excluded; both had IgG anti B. burgdorferi antibodies but their clinical presentation and imaging studies were compatible with alternative diagnoses (multiple sclerosis and brain neoplasm). Data on the remaining 30 patients was analyzed as pooled data.


Results
Baseline characteristics
Antibody subtypes directed against B burgdorferi in the thirty patients included in the study were detected as follows: seventeen patients (57%) had both IgM and IgG antibodies; six patients (20%) exhibited anti IgM antibodies only, and seven patients (23%) had only IgG anti-Borrelia antibodies. Patients ranged from 26 to 80 years of age, with a mean of 52.5 years; 60% were male. Twenty patients (67%) were resident of western counties of Ireland. Only one patient was resident outside the state. Recent travel outside Ireland was documented in seven cases. Nine patients (30%) had documented potential exposure to heavily wooded areas due to occupation or leisure activities. A history of tick bite was elicited in only one third of the patients. Lyme serology was requested by the patient’s general practitioner in twelve cases, by a consultant physician in thirteen cases and by a neurologist in five cases.
http://www.imj.ie//ViewArticleDetails.aspx?ArticleID=4785

wonderfullife
20-09-2011, 07:37 PM
Abstract

Lyme disease, caused by a tick-transmitted spirochete, typically begins with a unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin lesion, almost half developed multiple annular secondary lesions; some patients had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis, periorbital edema, or diffuse erythema. Skin manifestations were often accompanied by malaise and fatigue, headache, fever and chills, generalized achiness, and regional lymphadenopathy. In addition, patients sometimes had evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat, nonproductive cough, or testicular swelling. These signs and symptoms were typically intermittent and changing during a period of several weeks. The commonest nonspecific laboratory abnormalities were a high sedimentation rate, an elevated serum IgM level, or an increased aspartate transaminase level. Early Lyme disease can be diagnosed by its dermatologic manifestations, rapidly changing system involvement, and if necessary, by serologic testing.


Article and Author Information

▸From the Departments of Internal Medicine, Dermatology, and Pathology, Yale University School of Medicine; New Haven, Connecticut.


Grant support: in part by U. S. Public Health Service Grants AM-20358, AM-07107, AM-5639, RR-05443, and RR-00125; and the Arthritis Foundations and its Connecticut Chapter.


▸Requests for reprints should be addressed to Allen C. Steere, M.D.; Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street; New Haven, CT 06510.

http://www.annals.org/content/99/1/76.short

wonderfullife
20-09-2011, 07:39 PM
Lyme disease is a dangerous disease which is transmitted by ticks. Blood-sucking ticks ingest the agents that cause the disease – bacteria of the species Borrelia burgdorferi and its relatives – during a blood meal, and subsequently transmit them to the next victim they feast on, often a person. It is estimated that, in Western Europe, up to half of all ticks carry the bacteria. Although the early symptoms of the illness are quite mild, if left untreated, it can result in serious damage to the skin, the joints, the heart and the nervous system, and effective therapy becomes very difficult.

A team of researchers led by the veterinary bacteriologist professor Reinhard Straubinger at Ludwig-Maximilians Universität (LMU) München has now shown, in an animal model, that application of a gel containing the antibiotic azithromycin to the site of the bite rapidly terminates the infection. The efficacy of this local antibiotic therapy for the treatment of borreliosis in humans is now being tested in a Phase III clinical trial. In the meantime, though, patients must still undergo antibiotic treatment for several weeks and, in many cases, the drug must be administered intravenously – which is distressing not only for children. Furthermore, treatment measures are often initiated on suspicion, because the bacteria are not detectable in the blood soon after one has been bitten by an infected tick.

"Our approach simply involves applying a transparent, self-adhesive plaster to the site of the wound," says Straubinger. "Because the plaster contains very little antibiotic, the effects are localized and side-effects are negligible."

Reference: Knauer J, et al. Evaluation of the preventive capacities of a topically applied azithromycin formulation against Lyme borreliosis in a murine model. Journal of Antimicrobial Chemotherapy online, Sept. 15, 2011.
http://www.infectioncontroltoday.com/news/2011/09/reseasrchers-say-local-antibiotic-therapy-stops-lyme-disease.aspx

wonderfullife
20-09-2011, 07:43 PM
Abstract


Objectives Systemic antibiotic treatment of Lyme borreliosis is effective during the early stages of the infection, while chronic manifestations of the disease may remain refractory and difficult to treat. This study was carried out in order to evaluate the potential of topically applied azithromycin to eliminate the spirochaetal organisms in the skin of the freshly bitten host and thereby prevent Lyme borreliosis.


Methods Laboratory mice were challenged with Borrelia burgdorferi sensu stricto by needle inoculation or via infected ticks as vectors. Then, an azithromycin-containing formulation was applied once daily to the sites of exposure for three consecutive days. In the case of needle inoculation, a 5% azithromycin formulation was applied starting 1 h, 3 days and 5 days after infection. In the case of tick exposure, 4%, 10% and 20% azithromycin formulations were applied, starting directly after the detachment of the engorged ticks. Subsequently, the infection status of the mice was determined.


Results Concentrations of azithromycin in murine skin were >3800-fold higher than the published minimal inhibitory concentration for B. burgdorferi as soon as 3 h after the first application. After needle inoculation, spirochaetes were not detectable in all infected mice after treatment, if the first application started 1 h or even after 3 days post-infection. Furthermore, no borrelial organisms were detected after topical treatment when ticks were used for spirochaete inoculation.


Conclusions Our data indicate that topical treatment with a formulation containing azithromycin is a promising approach to prevent Lyme borreliosis shortly after a tick bite.
http://jac.oxfordjournals.org/content/early/2011/09/14/jac.dkr371

wonderfullife
20-09-2011, 07:52 PM
After being hunted to the edge of extinction in the 18th century, deer numbers have returned to levels not seen in Britain since the Norman conquest.

But now so many roam the countryside that they are fast becoming a menace, a Government study warned yesterday.


Herds are munching their way through undergrowth in important woodland habitats, threatening rare native species like nightingales, dormice and bluebells.


Numbers have risen to two million after the introduction of new species like muntjac, fallow and Chinese water deer that are smaller and breed faster.


Warmer winters, no natural predators, a fall in the number of people hunting and year-round crops mean numbers of native roe and red deer have also increased.


They eat the undergrowth in woodland taking out habitat for ground nesting birds, plants for insects and disturbing the ecosystem.


New research presented the British Ecological Society’s annual meeting found in certain areas of the country the problem is so bad that widespread culling will have to be introduced.

The research by Dr Emma Goldberg, of Natural England, looked at the impact of deer in 80 protected areas known as Sites of Special Scientific Interest (SSSIs).

She said deer browse out the undergrowth such as thickets of brambles and honeysuckle that birds nest in. The increasingly bare woodland floor can also impact on other mammals like dormice and insects like butterflies.

"The ecological knock-on impact is that it can have a direct impact on those shrubs, such as hazel, privet and some of the rarer shrubs, which may get browsed out of the woodland altogether,” she told the meeting in Sheffield.

“This has yet another knock-on impact for other species, like dormice or ground-nesting birds.

"Even butterflies can be affected because the shrub layer provides an important nectar source."

Ultimately, she said the deer threaten the woods themselves.

"As well as the shrub layer, the deer will actually eat the regenerating trees, so the long-term forecast of the woodland is unknown.

"If you do not have the regeneration of trees for the future, then that has a long-term impact."

In the countryside a major concern about deer is the spread of cattle disease like bovine tuberculosis and foot-and-mouth but in the city the worry is more about the growth in tick-bourn diseases like Lyme disease that can spread to pets and humans.

The National Deer Vehicle Collisions Project estimates estimate there are 74,000 accidents caused by deer every year, of which 44 per cent are in urban areas.

Peter Watson, of the Deer Initiative, said the effect on biodiversity is just the latest issue to come to light. He said the problem is worse in the east of England especially the East Midlands around Northampton and Corby, the Welsh marches around Herefordshire and Berkshire and Oxfordshire around the west side of London.

He said the problem has got worse because there is no coordinated approach across councils and other landowners to cull deer over a large area.

The Deer Initiative, which is a partnership between the Government, private sector and charities, is now working with landowners to carry out culls in those areas by trapping and shooting.

Mr Watson admitted that councils and charities are reluctant at first because of concerns about animal welfare.

But he pointed out that the Wildlife Trusts, RSPB and Woodland Trust are now all part of the initiative as they realise the deer population must be controlled for the good of wildlife.

Currently around 350,000 deer are killed in Britain every year, mostly by rifle, but it could be increased to 500,000.

Trained hunters carry out the culls and the venison can be sold for eating. However it is more difficult to cull deer in cities, where there is a growing problem with poaching and even hunting with dogs.

Even the RSPCA agrees culls may have to be carried out in certain areas, as long as deer fences and other preventive measures have been put in place first and the animals are killed humanely by trapping and shooting.

However many animal rights groups argue that deer are now a part of the urban and rural landscape like foxes that should be welcomed.

They insist that the animals can be stopped from causing a nuisance through control measures like contraception, relocation, ‘deer passes’ over motorways and fencing.
http://www.telegraph.co.uk/earth/earthnews/8765433/Deer-destroying-native-wildlife.html

wonderfullife
20-09-2011, 07:56 PM
Abstract

Background:Obesity is associated with increased health risk and has been associated with alterations in bacterial gut microbiota, with mainly a reduction in Bacteroidetes, but few data exist at the genus and species level. It has been reported that the Lactobacillus and Bifidobacterium genus representatives may have a critical role in weight regulation as an anti-obesity effect in experimental models and humans, or as a growth-promoter effect in agriculture depending on the strains.Objectives and methods:To confirm reported gut alterations and test whether Lactobacillus or Bifidobacterium species found in the human gut are associated with obesity or lean status, we analyzed the stools of 68 obese and 47 controls targeting Firmicutes, Bacteroidetes, Methanobrevibacter smithii, Lactococcus lactis, Bifidobacterium animalis and seven species of Lactobacillus by quantitative PCR (qPCR) and culture on a Lactobacillus-selective medium.Findings:In qPCR, B. animalis (odds ratio (OR)=0.63; 95% confidence interval (CI) 0.39-1.01; P=0.056) and M. smithii (OR=0.76; 95% CI 0.59-0.97; P=0.03) were associated with normal weight whereas Lactobacillus reuteri (OR=1.79; 95% CI 1.03-3.10; P=0.04) was associated with obesity.Conclusion:The gut microbiota associated with human obesity is depleted in M. smithii. Some Bifidobacterium or Lactobacillus species were associated with normal weight (B. animalis) while others (L. reuteri) were associated with obesity. Therefore, gut microbiota composition at the species level is related to body weight and obesity, which might be of relevance for further studies and the management of obesity. These results must be considered cautiously because it is the first study to date that links specific species of Lactobacillus with obesity in humans.International Journal of Obesity advance online publication, 9 August 2011; doi:10.1038/ijo.2011.153.
http://www.ncbi.nlm.nih.gov/pubmed/21829158

wonderfullife
20-09-2011, 07:59 PM
Anetoderma is an uncommon disease characterized by multiple
circumscribed atrophic, herniated skin lesions on trunk, thighs and
upper arms caused by loss of elastic fibers. Associations with
autoimmune diseases or infections, especially spirochetal infections,
have been described. We report a case of anetoderma with an increased
serum Borrelia burgdorferi IgM-titers. After treatment with doxycycline
200 mg/day for three weeks, the progression of the disease stopped and
no new lesions appeared.

wonderfullife
23-09-2011, 12:53 AM
A bacterin including effective immunizing amounts of two non-crossprotective isolates of inactivated Borrelia burgdorferi, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi isolates and a suitable carrier is provided herein. The bacterin may also contain a third non-crossprotective isolate. A bacterin including effective immunizing amounts of an antigenic subunit derived from a first Borrelia burgdorferi isolate and a second, non-crossprotective Borrelia burgdorferi isolate, an adjuvant in an amount effective to enhance the immunogenicity of the antigenic subunits and a suitable carrier is also provided. The bacterin may also contain an effective immunizing amount of an antigenic subunit of a third Borrelia burgdorferi. Further provided is a bacterin which includes effective immunizing amounts of two non-crossprotective isolates of inactivated Borrelia burgdorferi and one or more antigenic subunits from the non-crossprotective isolates, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi and antigenic subunits and a suitable carrier. Methods of immunizing an animal against Borrelia burgdorferi infection which comprise administering to the animal a dose of a bacterin provided herein are also provided.
Claims




What is claimed is:

1. A bacterin which comprises per dose an effective immunizing amount of two non-crossprotective inactivated Borrelia burgdorferi isolates, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi isolates and a suitable carrier, wherein one isolate is seroprotective group B strain C-1-11 of Borrelia burgdorferi having ATCC deposit designation PTA-1679 and the other isolate is selected from the group consisting of seroprotective group A Borrelia burgdorferi and seroprotective group C Borrelia burgdorferi.

2. The bacterin of claim 1, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is an amount from about 104 organisms to about 1010 organisms of each isolate.

3. The bacterin of claim 2, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is an amount from about 104 organisms to about 109 organisms of each isolate.

4. The bacterin of claim 3, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is an amount from about 104 organisms to about 108 organisms of each isolate.

5. The bacterin of claim 3 wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is about 107 organisms of each isolate.

6. The bacterin of claim 3 wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is about 5×107 organisms of each isolate.

7. The bacterin of claim 3 wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is about 5×108 organisms of each isolate.

8. The bacterin of claim 1, wherein the non-crossprotective isolates of Borrelia burgdorferi are inactivated by an agent selected from the group consisting of binary ethyleneimine, formalin and β-propriolactone.

9. The bacterin of claim 8, wherein the non-crossprotective isolates of Borrelia burgdorferi are inactivated by binary ethyleneimine.

10. The bacterin of claim 1, wherein the other isolate is of seroprotective group A Borrelia burgdorferi.

11. The bacterin of claim 10, wherein the seroprotective group A isolate of Borrelia burgdorferi is a strain selected from the group consisting of S-1-10 having ATCC deposit designati on PTA-1680, 297 and B31.

12. The bacterin of claim 11, wherein the seroprotective group A isolate of Borrelia burgdorferi is strain S-1-10 having ATCC deposit designation PTA-1680.

13. The bacterin of claim 1, wherein the adjuvant is selected from the group consisting of aluminum hydroxide, saponin, aluminum phosphate, carbopol and lipopolysaccharide.

14. The bacterin of claim 13, wherein the adjuvant is aluminum hydroxide.

15. The bacterin of claim 14, wherein the effective amount of the adjuvant is an amount from about 1.0% by volume to about 15% by volume.

16. The bacterin of claim 1, wherein the effective amount of the aluminum hydroxide adjuvant is an amount from about 5% by volume to about 10% by volume.

17. The bacterin of claim 16, wherein the effective amount of the adjuvant is about 7.5% by volume.

18. The bacterin of claim 1, wherein the suitable carrier comprises an aqueous buffer and preservatives.

19. The bacterin of claim 18, wherein the aqueous buffer is physiological saline.

20. The bacterin of claim 18, wherein the preservatives comprise gentamicin and nystatin.

21. The bacterin of claim 1, further comprising an effective immunizing amount of a third non-crossprotective isolate of inactivated Borrelia burgdorferi.

22. A method of immunizing an animal against infection by Borrelia burgdorferi which comprises administering to the animal a dose of the bacterin of claim 1.

23. The method of claim 22, wherein the animal is a mammal.

24. The method of claim 23, wherein the mammal is a human.

25. The method of claim 23, wherein the mammal is a dog.

26. The method of claim 25, wherein the dog is at least about six weeks old.

27. The method of claim 22, further comprising administering to the animal an additional dose of the bacterin at an interval of time after administration of the preceding dose.

28. The method of claim 27, wherein the interval of time is from about two weeks to about five weeks.

29. The method of claim 22, wherein the administration is by intramuscular injection.

30. The method of claim 22, wherein the administration is by subcutaneous injection.

31. A method of immunizing an animal against infection by Borrelia burgdorferi which comprises administering to the animal a dose of a bacterin which comprises an effective immunizing amount of at least two non-crossprotective isolates of inactivated Borrelia burgdorferi, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi and a suitable carrier for the immunization of animals against infection by Borrelia burgdorferi, wherein one isolate is seroprotective group B strain C-1-11 of Borrelia burgdorferi having ATCC deposit designation PTA-1679 and the other isolate is selected from the group consisting of seroprotective group A Borrelia burgdorferi and seroprotective group C Borrelia burgdorferi.

32. The method of claim 31, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is an amount from about 104 organisms to about 1010 organisms of each isolate.

33. The method of claim 31, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is an amount from about 104 organisms to about 109 organisms of each isolate.

34. The method of claim 31, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is an amount from about 104 organisms to about 108 organisms of each isolate.

35. The method of claim 31, wherein the effective immunizing amount of the non-crossprotective isolates of inactivated Borrelia burgdorferi is about 107 organisms of each isolate.

36. The method of claim 31, wherein the other isolate is of seroprotective group A Borrelia burgdorferi.

37. The method of claim 36, wherein the seroprotective group A isolate of Borrelia burgdorferi is a strain selected from the group consisting of S-1-10 having ATCC deposit designation PTA-1680, 297 and B31.

38. The method of claim 37, wherein the seroprotective group A isolate of Borrelia burgdorferi is strain S1-10 having ATCC deposit designation PTA-1680.
Description




BACKGROUND OF THE INVENTION

Lyme disease was first described by Steere et al. in 1977 who reported an epidemic of arthritis in Lyme, Old Lyme and East Haddam, Connecticut. In 1982, Dr. Willy Burgdorfer discovered a new spirochete in the midgut of Ixodes dammini ticks (see Burgdorfer, W. A. et al., (1982) Science 216: 1317-1319). This spirochete was subsequently shown to elicit an immune response in infected rabbits which paralleled that in humans with Lyme disease, and is now known to be the etiological agent of the disease. The spirochete was subsequently named Borrelia burgdorferi.

While Ixodes ticks are the most commonly encountered vectors of Borrelia burgdorferi, the spirochetes have also been found in deerflies, horseflies and mosquitoes. Spirochetes enter an animal host when the animal is bitten by the vector. The B. burgdorferi spirochetes reside in various tissues of the host animal, where they may lead to long term infection.

Borrelia burgdorferi have recently been shown to possess a unique type of extra chromosomal DNA, linear plasmids, which range in length from 0.5 to 50 kb (Bergstrom, S. et al., (1991) Scand. J. Infect. Dis.--Suppl. 77: 102-107). These plasmids contain the genes encoding the two major outer surface proteins (Osp) expressed by B. burgdorferi, OspA and Osp B (Bergstrom et al., 1991). These proteins are believed to be major antigens involved in the immunity to B. burgdorferi infection. Schwan and Simpson (Schwan, T. G. and Simpson, W. J., (1991) Scand. J. Infect. Dis.--Suppl. 77: 94-101) report heterogeneity of the Osp A and B proteins amongst different B. burgdorferi isolates, as well as on the same isolate grown at different temperatures in vivo and studies at different stages during the infection of mice.

The initial stage of Lyme disease is characterized by an expanding skin lesion, erythema chronicum migrans (Asbrink, E. and Hovmark, A.,(1988) Ann. N.Y. Acad. Sci. 539: 4-15; Halperin, J. J., (1991) Scand. J. Infect. Dis.--Suppl. 77: 74-80). Subjects also frequently develop arthritis. However, in only a small percentage of these subjects is the arthritis chronic (Steere, A. C., (1991) Scand. J. Infect. Dis.--Suppl. 77: 51-54). Borrelia burgdorferi may also infect the heart muscle. Cardiac involvement in Lyme disease has mainly been reported as transitory. However, animal studies revealed that skeletal and heart muscles are regularly affected and that the spirochetes appeared to be located within the muscle fibers. This observation suggests that the spirochetes are able to maintain long-term survival in hosts and may thus be able to cause chronic heart complications (Stanek, G. et al. (1991) Scand J. Infect. Dis.--Suppl. 77: 85-87).

B. burgdorferi also infects the nervous system in a high percentage of cases, leading to a wide range of acute, chronic and progressive central and peripheral nervous system disorders (Reik, L. et al. (1991) Ann. N.Y. Acad. Sci. 539: 1-3). Published reports have indicated that European populations afflicted with the disease experience dramatic clinical phenomena of neurological disorder, while North American patients develop milder forms of nervous system involvement. (Halperin, 1991; Halperin, J. J. et al., (1988) Ann. N.Y. Acad. Sci. 539: 24-34). However, Halperin (1991) report that it is becoming increasingly clear that at least as far as nervous system involvement is concerned, the same range of neurological phenomena occur in both populations. Diagnosis of Lyme disease depends upon a combination of the recognition of the clinical characteristics presented and also of the probability of exposure in endemically infected areas. However, the development of arthritis is often attributed to other causes and not correlated with a spirochete infection. The neurological symptoms which may be the result of B. burgdorferi infection can mimic a variety of other neurological conditions (Reik et al., 1988). Adding to these diagnostic complications is the difficulty of detecting the spirochetes in affected tissues.

Borrelia infection has been combatted with antibiotics, e.g., tetracycline, penicillin, amoxycilin, doxycilin, erythromycin and phenoxymethylpenicillin (Neu, H., (1988) Ann. N.Y. Acad. Sci., 539: 314-316; Skoldenberg, B. et al. (1988) Ann. N.Y. Acad. Sci. 539: 317-323; Weber, K. et al. (1988) Ann. N.Y. Acad. Sci. 539: 325-345; Luft., B. J. et al. (1988) Ann. N.Y. Acad. Sci, 539: 352-361). Ceftriaxone, and chemically similar compounds, have also been useful as chemotherapeutic agents (Neu, 1988). However, the establishment of protocols for effective chemical treatment of Lyme disease has been hampered by the lack of data with which an appropriate time period for treatment could be established. Additionally, there has been a lack of studies of the effectiveness of drugs in human patients. Further complicating the therapeutic picture is the need to establish and maintain sufficiently high tissue concentrations of antibiotics to combat chronic Borrelia infection (Neu, 1988; Skoldenberg et al., 1988).

Given this difficulty in the detection and treatment of Lyme disease, as well as the impracticability of managing the spread of spirochete vectors, there has been a recognized need for a vaccine capable of immunizing susceptible animals and humans against Borrelia burgdorferi infection. Vaccines have been studied in hamster (Johnson, R. C. et al. (1988) Ann. N.Y. Acad. Sci, 539: 258-263) and rat (Barthold, S. W. et al. (1988) Ann. N.Y. Acad. Sci. 539: 264-273) models. A whole cell Borrelia burgdorferi bacterin for use in domestic animals has been developed (U.S. Pat. No. 4,721,617). Vaccines based upon the B. burgdorferi Osp A and/or B proteins have also been developed. However, these whole cell and subunit vaccines contain, or are derived from, only one B. burgdorferi isolate. By contrast, the bacterin of this invention contains, or is derived from, at least two non-crossprotective B. burgdorferi isolates. The bacterin of this invention therefore will provide immune protection against two different types of B. burgdorferi isolate, while previously described bacterins provide protection against only one type of isolate. Accordingly, the bacterin provided by this invention will be more useful to vaccinate animals against Lyme disease.

SUMMARY OF THE INVENTION

This invention provides a bacterin which comprises per dose an effective immunizing amount of two non-crossprotective isolates of inactivated Borrelia burgdorferi, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi and a suitable carrier. The non-crossprotective isolates of Borrelia burgdorferi may be selected from the Wisconsin, Chicago and European seroprotective groups of Borrelia burgdorferi isolates. Presently preferred are isolates from the Wisconsin and Chicago groups. However, isolates belonging to other seroprotective groups may also be used. The bacterin may further comprise a third non-crossprotective inactivated Borrelia burgdorferi isolate.

This invention also provides a method of immunizing an animal against infection by Borrelia burgdorferi which comprises administering to the animal a dose of the bacterin provided. The animal may be a mammal including, but not limited to, humans and dogs. This invention contemplates administering an additional dose of vaccine to the animal at a suitable interval of time after administration of the preceding dose.

This invention further provides a bacterin which comprises per dose an effective immunizing amount of an antigenic subunit derived from a first Borrelia burgdorferi isolate, an effective immunizing amount of an antigenic subunit derived from a second, non-crossprotective Borrelia burgdorferi isolate, an adjuvant in an amount effective to enhance the immunogenicity of the antigenic subunits and a suitable carrier. The bacterin may further comprise an effective immunizing amount of an antigenic subunit of a third, non-crossprotective Borrelia burgdorferi isolate. This invention provides a method of immunizing an animal against disease caused by Borrelia burgdorferi which comprises administering to the animal a dose of the bacterin.

This invention also provides a bacterin which comprises per dose an effective immunizing amount of two noncrossprotective isolates of inactivated Borrelia burgdorferi and one or more antigenic subunits from the non-crossprotective isolates, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi and antigenic subunits and a suitable carrier.

This invention further provides for the use of a bacterin which comprises an effective immunizing amount of at least two non-crossprotective isolates of inactivated Borrelia burgdorferi, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi and a suitable carrier for the immunization of animals against infection by Borrelia burgdorferi.

The invention also provides for the use of a bacterin which comprises an effective immunizing amount of at least two non-crossprotective isolates of inactivated Borrelia burgdorferi and one or more antigenic subunits from the non-crossprotective isolates, an adjuvant in an amount effective to enhance the immunogenicity of the inactivated Borrelia burgdorferi and antigenic subunits and a suitable carrier for the immunization of animals against infection by Borrelia burgdorferi.
http://www.patentstorm.us/patents/6316005/fulltext.html

wonderfullife
23-09-2011, 12:56 AM
Abstract

Chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy and amyloid deposition in the atrophic form of general paresis. There is a significant association between Alzheimer disease (AD) and various types of spirochete (including the periodontal pathogen Treponemas and Borrelia burgdorferi), and other pathogens such as Chlamydophyla pneumoniae and herpes simplex virus type-1 (HSV-1). Exposure of mammalian neuronal and glial cells and organotypic cultures to spirochetes reproduces the biological and pathological hallmarks of AD. Senile-plaque-like beta amyloid (Aβ) deposits are also observed in mice following inhalation of C. pneumoniae in vivo, and Aβ accumulation and phosphorylation of tau is induced in neurons by HSV-1 in vitro and in vivo. Specific bacterial ligands, and bacterial and viral DNA and RNA all increase the expression of proinflammatory molecules, which activates the innate and adaptive immune systems. Evasion of pathogens from destruction by the host immune reactions leads to persistent infection, chronic inflammation, neuronal destruction and Aβ deposition. Aβ has been shown to be a pore-forming antimicrobial peptide, indicating that Aβ accumulation might be a response to infection. Global attention and action is needed to support this emerging field of research because dementia might be prevented by combined antibiotic, antiviral and anti-inflammatory therapy.
http://www.ncbi.nlm.nih.gov/pubmed/21933454

wonderfullife
23-09-2011, 12:57 AM
Seabirds and the Circulation of Lyme Borreliosis Bacteria in the North
Pacific.

Lobato E, Pearce-Duvet J, Staszewski V, Gómez-Díaz E, González-Solís
J, Kitaysky A, McCoy KD, Boulinier T

Vector Borne Zoonotic Dis 2011 09 15

Abstract Seabirds act as natural reservoirs to Lyme borreliosis
spirochetes and may play a significant role in the global circulation of
these pathogens. While Borrelia burgdorferi sensu lato (Bbsl) has been
shown to occur in ticks collected from certain locations in the North
Pacific, little is known about interspecific differences in exposure
within the seabird communities of this region. We examined the
prevalence of anti-Bbsl antibodies in 805 individuals of nine seabird
species breeding across the North Pacific. Seroprevalence varied
strongly among species and locations. Murres (Uria spp.) showed the
highest antibody prevalence and may play a major role in facilitating
Bbsl circulation at a worldwide scale. Other species showed little or no
signs of exposure, despite being present in multispecific colonies with
seropositive birds. Complex dynamics may be operating in this wide
scale, natural host-parasite system, possibly mediated by the host
immune system and host spe cialization of the tick vector.

wonderfullife
23-09-2011, 01:06 AM
EU ban may spell the end of Scotland’s purple hills

David Leask

21 Sep 2011

IT is the ruling that could turn Scotland’s purple hills a nasty shade
of green.

The European Parliament has outlawed the only chemical that kills
bracken, the prehistoric fern that would cover much of the country if
uncontrolled.

Horrified conservationists and farmers – who had forged an unlikely
alliance to fight the ban – last night warned the move would have a
devastating effect on Scottish uplands.

For years landowners have used the chemical Asulam – better known by its
trade name Asulox – to spray hills to kill off bracken and its
complicated and expansive root systems.

Simon Thorp, of charity The Heather Trust, said: “Without Asulox we are
going to see a huge expansion of bracken, especially on lower slopes of
hills. Bracken is going to replace heather.

“We like to think of the colour of Scottish hills as the purple of
heather. Well, that will now change.

“What people don’t seem to realise is that much of Scotland would be
naturally covered with bracken, by a plant so successful it was around
when the dinosaurs roamed the earth.”

The Heather Trust is one of scores of organisations as varied as
farmers’ union NFU Scotland, the Scottish Government, state environment
watchdogs SEPA and Scottish Natural Heritage, and the National
Gamekeepers Organisation which opposed the ban.

Most are not just worried about how Scotland will look without Asulox,
which is usually sprayed on an industrial scale from helicopters. They
are also concerned about the massive economic effects an expansion of
bracken would have on the country.

Outdoor pursuits such as hillwalking, shooting and deer-stalking are all
going to suffer, they have warned. So too will sheep farming.

NFU Scotland president Nigel Miller uses Asulox on his own Borders hill
farm. He said: “The lack of alternative products – particularly those
suitable for aerial spraying – means more of Scotland’s hills and
uplands run the risk of disappearing under a carpet of impenetrable
bracken.”

***Last night health concerns were also emerging about the decision –
bracken is rife with sheep ticks that can cause deadly Lyme disease.***

Crucially, MEPs backed the ban because Asulox has been found to be
unsafe for use as a herbicide on spinach crops, hardly an issue in Scotland.

It is understood to be perfectly safe to use on bracken, which isn’t
eaten and is widely believed to be carcinogenic itself.

Alyn Smith, the Scottish Nationalist MEP, has been warning of a problem
with the chemical since early this spring and said yesterday’s decision
was “no surprise”. Last night he was still hopeful something could be
done to fix the issue.

He said the manufacturer, India-based United Phosphorus Limited (UPL),
should have done more to make clear in its paperwork that the chemical
is for bracken, not spinach.

Mr Smith said: “This issue has been frustrating from the start, and I am
even more frustrated that I have to repeat the advice I gave the company
by letter back in early April. Advice they not only did not take but did
not even see fit to respond to.”

Asulox must now be withdrawn from sale by the end of the year and
farmers have until Hogmanay 2012 to use what stocks they have.

Rural Affairs Secretary Richard Lochhead said he was deeply disappointed
by the decision “not to support the continued use of asulam, which is
vitally important to control bracken on hill farms.

“Farmers will still be able to buy asulam up to December 31, 2011, and
store it for use up to December 31, 2012. From January 2013,
applications for an emergency authorisation for the use of asulam can be
made to the Chemicals Regulation Directorate until a longer term
solution is found.”

wonderfullife
23-09-2011, 01:08 AM
Prevalence of Anaplasma phagocytophilum and Coinfection with Borrelia
burgdorferi Sensu Lato in the Hard Tick Ixodes ricinus in the City of
Hanover (Germany).

Schicht S, Junge S, Schnieder T, Strube C

Vector Borne Zoonotic Dis 2011 09 15

Abstract The castor bean tick Ixodes ricinus has been found to be the
main vector for Lyme borreliosis spirochetes and Anaplasma
phagocytophilum in Central Europe. 1646 I. ricinus ticks from Hanover, a
city located in Northern Germany, were examined for infection with A.
phagocytophilum and coinfection with Borrelia burgdorferi sensu lato
(sl) to obtain so far missing prevalence data for this region. The total
A. phagocytophilum infection rate was 3.2% (52/1646 ticks), divided into
4.1% (32/777) adults and 2.3% (20/869) nymphs.
Coinfections with B. burgdorferi sl were found in 0.9% of all tick
stages. The detected genospecies were B. afzelii, B. garinii, B.
burgdorferi sensu stricto (ss), and B. garinii, which was the most
frequent species in coinfected ticks.

wonderfullife
23-09-2011, 01:10 AM
Evaluation of the preventive capacities of a topically applied
azithromycin formulation against Lyme borreliosis in a murine model.

Knauer J, Krupka I, Fueldner C, Lehmann J, Straubinger RK

J Antimicrob Chemother 2011 09 15

Objectives Systemic antibiotic treatment of Lyme borreliosis is
effective during the early stages of the infection, while chronic
manifestations of the disease may remain refractory and difficult to
treat. This study was carried out in order to evaluate the potential of
topically applied azithromycin to eliminate the spirochaetal organisms
in the skin of the freshly bitten host and thereby prevent Lyme borreliosis.

Methods Laboratory mice were challenged with Borrelia burgdorferi sensu
stricto by needle inoculation or via infected ticks as vectors. Then, an
azithromycin-containing formulation was applied once daily to the sites
of exposure for three consecutive days. In the case of needle
inoculation, a 5% azithromycin formulation was applied starting 1 h, 3
days and 5 days after infection. In the case of tick exposure, 4%, 10%
and 20% azithromycin formulations were applied, starting directly after
the detachment of the engorged ticks. Subsequently, the infection status
of the mice was determined.

Results Concentrations of azithromycin in murine skin were >3800-fold
higher than the published minimal inhibitory concentration for B.
burgdorferi as soon as 3 h after the first application. After needle
inoculation, spirochaetes were not detectable in all infected mice after
treatment, if the first application started 1 h or even after 3 days
post-infection. Furthermore, no borrelial organisms were detected after
topical treatment when ticks were used for spirochaete inoculation.

Conclusions Our data indicate that topical treatment with a formulation
containing azithromycin is a promising approach to prevent Lyme
borreliosis shortly after a tick bite.

wonderfullife
23-09-2011, 01:12 AM
Zoonotic Bartonella Species in Fleas and Blood from Red Foxes in Australia.

Kaewmongkol G, Kaewmongkol S, Fleming PA, Adams PJ, Ryan U, Irwin
PJ, Fenwick SG

Vector Borne Zoonotic Dis 2011 09 15

Abstract Bartonella are arthropod-borne, fastidious, Gram-negative, and
aerobic bacilli distributed by fleas, lice, sand flies, and, possibly,
ticks. The zoonotic Bartonella species, Bartonella henselae and
Bartonella clarridgeiae, which are the causes of cat scratch disease and
endocarditis in humans, have been reported from cats, cat fleas, and
humans in Australia. However, to date, there has been no report of B.
henselae or B. clarridgeiae in Australian wild animals and their
ectoparasites. B. henselae and B. clarridgeiae were detected in fleas
(Ctenocephalides felis) from red foxes (Vulpes vulpes), an introduced
pest animal species in Australia, and only B. clarridgeiae was detected
in blood from one red fox. Phylogenetic analysis of the ribosomal
intergenic spacer region revealed that the B. henselae detected in the
current study were related to B. henselae strain Houston-1, a major
pathogenic strain in humans in Australia, and confirmed the genetic
distinctness of B. clarridgeiae. The identification and characterization
of Bartonella species in red foxes in the Southwest of Western Australia
suggests that red foxes may act as reservoirs of infection for animals
and humans in this region.

wonderfullife
23-09-2011, 01:14 AM
Molecular characterization reveals distinct genospecies of Anaplasma
phagocytophilum from diverse North American hosts.

Rejmanek D, Bradburd G, Foley J

J Med Microbiol 2011 09 15

Anaplasma phagocytophilum is an emerging tick-borne pathogen that
infects humans, domestic animals, and wildlife throughout the Holarctic.
In the far-western United States multiple rodent species have been
implicated as natural reservoirs for A. phagocytophilum. However, the
presence of multiple A. phagocytophilum strains has made it difficult to
determine which reservoir hosts pose the greatest risk to humans and
domestic animals. Here we characterized three genetic markers (23S-5S
intergenic spacer, ank, and groESL) from 73 real-time Taqman
PCR-positive A. phagocytophilum strains infecting multiple rodent and
reptile species, as well as a dog and a horse, from California. Bayesian
and maximum likelihood phylogenetic analyses of all 3 genetic markers
consistently identified 2 major clades, one of which consisted of A.
phagocytophilum strains infecting woodrats and the other consisting of
strains infecting sciurids (chipmunks and squirrels) as well as the dog
and horse stra ins. In addition, analysis of the 23S-5S spacer region
identified two unique and highly dissimilar clades of A. phagocytophilum
strains infecting several lizard species. Our findings indicate that
multiple unique strains of A. phagocytophilum with distinct host
tropisms exist in California. Future epidemiological studies evaluating
human and domestic animal risk should incorporate these distinctions.

wonderfullife
23-09-2011, 01:16 AM
Absence of Lyme Disease Spirochetes in Larval Ixodes ricinus Ticks.

Richter D, Debski A, Hubalek Z, Matuschka FR

Vector Borne Zoonotic Dis 2011 09 16

Abstract To determine which kind of spirochete infects larval Ixodes
ricinus, we examined questing larvae and larvae derived from engorged
females for the presence of particular spirochetal DNA that permitted
species differentiation. Borrelia miyamotoi was the sole spirochete
detected in larval ticks sampled while questing on vegetation. Questing
nymphal and adult ticks were infected mainly by Borrelia afzelii,
whereas larval ticks resulting from engorged females of the same
population were solely infected by B. miyamotoi. Since larvae acquire
Lyme disease spirochetes within a few hours of attachment to an infected
rodent, questing larvae in nature may have acquired Lyme disease
spirochetes from an interrupted host contact. Even if transovarial
transmission of Lyme disease spirochetes may occasionally occur, it
seems to be an exceedingly rare event. No undisputable proof exists for
vertical transmission of Lyme disease spirochetes, whereas B. miyamotoi
appears to be readily passed between generations of vector ticks.

wonderfullife
23-09-2011, 01:18 AM
Primary lyme arthritis of the pediatric hip.

Glotzbecker MP, Kocher MS, Sundel RP, Shore BJ, Spencer SA, Kasser JR

J Pediatr Orthop 2011 09; 31 (7): 787-90

Lyme arthritis most commonly affects the knee. It is not commonly
considered in the differential diagnosis of monoarticular hip pain.
There are only a few case reports describing Lyme disease presenting
with isolated hip involvement. The purpose of this study is to review
our experience with primary Lyme arthritis of the hip.

wonderfullife
23-09-2011, 01:19 AM
Identification of Bacteria Infecting Ixodes ricinus Ticks by 16S rDNA
Amplification and Denaturing Gradient Gel Electrophoresis.

Tveten AK, Sjåstad KK

Vector Borne Zoonotic Dis 2011 09 16

Abstract Ticks harbor a complex microbial population, which they acquire
while feeding on a variety of mammalians and birds. Zoonotic diseases
transferred by ticks are an increasing problem and have become a burden
to the community. 16S rDNA amplification and denaturing gradient gel
electrophoresis (DGGE) enables detection of the broad spectrum of
bacteria that settles in the ticks. Profiling the complete microbial
population in ticks may provide a better understanding of the ticks'
potential to harbor and disperse pathogens. Separation of pathogenic
species by DGGE is based on variation in %GC content within the 16S rDNA
genetic region. Sequencing of these fragments allows identification of
bacterial species.

Present study identified some well-known tick-infecting bacteria, such
as members of genus Borrelia, Rickettsiales, and Pseudomonas, but also
less described tick-infecting bacteria such as Rhodococcus erythropolis,
Spiroplasma spp., and an endosymbiont of the microart hropod Folsomia
candida. This is the first report of Segniliparus rugosus-infected
Ixodes ricinus ticks. Also, it is the first report of several of these
pathogens in the Norwegian tick population.

wonderfullife
23-09-2011, 01:24 AM
First Molecular Evidence of Anaplasma ovis and Rickettsia spp. in Keds
(Diptera: Hippoboscidae) of Sheep and Wild Ruminants.

Hornok S, de la Fuente J, Biró N, Fernández de Mera IG, Meli ML,
Elek V, Gönczi E, Meili T, Tánczos B, Farkas R, Lutz H, Hofmann-Lehmann R

Vector Borne Zoonotic Dis 2011 09 16

Abstract To evaluate the presence of rickettsial agents in hippoboscid
flies with molecular methods, 81 sheep keds (Melophagus ovinus) were
collected from 23 sheep, 144 deer keds (Lipoptena cervi) were caught in
the environment, and a further 463 and 59 individuals of the latter
species were obtained from fresh carcasses of 29 red deer and 17 roe
deer, respectively. DNA was extracted individually or in pools.
Anaplasma ovis was demonstrated in all examined sheep keds, and from one
pool of free-living deer keds. Rickettsia helvetica or other,
unidentified rickettsiae were also present in one pool of sheep keds,
and in four pools of deer keds from both red deer and roe deer. This is
the first account of polymerase chain reaction positivity of hippoboscid
flies for A. ovis and rickettsiae. These results raise the possibility
that-apart from cattle and roe deer as already reported-sheep and red
deer might also play a reservoir role in the epidemiology of rickettsioses.
The sheep ked, Melophagus ovinus , is one of the most widely distributed
and important external parasites of sheep. There are also keds that
parasitize deer in North America ( Lipoptena depressa and Neolipoptena
ferrisi ).
Keds are wingless dipterans. The adult is ~7 mm long; a brown or reddish
color; and covered with short, bristly hairs. The head is short and
broad, and the legs are strong and armed with stout claws.
http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/71711.htm

wonderfullife
23-09-2011, 01:26 AM
Many clinical features of Lyme disease have been described in European case reports during the past 100 years (1). The name was not applied until 1975, however, when a cluster of cases was investigated in Old Lyme, Connecticut. The spirochaetal cause, Borrelia burgdorferi, was isolated in 1981 and subsequently identified in clinical material and ticks in Europe and the United States. A network of clinicans and scientists throughout Europe - the European Union Concerted Action on Lyme Borreliosis (EUCALB) - has set up programmes to formulate case definitions appropriate for European use and to improve and standardise the quality of laboratory diagnostic tests for Lyme disease (2). Case definitions covering presentations that affect the skin, nervous system, joints, and heart have been published (3). Definitions of the following conditions are all contingent on the patient having been exposed to ticks:

erythema migrans


borrelial lymphocytoma


acrodermatitis chronica atrophicans


early neuroborreliosis


chronic neuroborreliosis


Lyme arthritis


Lyme carditis



It is hoped that the application of standardised case definitions and improved diagnostic tests will enable the epidemiology of Lyme borreliosis and the burden of disease it causes to be better understood. Currently the most effective preventive measure is to raise public awareness about the disease and about how to avoid infection (2).

Lyme disease is a notifiable condition only in Slovenia and Scotland. EUCALB has gathered the limited data available, and a report is to be published soon (4). The disease is broadly commoner in eastern than in western Europe. Focal areas of higher incidence occur in countries where the incidence is generally low, however. These are usually in forested regions where there are many deer, which help to maintain the tick reproductive cycle.
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=1267

wonderfullife
23-09-2011, 01:29 AM
Eurosurveillance, Volume 16, Issue 27, 07 July 2011

Lyme borreliosis in Europe

A Rizzoli ()1,2, H C Hauffe1,2, G Carpi1, G I Vourc'h3, M Neteler1, R Rosà1

Department of Biodiversity and Molecular Ecology, Research and Innovation Centre, Fondazione Edmund Mach, San Michele all'Adige (Trento), Italy
Both authors contributed equally to this work.
Unité d'Epidémiologie Animale, Institut National de la Recherche Agronomique (INRA), St Genès Champanelle, France

LB risk is specifically linked to tick abundance and exposure. Therefore, although higher risk is no longer considered to be correlated with residency in rural areas, higher LB risk is associated with occupation (e.g. forestry work and farming) and especially with certain leisure activities (e.g. hunting, mushroom collecting and berry picking) and age (with two groups mainly affected: children aged 5–14 years and adults aged 50–64 years).

Since infection is correlated with tick abundance and exposure (and, therefore, tick activity), diagnosis of acute LB peaks in June and July in many northern and central countries of Europe, while a second smaller peak may occur in southern countries in late summer or early autumn; however, both erythema migrans and chronic forms of the disease can be diagnosed throughout the year [3]. Although the number of LB cases seems to be increasing in some areas, such trends are extremely heterogeneous and/or remain to be confirmed [3].

Clinical symptoms
The clinical presentation of LB ranges from acute to chronic illness, with wide variation attributed to the different Borrelia genospecies and/or genotypes implicated in the infection (as described above and in [44]), although the exact mechanisms maintaining chronic symptoms have yet to be confirmed. Diagnosis is primarily clinical and takes into account the risk of tick bite. Clinical case definitions for use in Europe – although not official European Union case definitions – are available in [45].

Briefly, several days or weeks after a tick bite, if Borrelia infection occurs, in 60–80% of cases this will be characterised by erythema migrans (the rash or patch on the skin about 10 cm across that may expand peripherally as a palpable band, and may or may not be itchy) [46], although early infection may be completely asymptomatic. Other early symptoms include influenza-like symptoms, fever, fatigue, headaches and muscle or joint pain. Several weeks or months after infection through a tick bite (with or without a previous history of erythema migrans), neuroborreliosis (noted in 10–20% of symptomatic patients) in the form of meningoradiculitis, meningitis or meningoencephalitis [47], Lyme arthritis or Borrelia lymphocytoma may occur [45]. Less frequently, multiple erythemata, or carditis are diagnosed [45,48]. Months or even years after Borrelia infection, acrodermatitis chronica atrophicans, lymphocytoma, chronic arthritis (fairly rare in Europe), encephalomyelitis or chronic neuroborreliosis (very rare in Europe) may be observed [45].
Microbial or serological confirmation of Borrelia infection is needed for all manifestations of the disease except for typical early skin lesions [49]. The diagnosis of some chronic forms of LB is currently controversial [50], and it has also been suggested that the overdiagnosis and overtreatment of LB may be an important problem [51].

Indirect diagnosis of B. burgdorferi sl
The complexity of the antigenic composition of B. burgdorferi sl and the temporal appearance of antibodies to different antigens at successive time intervals after Borrelia infection means the development of a serological test with high sensitivity and specificity is a challenge. The most commonly used serological methods for the detection of antibodies to B. burgdorferi sl include indirect immunofluorescent antibody assay (IFA) and an enzyme-linked immunosorbent assay (ELISA) [54]. Nevertheless, specific antibodies are often not detectable in the early stage of infection with the use of currently available test methods....

Testing

...In more than 50%of cases, diagnosis of LB can be made on the basis of an expanding erythema (confirmed after a one-week follow-up). In the absence of erythema migrans at least one other clinical manifestation must be noted and confirmed using serological diagnosis of Borrelia in blood or CSF. According to the most recent German Society for Hygiene and Microbiology (Deutsche Gesellschaft für Hygiene und Mikrobiologie, DGHM) guidelines [43], serological diagnosis for patients in Europe should follow a two-step procedure: (i) ELISA and if reactive, followed by (ii) an immunoblot, if possible using recombinant antigens (p100, p58, p41i, VlsE, OspC, DbpA), including those expressed primarily in vivo (VlsE and DbpA), instead of whole-cell lysate antigen blots. OspC and VlsE are the most sensitive antigens for IgM antibody detection [54]. European standardisation of these diagnostic tests and new markers for detecting active infections are urgently required [55].

Treatment

Treatment

Surprisingly, our review found that there is no European consensus on treatment and that economic considerations and national guidelines on avoidance of drug resistance also impact the current treatment of choice (no comparative costs are available). Treatment of the vast majority of LB cases is based on antibiotics, with drug type, dose, route (oral or intravenous) and duration varying with stage of the disease, as well as with symptoms. Treatment regimes and recommendations are summarised from the regularly updated European Union Concerted Action on Lyme Borreliosis (EUCALB) website [1] and [49], where doses can also be found. See also [49,51,56] for recent reviews on evaluation of treatments.

In general, in almost all LB cases, the disease is resolved with short courses of antibiotics [51,57], although longer courses are recommended for relapses or more serious and/or chronic forms. Some authors advocate that all symptomatic LB cases should be treated in order to avoid progression to later stages of the disease, and suggest that the earlier treatment begins, the less likely it is that more severe forms will follow [58]. However, overtreatment is considered a problem by others [51], although thus far, drug resistance has been noted only in vitro [59]. On the other hand, few data are available on the risk of long-term effects of non-treatment in asymptomatic LB patients [60]. Several studies have now shown that a few so-called chronic or `post-LB' forms of the disease do not respond to antibiotics, although the reason for this is subject to some debate [50,51,61].

The main risks involved in treatment appear to be inappropriate patient management following inaccurate diagnosis. As mentioned above, both over- and underdiagnosis of LB is suspected.

http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19906

wonderfullife
23-09-2011, 01:32 AM
Coll Antropol. 2011 Jan;35 Suppl 1:313-8.

Tremor, seizures and psychosis as presenting symptoms in a patient with
chronic lyme neuroborreliosis (LNB).

Markeljević J, Sarac H, Rados M.
Source

University of Zagreb, School of Medicine, Zagreb University Hospital
Centre, Department of Internal Medicine, Zagreb, Croatia.
[email protected]
Abstract

Lyme borreliosis is a multisystem disorder caused by Borrelia
burgdorferi (Bb). Neurological symptoms such as lymphocytic
meningoradiculoneuritis (Bannwart's syndrome), cranial neuritis
(II,III,IV,V,VI), encephalitis, transverse myelitis are found in about
10% of cases during the second phase of the disease. In the chronic
stage, many months or years after the initial infection, other
neurologic complications may occur, such as encephalomyelitis, epileptic
crises, cognitive impairment, peripheral neuropathy and psychiatric
disturbances such as depression, anxiety, panicc attacks, catatonia,
psychosis etc. Some patient continue to experience symptoms of fatigue,
insomnia or psychiatric disorder in the post borrelia syndrome. We
describe here a patient with a triad of unusual symptoms in chronic LNB
including tremor, seizures and psychosis. Standardized medical
interview, neurologic examination, neuroimaging, serum and CSF serology
as well as EEG and EMNG evaluation were performed. The patient was
treated with intravenous ceftriaxone and doxycycline and responded with
rapid clinical and functional improvement.Newertheless, he suffered from
multiple systemic and neurologic sequelas that influenced his daily
activities in post treatment period. Emphasis is placed on the atypical
onset and evolution, the difficulties encountered in formulating
diagnosis, early treatment and the uncertainties concerning the sequelae
after treatment. In patients with non-specific long lasting symptoms in
the absence of overt clinical signs suggesting CNS involvement, routine
treatment with i.v. ceftriaxone is not to be encouraged.

PMID:
21648354
[PubMed - indexed for MEDLINE]

wonderfullife
23-09-2011, 01:59 AM
Eur J Neurol. 2011 Apr;18(4):547-55. doi:
10.1111/j.1468-1331.2010.03229.x. Epub 2010 Oct 27.

The diagnostic spectrum in patients with suspected chronic Lyme
neuroborreliosis--the experience from one year of a university
hospital's Lyme neuroborreliosis outpatients clinic.

Djukic M, Schmidt-Samoa C, Nau R, von Steinbüchel N, Eiffert H, Schmidt H.
Source

Department of Neurology, University of Goettingen, Goettingen, Germany.
Abstract
BACKGROUND AND PURPOSE:

Studies addressing the diagnostic relevance of anti-Borrelia burgdorferi
(BB) serum antibodies in patients with non-specific symptoms and
suspected chronic Lyme neuroborreliosis (LNB) are scarce.
METHODS:

In this study, we enrolled within 1 year 122 patients with suspected
chronic LNB. One hundred and fourteen patients had previously tested
positive for BB. All patients had previously received antibiotic
treatment. Each patient received a clinical examination and measurement
of BB-specific antibodies. The diagnosis of neuroborreliosis was made
according to the national guidelines of the German Society of Neurology.
Nine patients had acute borreliosis. One of the nine met the criteria of
acute LNB. Of the remaining 113 patients, 85 patients underwent a lumbar
puncture. Ten seronegative subjects without lumbar puncture were also
considered. In 61.8% of these 95 patients the quality of life, of sleep,
mood, and anxiety were assessed.
RESULTS:

Of 95 patients, 25.3% had symptoms without a somatic cause or evidence
of borreliosis, 38.9% had a well-defined illness unrelated to BB
infection, and 29.5% suffered from symptoms without a detectable somatic
cause, displaying antibodies against BB. Six patients were grouped as
post-LNB syndrome. Most common symptoms in all categories were
arthralgia, myalgia, dysaesthesia, depressive mood and chronic fatigue.
CONCLUSION:

Patients with persistent symptoms with elevated serum antibodies against
BB but without signs of cerebrospinal fluid inflammation require further
diagnostic examinations to exclude ongoing infection and to avoid
co-infections and other treatable conditions (e.g. autoimmune diseases).
One patient with acute LNB, who was treated with ceftriaxone for 3 weeks
suffered from LNB with new headaches and persistent symptoms 6 months
later. These data should encourage further studies with new experimental
parameters.

© 2010 The Author(s). European Journal of Neurology © 2010 EFNS.

PMID:
20977545
[PubMed - indexed for MEDLINE]

wonderfullife
23-09-2011, 02:01 AM
Przegl Epidemiol. 2009;63(4):539-43.

[Evaluation of the usefulness cerebrospinal fluid myelin basic protein
(MBP) concentration examination in patients with Lyme
neuroborreliosis--preliminary study].

[Article in Polish]

Kepa L.

Source

Oddział Chorób Zakaźnych Slaskiego Uniwersytetu Medycznego w Bytomiu,
przy Klinice Chorób Płuc i Gruźlicy Slaskiego Uniwersytetu Medycznego w
Zabrzu.
Abstract

The aim of the study was evaluation of usefulness of cerebrospinal fluid
(CSF) myelin basic protein (MBP) level examination in diagnostics of
Lyme neuroborreliosis. The study was performed in 24 subjects. In all
individuals CSF MBP concentration was estimated on the 1st day of
hospitalization. In patients with depressive and cognitive impairments,
proved in neuropsychological tests (group I), mean CSF MBP concentration
was 3.1 ng/mL, whereas in subjects without abnormalities in tests (group
II), respectively, 1.2 ng/mL. The difference of mean CSF MBP levels was
statistically significant (p<0.01). The obtained results indicate
usefulness of this CSF parameter, besides neuropsychological tests, in
objective evaluation of clinical state in patients with **chronic Lyme
neuroborreliosis**.

PMID:
20120953

wonderfullife
23-09-2011, 02:02 AM
Regional cerebral blood flow and cognitive deficits in **chronic Lyme
disease**.

Fallon BA, Keilp J, Prohovnik I, Heertum RV, Mann JJ.
Source

The NYS Psychiatric Institute, New York, New York 10032, USA.
Abstract

This study examined brain functioning in patients with Lyme
encephalopathy. Eleven patients underwent neuropsychological tests and
Xenon(133)-regional cerebral blood flow (rCBF) studies, using an
external detector system. Each rCBF scan was age- and sex-matched to two
archival, normal controls. While few differences were noted on
gray-matter flow indices (ISI, fg), Lyme patients demonstrated
significant flow reductions in white matter index (k(2)) (p=.004),
particularly in the posterior temporal and parietal lobes bilaterally
(p=.003). Flow reductions in white matter areas were significantly
associated with deficits in memory (r=.66, p=.027) and visuospatial
organization (r=.62, p=.041). Results suggest that Lyme encephalopathy
may be a disease primarily affecting the cerebral white matter.

PMID:
12928508
[PubMed - indexed for MEDLINE]

wonderfullife
23-09-2011, 02:06 AM
Rev Med Chir Soc Med Nat Iasi. 2008 Apr-Jun;112(2):496-501.

[Results of etiologic diagnosis in clinical syndrome consistent with
acute and **chronic borreliosis**].

[Article in Romanian]
Persecă T, Feder A, Molnar GB.

Source

Institutul de Sănătate Publică, Prof. Dr. Iuliu Moldovan" Cluj Napoca.
Abstract

Borreliosis is a multisystem infection, which in the absence of adequate
diagnosis and clinical management, may develop towards various clinical
forms of chronic pathology. Due to the heterogeneity of clinical
manifestations it is known under more names: erythema migrans, Lyme
disease, neuroborreliosis etc. MATERIAL AND METHOD: Taking into account
the present interest and the weight in pathology of syndromes consistent
with the suspicion of a Borrelia spp. infection, since 2002 we applied
in current practice the investigation of this etiology. There have been
investigated 481 subjects, clinically suspected of Borrelia spp.
infection that had historical risk of tick bite and cases of serous
meningitis, after exclusion of usual etiology. Tests were performed on
ELISA kits with standardised immunoreagents and recently, for result
validation, on Western immunoblot kits (WB). RESULTS: Our results
revealed the Borrelia etiology in 32% of cases (27.96-36.29% CI = 95%)
at the screening, value expressed by the persistent positivity of the
specific immunoglobulins (Ig) IgM (80.5%) and IgM+IgG (19.5%). Historic
infection, represented exclusively by IgG positivity, was present in
8.6% (5.87-11.98% CI = 95%) from the cases that were negative for IgM
(68%, 63.71-72.04%, CI = 95%). This weight is superposable with the

results obtained in investigating a comparable sample of healthy
individuals (193 subjects with 6.74% historical IgG, 3.79-10.96%, CI =
95%). Based on these results, it can be considered that ELISA procedure
is useful and of reliable prognosis value for screening the Borrelia
spp. etiology, the next step, taking into account the higher sensitivity
of WB, being WB procedure which is useful for confirmation of ELISA
positive cases and for treatment efficiency surveillance. The results
prove that Borrelia spp. infections are a public health issue, which due
to the diversity of clinical manifestations and diagnosis difficulties
need repeated and complex laboratory investigations.

PMID:
19295026
[PubMed - indexed for MEDLINE]

wonderfullife
23-09-2011, 02:11 AM
J Neuropathol Exp Neurol. 2011 Sep;70(9):748-757.

Long-Term Intrathecal Infusion of Outer Surface Protein C From Borrelia
burgdorferi Causes Axonal Damage.

Tauber SC, Ribes S, Ebert S, Heinz T, Fingerle V, Bunkowski S,
Kugelstadt D, Spreer A, Jahn O, Eiffert H, Nau R.

Source

From the Department of Neurology (SCT), RWTH Aachen University
Hospital, Aachen; Departments of Neuropathology (SR, SB, RN), Neurology
(SE, TH, AS), and Medical Microbiology (HE), Georg-August-University,
Gottingen; National Reference Centre for Borrelia (VF), Bavarian Health
and Food Safety Authority, Munich; Sekisui Virotech GmbH (DK),
Rüsselsheim; Max Planck Institute of Experimental Medicine (OJ); and
Department of Geriatrics (RN), Evangelisches Krankenhaus
Gottingen-Weende, Gottingen, Germany.
Abstract

Lyme neuroborreliosis (LNB) is the most frequent tick-borne infectious
disease of the central nervous system. In acute LNB and the rare
**chronic state of infection**, patients can experience cognitive
deficits such as attention and memory disturbances. During LNB, single
compounds of Borrelia burgdorferi sensu lato are released into the
subarachnoid space.To investigate the pathogenesis of neurologic
dysfunction in LNB, we determined that the outer surface protein C
(OspC), a major virulence factor of B. burgdorferi, stimulated mouse
microglial cells in a dose-dependent manner to release nitric oxide
(EC50 = 0.24 mg/L) in vitro. To mimic pathophysiologic conditions of
long-term release of this bacterial component in vivo, we treated
C57BL/6 mice with recombinant OspC from Borrelia garinii or buffer by
intraventricular infusion and tested them for behavioral deficits. After
4weeks, brains were examined by routine histology and
immunohistochemistry. Assessment of spatial learning and memory of
treated mice during OspC exposure did not reveal significant differences
from controls. Continuous exposure to intrathecal B. burgdorferi OspC
led to activation of microglia and axonal damage without demonstrable
cognitive impairment in experimental mice. These results suggest that
long-term intrathecal exposure to OspC resulted in axonal damage that
may underlie the neurologic manifestations in chronic LNB.

PMID:
21865883
[PubMed - as supplied by publisher]

wonderfullife
23-09-2011, 02:13 AM
Neuroinflammation. 2008 Sep 25;5:40.

Persisting atypical and cystic forms of Borrelia burgdorferi and local
inflammation in Lyme neuroborreliosis.

Miklossy J, Kasas S, Zurn AD, McCall S, Yu S, McGeer PL.

Source

Kinsmen Laboratory of Neurological Research, University of British
Columbia, Vancouver, BC, Canada. [email protected]
Abstract
BACKGROUND:

The long latent stage seen in syphilis, followed by chronic central
nervous system infection and inflammation, can be explained by the
persistence of atypical cystic and granular forms of Treponema pallidum.
We investigated whether a similar situation may occur in Lyme
neuroborreliosis.
METHOD:

Atypical forms of Borrelia burgdorferi spirochetes were induced exposing
cultures of Borrelia burgdorferi (strains B31 and ADB1) to such
unfavorable conditions as osmotic and heat shock, and exposure to the
binding agents Thioflavin S and Congo red. We also analyzed whether
these forms may be induced in vitro, following infection of primary
chicken and rat neurons, as well as rat and human astrocytes. We further
analyzed whether atypical forms similar to those induced in vitro may
also occur in vivo, in brains of three patients with Lyme
neuroborreliosis. We used immunohistochemical methods to detect evidence
of neuroinflammation in the form of reactive microglia and astrocytes.
RESULTS:
Under these conditions we observed atypical cystic, rolled and granular
forms of these spirochetes. We characterized these abnormal forms by
histochemical, immunohistochemical, dark field and atomic force
microscopy (AFM) methods. The atypical and cystic forms found in the
brains of three patients with neuropathologically confirmed Lyme
neuroborreliosis were identical to those induced in vitro. We also
observed nuclear fragmentation of the infected astrocytes using the
TUNEL method. Abundant HLA-DR positive microglia and GFAP positive
reactive astrocytes were present in the cerebral cortex.
CONCLUSION:
The results indicate that atypical extra- and intracellular pleomorphic
and cystic forms of Borrelia burgdorferi and local neuroinflammation
occur in the brain in **chronic Lyme neuroborreliosis**. The persistence
of these more resistant spirochete forms, and their intracellular
location in neurons and glial cells, may explain the long latent stage
and persistence of Borrelia infection. The results also suggest that
Borrelia burgdorferi may induce cellular dysfunction and apoptosis. The
detection and recognition of atypical, cystic and granular forms in
infected tissues is essential for the diagnosis and the treatment as
they can occur in the absence of the typical spiral Borrelia form.

PMID:
18817547
[PubMed - indexed for MEDLINE]
PMCID: PMC2564911

wonderfullife
24-09-2011, 04:44 PM
Lyme Disease: Challenges and Innovations

Lyme disease is one of the most rapidly emerging infectious diseases in North America and Europe. In 2009, nearly 30,000 confirmed and more than 8,500 probable cases of Lyme disease were reported to the CDC in the United States alone. Named after a small Connecticut town, Lyme disease is transmitted to humans by the bite of ticks infected with the bacterium Borrelia burgdorferi. This multi-system infection typically occurs in stages with different clinical manifestations at each stage. While it can be treated effectively with antibiotics, in some cases recovery may be incomplete - although there is no evidence that any of these post-Lyme disease syndromes respond to further courses of antibiotic therapy.

On May 19, 2011, Dr. Allen Steere, the renowned discoverer of Lyme disease, joined an esteemed panel of Grand Rounds speakers to explore the clinical manifestations and treatment of Lyme disease, innovations in laboratory testing, prevention strategies, and national trends of disease emergence. The session gave a rare glimpse into the front lines of those battling and treating Lyme disease while addressing the data gaps, unmet needs, and overall challenges and opportunities for its prevention and control.
http://www.cdc.gov/about/grand-rounds/archives/2011/May2011.htm?source=govde

wonderfullife
24-09-2011, 04:46 PM
Abstract

The most common clinical manifestation of Lyme disease is the characteristic rash, erythema migrans (EM). In the 1980s EM-like eruptions were reported in Missouri and other southeastern states. The EM-like eruptions, which were of unknown etiology, often followed the bite of the Lone Star tick (Amblyomma americanum) and the rash is called STARI (southern tick-associated rash illness). Although the Lone Star tick is found in the Lyme disease–endemic areas of New England and Mid-Atlantic regions of the United States, STARI has been reported only once from the Northeast and Mid-Atlantic regions. We report a child from Connecticut who visited Long Island, New York, and developed a rash that was thought to be EM. Because the patient failed to respond to antibiotics used to treat Lyme disease, an investigation ensued, and the diagnosis of STARI was established.

http://cid.oxfordjournals.org/content/early/2011/09/21/cid.cir553

wonderfullife
24-09-2011, 04:57 PM
Abstract

AIM:

Although intravenous antibiotic therapy is recommended for neurologic Lyme disease, safety concerns have been raised about treatment beyond 30 days in patients with persistent neurologic symptoms. The goal of our study was to evaluate the safety of extended intravenous antibiotic therapy in patients referred for treatment of neurologic Lyme disease.

METHODS:

We enrolled 200 consecutive patients with significant neurologic symptoms and positive testing for Borrelia burgdorferi. Patients were treated with intravenous antibiotics using various intravascular devices (IVDs). Standard IVD care was administered to all patients, and monitoring for medication reactions and IVD complications was performed on a weekly basis.

RESULTS:

The mean length of intravenous antibiotic treatment was 118 days (range, 7-750 days) representing 23,654 IVD-days. Seven patients (3.5%) experienced allergic reactions to the antibiotic medication, and two patients (1.0%) had gallbladder toxicity. IVD complications occurred in 15 patients (7.5%) representing an incidence of 0.63 per 1,000 IVD-days. The IVD problems occurred an average of 81 days after initiation of treatment (range, 7-240 days). There were six suspected line infections for an incidence of 0.25 per 1,000 IVD-days. Only one of the IVD infections was confirmed, and no resistant organisms were cultured from any patient. None of the IVD complications were fatal.

CONCLUSION:

Prolonged intravenous antibiotic therapy is associated with low morbidity and no IVD-related mortality in patients referred for treatment of neurologic Lyme disease. With proper IVD care, the risk of extended antibiotic therapy in these patients appears to be low.

wonderfullife
24-09-2011, 05:04 PM
Chronic spirochetal infection can cause slowly progressive dementia, cortical atrophy and amyloid deposition in the atrophic form of general paresis. There is a significant association between Alzheimer disease (AD) and various types of spirochete (including the periodontal pathogen Treponemas and Borrelia burgdorferi), and other pathogens such as Chlamydophyla pneumoniae and herpes simplex virus type-1 (HSV-1). Exposure of mammalian neuronal and glial cells and organotypic cultures to spirochetes reproduces the biological and pathological hallmarks of AD. Senile-plaque-like beta amyloid (Aβ) deposits are also observed in mice following inhalation of C. pneumoniae in vivo, and Aβ accumulation and phosphorylation of tau is induced in neurons by HSV-1 in vitro and in vivo. Specific bacterial ligands, and bacterial and viral DNA and RNA all increase the expression of proinflammatory molecules, which activates the innate and adaptive immune systems. Evasion of pathogens from destruction by the host immune reactions leads to persistent infection, chronic inflammation, neuronal destruction and Aβ deposition. Aβ has been shown to be a pore-forming antimicrobial peptide, indicating that Aβ accumulation might be a response to infection. Global attention and action is needed to support this emerging field of research because dementia might be prevented by combined antibiotic, antiviral and anti-inflammatory therapy.
http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=8385895

creation
24-09-2011, 05:04 PM
Ok wonderfullife you can stop posting now.

wonderfullife
24-09-2011, 05:17 PM
Ok wonderfullife you can stop posting now.

Why?
Many are ill with this illness, they want information need information.
More and more will get ill with this emerging plague and will be debilitated by it and never know why.
I wish i had known about it 30 years ago I wish my dead family and friends had known and they would still be with us now.

wonderfullife
24-09-2011, 07:03 PM
Dashing the hopes of many people with chronic fatigue syndrome, an eagerly awaited study coordinated by government health agencies has not confirmed a link between the illness and a virus called XMRV or others from the same class of mouse leukemia viruses.
Two research groups had earlier reported an association between chronic fatigue syndrome and the group of viruses, known as murine leukemia viruses, or M.L.V.’s, raising hopes that a treatment or cure could be found. But later studies did not substantiate the link, and many researchers suggested that that the initial findings were the result of contamination of laboratory samples or equipment.

The new multilab study, published online Thursday in the journal Science, was designed to answer some of the questions about these unusual viruses and determine whether they posed a risk to the blood supply.

Results from another government-sponsored study of M.L.V.’s, with a much larger sample size, are expected early next year. But Thursday’s report appeared to leave little room for continued optimism.

Of the nine labs that received blinded blood samples from 15 people previously reported to have been infected with M.L.V.’s and 15 healthy controls, only two reported finding evidence of the viruses in any of the samples. And the results from those two labs — which were the only two to find positive results in the original studies — contradicted not only each other this time, but some of their own earlier findings as well.

“These results indicate that current assays do not reproducibly detect XMRV/M.L.V. in blood samples and that blood donor screening is not warranted,” reported the new study, written by researchers participating the Blood XMRV Scientific Working Group.

But the scientists also said they could not “definitively exclude” the possibility that levels of viral markers in the blood might fluctuate over time and become undetectable at certain periods.

Also on Thursday, researchers from the original study linking XMRV to chronic fatigue syndrome, which was published in Science in October 2009, retracted a portion of their data — but not their conclusions — because of evidence of contamination in one lab involved in the study.

Vincent Racaniello, a microbiology professor at Columbia University who has covered the controversy on his popular virology blog, said the XMRV/M.L.V. hypothesis was now dead. “It’s clearly time to move on in the study for the origin of this disease,” he wrote in an e-mail message.

An estimated one million Americans suffer from chronic fatigue syndrome. Countless studies have documented immunological, neurological and other physiological abnormalities. Despite the name of the illness, patients have long reported that simple fatigue is not their cardinal symptom but rather what researchers call postexertional exhaustion — a profound depletion of energy after even minimal exercise or activity.

Recently, a panel of top researchers proposed a new definition of the illness that requires the presence of postexertional exhaustion, rather than the six months of unexplained fatigue required under the standard definition.

The group also recommended changing the name to myalgic encephalomyelitis, a virtually identical illness long recognized by the World Health Organization.

Dr. Nancy Klimas, an immunologist at the University of Miami, said that the two-year debate over M.L.V.’s had raised the profile of the disease and brought attention to the likely role of infectious agents in chronic fatigue syndrome.

“Internationally recognized experts have looked at the immune data and concluded that there very well may be a pathogen or pathogens involved in the persistence of this illness,” Dr. Klimas wrote in an e-mail message.

The new findings will also be presented Friday in Ottawa at the annual conference of the International Association for Chronic Fatigue Syndrome/ME, a leading scientific organization.
http://www.nytimes.com/2011/09/23/health/research/23fatigue.html?_r=3&emc=tnt&tntemail1=y

wonderfullife
24-09-2011, 07:08 PM
The number of cases of borreliosis - Class of infectious diseases, including including Lyme disease, caused by bacteria with natural reservoirs for small rodents and transmitted by ticks or lice - seems to be increasing rapidly in recent decades. En Autriche, quelques 50.000 personnes sont ainsi infectées chaque année. In Austria, some 50,000 people are infected each year as well. Or l'Université de Médecine de Vienne a mis au point un gel qui permet de réduire le taux d'infection après morsure de tique, chez l'animal, de 33% à 0% - et ce même si le gel est appliqué de manière prophylactique jusqu'à trois jours après la morsure. Now the Medical University of Vienna has developed a gel that reduces the rate of infection after tick bite, in animals, from 33% to 0% - even if the gel is applied prophylaxis until three days after the bite.
Promising results


http://translate.google.com/translate?sl=fr&tl=en&js=n&prev=_t&hl=en&ie=UTF-8&layout=2&eotf=1&u=http%3A%2F%2Fwww.bulletins-electroniques.com%2Factualites%2F67730.htm

wonderfullife
24-09-2011, 08:04 PM
http://www.natcaplyme.org/

Good site

multiverse
30-09-2011, 09:11 PM
Please watch if you haven't seen it already.

~7~ SEVEN LYME FACTS THAT COULD HAVE SAVED ME!!! - YouTube

wonderfullife
01-10-2011, 08:21 PM
A flawed study claiming prevention of Lyme spirochete infection with topical antibiotics
Two recent papers tested the effectiveness of topical antibiotics in preventing Borrelia burgdorferi infection in mice following a tick bite. Infection by the Lyme disease spirochete was successfully halted in the Knauer et al. study from Germany1 but not in the Wormser et al. study conducted in New York.2 However a flaw in the Knauer study may have unfairly tipped the outcome in the antbiotic's favor. (I'll save the Wormser study for another post.)
The paper by Knauer and colleagues1 presented two trials, which differed in how the mice were inoculated with B. burgdorferi, In the first trial the spirochetes were injected into the skin, and azithromycin was applied topically one hour, three days, and five days later at the injection site. In the second trial infected ticks transmitted the spirochetes to the mice. Azithromycin was applied topically to the feeding site immediately after the ticks stopped feeding. In both trials azithromycin was dissolved in ethanol for application to the inoculation site. Disseminated infection of the mice was assessed by culturing the heart, bladder, ear, and tarsus 56 days after inoculation.

The results from the first trial reveals the problem with the study (Table 1). Among the ten mice in the placebo group (first row), which received only ethanol, only one (10%) had any culture positive organs 56 days later. The spirochetes failed to establish a persistent infection in the other nine mice, suggesting that the investigators were working with a weakened strain of B. burgdorferi. The ethanol could have had a slight killing effect (see the second trial) yet could not have accounted for the poor infection rate in the placebo group.

Wednesday, September 28, 2011
A flawed study claiming prevention of Lyme spirochete infection with topical antibiotics
Two recent papers tested the effectiveness of topical antibiotics in preventing Borrelia burgdorferi infection in mice following a tick bite. Infection by the Lyme disease spirochete was successfully halted in the Knauer et al. study from Germany1 but not in the Wormser et al. study conducted in New York.2 However a flaw in the Knauer study may have unfairly tipped the outcome in the antbiotic's favor. (I'll save the Wormser study for another post.)

The paper by Knauer and colleagues1 presented two trials, which differed in how the mice were inoculated with B. burgdorferi, In the first trial the spirochetes were injected into the skin, and azithromycin was applied topically one hour, three days, and five days later at the injection site. In the second trial infected ticks transmitted the spirochetes to the mice. Azithromycin was applied topically to the feeding site immediately after the ticks stopped feeding. In both trials azithromycin was dissolved in ethanol for application to the inoculation site. Disseminated infection of the mice was assessed by culturing the heart, bladder, ear, and tarsus 56 days after inoculation.

The results from the first trial reveals the problem with the study (Table 1). Among the ten mice in the placebo group (first row), which received only ethanol, only one (10%) had any culture positive organs 56 days later. The spirochetes failed to establish a persistent infection in the other nine mice, suggesting that the investigators were working with a weakened strain of B. burgdorferi. The ethanol could have had a slight killing effect (see the second trial) yet could not have accounted for the poor infection rate in the placebo group.




The table legend claims that the difference between the placebo and treatment groups was significant, but the statistics were done on the numbers in the column labeled "Infection Status." According to the text of the paper, a positive "Infection Status" refers to those animals that managed to produce antibodies against B. burgdorferi antigens. Infection status is therefore not the proper metric to assess the infectivity of B. burgdorferi. When the statistics are performed with the appropriate numbers, located in the column under "Culture," the effect of azithromycin (1/10 culture positive in control group vs. 0/10 culture positive in any treatment group) is not significant (P = 0.9 for control vs. any treatment group).

Results from the second trial are shown in Table 2. This trial included an extra control group ("No treatment") that received neither antibiotic nor ethanol. Four of the seven mice in the untreated group (57%) ended up culture positive. This is still a low infection rate compared to the rates observed in other studies, in which 90-100% of the control animals end up infected following tick inoculation of B. burgdorferi. Two of the nine mice treated with ethanol alone (placebo) were culture positive, suggesting that ethanol alone helps prevent infection (57% culture positive in "no treatment" group vs. 22% in placebo group, P = 0.152), although the experiment would need to be repeated with larger groups of animals to make a statistically convincing case.

None of the animals treated with azithromycin were culture positive. However the number of animals was again too low to conclude that antibiotic treatment was effective (2/9 culture positive in placebo group vs. 0/9, 0/8, and 0/5 in the treatment groups, P > 0.4 for comparison of each treatment group with placebo group). The authors were able to claim statistical significance by combining the two control groups (no treatment and placebo) and the treatment groups. However it is inappropriate to combine groups in this manner to attain statistical significance.

Even if the investigators had used a larger number of animals, the problem of their weakened challenge strain remains. Application of topical antibiotics may turn out to be effective in preventing Lyme disease after a tick bite, but the study presented by Knauer and colleagues was not a fair test of this treatment approach.

http://spirochetesunwound.blogspot.com/2011/09/flawed-study-claiming-prevention-of.html

wonderfullife
01-10-2011, 08:59 PM
I am on session 7 and boy there is a diffrence!

I am more mobile more energy mood better brain function better.

If you do have Lyme or BB why not try it out?

I shall see how I am tommorow because Sunday is my longest working day and i was getting to the point where I was going to give up work because i just was not coping.

BTW always buy your own mask which you can buy at the centre because i got infected with a cold so now i have my own mask.

wonderfullife
01-10-2011, 09:30 PM
A new tick-dwelling bacterium related to the one that causes Lyme disease has been discovered in Canada and the northeastern United States.

Studies conducted by the Public Health Agency of Canada and Yale University have identified the bacterium, Borrelia miyamotoi, in deer ticks, the most common transmitter of Lyme disease, a flu-like illness that can lead to irregular heartbeat and nerve damage.

Deer ticks are found in southwestern and eastern Ontario, as well as parts of British Columbia, Manitoba, Quebec and Nova Scotia. The fully-engorged insects are no larger than a dime.

A March 2011 Public Health Agency study of 309 Canadian deer ticks, published by the American Society for Microbiology, found Borrelia miyamotoi in six specimens. The Yale report, in the journal Emerging Infectious Disease last week, determined roughly two per cent of deer ticks in the northeastern U.S. and upper Midwest carry the bacterium.

Borrelia miyamotoi is thought to cause a disease characterized by high fever, which fades without medical treatment. To identify the effects of the new bacterium, Yale scientists compared symptoms in infected patients in Russia with Lyme disease patients in the U.S.

Public Health Ontario does not test for the disease, meaning it’s not reportable by Toronto Public Health.

As of July, only nine Lyme disease cases have been reported by Toronto Public Health this year. Most of the confirmed cases are travel-related, meaning the illness was acquired outside the city.

The Public Health Agency of Canada recommends those at risk of tick-borne diseases cover exposed skin, and change and wash clothing frequently
http://www.thestar.com/news/article/1060669

wonderfullife
01-10-2011, 09:39 PM
Risk of exposure to nymphal Ixodes pacificus Cooley and Kohls ticks was investigated at 7 picnic areas in Tilden Regional Park, a heavily used recreation area of over 2000 acres in northwestern California, east of San Francisco Bay. Wooden picnic tables, tree trunks, logs, leaf litter, surrounding vegetation, and rock walls were checked for ticks using standard 1-m2 flannel tick flags at biweekly intervals from March to August 2008. Results indicate that nymphal I. pacificus were commonly found on wooden picnic tables and other wooden materials, such as tree trunks and logs, at an equal proportion to those found in leaf litter. Nymphal I. pacificus in picnic areas peaked in April, with a secondary peak in early June. Five of 170 (2.9%) nymphal I. pacificus collected at picnic sites were positive for Borrelia spirochetes, of which 3 (1.8%) were identified as B. burgdorferi sensu stricto using molecular techniques. In addition, a nymphal I. auritulus collected from a rock wall in a picnic area tested positive for a mixture of B. burgdorferi and B. bissettii; this tick species feeds exclusively on birds. This study indicates a moderate risk of acquiring a nymphal tick at Tilden Park picnic areas, but due to the low B. burgdorferi infection prevalence, the risk of acquiring Lyme disease appears to be low.
http://www.sciencedirect.com/science/article/pii/S1877959X11000550

wonderfullife
01-10-2011, 09:45 PM
Lichen sclerosus et atrophicans (LSA) is a chronic, inflammatory skin disease of unknown etiology, characterized by atrophy. We report a case of LSA with frontoparietal distribution, mimicking scleroderma en coup de sabre, causing scarring alopecia. The case was associated with Borrelia infection. The lesion improved with 2 cycles of antibiotic therapy with ceftriaxone 2 gr /day i.v for 21 days associated with UVA-1 therapy and local and systemic vitamin E supply (400 mg 2x/day per os for 3 months). This case stresses the importance of identifying clinical manifestations associated with Lyme disease and the use of tissue PCR to detect borrelial DNA in patients with these lesions, but characterized by negative serology for Borrelia.

http://www.pagepress.org/journals/index.php/dr/article/view/dr.2011.e27

wonderfullife
01-10-2011, 09:59 PM
http://www.publichealthalert.org/pdf/2011_09.pdf

Very good read

wonderfullife
01-10-2011, 10:05 PM
[Differential aspects of multiple sclerosis and chronic borrelial
encephalomyelitis.]

Spirin NN, Baranova NS, Fadeeva OA, Shipova EG, Stepanov IO

Zh Nevrol Psikhiatr Im S S Korsakova 2011 9; 111 (7): 8-12

The Yaroslavl region is an endemic area for Lyme disease (LD) with one
of the highest levels of morbidity in Russia. Chronic neuroborreliosis
can mimic multiple sclerosis and cause considerable difficulties in
differential diagnosis. A comparative clinical-instrumental analysis of
patients with definite multiple sclerosis (n=65) and chronic borrelial
encephalomyelitis (n=11) was carried out. The key
differential-diagnostic features of multiple sclerosis and borrelial
encephalomyelitis were specified. Migrating erythema and tick's bite in
the anamnesis, combined with lesions of the central and peripheral
nervous systems, the absence of retrobulbar neuritis in the anamnesis,
artralgia and myalgia, the high blood sedimentation rate were not
characteristic of multiple sclerosis. A patient with above mentioned
findings should be tested for the presence of antibodies to Borrelia
burgdorferi in the blood serum and, if necessary, in the cerebrospinal
fluid to exclude the diagnosis o f Lime disease.

wonderfullife
01-10-2011, 10:07 PM
Interleukin-10 Alters Effector Functions of Multiple Genes Induced by
Borrelia burgdorferi in Macrophages to Regulate Lyme Disease Inflammation.

Gautam A, Dixit S, Philipp MT, Singh SR, Morici LA, Kaushal D, Dennis VA

Infect Immun 2011 09 26

Interleukin-10 (IL-10) modulates inflammatory responses elicited in
vitro and in vivo by Borrelia burgdorferi, the Lyme disease spirochete.
How IL-10 modulates these inflammatory responses still remains elusive.
We hypothesize that IL-10 inhibits effector functions of multiple genes
induced by B. burgdorferi in macrophages to control concomitantly
elicited inflammation. Because macrophages are essential in the
initiation of inflammation, we used mouse J774 macrophages and live B.
burgdorferi as the model target cell and stimulant, respectively. First
we employed transcriptome-profiling to identify genes induced by
stimulation of cells with live spirochetes, and which were perturbed by
addition of IL-10 to spirochete cultures. Spirochetes significantly
induced up-regulation of 347 genes at both the 4 h and 24 h time-points.
IL-10 inhibited the expression levels, respectively of 53 and 65 of the
4 h and 24 h genes, and potentiated, respectively at 4 h and 24 h, 65
and 50 gene s. Prominent among the novel identified IL-10-inhibited
genes also validated by qRT-PCR were TLR1, TLR2, IRAK3, TRAF1, IRG1,
PTGS2, MMP9, IFI44, IFIT1 and CD40. Proteome analysis using multiplex
ELISA revealed the IL-10 modulation/and or potentiation of RANTES/CCL5,
MIP-2/CXCL2, IP-10/CXCL10, MIP1-α/CCL3, G-CSF/CSF3, CXCL1, CXCL5, CCL2,
CCL4, IL-6, TNF-α, IL-1α, IL-1β, IFN-γ and IL-9. Similar results were
obtained using sonicated spirochetes or lipoprotein as stimulants. Our
data show that IL-10 alters effectors induced by B. burgdorferi in
macrophages to control concomitantly elicited inflammatory responses.
Moreover, for the first time, this study provides a global insight into
potential mechanisms used by IL-10 to control Lyme disease inflammation.

wonderfullife
01-10-2011, 10:09 PM
Epidemiology and etiology of mantle cell lymphoma and other
non-Hodgkin lymphoma subtypes.

Smedby KE, Hjalgrim H

Semin Cancer Biol 2011 09 18

We aimed to give an overview of the descriptive epidemiology and
etiology of mantle cell lymphoma (MCL) in the context of all non-Hodgkin
lymphoma (NHL) and major NHL subtypes, based on available published
reports. In retrospective case series, MCL cases represent between 2 and
10% of all NHL. Population-based studies of MCL incidence by basic
demographic characteristics are limited to the past 15-20 years and to
Europe and the US. In both regions, average incidence rates of
approximately 0.5 cases per 100000 person-years were reported, with a
male-to-female ratio of 2.3-2.5:1, and a median age at diagnosis of
close to 70 years. Some data suggest a possible increase in MCL
incidence over the last two decades, but the observation may also
reflect improved diagnostics. The causes of MCL are not known. Studies
of potential risk factors of MCL are few and conducted primarily within
the framework of all NHL. Moderate associations with MCL risk have been
reported for Borrelia burgdorferi infection, family history of
hematopoietic malignancies, and genetic variation in the interleukin-10
and tumor necrosis factor genes, but findings remain unconfirmed. Large
multicenter studies are needed to address these and other factors in
risk of MCL with sufficient statistical power in the future.

wonderfullife
01-10-2011, 10:11 PM
Cutaneous Manifestations of B-Cell Chronic Lymphocytic Leukemia
Associated With Borrelia burgdorferi Infection Showing a Marginal Zone
B-Cell Lymphoma-Like Infiltrate.

Kash N, Fink-Puches R, Cerroni L

Am J Dermatopathol 2011 10; 33 (7): 712-715

We report on a 69-year-old female patient with specific cutaneous
manifestations of B-cell chronic lymphocytic leukemia that arose at the
site of erythema chronicum migrans due to Borrelia burgdorferi
infection. Histological examination revealed the presence of dense
infiltrates of small hyperchromatic lymphocytes admixed with clusters of
plasma cells. Immunohistology showed a CD5+/CD20+ phenotype of the
lymphocytes and monoclonal expression of kappa immunoglobulin light
chain by the plasma cells. Presence of Borrelia DNA was confirmed by
polymerase chain reaction studies. The unusual histopathological and
phenotypic findings described in this case of cutaneous manifestations
of B-cell chronic lymphocytic leukemia associated with Borrelia
burgdorferi infection may lead to the misdiagnosis of cutaneous marginal
zone B-cell lymphoma.

wonderfullife
01-10-2011, 10:16 PM
Lyme Disease

Since the Well-One Clinic started work I have become very interested in Lyme disease, as patients who cannot get any help from the NHS are beginning to visit the clinic. This is an infection by the bacteria, Borrelia burgdorferi, a spirochaete, which is transferred to the blood by a tick bite

At present there seems to be no reliable testing for such parasites in the UK. To diagnose these cases blood is often sent to California and diagnosis and treatment is rare in the NHS, although about 3,000 cases a year are said to occur.

The initial signs and symptoms often comprise a red spot or rash at the location of the tick bite known as Erythema migrans. This may be associated with fatigue, joint and muscle pain (e.g. arthritis), mild fever, headaches, drowsiness and swollen lymph glands etc.

Symptoms may not show for many years: the organism can lie dormant until a particular life event such as a period of extreme stress or another infection that alters the immune response. Other symptoms may not appear for some time but often lead to serious diseases of the head, face and neck (e.g Bell’s palsy). The eyes, musculoskeletal system, neurological system, psychological well-being cognitive function and general well-being are under attack.

Diagnosis

Currently methods for the diagnosis of Lyme disease rely on the detection of the Borrelia bacteria itself or the detection of blood-borne antibodies to certain portions of the bacteria. These have resulted in methods such as dot-blot, PCR, ELISA and Western blot. Of all the methods, the most definitive is Western blot.

Treatment

Treatment should start immediately after the tick bite and many people are now recomending a large dose of antibiotics immediately after a bite for at least one month. In the NHS it is only recommended to treat when there is a positive Elisa test and treatment should be for one month with mainly doxycycline in a higher than average dose. For those who are not diagnosed until later the antibiotic treatment needs to be much more intensive and long lasting. Often a cocktail of three anitbiotics is used. Treatments can include some herbal remedies and other alternative treatments. The illness is often prolonged and progressive and patients need much supporting therapy.

Research

The Well - One Clinic, Cytogenex Lab and Jacob’s Well Appeal are jointly researching best methods of diagnosis and studying best methods of treatment. The research is ongoing and dependant on funding.
http://www.welloneclinic.org.uk/services.html#Lyme

May not be everyones bag but good to know about it.

wonderfullife
01-10-2011, 10:21 PM
Lyme Disease and Bipolar, OCD, Schizophrenia, other Mental Illness - YouTube

wonderfullife
01-10-2011, 10:23 PM
Microbes are the greatest predator of man. As medical technology improves, there is increasing recognition that infectious disease contributes not only to acute, but also chronic relapsing illness and mental illness. -Robert C. Bransfield, M.D.

Probably the biggest challenge facing those sick with Lyme disease manifesting with psychiatric symptoms is to get the Lyme disease diagnosis in the first place. Many people with Lyme and associated mental dysfunction (this is about 95% of all Lyme sufferers) never get diagnosed properly and are left to struggle with palliative treatment, institutionalization, and basically a life sentence of obscurity and panic.

Even for those with the right diagnosis, for example, Lyme disease infection, symptoms of mental illness are obviously still devastating. I created this video to address some of the common experiences, and some useful solutions / tips, for people who meet this description. Below the video is an excerpt from a book I wrote in 2007 entitled The Lyme-Autism Connection, which further addresses the topic of the connection between Lyme disease and mental illness.
Excerpt: Mental Illnesses and Autism, Lyme Disease
From the book, The Lyme Autism Connection

Symptom similarities between Lyme disease and autism, especially in children, are astounding. Obviously, symptom similarity alone is not a strong enough scientific indicator to implicate Lyme disease in the autism epidemic. However, when considered within the framework of the other arguments presented in this book, symptom similarity becomes an important, central piece of the puzzle.

This chapter was written with three primary goals. First, we will look at the diagnostic procedures used in classifying mental illnesses. Then we will show that a Lyme disease diagnosis overlaps with numerous other mental disorders. Finally, we will show that an autism diagnosis not only overlaps with a variety of different mental illnesses as well, but that they happen to be, in many cases, the same mental illnesses which overlap with Lyme disease. Additionally, the chapter will also cover various data which support the above three points.

Symptoms vs. Syndromes

At first glance, the obvious question to ask in this chapter is whether or not the symptoms of Lyme disease overlap with the symptoms of autism. As you will see, however, this question is much too broad. You will see that Lyme disease is known as the “great imitator” because it can mimic dozens of seemingly unrelated health problems. Lyme disease symptoms overlap with just about every mental illness, so it is not very impressive to show that they also overlap with autism.

For this reason, we will instead take a narrower look at the symptom similarities between Lyme disease and autism, and delve further into analyzing the overlap. Namely, we will not look at individual symptoms the diseases share in common, but instead at entire disease syndromes which the two diseases share in common. For example, we will go further than to just say “Lyme disease and autism both cause headaches.” Rather, we will say that “Lyme disease and autism both manifest as schizophrenia.” A headache is an individual symptom, while schizophrenia is a complex syndrome.

For our purpose of further analyzing the Lyme-autism connection, it is more helpful to look at overlapping disease syndromes instead of just overlapping symptoms because disease syndromes are much more complex, specific, and isolated than are individual symptoms. Many things can cause a headache, such as fatigue, a bad lunch, or a fight with a spouse. So, demonstrating that Lyme disease and autism both cause headaches does not add much support to the Lyme-autism connection. Schizophrenia, on the other hand, is not caused by many factors, and cannot be confused with simple triggers like a bad hamburger or emotional stress. By narrowing the comparison down to specific disease syndromes, we can build a much stronger case for the Lyme-autism connection.

Blurred Lines Between Disease Labels

In order to show that both Lyme disease and autism share in common numerous disease syndromes, we must first accept the fact that the diagnostic lines are blurred between autism, Lyme disease, and numerous other mental illnesses, leading to somewhat arbitrary and meaningless guidelines for diagnosing the diseases. For example, someone diagnosed with the label “schizophrenia” may in fact be suffering from Lyme disease, autism, or both. “Schizophrenia” is not a disease; instead it is a disease presentation. The label schizophrenia says nothing about the reason for the disease, or the cause, but instead simply says that a given person is suffering from a collection of physiologic and symptomatic dysfunctions.

It is important to keep this in mind as you think about Lyme disease, autism, and the list of mimicking diseases. You have to ask yourself, “Does the disease label in question tell me anything about what is actually causing this health problem?” Understanding that many of the disease labels used by conventional medicine are actually not indicative of the cause of the disease will help you learn how to adjust your thinking process and see that many “diseases” do not in fact have established, defined boundaries separating them from other “diseases,” but are instead simply a melting pot of symptomatic and physiological characteristics.

Why is this important? Let’s again use the example of a headache. When someone says, “I have a headache,” you would never jump to a conclusion about what is causing the headache unless you knew more about the person’s current circumstances. A headache is not a disease in and of itself; instead it is a list of symptomatic and physiologic properties, namely, pain in the head, and typically, inflammation in the head. We all know that many things can cause headaches, hence, if someone mentions their headache, the next thing you might try to do is play detective to discover what is causing the headache. You might ask the person what they ate for lunch, how much sleep they are getting, or what is happening at work. You would never assume that the cause of their headache is the headache itself. Headaches always have underlying, root causes.

In the same way, if someone has schizophrenia or autism, you should train your mind to play the same detective role. Schizophrenia and autism are no more the cause of a health problem than is a headache. Instead, schizophrenia and autism are just labels for a set of symptomatic and physiologic characteristics. When you begin to adopt this way of thinking, you can see that the lines between various diseases can easily become blurred.

When autism is seen as a set of symptoms rather than a defined “disease,” it leaves a lot more room for questions—questions which can ultimately lead to a better understanding of the disease and its cause(s). Do not passively accept a diagnosis of autism as the final description of your child’s health. You should empower yourself to play detective and get to the bottom of the symptoms, instead of simply accepting the diagnosis and giving up.

If you think about Lyme disease and autism as separate diseases, with distinct boundaries, then the Lyme-autism connection seems improbable. However, if you think of the two diseases accurately, as nothing more than arbitrary labels which encompass a grouping of symptoms, some of which overlap, then the question arises and must be answered: what is the root cause of the disease syndromes? Is the root cause potentially the same?

Now, a clarifying point is in order here. Some diseases certainly do include causative factors in their label. For example, strep throat is caused by…strep bacteria in the throat. The disease label “strep throat” is one which is accurate in its description of causality. Similarly, Lyme disease is caused by Lyme disease bacteria (the scientific name for which is Borrelia burgdorferi). So, when we are looking at the Lyme-autism connection, what we are really asking is whether or not autism shares the same root cause as Lyme disease, namely, a Borrelia infection.

Ok, so this all sounds good in theory, but where is the evidence? Let’s now turn our attention to several scientific studies which provide objective substantiation for the theory we just talked about—the theory that mental disorders have blurred diagnostic lines.

Lyme Disease: The Great Imitator

To substantiate the theory that disease labels are relatively arbitrary and have blurred defining lines, let’s begin by looking at Lyme disease and the many diseases which it mimics.

The Journal of Neuropsychiatry in 2001 published an article in which it was stated that “Children with Lyme disease have…cognitive and psychiatric disturbances…resulting in psycho-social and academic impairments.” According to Dr. Frederic Blanc, of the University of Strasbourg, France, “The neurological and psychiatric manifestations of Borrelia are so numerous that it is called the ‘new great imitator.’ Every part of the nervous system can be involved: from central to peripheral.”

It is difficult to convey just how broad and diverse Lyme disease symptoms can be. As the “new great imitator” (Syphilis was considered the original great imitator), Lyme disease mimics dozens of seemingly unrelated illnesses, from physical disorders such as chronic fatigue syndrome and arthritis, to psychiatric disorders including schizophrenia, obsessive compulsive disorder, Tourette syndrome, depression, bipolar disorder, and more. According to psychiatrists at Columbia University, as published in 1994 in the American Journal of Psychiatry:

“Lyme disease can trigger a broad range of psychiatric reactions, including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa and obsessive–compulsive disorder.”

As you can see, Lyme disease is often the root cause of a long list of diseases. In these cases, there is in fact zero separation between the seemingly distinct diseases on the list—the lines are blurred beyond recognition. A variety of mental disorders can potentially all have the same root cause.

Antiquated belief that Lyme disease is characterized by a limited set of mostly benign symptoms is rapidly being replaced by modern, increasingly accurate models of Lyme disease symptomology that encompass a vast diversity of symptomology in numerous body systems. So, if you are doubtful that a simple bacterial infection can cause such diverse symptoms as are present in autism, be forewarned—Lyme disease is a highly advanced neuropsychiatric disease with complicated and poorly understood effects on the brain. The combination of wide-ranging symptoms and the prevalence of false-negative laboratory test results means that Lyme disease may be one of the most rampant, yet under-diagnosed, infections on the planet. And, when the Lyme infection occurs in the womb, a new set of variables and complexities are introduced to the scene which further broaden the potential neurological effects of Lyme disease.

Still, the fact that Lyme disease is a great imitator is nothing worth writing home about—this has become accepted science in both mainstream and alternative medicine. Therefore, we will not belabor this point here. To learn more about Lyme disease as a great imitator, read Appendix B and consult available Lyme disease literature.

The real point we are tracking down in this chapter is not merely the fact that Lyme disease shares blurred lines with many mental illnesses, but, more importantly, the fact that autism also shares blurred lines with a variety of mental disorders. Even more important yet is the paramount question of whether or not Lyme disease and autism share blurred lines with the same set of mental illnesses.

Autism: The Next Great Imitator?

You may be surprised to learn that just as Lyme disease is a great imitator, so also is autism.

Many autistic people have a broad range of psychological symptoms, not just those few which have historically defined “classic” autism. Autism is currently being re-defined as a multi-systemic, multi-factorial disease. In this section, we will examine some of the science surrounding autism as a great imitator. For each of the scientific studies below, we will note their relevance to the Lyme-autism connection.

Swedish researchers have observed a fascinating overlap between symptoms of autism and other mental illnesses. In 2004, the Department of Child and Adolescent Psychiatry, at Göteborg University, Sweden, published findings in the Journal of Neural Transmission indicating that patients suffering from autism also sometimes have symptoms of schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder (AD/HD). The Swedish researchers don’t offer an explanation for this symptom overlap, but they do acknowledge it, and conclude their study by stating that “Current diagnostic criteria have to be revised to acknowledge the co-morbidity of autism with bipolar disorder, AD/HD, schizophrenia, and other psychotic diseases.”

The connection: Of the mental illnesses which Lyme disease mimics, schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder are at the top of the list.

Researchers at the University of Michigan published a study in 2004 in the Journal of Autism and Developmental Disorders which concluded with the following statement: “This study lends support to the validity of depression as a distinct condition in some children with autism/PDD and suggests that, as in the normal population, autistic children who suffer from depression are more likely to have a family history of depression.”

The connection: These findings are significant for two reasons: first, the study indicates that depression is part of the autism complex of symptoms, and second, this depression can be found in family history. Both of these points are true of Lyme disease, as well.

In London, similar conclusions are being reached. The Genetic and Developmental Psychiatry Research Centre published in 1998 a study entitled “Autism, affective and other psychiatric disorders: patterns of familial aggregation.” The report was released by Cambridge University Press in the Journal of Psychological Medicine. In addition to finding a correlation between familial mental disorders and autism, researchers also discovered that “Individuals with a singular diagnosis of obsessive-compulsive disorder were more likely to exhibit autistic-like social and communication impairments.”

The connection: This finding is fascinating because it tells us that not only does autism involve symptoms of other, previously believed separate diseases, but the converse of this is also true; that those separate diseases also sometimes include symptoms known to occur in autism. This further blurs the lines between different mental disorders. This is another piece of the puzzle that shatters the previous belief that autism is completely distinct and separate from other psychiatric diseases. Modern medicine likes to put these diseases in their own neatly organized, unrelated files, but reality just won’t comply with such an organizational strategy.

City of Hope National Medical Center in California published findings that link autism and Tourette syndrome. Researchers found that “there is an intimate genetic, neuropathologic relatedness between some cases of [autism] and Tourette syndrome.” Additionally, these researchers noted frequent family groupings of the two afflictions, with obsessive compulsive disorder also showing up frequently.

The connection: The Lancet in 1998 published a study linking Lyme disease with Tourette syndrome. A 4-year old boy developed typical Tourette symptoms and was subsequently diagnosed with Lyme disease by ELISA IgG antibody testing. Upon antibiotic treatment, all symptoms resolved. From the Lancet: “Rapid efficacy of antibiotic treatment followed by a decrease in Borrelia-specific antibody titres suggests that the multiple motor and vocal tics [in this 4-year old boy] were at least partially caused by the tertiary stage of Borreliosis.” Therefore, both autism and Lyme disease share in common blurred lines with Tourette syndrome.

The lines between autism and other mental disorders are further blurred when considering the methods used to diagnose autism. This is an important area to examine because the diagnostic model used in categorizing childhood mental disorders is the primary determinant of the next twenty or more years of treatment decisions. Consider this carefully—if a child is diagnosed with autism but Lyme disease is really the root problem, then parents will spend thousands (or maybe millions) of dollars, thousands of hours, and incalculable stress, pursuing the wrong course(s) of treatment. Hence, proper diagnostic procedures, or at least, proper understanding of the limitations of modern diagnostic capabilities, is essential for ensuring that a lifetime of energy is focused in the right direction. This statement is substantiated by the experiences of numerous mothers, whose stories appear in Appendix E. These mothers only received desirable treatment results after discovering the Lyme infection in their children. Prior to the discovery, they wasted incalculable time, energy and money chasing palliative treatments.

Alarmingly, the diagnostic model used for autism can be relatively unreliable. The Indiana University School of Medicine in 1971 evaluated 5 diagnostic systems designed to differentiate infantile autism and early childhood schizophrenia and published their findings in the Journal of Autism and Developmental Disorders. Diagnostic scores from 44 children were examined. Some of the five diagnostic systems contradicted the others, leading to a confusing and disturbing debate about the definitions of autism and schizophrenia. So similar are the two diseases that the lines between them become blurred when using these diagnostic systems, and the results of the diagnostic procedures become relatively meaningless. Obviously, diagnostic systems have improved exponentially since 1971. However, even today, the same symptom similarities exist between autism and schizophrenia, resulting in debate and disagreement about proper courses of treatment for the two disorders, not to mention heated arguments between parents and physicians about which treatments are most logical to pursue. Modern medicine’s appearance of having everything figured out, with white-coated, authoritative doctors passing down final diagnostic decrees to parents, is riddled with an uncertain and ambiguous past.

The tendency to over-compartmentalize diseases without sufficient data is not limited to just the commercial medical industry—non-profit research organizations dedicated to healing schizophrenia and autism also suffer the effects of arbitrarily separating autism from schizophrenia when conducting research and presenting information. The reality is that autism and schizophrenia are intimately related, and only when this fact is accounted for will true breakthrough occur in the research of the two conditions. Autism and schizophrenia are not two separate entities like the colors black and white. They resemble more closely a shade of grey, mixing some amount of black and some amount of white. When researchers only look at the black, they miss the big picture, and when they only look at white, they don’t see all of the facts. Only when shades of grey are acknowledged, will the mechanisms behind the afflictions become more apparent.

Any parent with an autistic child knows that their child exhibits a wide array of symptoms and that no two days are alike. Unlike high cholesterol or diabetes, which are fairly constant disorders with very few variations in symptoms and presentation, autism is a wildly variable condition that seems to follow no particular pattern or predictable course.

Thus far in this chapter, we have worked to establish that not only do Lyme disease and autism act like great imitators, but the diseases which they imitate happen to be the same diseases—namely, mental disorders such as schizophrenia, obsessive compulsive disorder, depression, Tourette syndrome, AD/HD, and others. Although this overlap in associated disease syndromes (and, more broadly, associated individual symptoms) is not sufficient evidence to stand alone as the foundation for the Lyme-autism connection, this observation is, again, one more piece of the puzzle.

It really is shocking and insightful to discover that Lyme disease and autism are separated by much less space than medical schools and textbooks teach. If these broad similarities are not explained by an underlying Lyme disease infection, then what is the explanation? Isn’t it a bit improbable that two supposedly separate diseases are so intimately related in so many ways?

Before concluding this chapter, we will briefly introduce one more area of overlap: autoimmunity.

Autoimmunity

Lyme disease and autism not only share numerous similarities with regard to psychiatric symptoms and syndromes, but also autoimmunity.

The number of studies linking both Lyme disease and autism to autoimmune dysfunction is vast, encompassing dozens of published articles released by several research institutions. For specific studies, visit MEDLINE at www.ncbi.nlm.nih.gov/PubMed and search for keywords autism autoimmune and lyme disease autoimmune. At the time of this writing, the first search string yielded 86 studies and the second string yielded 123 studies.

The fact that Lyme disease and autism share autoimmunity in common is, of course, fascinating, and lends credit to the Lyme-autism hypothesis. However, the link becomes even stronger in light of the fact that new research is revealing that many autoimmune disorders are caused by stealth infections. Recent research has found that treatments aimed at eradicating stealth infections happen to also provide relief, and in some cases, remission or cure, for autoimmune diseases.

One such cutting-edge treatment is the Marshall Protocol, discussed at length in The Top 10 Lyme Disease Treatments. The Marshall Protocol is significant in this context because it defines and reveals the mechanism by which symptoms of autoimmunity can really be an indication of underlying infection. Patients experiencing healing on the Marshall Protocol suffer from a wide range of autoimmune disorders—and healing is taking place via the anti-infective treatments that comprise the protocol. Autoimmunity is defined as the body attacking its own cells. But why would it do that? The new, prevailing theory is that there is a stealth infection inhabiting body tissues and when the immune system attempts to attack that infection, it mistakenly attacks its own proteins which might look similar to the proteins that compose the infectious microorganisms. This new theory of autoimmunity is gaining momentum.

It shouldn’t surprise us that autoimmunity is involved in Lyme disease. After all, Lyme disease is known to be caused by an infection. However, what about autism? Why is there autoimmunity in autism? Is there an underlying infection? If, in fact, autoimmunity is caused by an infectious process, then the autoimmune link between Lyme disease and autism becomes quite telling and is, yet again, just another piece of the puzzle.

Where the Rubber Meets the Road

Hopefully, this chapter has given you a new perspective on childhood developmental disorders. Remember, if your child gets diagnosed with any of the disease labels we have just looked at, do not be satisfied with the diagnosis. Being diagnosed with attention deficit disorder is like being diagnosed with a headache. A headache is not a diagnosis, it is a symptom. A headache is the beginning of the diagnostic journey, not the end. The same can be said of attention deficit disorder.

The minute you start treating your child’s attention deficit disorder (or autism, or schizophrenia, or fill-in-the-blank disorder) as if it is a complete diagnosis, you are beginning a losing battle. Why? The reason is logical and simple. Since these disease labels do not factor in the true cause(s) of the disease (whatever the cause(s) may be), the only treatment modern medicine can offer you is palliative treatment. Palliative treatment is that which covers symptoms instead of addressing cause. The word palliative is derived from the Latin word palliare, which means “to cloak.”

Antidepressant drugs are an example of a palliative treatment, and, not surprisingly, antidepressant drugs are the treatment most often given for childhood developmental disorders. Other palliative drugs include anti-psychotic, anti-anxiety, and sedative. These drugs only temporarily snuff out the symptoms of the underlying problem. And, these drugs have ghastly, brutal side effects of which the public is becoming increasingly aware—such as aggressive behavior, suicidal thoughts and ideation, and decline in intellect. Are these horrendous side effects justified given that the drugs are not even addressing the cause of the disease?

Most of the autism treatment programs and centers in the United States (at least among mainstream medicine) do nothing but offer palliative, or “behavioral” treatment. The government, non-profit research organizations, and parents spend millions of dollars on palliative treatments for childhood developmental disorders. What would happen if some of that money were actually spent on what really matters; that is, trying to locate and treat the cause? Would you offer physical therapy to someone suffering from a broken leg, or would you repair the broken leg?

Now that you are equipped with knowledge, and you know that childhood developmental disorders do in fact have underlying, scientific, physiological causes (even though these causes are sometimes elusive and difficult to isolate), you can begin to play detective with your child and treat the causes, not the symptoms, of their disease. Palliative treatments are useful to increase quality of life during the discovery process. But the palliative treatments themselves are not the end goal.

Maybe your child’s disorder is caused by an imbalance of intestinal microflora. In this case, you might consider using probiotics, diet, and herbs to correct the problem. Or maybe, it is mercury poisoning, for which you could use chelation. Or possibly, your child’s disorder is caused by food allergies, which you might alleviate by an elimination diet. Or, as this book proposes, maybe your child’s autism is caused by Lyme disease, in which case you may decide to undergo Lyme treatment. Whatever the underlying cause, the thought pattern is the same: you, as the parent, must step up to the plate, take responsibility, reject the “diagnosis” your child was given, and search for the underlying cause.

A good friend of mine (Bryan) suffered from migraine headaches for years. She drained her bank account trying the strongest painkillers and anti-migraine medications available. She endured the side effects of powerful, dangerous pharmaceuticals. She only received minimal relief, and suffered greatly. One day, a thinking physician inquired about her diet and discovered that she consumed diet soda pop once or twice a day, every day of her life. In fact, if she ran out of soda, she would make a special trip to the store to replenish her stock. After she objected vehemently, he finally convinced her to go without the soda for a few weeks. Bingo! The headaches disappeared, almost overnight. The palliative, symptom-covering painkillers were not the answer (although they did make a few CEOs and stockholders richer). Eliminating the root cause was the answer.

I do not want to oversimplify childhood developmental disorders. In most cases, the detective work necessary is much more difficult than the experience my friend had with her headaches. However, you owe it to yourself and your child to at least try the detective strategy. In the best case scenario, you will cure your child, and in the worst case scenario, you will at least become educated about your son or daughter’s body, and provide him or her with some level of relief, however minor. But most importantly, taking a detective approach will ensure that you are doing absolutely everything you can to be a good parent.

You, as a thinking, caring, intelligent parent, have what it takes to be a detective and to reject the superficial diagnosis given by a doctor whose thinking is victim of the dogmatic, palliative treatment paradigm that currently rules American medicine.

http://www.lymebook.com/lyme-disease-mental-illness-schizophrenia-bipolar-ocd

wonderfullife
01-10-2011, 10:26 PM
"... To our knowledge this is the first reported case with an exclusive
psychiatric manifestation of Lyme disease...."

Biol Psychiatry 1999 Mar 15;45(6):795


Borrelia burgdorferi central nervous system infection presenting as an organic
schizophrenialike disorder.


Hess A, Buchmann J, Zettl UK, Henschel S, Schlaefke D, Grau G, Benecke R
Department of Neurology, University of Rostock, Germany.


BACKGROUND: We report on a 42-year-old female patient who presented with a
schizophreniform disorder and complete relief of symptoms after specific
therapy. METHODS: Cerebrospinal fluid and magnetic resonance imaging findings
led to the diagnosis of Lyme disease. RESULTS: To our knowledge this is the
first reported case with an exclusive psychiatric manifestation of Lyme
disease. CONCLUSIONS: In case of first manifestation of psychotic disorder,
although neurological symptoms are lacking, Lyme disease should be considered
and be excluded by cerebrospinal fluid analysis.


PMID: 10188012, UI: 99203827


Title: Untreated neuroborreliosis: Bannwarth's syndrome evolving into acute
schizophrenia-like psychosis. A case report.
Authors: Roelcke U, Barnett W, Wilder-Smith E, Sigmund D, Hacke W
Source: J Neurol 1992 Mar;239(3):129-31
Organization: Neurologische Klinik Universitat Heidelberg Federal Republic of
Germany.


Abstract:
In general, meningopolyradiculitis (Bannwarth's syndrome, stage 2 of
neuroborreliosis) follows a predictable monophasic self-limiting course. In
contrast, we report the case of a patient with an untreated
meningopolyradiculitis which evolved into acute schizophrenia-like psychosis
due to persistent infection with Borrelia burgdorferi. The psychosis resolved
within 1 week of treatment with ceftriaxone. This case shows that the usually
benign monophasic meningopolyradiculitis may progress to severe CNS
complications, which may have implications on current pathophysiological
beliefs.


Keywords:
Acute Disease, Antibodies, Bacterial, CF, Borrelia burgdorferi, IM, IP, Case
Report, Ceftriaxone, TU, Chronic Disease, Diagnosis, Differential,
Encephalitis, CF, CO, DT, MI, Human, IgG, CF, Lyme Disease, CF, CO, DT, PX,
Male, Meningitis, CF, CO, DT, MI, Middle Age, Organic Mental Disorders,
Psychotic, CF, DI, ET, Polyradiculitis, CO, DT, MI, Schizophrenia, DI,
Syndrome, Medline File


Language: German


Title: [Endogenous paranoid-hallucinatory syndrome caused by Borrelia
encephalitis]
Authors: Barnett W, Sigmund D, Roelcke U, Mundt C
Source: Nervenarzt 1991 Jul;62(7):445-7
Organization: Psychiatrische Universit:atsklinik, Heidelberg.


Abstract:
We describe a case with no neurological signs but marked psychiatric symptoms
induced by borrelia burgdorferi, whose clinical picture was indistinguishable
from an endogenous schizophrenia. The symptoms within one week under antibiotic
treatment with ceftriaxon, but afterwards the patient showed a mild organic
brain syndrome. The case demonstrated the aetiologic nonspecificity of paranoid
symptoms and hallucinations and emphasizes that in psychotic patients without
psychiatric history additional diagnostic measures should be performed.


Keywords:
Brain Damage, Chronic, DIAGNOSIS, PSYCHOLOGY, Case Report, Diagnosis,
Differential, Encephalitis, DIAGNOSIS, PSYCHOLOGY, English Abstract, Human,
Lyme Disease, DIAGNOSIS, PSYCHOLOGY, Male, Middle Age, Neuropsychological
Tests, Schizophrenia, Paranoid, DIAGNOSIS, PSYCHOLOGY, Syndrome


Language: Ger


Unique ID: 92018508


Title: Lyme disease: a neuropsychiatric illness.
Authors: Fallon BA, Nields JA
Source: Am J Psychiatry 1994 Nov;151(11):1571-83
Organization: Department of Psychiatry, College of Physicians and Surgeons,
Columbia University, New York.


Abstract:
OBJECTIVE: Lyme disease is a multisystemic illness that can affect the central
nervous system (CNS), causing neurologic and psychiatric symptoms. The goal of
this article is to familiarize psychiatrists with this spirochetal illness.
METHOD: Relevant books, articles, and abstracts from academic conferences were
perused, and additional articles were located through computerized searches and
reference sections from published articles. RESULTS: Up to 40% of patients with
Lyme disease develop neurologic involvement of either the peripheral or central
nervous system. Dissemination to the CNS can occur within the first few weeks
after skin infection. Like syphilis, Lyme disease may have a latency period of
months to years before symptoms of late infection emerge. Early signs include
meningitis, encephalitis, cranial neuritis, and radiculoneuropathies. Later,
encephalomyelitis and encephalopathy may occur. A broad range of psychiatric
reactions have been associated with Lyme disease including paranoia, dementia,
schizophrenia, bipolar disorder, panic attacks, major depression, anorexia
nervosa, and obsessive-compulsive disorder. Depressive states among patients
with late Lyme disease are fairly common, ranging across studies from 26% to
66%. The microbiology of Borrelia burgdorferi sheds light on why Lyme disease
can be relapsing and remitting and why it can be refractory to normal immune
surveillance and standard antibiotic regimens. CONCLUSIONS: Psychiatrists who
work in endemic areas need to include Lyme disease in the differential
diagnosis of any atypical psychiatric disorder. Further research is needed to
identify better laboratory tests and to determine the appropriate manner
(intravenous or oral) and length (weeks or months) of treatment among patients
with neuropsychiatric involvement.


Keywords:
Case Report, Comorbidity, Diagnosis, Differential, Female, Human, Lyme Disease,
DIAGNOSIS, EPIDEMIOLOGY, Male, Nervous System Diseases, DIAGNOSIS,
EPIDEMIOLOGY, Neuropsychological Tests, Organic Mental Disorders, DIAGNOSIS,
EPIDEMIOLOGY, Prevalence, Recurrence, Support, Non-U.S. Gov't, United States,
EPIDEMIOLOGY


Language: Eng


Unique ID: 95030026


Country: China,Nei Menggu
Abstract journal details: 2T09604Language: ChOther info: 8 ref.
Authors affiliation: Central Hospital of Forestry Industry, Greater Xing-An
Mountains, Nei Menggu, 022150, China.CABICODES: VV200


Abstract:
A serological survey to detect antibodies against Borrelia burgdorferi was
carried out in 134 cases of schizophrenia and 90 normal control subjects by IFA
in Nei Menggu, China. The results revealed that positive antibody detection was
38.9% in schizophrenics, much higher than in the control group, and
spirochaetes were isolated from a patient with schizophrenia. This indicated
that B. burgdorferi may be an aetiologic agent of schizophrenia (chronic
neurologic manifestations).Descriptors:
Lyme disease,antibodies,Borrelia burgdorferi,serological surveys,man,human
diseases,schizophrenia,nervous system diseasesAbstract no: 990500358
http://neurotalk.psychcentral.com/thread35017.html

wonderfullife
01-10-2011, 10:42 PM
Hyperbaric Oxygen Therapy Lyme Disease Part 1 - YouTube

wonderfullife
02-10-2011, 12:44 AM
Lyme Disease Destroys The Mind - YouTube

wonderfullife
02-10-2011, 07:54 PM
http://naturalnews.tv/v.asp?v=13EAAF22CDA367BB3C2F94D2CD90EF7B

wonderfullife
02-10-2011, 08:11 PM
(NaturalNews) One of the most prominent vaccine scientists in the history of the vaccine industry -- a Merck scientist -- made a recording where he openly admits that vaccines given to Americans were contaminated with leukemia and cancer viruses. In response, his colleagues (who are also recorded here) break out into laughter and seem to think it's hilarious. They then suggest that because these vaccines are first tested in Russia, they will help the U.S. win the Olympics because the Russian athletes will all be "loaded down with tumors." (Thus, they knew these vaccines caused cancer in humans.)

This isn't some conspiracy theory -- these are the words of a top Merck scientist who probably had no idea that his recording would be widely reviewed across the internet (which didn't even exist when he made this recording). He probably thought this would remain a secret forever. When asked why this didn't get out to the press, he replied "Obviously you don't go out, this is a scientific affair within the scientific community."

In other words, vaccine scientists cover for vaccine scientists. They keep all their dirty secrets within their own circle of silence and don't reveal the truth about the contamination of their vaccines.

You can hear this interview at:
http://naturalnews.tv/v.asp?v=13EAA...

Here is the full transcript. (Thanks are due to Dr. Len Horowitz for finding this recording and making it publicly available.)

Transcript of audio interview with Dr. Maurice Hilleman
Dr. Len Horowitz: Listen now to the voice of the worlds leading vaccine expert Dr Maurice Hilleman, Chief of the Merck Pharmaceutical Company's vaccine division relay this problem he was having with imported monkeys. He best explains the origin of AIDS, but what you are about to hear was cut from any public disclosures.

Dr Maurice Hilleman: and I think that vaccines have to be considered the bargain basement technology for the 20th century.

Narrator: 50 years ago when Maurice Hilleman was a high school student in Miles City Montana, he hoped he might qualify as a management trainee for the local JC Penney's store. Instead he went on to pioneer more breakthroughs in vaccine research and development than anyone in the history of American medicine. Among the discoveries he made at Merck, are vaccines for mumps, rubella and measles…

Dr Edward Shorter: Tell me how you found SV40 and the polio vaccine.

Dr Maurice Hilleman: Well, that was at Merck. Yeah, I came to Merck. And uh, I was going to develop vaccines. And we had wild viruses in those days. You remember the wild monkey kidney viruses and so forth? And I finally after 6 months gave up and said that you cannot develop vaccines with these damn monkeys, we're finished and if I can't do something I'm going to quit, I'm not going to try it. So I went down to see Bill Mann at the zoo in Washington DC and I told Bill Mann, I said "look, I got a problem and I don't know what the hell to do." Bill Mann is a real bright guy. I said that these lousy monkeys are picking it up while being stored in the airports in transit, loading, off loading. He said, very simply, you go ahead and get your monkeys out of West Africa and get the African Green, bring them into Madrid unload them there, there is no other traffic there for animals, fly them into Philadelphia and pick them up. Or fly them into New York and pick them up, right off the airplane. So we brought African Greens in and I didn't know we were importing the AIDS virus at the time.

Miscellaneous background voices:…(laughter)… it was you who introduced the AIDS virus into the country. Now we know! (laughter) This is the real story! (laughter) What Merck won't do to develop a vaccine! (laughter)

Dr Maurice Hilleman: So what he did, he brought in, I mean we brought in those monkeys, I only had those and this was the solution because those monkeys didn't have the wild viruses but we…

Dr Edward Shorter: Wait, why didn't the greens have the wild viruses since they came from Africa?

Dr Maurice Hilleman: …because they weren't, they weren't, they weren't being infected in these group holding things with all the other 40 different viruses…

Dr Edward Shorter: but they had the ones that they brought from the jungle though...

Dr Maurice Hilleman: …yeah, they had those, but those were relatively few what you do you have a gang housing you're going to have an epidemic transmission of infection in a confined space. So anyway, the greens came in and now we have these and were taking our stocks to clean them up and god now I'm discovering new viruses. So, I said Judas Priest. Well I got an invitation from the Sister Kinney Foundation which was the opposing foundation when it was the live virus…

Dr Edward Shorter: Ah, right…

Dr Maurice Hilleman: Yeah, they had jumped on the Sabin's band wagon and they had asked me to come down and give a talk at the Sister Kinney Foundation meeting and I saw it was an international meeting and god, what am I going to talk about? I know what I'm going to do, I'm going to talk about the detection of non detectable viruses as a topic.

Dr Albert Sabin …there were those who didn't want a live virus vaccine… (unintelligible) …concentrated all its efforts on getting more and more people to use the killed virus vaccine, while they were supporting me for research on the live viruses.

Dr Maurice Hilleman: So now I got to have something (laughter), you know that going to attract attention. And gee, I thought that damn SV40, I mean that damn vaculating agent that we have, I'm just going to pick that particular one, that virus has got to be in vaccines, it's got to be in the Sabin's vaccines so I quick tested it (laughter) and sure enough it was in there.

Dr Edward Shorter: I'll be damned

Dr Maurice Hilleman: … And so now…

Dr Edward Shorter: …so you just took stocks of Sabin's vaccines off the shelf here at Merck…

Dr Maurice Hilleman: …yeah, well it had been made, it was made at Merck…

Dr Edward Shorter: You were making it for Sabin at this point?

Dr Maurice Hilleman: …Yeah, it was made before I came…

Dr Edward Shorter: yeah, but at this point Sabin is still just doing massive field trials…

Dr Maurice Hilleman: …uh huh

Dr Edward Shorter: okay,

Dr Maurice Hilleman: …in Russia and so forth. So I go down and I talked about the detection of non detectable viruses and told Albert, I said listen Albert you know you and I are good friends but I'm going to go down there and you're going to get upset. I'm going to talk about the virus that it's in your vaccine. You're going to get rid of the virus, don't worry about it, you're going to get rid of it… but umm, so of course Albert was very upset...

Dr Edward Shorter: What did he say?

Dr Maurice Hilleman: …well he said basically, that this is just another obfuscation that's going to upset vaccines. I said well you know, you're absolutely right, but we have a new era here we have a new era of the detection and the important thing is to get rid of these viruses.

Dr Edward Shorter: Why would he call it an obfuscation if it was a virus that was contaminating the vaccine?

Dr Maurice Hilleman: …well there are 40 different viruses in these vaccines anyway that we were inactivating and uh,

Dr Edward Shorter: but you weren't inactivating his though…

Dr Maurice Hilleman: …no that's right, but yellow fever vaccine had leukemia virus in it and you know this was in the days of very crude science. So anyway I went down and talked to him and said well, why are you concerned about it? Well I said "I'll tell you what, I have a feeling in my bones that this virus is different, I don't know why to tell you this but I …(unintelligible) …I just think this virus will have some long term effects." And he said what? And I said "cancer". (laughter) I said Albert, you probably think I'm nuts, but I just have that feeling. Well in the mean time we had taken this virus and put it into monkeys and into hamsters. So we had this meeting and that was sort of the topic of the day and the jokes that were going around was that "gee, we would win the Olympics because the Russians would all be loaded down with tumors." (laughter) This was where the vaccine was being tested, this was where… so, uhh, and it really destroyed the meeting and it was sort of the topic. Well anyway…

Dr Edward Shorter: Was this the physicians… (unintelligible) …meeting in New York?

Dr Maurice Hilleman …well no, this was at Sister Kinney…

Dr Edward Shorter: Sister Kinney, right…

Dr Maurice Hilleman: …and Del Becco (sp) got up and he foresaw problems with these kinds of agents.

Dr Edward Shorter: Why didn't this get out into the press?

Dr Maurice Hilleman: …well, I guess it did I don't remember. We had no press release on it. Obviously you don't go out, this is a scientific affair within the scientific community…

Voice of news reporter: …an historic victory over a dread disease is dramatically unfolded at the U of Michigan. Here scientists usher in a new medical age with the monumental reports that prove that the Salk vaccine against crippling polio to be a sensational success. It's a day of triumph for 40 year old Dr. Jonas E Salk developer of the vaccine. He arrives here with Basil O'Connor the head of the National Foundation for Infantile Paralysis that financed the tests. Hundreds of reporters and scientists gathered from all over the nation gathered for the momentous announcement….

Dr Albert Sabin: …it was too much of a show, it was too much Hollywood. There was too much exaggeration and the impression in 1957 that was, no in 1954 that was given was that the problem had been solved , polio had been conquered.

Dr Maurice Hilleman: …but, anyway we knew it was in our seed stock from making vaccines. That virus you see, is one in 10,000 particles is not an activated… (unintelligible) …it was good science at the time because that was what you did. You didn't worry about these wild viruses.

Dr Edward Shorter: So you discovered, it wasn't being inactivated in the Salk vaccine?

Dr Maurice Hilleman: …Right. So then the next thing you know is, 3, 4 weeks after that we found that there were tumors popping up on these hamsters.

Dr. Len Horowitz: Despite AIDS and Leukemia suddenly becoming pandemic from "wild viruses" Hilleman said, this was "good science" at that time.

NaturalNews wishes to thank Dr. Len Horowitz for uncovering this interview from the national archives, and for getting it released so the public can learn the truth behind the deadly vaccine industry.



Learn more: http://www.naturalnews.com/033584_Dr_Maurice_Hilleman_SV40.html#ixzz1ZeVoG8rr

wonderfullife
03-10-2011, 12:19 AM
I am on session 7 and boy there is a diffrence!

I am more mobile more energy mood better brain function better.

If you do have Lyme or BB why not try it out?

I shall see how I am tommorow because Sunday is my longest working day and i was getting to the point where I was going to give up work because i just was not coping.

BTW always buy your own mask which you can buy at the centre because i got infected with a cold so now i have my own mask.

Well I finshed work at 11pm tonight (Sunday) and it was a very busy day at that.
I am amazed at the diffrence wow! I wasn't extremly tired I was able to finish work on a high note rather than a low i.e deppressed sleepy etc.
pain is very minimal yes i would recommend oxygen therapy.

wonderfullife
05-10-2011, 05:08 PM
Abstract

ABSTRACT: A 90-year-old woman presented with subacute painless left ptosis. Examination of the left eye revealed ptosis with loss of the superior eyelid sulcus, 2 mm of proptosis, mild tenderness with retropulsion, and optic disc edema. Levator function and extraocular movements were normal, and there was no relative afferent pupillary defect. MRI demonstrated thickening of the extraocular muscles in the left orbit with lacrimal gland enlargement and mild enhancement of the optic nerve sheath. Serology revealed a positive enzyme-linked immunosorbent assay for Lyme antibodies and a positive Western blot of Lyme IgG titer. The patient recalled a tick bite 6 months earlier, at which time Lyme serologies were negative. After 3 weeks of intravenous ceftriaxone, she had a significant improvement and a full recovery by 3 months. Lyme disease should be included in the differential diagnosis of orbital inflammation, especially in Lyme-endemic areas

http://www.ncbi.nlm.nih.gov/pubmed/21956017

wonderfullife
05-10-2011, 05:09 PM
Cat Scratch Neuroretinitis: The Role of Acute and Convalescent Titers for Diagnosis.

Gulati A, Yalamanchili S, Golnik KC, Lee AG.


Source

Department of Ophthalmology, The Methodist Hospital (AGL), Houston, Texas Departments of Ophthalmology, Neurology, and Neurosurgery, Weill Cornell Medical College (AGL, SY), New York, New York Department of Ophthalmology, University of Iowa Hospitals and Clinics (AGL), Iowa City, Iowa Department of Ophthalmology, University of Texas Medical Branch (AGL), Galveston, Texas Baylor College of Medicine (AG, AGL) Department of Ophthalmology, University of Cincinnati (KCG), Cincinnati, Ohio.


Abstract

ABSTRACT: Cat scratch neuroretinitis (CSN) is a clinical diagnosis supported by serological testing. We present 2 cases of CSN in which initial acute titers were negative or equivocal for Bartonella henselae while convalescent titers were shown to be positive. We report these cases to emphasize that a single acute negative titer is insufficient to exclude the diagnosis of CSN and that convalescent titers should be obtained in patients for whom there is a high clinical suspicion of the disease.


PMID: 21941214 [PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/21941214

wonderfullife
05-10-2011, 05:12 PM
HOUSTON (KTRK) -- Lyme disease is an infection spread by tick bites. It's curable when it's caught early, but when it's not, that's when the treatment becomes controversial.
Sharon Abercia runs Au Bon Pain, her family's restaurant. It's a long way from her life when Lyme disease made her an invalid.

"I was bedridden for almost a year," she said.

It started with flu-like symptoms.

"The next morning, I got up and I had bells palsy all on the right side of my body. I went to the doctor and they said maybe I had a stroke, and I met someone who asked me if I had ever been bit by a tick," Abercia said.

She had. Lyme infection is transmitted by the deer tick. In Texas, the Lone Star tick can cause Lyme-like symptoms.

Lyme causes a red bull's eye-like rash and symptoms of fatigue, chills, fever, headache, and muscle and joint aches.

Untreated, the Center for Disease Control and Prevention says, Lyme can cause facial palsy, spinal cord inflammation, joint pain, and heart palpitations. There is no doubt Lyme disease can be devastating. It's the treatment that has become controversial.

It's the topic of documentaries like "Under Our Skin," and the question, if patients who don't get better on the first round of antibiotics, should they keep taking them?

Abercia took IV antibiotics for three years.

"I'm here to tell you that if he hadn't given me that, Christi, I'd probably be dead or I'd be in a wheelchair for sure," she said.

"Longer courses of antibiotics have been studied, they don't help," said Dr. Charles Ericsson, head of UTHealth Infectious Diseases department.

Today, most doctors only give antibiotics for a few weeks and only if you test positive. At UT Houston medical school, researchers developed a blood test to accurately diagnose Lyme within hours.

"Today there are 13 companies that use this protein that we found for the diagnosis of Lyme disease," said Dr. Steven Norris, who developed a Lyme disease test.

If the blood test is negative...

"Something else is probably going on and that's what you need to diagnose," Dr. Ericsson said.

But doctors and patients agree on one thing: if you get a tick bite with a bulls eye rash...

"Get on six weeks of IV treatment and then you'll knock it out and you'll never have to worry," Abercia said.

The CDC reports that 10 to 20 percent of Lyme disease patients continue to have symptoms years later.

The local chapter of the Texas Lyme Disease Association meets 3-5pm the second Saturday of each month at the Kindred Hospital cafeteria, 11297 Fallbrook. Call 281-517-1000 or visit www.txlda.org for more information.




(Copyright ©2011 KTRK-TV/DT. All Rights Reserved.)



http://abclocal.go.com/ktrk/story?section=news/health&id=8377098

wonderfullife
05-10-2011, 05:18 PM
Breaking news. The entire WPI research program has been closed by the institute's CEO, and the facility is now locked down. It's former principle investigator, Dr. Judy Mikovits, is in active discussions concerning institutions to which she may move to continue her grant-funded research. The institutions must remain unidentified, for obvious reasons, but it’s important for patients to know that she remains committed to continuing this critical work.

So now, on top of everything else, a divorce at the WPI. Yet to come are all the things that can happen in such messy situations. Meanwhile, there is no Mikovits-led research at the WPI or any research institution at the moment. An enormous loss of possibility. I've done a lot of soul searching about whether to write this blog or not. My motivation for writing all along has been to make things better, to inform, alleviate isolation, share ideas that I hoped would be useful. This is different. Writing this entry, I feel like I'll be taking away hope, which is anathema to me. But at this time, withholding the information I have would be dishonest. I don't know what else to do, except tell it the way I see it.


Here is the reality and the context for why I write this particular blog entry: My email inbox is filled with so much pain and confusion, as patients try to figure out what the BWG study means to them. I feel it is my obligation to both these patients and the larger community to share my opinions. I think what the BWG results mean is that all the XMRV/HGRV testing done at VIP Dx has been and is now null and void. Keep in mind that Dr. Mikovits works at the WPI research lab, which is a separate lab from the clinical, commercially-oriented VIP Dx lab. She believes that she has reproduced her original work many times and found evidence of infection in the patients who were previously found XMRV positive. But she never found any single patient positive on every date tested by every assay. So there has been an assumption that there were false negatives in the WPI research lab for some time. Another important thing to keep in mind is that WPI routinely used several tests on each sample, whereas VIP Dx used different, more limited testing, on the samples they received, testing that apparently was never truly validated against WPI methods or performed with appropriate controls. I personally don't know why this was the case or how it happened. Obviously the decision to sell a test was a very poor one, hindsight being 20/20. It left the institute with a difficult conflict of interest.


I have watched this whole thing unfold and kept quiet because I hoped that management at the WPI would come to their senses, before it was too late. They have not, so I now feel obligated to share what I know.


Dr. Mikovits is a personal friend of mine. We've spent time together in Reno. We were excited about our collaboration. We still speak and email regularly. Because I know her so well, I can tell you first hand that she never thinks of or spares herself, and instead gives her all to the research and the patients who need it so badly. She has been criticized for the unorthodox step she took of allowing patients to gain access to her, a step that was life-saving for some, though it turned her into the ME/CFS hotline.


In terms of the BWG: I was told that the BWG specimens were being run in both the WPI research lab and the VIP Dx clinical lab. Though the labs were kept separate, and cooperation between the two labs was already very troubled, Dr. Mikovits believed that VIP Dx would succeed, and everything would be doubly validated.


When the results of the BWG were uncoded and revealed to all nine labs (but not yet made public), in early August, WPI was left in a bad place. Dr. Mikovits says that at that time she asked WPI management to stop offering the XMRV test at VIP Dx. But the testing was not stopped. Why?


Then, when the BWG results were finally made public on September 22, Dr. Mikovits was quoted as saying, "VIPdx lab will NOT continue XMRV-testing because it hasn't been shown to be reproducible in [the] BloodWorkingGroup". Shortly after she said this, cooperation between the two labs ceased completely and the research lab was closed. Why?


It is important to know that Dr. Mikovits stands by her work at the WPI research lab, which is all she can vouch for. She cannot account for what happened at VIP Dx. It was in a different location, under different leadership: Dr. Lombardi was in charge at VIP Dx.


Now it appears the WPI research program is getting thrown under the bus, but VIP Dx is still up and running, now minus XMRV testing. None of this means that we don't have HGRV's, or that some of the work that came out of the Mikovits-led research lab wasn't correct. What it does mean is that there is no validated test for clinical, commercial use. And it means we are now at risk of losing all the gains we've made because of poor managerial decisions.


My next blog will be to repost Dr. Mikovits' slides from Ottawa, this time with her comments and a summary from me, making the case for HGRV's. Culture contamination with VP62 doesn't explain away her findings. She was finding variants of XMRV. The serology test used in the BWG and published in Lombardi et al is picking up something that is at least very close to, if not antibodies to, MLV proteins. Someone needs to find out what those proteins are. There were electron micrographs from patients showing retroviruses. Pictures. Frank Ruscetti has been studying retroviruses since the beginning of the field and he believes he has been looking at something real. And there have been clinical responses to antiretrovirals, including ours, that are hard to explain away, other than that they are doing what they are supposed to do, inhibiting the replication of retroviruses. Please read Dr. Snyderman's posts and comments again: A Reason For Hope.


As sometimes happens with divorce, we now find ourselves in a position where we have to take sides. The science, not the institution, is the child that must be protected somehow in the ensuing custody fight.


For the record. As we descend back into darkness... I wrote the below text a few weeks ago, but didn't post it. I have confronted these issues directly with WPI management and not gotten an adequate response.
http://treatingxmrv.blogspot.com/2011/10/square-one.html

wonderfullife
05-10-2011, 05:19 PM
Nervous system Lyme disease: is there a controversy?

Halperin JJ

Semin Neurol 2011 07; 31 (3): 317-24

Infection with the tick-borne spirochete, BORRELIA BURGDORFERI, affects
the nervous system in well-defined ways. Accurate diagnostic tools and
effective therapeutic regimens are now well established. Persistent
misconceptions about (1) the role and interpretation of laboratory
tests, (2) what is and is not evidence of nervous system infection, and
(3) what constitutes an expected response to treatment have fostered
widespread perceptions that this disease is highly controversial.
Infection causes the classically described triad of meningitis,
radiculoneuritis, and cranial neuritis; however, virtually every known
neurologic disorder has been blamed on this infection. For most
(multiple sclerosis, amyotrophic lateral sclerosis, Alzheimer disease,
Parkinson disease), evidence is scant, nonexistent, or coincidental. For
some (cerebral vasculitis with stroke, optic neuritis) a few case
reports suggest a rare possible causal link.

wonderfullife
05-10-2011, 05:31 PM
In 2009 prior to the IDSA hearing, CALDA wanted patient voices to be heard and conducted a survey that drew over 4,000 responses. It ended up being the largest survey of Lyme patients ever conducted in the United States. Today, the results of this survey were published in Health Policy in a study by Johnson, Aylward and Stricker. Health Policy is a highly regarded peer-reviewed journal that explores health policy issues. This survey focused on 2,424 respondents whose clinical diagnosis was supported by positive test results. The study examines problems with access to healthcare and burden of illness, and it found that although patients with Lyme disease suffered a substantial burden of illness, they had significant barriers to healthcare access. Specifically, patients with Lyme disease had difficulty obtaining diagnosis and treatment for their illness, traveled great distances to receive healthcare, were turned down for health insurance based on their illness, and had difficulty receiving care at local hospitals.

The burden of illness of these patients was substantial: Roughly 26% had been on disability, with a majority receiving support for more than 2 years. Over half had visited an emergency room as a result of their illness, 15% had done so three to five times, and 9% had done so six or more times. These findings indicate that Lyme patients have significant delays in diagnosis and that there is a critical need for healthcare reform in order to reduce the burden of illness and improve access to medical care for Lyme disease.

The study concludes:

“An influential medical society considers Lyme disease to be “rare” and has issued restrictive treatment guidelines. Our study raises concerns that these restrictions lead to delayed and inadequate treatment of patients with Lyme disease, resulting in concomitant reductions in health benefits and increases in economic costs. Our findings therefore indicate that there is substantial need for reform of the healthcare approach to Lyme disease in the United States.”

Access to healthcare:

More than half of patients saw 7 or more physicians to obtain a diagnosis; over a third saw 10 or more physicians.

Nearly half of these Lyme patients had traveled over 50 miles to receive healthcare; 30% had traveled more than 100 miles; and 9% had traveled over 500 miles.(Travel distances of 30 miles or more are considered to impose a high healthcare access burden on a patient.)

Roughly 40% had sought services at their local hospital, and approximately 82% of these Lyme patients had difficulty obtaining care.

Of those who applied for health insurance after being diagnosed with Lyme disease 40% were denied coverage because of their prior diagnosis.

13% of those with medical insurance were told to see an infectious disease specialist in order to obtain medical reimbursement for medical costs.

31% of those responding had applied for disability insurance and 39% of these had been denied benefits based on failure to conform to Infectious Diseases Society of America (IDSA) guidelines.

Burden of Illness:

25% had received disability or public support, with a majority receiving support for two or more years; 37% for more than 5 years.

39% of those who applied for disability benefits were denied support based on IDSA guidelines.

Study Population:

Patients had been ill a long time. 95% had had Lyme disease for more than 2 years.

95% had received at least 21 days of antibiotics and reported chronic symptoms of 6 months or more.

Centers for Disease Control (CDC) versus other testing results: Patients were clinically diagnosed with supporting lab tests. The diagnosis of 1,000 patients was confirmed by CDC two-tiered criteria or CDC Western blot criteria, while the diagnosis of 1,424 patients was confirmed by other lab methods (including positive PCR, cerebrospinal fluid tests, or positive ELISA or Western blots interpreted using non-CDC criteria). Aside from delay in diagnosis, there were no significant differences in the patients whose diagnosis was confirmed with tests meeting CDC surveillance criteria and those whose supporting tests did not meet CDC criteria. Those without CDC-based positive tests saw more physicians before they were diagnosed.
http://www.lymedisease.org/news/lymepolicywonk/750.html

wonderfullife
05-10-2011, 05:36 PM
Retrospective evaluation of laboratory data on canine vector-borne
infections from the years 2004-2008.

Röhrig E, Hamel D, Pfister K

Berl. Munch. Tierarztl. Wochenschr. 2011 09; 124 (9-10): 411-8

The detection and therapy of canine vector-borne diseases in imported
dogs are of major importance in small animal practice. Over the last
years, the import of dogs from the Mediterranean region and Southeast
Europe has increased, countries often endemic for a variety of
vector-borne diseases such as babesiosis, hepatozoonosis, leishmaniosis,
dirofilariosis or ehrlichiosis. This retrospective study presents the
evaluation of data from our diagnostic laboratory on vector-borne
infections in imported dogs from the years 2004-2008. Specific
antibodies were detectable in 20.5% of all samples with individual
detection rates of 8.9%, 9.6% and 10.8% for Babesia canis ssp.,
Leishmania spp. and/or Ehrlichia canis. A total of 5.5% of all samples
tested by direct methods were positive. Up to 1.1% of Giemsa-stained
blood/buffy coat smears were positive for B. canis ssp., Rickettsia spp.
or Hepatozoon spp. Microfilariae were detectable by the Knott's Test in
6.4% and heartworm antigen w as detectable using the DiroChek-ELISA in
3% of the examined samples. EDTA-blood samples were positive for
Leishmania spp.-(14.9%), E. canis- (5.3%) and A. phagocytophilum-DNA
(5.0%) by PCR. Therewith, imported dogs have a high chance of being
carriers of pathogens. As some diseases may also be of a zoonotic
concern, in case of the availability of competent vectors, the key focus
in the future should be aimed at the prevention of importing infected
dogs or at compulsory diagnostic screening and treatment of infected
dogs at the time of import.

wonderfullife
05-10-2011, 05:39 PM
Hamel D, Silaghi C, Lescai D, Pfister K

Parasitol Res 2011 09 27

Canine arthropod-borne infections are of major interest in small animal
practice and have been widely investigated in Central and Western
Europe. However, only limited epidemiological data are available from
South-Eastern European countries, although diseases including babesiosis
or dirofilariosis are widely recognised as important canine infections
in these countries. A steadily increasing number of dogs imported from
South-Eastern Europe into Germany require particular attention by small
animal practitioners. In this study, a total of 216 dogs [29 local
Romanian pet dogs presented at Salvavet Veterinary Clinic in Bucharest,
Romania, and 187 imported stray dogs from Romania (n = 109) and Hungary
(n = 78) into Germany] were screened by molecular biological,
serological and haematological methods for canine arthropod-borne
infections. Eleven different parasitic and bacterial vector-borne
pathogens-Babesia canis canis, Babesia canis vogeli, Babesia gibsoni,
Babesia fe lis-like, Hepatozoon canis, Leishmania spp., Dirofilaria
immitis, Dirofilaria repens, Acanthocheilonema reconditum, Anaplasma
phagocytophilum and Mycoplasma haemocanis-were detected. Fifty-six
percent of the dogs were positive by direct methods. B. canis canis was
the most prevalent pathogen in dogs imported to Germany (42.8%) and dogs
submitted for clinical consultation in Bucharest (44.8%). Our data
strongly suggest the introduction of an adjusted screening panel in dogs
from South-East Europe in view of increasing importation of dogs into
Germany.

wonderfullife
05-10-2011, 05:40 PM
Lempereur L, Lebrun M, Cuvelier P, Sépult G, Caron Y, Saegerman C,
Shiels B, Losson B

Parasitol Res 2011 09 27

Anaplasmosis and babesiosis are major tick-borne diseases with a high
economic impact but are also a public health concern. Blood samples
collected in the spring, summer, and autumn of 2010 from 65 cows in
seven different farms in Belgium were monitored with an indirect
immunofluorescence antibody test to assess seroprevalence against these
pathogens. Seroprevalences to Babesia spp. were measured as 10.7%, 20%,
and 12.3% in spring, summer, and autumn, respectively, whereas
seroprevalences to Anaplasma phagocytophilum were 30.8%, 77%, and 56.9%,
respectively. A total of 805 Ixodes ricinus ticks were collected at the
same time from both cattle (feeding ticks) and grazed pastures (questing
ticks). The infection level of ticks, assessed by PCR assay, for Babesia
spp. DNA was 14.6% and 7.9% in feeding and questing ticks, respectively,
whereas 21.7% and 3% of feeding and questing ticks were found be
positive for A. phagocytophilum cDNA. Fifty-five PCR-positive samples
were identified by sequencing as Babesia sp. EU1, of which five from
feeding ticks were positive for both A. phagocytophilum and Babesia sp.
EU1. The high density of wild cervids in the study area could explain
these observations, as deer are considered to be the main hosts for
adults of I. ricinus. However, the absence of Babesia divergens both in
feeding and questing ticks is surprising, as the study area is known to
be endemic for cattle babesiosis. Increasing cervid populations and
comorbidity could play an import role in the epidemiology of these
tick-borne diseases

wonderfullife
05-10-2011, 05:41 PM
Procajło A, Skupień EM, Bladowski M, Lew S

Pol J Vet Sci 2011 09; 14 (3): 515-20

Ehrlichiosis is the multiorgan infectious disease caused by small,
intracellular rickettsias from the genus Ehrlichia. These microorganisms
are known as an etiologic factor of infections world wide in humans and
in different species of animals. Dog ehrlichiosis can be caused by
several species of Ehrlichia attacking different groups of blood cells,
but most often an infection by Ehrlichia canis is diagnosed with special
relation to monocytes. A vector for E. canis are Rhipicephalus
sanguineus and Ixodes ricinus, commonly occurring in Poland. Disease
caused by E. canis is known as Canine Monocytic Ehrlichiosis (CME). The
disease most often has an asymptomatic course which can, in favourable
circumstances, run into acute or chronic forms. The acute form of CME
proceeds usually with fever, apathy, weakness and accompanying
respiratory symptoms, lameness and disturbances in blood coagulation. In
laboratory examinations thrombocytopenia, anemia and leucopenia are
ascertained. Th e chronic form of CME proceeds among gentle, unspecific
symptoms which may last even 5 years. The CME diagnosis is difficult and
often demands parallel different diagnostic methods. A medicines of
choice in the ehrlichiosis treatment are antibiotics from the group of
tetracyclines, given at least for 28 days. They are largely efficient
during treatment of the acute CME, causing the quick improvement.
Instead, in the case of chronic form, answer for treatment can be weak,
and cases of resistance to antibiotics ave known.

wonderfullife
05-10-2011, 05:44 PM
Serological response to Bartonella species in febrile patients from Nepal.

Myint KS, Gibbons RV, Iverson J, Shrestha SK, Pavlin JA,
Mongkolsirichaikul D, Kosoy MY

Trans R Soc Trop Med Hyg 2011 09 26

The Bartonella-associated illnesses are spread world-wide and involve a
broad spectrum of signs and symptoms in humans. Several Bartonella
species have been shown to be responsible for cases of febrile
illnesses. Little information exists on distribution of Bartonella
species and their role in human diseases in Nepal. Our preliminary
study, a retrospective serological survey of archived specimens,
suggests that Bartonella antibodies are prevalent among febrile patients
in the Kathmandu Valley of Nepal.

wonderfullife
05-10-2011, 05:45 PM
Evaluation of skin thickness lesions in patients with Lyme disease
measured by modified Rodnan total skin score.

Moniuszko A, Gińdzieńska-Sieśkiewicz E, Pancewicz SA, Czupryna P,
Zajkowska J, Sierakowski S

Rheumatol Int 2011 09 30

Recently, a possible etiological connection between infection with
Borrelia burgdorferi and various skin lesions, including morphea and
systemic sclerosis (SSc), has been discussed. The aim of our study was
the evaluation of frequency of skin thickening typical of SSc or morphea
in the group of patients with Lyme disease (LD) with frequent exposition
to tick bites. The group consisted of 110 patients with LD frequently
exposed to tick bites form the northeastern Poland, which is an endemic
area for this disease. To measure the skin lesions, the modified Rodnan
total skin score (RTSS) was used. In the analyzed group, no skin changes
typical of morphea or skin thickening were found. According to RTSS, all
patients scored 0 points. Raynaud's phenomenon in all patients was not
found. The relationship between scleroderma or morphea and LD is still a
matter of controversy. Described by some authors, cases with LD and
scleroderma may be associated with co-existence of B. burgdorfe ri
infection with autoimmune process.

wonderfullife
05-10-2011, 05:47 PM
Lyme-Associated Orbital Inflammation Presenting as Painless Subacute
Unilateral Ptosis.

Xu L, Winn BJ, Odel JG

J Neuroophthalmol 2011 09 27

ABSTRACT: A 90-year-old woman presented with subacute painless left
ptosis. Examination of the left eye revealed ptosis with loss of the
superior eyelid sulcus, 2 mm of proptosis, mild tenderness with
retropulsion, and optic disc edema. Levator function and extraocular
movements were normal, and there was no relative afferent pupillary
defect. MRI demonstrated thickening of the extraocular muscles in the
left orbit with lacrimal gland enlargement and mild enhancement of the
optic nerve sheath. Serology revealed a positive enzyme-linked
immunosorbent assay for Lyme antibodies and a positive Western blot of
Lyme IgG titer. The patient recalled a tick bite 6 months earlier, at
which time Lyme serologies were negative. After 3 weeks of intravenous
ceftriaxone, she had a significant improvement and a full recovery by 3
months. Lyme disease should be included in the differential diagnosis of
orbital inflammation, especially in Lyme-endemic areas

wonderfullife
05-10-2011, 06:03 PM
In the 1950s, Willy Burgdorfer, who isolated the tick-vectored Lyme disease spirochete and for whom the causative Borrelia is named,[i] worked on artificially forcing Borrelia disease agents (like relapsing fever Borrelias) to infect new tick vectors. (Burgdorfer then used these artificially infected ticks in attempts to infect lab animals.[ii])



He also published papers describing the "occult infections" due to these relapsing fever spirochete disease agents.[iii] In parallel with these studies, he developed production-like methods for transferring diseases to Ixodid ticks,[iv] the same species that spreads the occult Borrelia infection initially called Lyme disease, which Burgdorfer later compared to the relapsing fever Borrelias he had studied.[v]



The lab he conducted this research in and which later isolated the Lyme spirochete[vi] is now a “biosafety level 4” biowarfare research facility,[vii] just like the biowarfare lab at the epicenter of the Lyme Epidemic (Plum Island Animal Disease Center), which conducted outdoor tick research and is suspected of being the source of the Lyme Epidemic. [viii]



Given the manner in which Lyme disease broke out and the deadly manner in which it has been intentionally mismanaged ever since, hard questions must be asked:



When Burgdorfer was developing techniques to artificially expand the host-range of Borrelias to new tick species, and then to lab animals, was he in fact conducting biological warfare research at the Rocky Mountain Laboratory?


Did this research feed in to the tick research that was conducted at Plum Island Animal Disease Center, the outdoor biowar test facility for such insect vectors? And was Plum Island,the outdoor test facility for Fort Detrick, the center of the U.S. biological warfare effort?


Was the causative agent of Lyme disease later “discovered” by a military epidemiologist as part of a suspected public relations/containment effort to control information about the burgeoning epidemic and its ties to the military?


Did this effort surrounding the so-called "natural" outbreak of a zoonotic agent lead to an experimental vaccine effort (orchestrated by CDC/EIS biowarfare agents) similar to that which happened in Egypt, when human vaccine experiments were conducted after the "natural" outbreak of Rift Valley fever virus, an outbreak that occurred in the same time-frame as the Lyme disease outbreak?


In the time period leading up to the Lyme Epidemic, Burgdorfer worked for the military in a capacity consistent with this hypothesis: He was a member of the Armed Forces Epidemiology Board investigating insect vectored diseases.[ix] The disastrous non-response to the Lyme Epidemic has been orchestrated by military epidemiologists using their influence in the government, medical infrastructure and media. Was Willy Burgdorfer part of this non-response to the devastating disease named after him?



At a time when desperate patients and persecuted doctors need all the information they can get about the true nature of Lyme disease, Willy Burgdorfer has coyly stated, on film, that he hasn’t told us everything he knows about the disease.



What are you hiding Willy?



Why don’t you tell us what you know?



Until you do, you have the Borrelia BURGDORFERi-infected blood of millions on your hands.

https://sites.google.com/site/jerryleonard999/home/burgdorfer

wonderfullife
05-10-2011, 06:13 PM
Careful investigation supports the theory that the epidemic of ignorance and corresponding lack of treatment has been perpetuated by the CDC as part of Phase II of the deadly Tuskegee Experiment.



Even worse, Phase II is being carried out by the CDC with the aid of its secretive biological warfare group. Where the Phase I experiment denied isolated patients from seeing non-CDC-approved doctors,[i] Phase II involves preventing doctors from treating patients (or even providing an accurate diagnosis--recall the Tuskegee diagnosis of syphilis as “bad blood”[ii]) outside of CDC-approved guidelines published by a medical society known as the IDSA (Infectious Disease Society of America), on an international basis.



The CDC’s own history of the Tuskegee Experiment describes how the CDC worked with prominent medical societies to gain support for the multi-decade experiment in medical malpractice:



“1969 CDC reaffirms need for study and gains local medical societies' support (AMA and NMA chapters officially support continuation of study).”



So the national agency that was supposed to be protecting the public from a deadly disease was actually in favor of letting it go untreated for experimental reasons and worked with prestigious medical societies to that end!



Tuskegee Phase II is being conducted in a similar manner, including the direct assistance of prominent medical societies through IDSA treatment guidelines[iii] enforced by CDC insiders, who are regularly found to be on the payroll of the pharmaceuticals and insurance industries--both of which can profit enormously[iv] [v] by not treating the many symptoms[vi] caused by the disease.





“One way drug companies have marketed their products is by funding the implementation of guidelines…”

--Civil Action No. 08 CA 11318 DPW





The CDC has used the non-specificity of Lyme symptoms (except for those fortunate enough to manifest the Bull’s Eye rash at the onset of infection[vii]) as an excuse to mislabel the disease and thereby prevent effective diagnosis and treatment.[viii] [ix] As Dr. Brian Fallon summarized:



“Incorrectly labeling these patients as having a functional illness, such as depression, hypochondriasis or a somatization disorder, may result in a delay in the initiation of antibiotic treatment. Such delay may lead to further dissemination of the infection, and in some cases severe disability and possibly chronic neurologic damage.”



The further dissemination of symptoms is highly profitable for pharmaceutical companies, while treating the root cause of the disease with off-patent antibiotics is not.[x]
https://sites.google.com/site/jerryleonard999/subversion-of-modern-medicine-through-treatment-guidelines/allen-steere-psychopath-at-large

wonderfullife
06-10-2011, 08:51 PM
Study shows Lyme testing has long way to go
by Pam Rogers

Pam Rogers is a senior microbiologist at the Wisconsin State Laboratory of Hygiene (WSLH). She coordinates the WSLH’s proficiency testing program for Lyme disease, as well as the immunoserology and immunoprotein PT programs. She graduated from UW-LaCrosse with a bachelor’s degree in microbiology.

The following is a summary of a new study 1 conducted by Lori Bakken†, Steven Callister, Ph.D.,††, Philip Wand¥ and Ronald Schell, Ph.D.,¥ ¥ which was published in the March 1997 issue of the Journal of Clinical Microbiology. The purpose of the recent study was to determine if the accuracy of Lyme disease tests has improved since 1991.

Data collected in 1991 showed that there was significant inter- and intra-laboratory variation among laboratories that performed tests for Lyme disease. Up to 55 percent of laboratories examined in that study could not identify positive, case-defined, serum samples which contained antibodies to Borrelia burgdorferi. False positive test results on serum samples which were obtained from individuals with no known exposure to B. burgdorferi were reported by two to seven percent of the study participants. This study, published in 1992 in the Journal of the American Medical Association, was the basis for the development of a national Lyme proficiency testing program co-sponsored by the Wisconsin State Laboratory of Hygiene (WSLH) and the College of American Pathologists (CAP).

The recent paper reports that 50 serum samples, 22 from individuals with no history of Lyme borreliosis and 28 from Lyme disease patients, were randomly selected and sent to 516 participant laboratories through the WSLH/CAP Lyme proficiency testing program from 1992 through 1995.

Data obtained indicate that there was no improvement in the serodiagnosis of Lyme disease. Specificity* of tests fell to 81 percent and sensitivity** fluctuated between 75-93 percent (see figures 3 and 4).

Specificity of polyvalent, IgM and IgG conjugate-specific tests for identification of serum samples from healthy donors for 1992 (n=516), 1993 (n=515) and 1994 (n=496) as indicated by the bars from left to right, respectively.

Sensitivity of polyvalent, IgM and IgG conjugate-specific tests for identification of CDC case-defined serum samples for 1992 (n=516), 1993 (n=515) and 1994 (n=496) as indicated by the bars from left to right, respectively.

Since ASTPHLD recommends that Lyme testing be a two-tiered process—testing all samples by EIA, and then testing positive samples with a Western Blot—study data suggests that the current tests are neither sensitive enough nor specific enough to support ASTPHLD’s two-tier approach.

Data collected also demonstrate that the performance of participating laboratorieschanges drastically with the selection of serum samples. Commercially available kits for B. burgdorferi appear to perform well if high levels of antibody are present. Samples chosen because they had high concentration of antibody to B. burgdorferi or samples which were chosen for their lack of interfering or cross-reacting substances were rarely missed. When the levels of anti-B. burgdorferi antibodies were low, the commercially available kits failed to identify as positive sera from patients with Lyme disease.

These clear-cut samples do not reflect the spectrum of patients with Lyme disease or their test results. Although CLIA ‘88 regulations require that proficiency testing programs provide a wide range of challenges, the mechanism needed to evaluate samples (>90 percent consensus among participant labs) does not allow low levels of antibody to be appropriately evaluated. This gives the laboratory a false sense of security since the most difficult samples, which lack participant consensus, are not scored or evaluated.

The paper concludes:

“In conclusion, our results suggest that stronger measures need to be taken by the Food and Drug Administration to control the quality of commercially available Lyme disease assay kits. One solution is to force all currently used or approved assay systems through an evaluation with sera obtained from culture-positive patients. An arbitrary sensitivity of 90% could be selected. The specificity could also be set at 95%. Commercially available tests that did not reach these performance levels would be removed from the market. Although this is a drastic solution, its time has come. This measure would lessen the overdiagnosis of Lyme disease and prevent the use of costly laboratory solutions, like Western immunoblotting, to make a serodiagnosis of Lyme disease.”

Study Author Credits: Departments of †Continuing and Vocational Education, ¥ ¥Medical Microbiology and Immunology , ¥Wisconsin State Laboratory of Hygiene , University of Wisconsin-Madison; ††Microbiology Research Laboratory, Gundersen Medical Foundation, LaCrosse, Wisconsin

Sources

1 Bakken, L.L., S.M. Callister, P.J. Wand, and R.F. Schell. 1997. Interlaboratory Comparison of Test Results for Detection of Lyme Disease by 516 Participants in the Wisconsin State Laboratory of Hygiene/College of American Pathologists Proficiency Testing Program. J. Clin. Microbiol. 35:537-543.

2 Bakken, L.L., K.L. Case, S.M. Callister, N.J. Bourdeau, and R.F. Schell. 1992. Performance of 45 Laboratories Participating in a Proficiency Testing Program for Lyme Disease Serology. JAMA 268:891-895.

--------------------------------------------------------------------------------

Wisconsin State Laboratory of Hygiene Results Summer 1997

Abstract:

In 1991, we reported that 55% of laboratories participating in the Wisconsin Proficiency Testing Program could not accurately identify serum samples from Lyme disease patients containing antibody against Borrelia burgdorferi. The purpose of this study was to determine whether the accuracy of Lyme disease test results reported by approximately 500 participants in the Wisconsin State Laboratory of Hygiene/College of American Pathologists Lyme Disease Survey had improved.

From 1992 through 1994, 50 serum samples were sent to participants of the survey. Each laboratory received 28 serum samples from individuals with Lyme disease according to the case definition of the Centers for Disease Control and Prevention and 22 serum samples from healthy individuals.

Unfortunately, the serodiagnosis of Lyme disease by participants had not improved.

The specificity of the Lyme disease assays steadily decreased from approximately 95% to approximately 81% during the 3-year period of the survey. False-positive test results approached 55% with some of the serum samples from healthy donors. A serum sample containing antibody against Treponema pallidum was reported as positive by 70% of the participants.

In addition, the sensitivity fluctuated between 93 and 75%, depending upon the conjugate used by the laboratories. These results suggest that stronger criteria must be applied for approving and continuing to approve commercially available kits for the serodiagnosis of Lyme disease.

Keywords: Antibodies, Bacterial, BLOOD, Bacteriology, STATISTICS & NUMER DATA, STANDARDS, Borrelia burgdorferi, IMMUNOLOGY, Comparative Study, Data Collection, False Negative Reactions, False Positive Reactions, Human, IgG, BLOOD, IgM, BLOOD, Laboratories, STANDARDS, Lyme Disease, DIAGNOSIS, IMMUNOLOGY, Quality Control, Reference Standards, Sensitivity and Specificity, Serodiagnosis, STATISTICS & NUMER DATA, STANDARDS, Wisconsin
http://www.canlyme.com/516labs.html

wonderfullife
06-10-2011, 08:56 PM
Evolution of antigen variation in the tick-borne pathogen Anaplasma
phagocytophilum.

Rejmanek D, Foley P, Barbet A, Foley J

Mol Biol Evol 2011 09 28

Anaplasma phagocytophilum is an obligately intracellular,
tick-transmitted, bacterial pathogen of humans and other animals. During
the course of infection, A. phagocytophilum utilizes gene conversion to
shuffle ∼100 functional pseudogenes into a single expression cassette of
the msp2(p44) gene, which codes for the major surface antigen, major
surface protein 2 (Msp2). The role and extent of msp2(p44)
recombination, particularly in hosts that only experience acute
infections, is not clear. In the present study, we explored patterns of
recombination and expression of the msp2(p44) gene of A. phagocytophilum
in a serially infected mouse model. Even though the bacterium was passed
rapidly among mice, minimizing the opportunities for the host to develop
adaptive immunity, we detected the emergence of 34 unique msp2(p44)
expression cassette variants. The expression of msp2(p44) pseudogenes
did not follow a consistent pattern among different groups of mice,
although some pseudog enes were expressed more frequently than others.
In addition, among 263 expressed pseudogenes, 3 mosaic sequences each
consisting of 2 different pseudogenes, were identified. Population
genetic analysis showed that genetic diversity and subpopulation
differentiation tended to increase over time until stationarity was
reached but that the variance that was observed in allele (expressed
pseudogene) frequency could occur by drift alone only if a high variance
in bacterial reproduction could be assumed. These findings suggest that
evolutionary forces influencing antigen variation in A. phagocytophilum
may comprise random genetic drift as well as some innate but apparently
non-purifying selection prior to the strong frequency-dependent
selection that occurs cyclically after hosts develop strong adaptive
immunity

wonderfullife
06-10-2011, 08:58 PM
Pediatrics. 2011 Oct 3. [Epub ahead of print]

Ceftriaxone-Induced Hemolysis in a Child With Lyme Arthritis: A Case for
Antimicrobial Stewardship.

Boggs SR, Cunnion KM, Raafat RH.

Children's Hospital of The King's Daughters and Eastern Virginia Medical
School, Norfolk, Virginia.

Abstract

Guidelines for the treatment of Lyme arthritis were published by the
Infectious Diseases Society of America in 2006 and recommended oral
doxycycline for initial therapy. We report here the case of a young girl
treated with intravenous ceftriaxone who subsequently developed
drug-induced autoimmune hemolytic anemia and renal failure. Her severe
sequelae highlight the importance of antimicrobial stewardship. We
review here the goals of antimicrobial stewardship and several
strategies for achieving them. In addition, we briefly discuss the rare
adverse drug event experienced by our patient.

PMID:
21969285
[PubMed - as supplied by publisher]

wonderfullife
06-10-2011, 09:46 PM
Fall 2011- The Lyme Disease Education and Support Groups of Maryland would like to update healthcare providers and the public regarding a newly discovered disease found in ticks that also carry Lyme disease (Borrelia burgdorferi). The inability of commercial tests to detect the new infection is of concern, as is the fact that a curative treatment protocol, if one exists, has yet to be established.

Borrelia miyamotoi, reported in Japan in 1995, causes a prolonged, relapsing bacterial infection in humans that may last for months. The organism has been detected in ticks, animals and humans across the United States, especially along the Atlantic flyways, and seven different countries, including Canada. US researchers report Borrelia miyamotoi was seen frequently in ticks carrying Lyme disease, and the presence of multiple genotypes of Lyme disease (Borrelia burgdorferi), even in the same tick, were also noted.

Similar to Lyme disease, Borrelia miyamotoi is characterized by a flu-like illness, headache, chills, fatigue, vomiting, myalgias, neck stiffness, and a high fever. Only 9% of study participants reported a rash. Additional symptoms can include ocular, neurologic, respiratory, cardiac, and pregnancy complications associated with relapsing fevers.

As the fall hunting season approaches, it is important to note the University of Tennessee reported 58% of the turkeys harvested in 2009 tested positive for B. miyamotoi, with a higher percentage of organisms detected in tissue than blood. Fisheries and Wildlife at University of Michigan have also detected the organism it its wildlife. Borrelia miyamotoi has also been found in NY, RI, NJ, CT, and CA. The responsible bacteria appear to be readily passed between generations of ticks, without requiring deer as hosts to sustain its life cycle.

Researchers in the United States report it is possible that “some prolonged episodes of illness attributed to Lyme disease and designated as "chronic Lyme disease" are due to B. miyamotoi infection.” Patients may remain undiagnosed because the disease can, like Lyme disease, be confused with any number of illnesses (MS, Parkinson’s, ALS, fibromyalgia, Alzheimer’s, autoimmune diseases, heart disease, etc), including infections caused by any of the 300+ known strains of Borrelia that may or may not cause serious human or animal disease.

The number of identifiable vector-borne pathogens is steadily increasing, however, many of the resulting diseases are undetectable, as there are currently no commercial tests available. Various species, strains and genotypes of Anaplasmosis, Ehrlichiosis, Bartonellosis, Q-fever, Southern Tick Associated Rash Illness (STARI- Borrelia lonestari), viral infections, Tularemia, Brucellosis, Parvo B-19, and Rocky Mountain Spotted Fever (RMSF) have been detected in patients, pets and wildlife in Maryland, with a growing number of patients being found to be multiply coinfected.

A new RMSF-like organism, Rickettesia amblyommii, was discovered in Maryland ticks (2008) by US Army researchers at Aberdeen Proving Ground. Cases of Babesiosis, responsible for a growing number of blood-transfusion deaths, is caused by Babesia microti and what was once thought to be a “west-coast” strain of Babesia (Babesia duncani). Both are increasing in Maryland.

For more information on tick & vector borne diseases, please visit www.MarylandLyme.org Contact Person: Lucy Barnes, Lyme Disease Education and Support Groups of Maryland.

Email- [email protected] Website- www.MarylandLyme.org

https://sites.google.com/site/getitrighttreatthebite/health-alert

wonderfullife
06-10-2011, 10:13 PM
Transfusion-Associated Babesiosis in the United States: A Description of Cases

Barbara L. Herwaldt, MD, MPH;
Jeanne V. Linden, MD, MPH;
Elizabeth Bosserman, MPH;
Carolyn Young, MD;
Danuta Olkowska, MD; and
Marianna Wilson, MS

+ Author Affiliations

From the Centers for Disease Control and Prevention, Atlanta, Georgia; New York State Department of Health, Wadsworth Center, Albany, New York; and Rhode Island Blood Center, Providence, Rhode Island.





Next Section
Abstract


Background: Babesiosis is a potentially life-threatening disease caused by intraerythrocytic parasites, which usually are tickborne but also are transmissible by transfusion. Tickborne transmission of Babesia microti mainly occurs in 7 states in the Northeast and the upper Midwest of the United States. No Babesia test for screening blood donors has been licensed.


Objective: To ascertain and summarize data on U.S. transfusion-associated Babesia cases identified since the first described case in 1979.


Design: Case series.


Setting: United States.


Patients: Case-patients were transfused during 1979–2009 and had posttransfusion Babesia infection diagnosed by 2010, without reported evidence that another transmission route was more likely than transfusion. Implicated donors had laboratory evidence of infection. Potential cases were excluded if all pertinent donors tested negative.


Measurements: Distributions of ascertained cases according to Babesia species and period and state of transfusion.


Results: 159 B. microti transfusion-associated cases were included; donors were implicated for 136 (86%). The case-patients' median age was 65 years (range, <1 to 94 years). Most cases were associated with red blood cell components; 4 were linked to whole blood–derived platelets. Cases occurred in all 4 seasons and in 22 (of 31) years, but 77% (122 cases) occurred during 2000–2009. Cases occurred in 19 states, but 87% (138 cases) were in the 7 main B. microti–endemic states. In addition, 3 B. duncani cases were documented in western states.


Limitation: The extent to which cases were not diagnosed, investigated, reported, or ascertained is unknown.


Conclusion: Donor-screening strategies that mitigate the risk for transfusion transmission are needed. Babesiosis should be included in the differential diagnosis of unexplained posttransfusion hemolytic anemia or fever, regardless of the season or U.S. region.
http://www.annals.org/content/early/...180-00362.full

wonderfullife
08-10-2011, 07:32 PM
Bouvresse S, Socolovshi C, Berdjane Z, Durand R, Izri A, Raoult D,
Chosidow O, Brouqui P

Comp Immunol Microbiol Infect Dis 2011 10 3

The human body louse is the only known vector of Bartonella quintana.
However, the presence of this bacterium has recently been detected in
the head lice of homeless individuals and Nepalese slum children.
Previous studies have reported the isolation of Acinetobacter baumannii
from the body lice of homeless individuals. An epidemiological survey
including 74 schools was conducted between 2008 and 2009 in Paris. After
a first visual examination, the hair of children with suspected
pediculosis was combed with a fine-tooth comb to collect live adult head
lice. Molecular studies were performed on randomly selected DNA samples
to detect B. quintana and A. baumannii by specific quantitative
real-time PCR. Among a collection of 288 DNA samples, B. quintana was
not detected, but A. baumannii was detected in 95 DNA samples (33%).
Further study is needed to determine the significance of the finding of
A. baumannii in head lice.

wonderfullife
08-10-2011, 07:37 PM
Fritzen CM, Huang J, Westby K, Freye JD, Dunlap B, Yabsley MJ,
Schardein M, Dunn JR, Jones TF, Moncayo AC

Am. J. Trop. Med. Hyg. 2011 10; 85 (4): 718-23

Abstract. Rocky Mountain spotted fever, Lyme disease, and ehrlichiosis
are tick-borne diseases that are reported annually in Kentucky. We
conducted a survey to describe infection prevalence of tick-borne
pathogens in Amblyomma americanum and Dermacentor variabilis ticks
collected in Kentucky. During 2007-2008, we collected 287 ticks (179 D.
variabilis and 108 A. americanum) from canine, feral hog, horse,
raccoon, white-tailed deer, and human hosts in six counties in Kentucky.
Ticks were screened for Rickettsia spp., Borrelia spp., and Ehrlichia
spp. by using polymerase chain reaction. Forty-one (14.3%) ticks (31 A.
americanum and 10 D. variabilis) were polymerase chain reaction-positive
for a Rickettsia spp. Fourteen (4.9%) ticks (6 A. americanum and 8 D.
variabilis) were positive for E. chaffeensis, and 4 A. americanum (1.4%)
were positive for E. ewingii. One (0.4%) A. americanum was positive for
Borrelia lonestari. Although Rocky Mountain spotted fever is diagnosed
in Kentucky, no R. rickettsii was found in ticks in this study.

wonderfullife
08-10-2011, 07:43 PM
Seabirds act as natural reservoirs to Lyme borreliosis spirochetes and may play a significant role in the global circulation of these pathogens. While Borrelia burgdorferi sensu lato (Bbsl) has been shown to occur in ticks collected from certain locations in the North Pacific, little is known about interspecific differences in exposure within the seabird communities of this region. We examined the prevalence of anti-Bbsl antibodies in 805 individuals of nine seabird species breeding across the North Pacific. Seroprevalence varied strongly among species and locations. Murres (Uria spp.) showed the highest antibody prevalence and may play a major role in facilitating Bbsl circulation at a worldwide scale. Other species showed little or no signs of exposure, despite being present in multispecific colonies with seropositive birds. Complex dynamics may be operating in this wide scale, natural host–parasite system, possibly mediated by the host immune system and host specialization of the tick vector.
http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0267

wonderfullife
08-10-2011, 07:48 PM
Misty Brown was a success story, in theory.

After years of misdiagnoses and physicians just throwing up their hands in confusion, she was finally diagnosed with Lyme disease in 2006 — a disease more commonly associated with New England and the Mid-Atlantic region — mere weeks after doctors said she was out of time.

“They took my husband aside and told him, ‘You need to get your wife’s stuff together. She’s not going to make it.’”

She believes she was infected by a tick that bit her as she moved her husband’s hunting equipment while preparing for a garage sale. The two years that followed allowed the disease to ravage her system, leading to heart failure, seizures, vision, balance and speech problems.

“It was ‘check, check, check’ as far as the symptoms, “because Lyme disease has three stages and I was so far into the third stage.”

But she wasn’t too far gone to come back, according to a Lyme disease specialist in Nevada City.

“’I just want you to know,’” Brown recalls him saying, “You’ll be OK. I know they’ve told you that you’re going to die, but you’re going to be OK.”

After a year of aggressive treatment, she was able to walk again, could talk clearly and was back working several days a week at the family hair salon.

“I was like 60 percent better,” she said. After having written letters to her daughter to be read after Brown assumed she’d be dead, that alone was a gift. “I was able to walk my daughter to her first day of kindergarten.”

But the aggressive treatment had a downside.

“Six years of harsh, harsh medication was starting to damage my body,” she said.

Brown’s kidneys and liver were failing.

“When you have Lyme, you have to accept that your life will be (spent on) medication.”

But if her liver and kidneys failed, she might not have much life left. Brown’s vision was going, her hair was falling out and she had lost her sense of smell.

The family found a treatment center — the Hansa Center for Optimum Health in Wichita — that they believed could help undo much of the damage done by her Lyme disease treatment, but it would cost more than they had left, after years of medical struggles.

“Through this process, I had to go so far out of my insurance,” she said. “We lost cars, houses.”

Out at dinner with friends, they mentioned their dilemma and how they were trying to come up with the $10,000 they’d need for the treatment. A few days later, Shelley Keller, the daughter of Boulder Creek Ranch owners Jim and Gail Hasty, called back and said that, after their dinner conversation, the Hasty family wanted to help.

The 2010 Harvest Festival at Boulder Creek raised a total of about $8,000 toward her $10,000 treatment.

“You get well if you have money,” said Brown, who has only recently returned from the Hansa Center, as she and her husband spent a few more months finding the remaining $2,000 they needed. “If you have anything crazy, your insurance won’t cover it.”

Fortunately, the treatment worked, and Brown’s condition started to improve.

“Within the first two days, all the bags and circles (under her eyes) disappeared,” she said. “I could see again. I could smell again. I regained my balance. ... I’m running again. I’m talking again.”

Although her Lyme disease specialist continues to monitor her condition, and she will be making annual pilgrimages back to the Hansa Center, she’s now off her medication and returning to a normal life she thought she’d never have again.

Last year, she held a Lyme Disease Awareness Walk and will be helping run the charity event for a new charity benefiting orphans, at this year’s Harvest Festival.

“In the midst of all the hustle and bustle” at last year’s event, “my life was genuinely changed. ... I just want to thank each and every person who contributed.”

Beau Yarbrough may be reached at (760) 956-7108 or at [email protected] Follow us on Facebook at Facebook.com/Hesperia.Star.

http://www.hesperiastar.com/news/dis...ing-misty.html

wonderfullife
09-10-2011, 02:11 PM
Can't lie to ya. Rough road ahead. In fact, getting well may be about
the hardest and most difficult thing you'll ever do. But it's worth
it! Stick with it! Never give up hope!The first thing you should know is that it gets worse before it gets better. It can in fact get a lot worse before it gets better. Itdepends on how long you've had it, how much of the bacteria has builtup, what strain you have, and many other factors as well.

The Lyme bacteria gives off a chemical toxin when it dies. When the antibiotics start killing them, the toxin levels in your body will soar and the symptoms can become intense. Physical symptoms includepain, numbness, swelling, tremors, and a myriad of others if internalorgans are significantly affected. The toxin affects your mind aswell. Typical symptoms include insomnia, confusion, disorientation,depression, anxiety and panic attacks. These will all go away as youget well!

As if the toxin effects weren't good enough, another fact about theLyme bacteria is that it grows and reproduces slowly. At first thatmay seem a good thing, except that antibiotics are generally able tokill it only during certain stages of it's life cycle. The end resultbeing that it takes a long time to get well. usually months. Therehave been cases of "miracle" cures in just a couple weeks, but theseare rather rare. Just don't give up hope! Keep at it! Keep trying! Ittakes a long time, but being happy and healthy again is worth it!

Of course we'd all probably like to have our mind functioning properly again as the first step in getting well. Unfortunately, that won't happen. Your mind returns last, when just about all the bacteria are dead. Physical symptoms like pain and numbness go first, then the bacteria that didn't cause pain, and then, finally, your
head begins to clear up. This can be very disconcerting when your body feels good but your head is still reeling. Hang in there!
When you first start on effective antibiotics, you'll be in for quite an unpleasant surprise. Within a day or two you'll feel like you've been hit by a fully loaded military cargo jet flying at full
throttle.
Your symptoms, including the ones you didn't even know you had, will flare up intensely. Try hard to tough it out. But if you find that you absolutely positively can't, and this is not too
unusual, ask your doctor about lowering the dosage for a while, or pulsing on and off until you get through the worst of it. Sticking on the medication as prescribed, always taking them right on time, is your best bet for getting through it as quickly as possible. Don't give those nasty little bacteria an inch! This can be really tough, because it takes at least a few weeks (6-8), and sometimes much more to get through the brutally hard part.

If when you start your antibiotics, your symptoms don't flare severely, including ones you didn't know you had, then you may have astrain that is resistant to that particular antibiotic.Or, perhaps, your body is fighting the antibiotic and not letting it do its job properly. This is one reason that two antibiotics are often used at the same time. It is a judgment call between you and your doctor as to whether the antibiotics are being effective, and what might need to be done if they aren't.

Which set of symptoms, the physical or the psychological, will be the
most difficult to handle is entirely up to the individual. Are you
more physically oriented? Or are you a thinker?
Some people are so happy-go-lucky and full of faith that nothing at all bothers them. In fact, many people are. You can be like them too. Just don't bother to worry about it! You're on the right road. The road to being happy, healthy and normal again!

Is it contagious?
The answer is: no one knows. Spouses and siblings tend to all travel in the same places, so it is hard to tell if the disease was transmitted person to person or just infectious bites by
different ticks. The long answer is: that since it's a blood-borne disease, as long as you don't go around biting people and bleeding on them, then no, it's not. As always though, better safe than sorry.

A few annoyances you may encounter along the way, and should be made
aware of if you're the worrying sort:

1. Confusion/Disorientation. Your short-term memory will probably be taking a nice long vacation. You may find yourself confused about where you are and what you're doing every time the scenery changes. Like when walking from one room to another, or driving (DON'T!). Sometimes even when just sitting or lying around doing nothing. It could also be even more intense, with temporary bouts of amnesia. But it's a fact of life that vacations do end. This one tends to be about the most disconcerting psychological symptom for most people. Again
though, it's caused by the toxin release from the dying bacteria. It
will get better and eventually go away!

2. Numbness. Various parts of your body, both those you knew were infected and those you didn't, may go numb for a period of time. Quite often it's just for a day or so, but can also last for many weeks, until enough of the bacteria in that location have been killed that the toxin level finally drops. Don't panic! They all come back! (The numb body parts, that is!) They'll eventually switch from numb to painful, and then finally to normal.

3. Pain. Same as 2), but may be sporadic pains instead of numbness.

4. It's in more places than you know. While you are on effective antibiotics the bacteria are NOT spreading. Never had a problem with your back, but now it hurts? Forearms maybe? Wrists? They hurt now because the bacteria were there all along, and now that they're dying they're releasing toxins. It's the toxin from the dying bacteria that causes the numbness and pain. Dead bacteria is a good thing!

5. Insomnia. And not just at night either. You may find it impossible to nap during the day at all. You may get to enjoy every last minute of the worst part. As the toxin levels fall though, you'll be able to sleep better and better.

6. Hallucinations and voices. These can occur during times when your mind and body are exhausted but the toxins won't let you sleep. You may be trying to rest, but your brain gets stuck halfway between sleep and awake, dreams and reality mix. Better sleep at night, along with less activity during the day, should help these symptoms disappear. Ask your Doctor about sleeping aids you can use if necessary. However, if you get these symtpoms while you're wide awake and have gotten reasonable sleep, consult your doctor immediately.

7. Tremors, shakes, and spasms. Can occur in various places to varying degrees. The length of time they last varies as well. These may be caused by bacteria dying near, and hence irritating, a nerve which controls motion.

8. Sweats, hot, cold, day and night. Get used to them. You might consider adding just a bit of extra salt to your diet so that you don't become salt/sodium deficient.

9. Fireworks, popcorn, or pin-cushion pains. These tend to feel like someone has picked a part of your body and decided to jab it with a pin a few times. Then they go and pick another spot. These are probably just irritations of pain nerves, or perhaps bacteria dying inside a nerve itself. You might notice that they tend to occure in
your most affected areas, and that more effective antibiotics cause more of them.

10. Heart palpitations or irregularities. Notify your doctor immediately so that they can determine if the irregularities are severe enough to be dangerous. In some extreme cases, people have been put on a temporary pace maker until the worst of the symptoms have disappeared

11. Dizziness and Vertigo. It's everywhere else, why be surprised that it's in your ears? Symptoms here can range from a feeling of "walking through jello" to complete loss of orientation.

12. Temporary Amnesia. Really this is just an extension of memory loss symptoms, except that instead of just losing your short-term memory, mid and sometimes long-term memory can go for a hike as well. These symptoms can last anywhere from just a few minutes, to a few weeks, and will probably only occur during the first month or so of treatment.

13. Aliens Under My Skin. usually felt in the forearms or shins, but can occur anywhere, this feels for all the world like little turtle- shaped aliens crawling around in the affected area. These are actually associated with an attack by your own immune system against the bacteria, and are probably the result of localized swelling and toxin releases from the bacteria dying under the attack.

14. Sudden bouts of weakness and symptoms flares. Your body is fighting the bacteria alongside the antibiotics. But your body isn't
always a nice steady predictable stream. Occasionally, and even frequently during the first cycle or two, your body will attack. Sometimes with an all-out-vengeance that will literally leave your knees weak and you panting for breath. In extreme cases, this can actually cause fainting. This can be very disconcerting if your're not expecting it. As long as your heart rate and blood pressure are OK, then you're' probably fine. Go over your drug allergy checklist and consult your doctor if you think it might be a delayed reaction to antibiotics. Normally, this feeling will drop in intensity withina few minutes.

15. Headaches. Can range from not at all if you're really lucky, tosome really intense head-splitters. Do whatever you can to survive them.

16. Disconnection. Close your eyes, now where is your arm? OK, look at it now. Doesn't really feel like it looks where it is, does it? The extreme of this symptom is a complete out-of-body experience. As toxin levels fall, you should become more and more re-connected to your body again. And there you were thinking that you were just getting really good at your Yoga exercises.......

17. Panic Attacks. You don't want to get these, really, you don't. It's a feeling of "Oh my God, I'm going to be like this forever, I can't take it please, somebody just kill me and get it over with..." The only possible good thing about this symptom is that it goes away.

18. Bright Colours. Your pupils may dilate a bit. Indeed, you may find yourself wearing sunglasses, inside!

19. Hypersensitive Hearing. Your ears may become hypersensitive to sound. In extreme cases, sound, even very quiet ones, can become painful.

20. Mood Swings, Irritability/Short Temper, Erratic Behaviour. Again, all due to the toxin's effect on your mind. These will all clear up as you get well. These symptoms can be especially difficult for those around you to deal with.

21. Yo-Yo. You'll be feeling like one. Up one minute, down the next. You might wake up feeling great one day, only to find that a couple hours later you're back feeling horrible again. UP, down, up, down, all around. Slowly, month after month, the downs will stop being quite so low, and eventually go away.

22. Whatever Else. Everyone is different, and the disease is quite well known these days for just how differently it affects different people. Any other significant symptoms that you are concerned about should be discussed with your doctor.

wonderfullife
09-10-2011, 03:15 PM
1. You may need help to get through this. You should not be left alone for long periods of time. Someone needs to be around to help encourage and reassure you along your rough road back to wellness. Your mind will not be working properly, and it's easy to become confused, terrified, and discouraged. Make sure you have someone to talk to when you need them. Just a phone call can help tremendously! Emotional release, if needed, can be good for you! Rare are the ones who can make the journey back to wellness without a few breakdowns along the way. Call around, ask around, find your local lyme disease support groups. Talk to them. That's why they're there. They want to help!

2. Eat! When you finally get through this, you'd certainly like to enjoy life again as soon as possible, wouldn't you? Well you can't do that if you're a shriveled-up little mess. Solid food is best, but may prove difficult for a while.Liquid foods like "Ensure Plus" and "Instant Breakfast" can help keep your calorie intake up. Don't forget your basic "Multi-vitamin & Minerals" either. And eating does much more than just keep your weight up. It provides energy for: your own immune system so it can fight too, for all the healing that has to take place, and energy to help your body process the toxins out.
Eat, and you'll be healthy and happy again that much sooner.

3. Move and Stretch. The worst ting you can do is just sit or lie around all day. Lyme Disease is a deep tissue bug as well as not-so- deep tissue. It likes to hide and live in places that are hard to reach, both for your body and the antibiotics. Stretching and moving around does a number of things: such as providing circulation going and flushing toxins out, you help prevent toxic bulid-up and subsequent possible permanent damage. So if it hurts, stretch it
(gently), move it around, get some circulation in there! You should be gently stretching everything from your nose to your toes at least once an hour while you're awake. Go for a short walk... Even just up and down the driveway, or around the living room a few times will do a world of good. This is extremely important during the first few weeks or so when the toxin levels will sky-rocket!

4. Sleeping aids. Do not use sleeping aids during the first couple weeks or so. As long as you have extreme pain or numbness somewhere that needs to be moved around occasionally you're probably better off rolling around and tossing and turning all night. Once you feel like you can go the night without accumulating severe pain somewhere, then sleeping aids are OK. Naturally, use as little as possible. You do need sleep but you also don't want
permanent toxin damage.

5. Take your medication on time, every time, religiously. Some bacteria takes days to kill. A missed dose may let them recover and restart the clock all over again. Unless, of course, you like suffering......

6. Don't stop once you feel good. Lyme Disease is very slow growing, but the longer you've had it, the deeper into your system it gets. Deep enough such that even the "instant kill" family of cephalosporins antibiotics take time to kill it. Thus it is generally good practice for Lyme patients to continue effect antibiotics for a number of months after symptoms have (seeminglydisappeared. Taking medication when you feel good can be an annoyance, but when you consider what you're going through now, do you really want to do it again?

7. Lyme Disease doesn't just grow in the bloodstream. It tends to enter inside your cells and grow there too. Not all antibiotics can penetrate cell walls to effectively kill the bacteria there. Fortunately, there are a number that can: Suprax, Flagyl, and Biaxin for example. One might consider some time spent on these to help kill any bacteria which might have crossed inside the cell wall barrier.

8. Know the signs of a drug reaction for those drugs you haven't had before. Sometimes it can be difficult to distinguish between a drug reaction and standard Lyme symptoms. Discuss any concerns or unusual symptoms with your doctor.

9. Avoid any anti-inflammatory and anti-pain medication. Mostly at the start of treatment. Inflammation is your body's way of increasing circulation to affected areas. Circulation is what brings the antibiotics in to where they need to go and takes the toxins away. Pain is your body's way of saying "Hey stupid! Move this part around a bit!" You might actually find that anti-inflammatories, though, during the first month or so of treatment, will tend to make joint pains worse. Once past the hard part though, a bit of anti- inflammatory and anti-pain medication is OK.

10. Antibiotic Soap. For shower or bath. Not proven to actually do
anything, but may help to kill the bacteria hiding in the pores of your skin.

11. Contact Lenses. Take them out! Never nap or sleep with your contacts in! It is just as likely that the bacteria is in your eyes, as well as everywhere else. A die-off in your eyes can raise the local toxin levels, but with your contacts in your body, is hindered from flushing it away. The result build-up may cause damage to your eyes. Better safe than sorry! Dig up that dusty old pair of glasses!

12. Depression. Nobody likes feeling depressed. Problem is, that a fair number of people just get that way after fighting the disease for a seeming eternity and still not feeling a whole lot better. Try to find things you can do to occupy yourself and keep your mind off it. Do whatever you can, naturally, to lift your spirits and keep them up. Failing that, it is not out of the question to ask you doctor for a little help. Make sure to avoid anti-depressants that
can add to your insomnia!

13. B-Complex Vitamins. Thse have been shown to significantly help psychological symptoms. They also help the brain repair and protect itself from toxin damage.

14. Injuries. Try to avoid them. The Lyme bacteria thrive on injured body parts. Bruises, sprains, etc., are a feast with an open all-you- can-eat invitation. You might, to amuse yourself once you know the exact length of your cycle, try mapping back specific short-lived pains to the event which caused them!

15. Exercise. Gentle stretching and low-level workouts are OK. But remember that strenuous exercise and hard workouts are actually controlled injury...and injury feeds the bacteria.

16. Yeast Infections - in throat and/or digestive tract. Some antibiotics are more prone than others to causing yeast infections by killing off all your good bacteria. Your doctor should question you about sore throats and intestinal problems each time you visit. These infections can be cured with yet more drugs, or avoided all together by simply asking your pharmacist for "good tummy bacteria", the live ones". Lactobacillus Acidophilus (they're non-prescription) Live Culture yogurt does essentially the same thing, as it contains the very same live bacteria. In either case, make sure to rinse your mouth and throat with water immediately after you eat or drink anything, then swish a bit of your live good bacteria around in your mouth and swallow.

17. Antihistamines. No. No. No. No. No. And most especially not whenon one of the 'Cyclene family of antibiotics. Your immune system is one of the biggest factors in your recovery, one of the big superpowers in the war against disease. The antibiotics will kill some percentage of the bacteria each cycle while your immune system kills off the ones that were weakened. Together, the antibiotics and your body create a team to defeat the bacteria. Antihistamines, like Benadryl, turn off your immune system! All they do is make sure that you suffer longer! Further, the cyclene family of antibiotics doesn't actually kill the bacteria, but rather just stops them from growing and relies on your immune system to kill them.

18. Natural herbs and such. A stroll through your local herbal and natural foods shop will provide you with an amazing array of itmes which claim to do all sorts of good things. Anything that says "boosts your immune system" might be a good idea. Purely optional, although a number of herbal concoctions have actually been shown to do as they claim.

19.Caffeine. Suppresses the immune system, which is very bad. Give up that morning coffee and that afternoon coke.

20. Alcohol. Worse for you than caffeine. Unless you just want to be sick longer, no alcohol!

21. Smoking. Haven't you been lectured about this enough yet? Now
would be a really good time to quit.

22. Rest. You're going to need a lot of it. Even after you begin to feel better, remember your body is still fighting off a rather nasty infection. Don't overdo it. Without sufficient rest, recovery just takes longer.

23.Hot drinks. Let them cool off to luke-warm first. Hot fluids tend to make the dead layers of cells on your tongue rather thick to protect them from the scalding heat. This means more stuff for yeast infections to grow in.

wonderfullife
09-10-2011, 04:09 PM
Chart it!

Make a chart of your symptoms! Get some graph paper, on the left-hand column list your symptoms and various affected body parts, and then across the top number the days. Each day, fill in the appropriate squares with the severity of your symptoms. Hurts like crazy? Fill that square in. Hurts just a little? Maybe just put a line across the bottom of the square. Record the worst of each symptom each day. You'll notice that some move gradually up and down, some might appear constant, and others can blink in and out in just a day. Now you have a record. With this record, you can help you and your doctor figure out exactly what to expect when, and even make a prediction on when you'll feel 100% normal again! Instead of being at the mercy of the disease, waking up each morning and wondering "what's the torture of the day going to be?", or wondering "When is it ever going to end?", you could be looking at your chart and knowing exactly what to expect and when! Of course, you still have to map that first cycle, but from there on out you're not just blindly muddling along!

Sometimes interpreting your chart can be difficult. For instance, some body parts may feel fine during the first month or two, only to become painful later on. Reason being, is that they started out numb, and as the bacteria died away the feeling came back to that area. Physical symptoms that started out painful should show themselves fading away with each cycle. Basic energy level should rise each month, although there may only be a slight increase between the first two cycles. Neuro symptoms should also improve slightly each month, but they will be the last ones to finally clear up.

The Lyme bacteria appears to stick very tightly to its cyclical schedule. These cycles tend to be about 21 days in men, 30 days in women. If your symptoms don't appear to be going down with each cycle, then consult your doctor about increasing the antibiotic levels, adding another, switching, or whatever the attack plan they might suggest.

Because the physical symptoms disappear first and the psychological ones are sometimes difficult to measure, your doctor may ask you to begin recording your temperature a few times a day once your symptoms are nearly cleared. When you've gone through a few full cycles without sign of a fever, you're done!

The Lyme bacteria will typically have a peak intensity sometime during its cycle each month. Beginning, middle, or end is a matter of chance and at what point you start your charting. But it can be very frustrating to start your antibiotics on the low end of a cycle, only to find yourself feeling worse and worse as the days go by. Which is why you are keeping a chart! It is completely irrelevant to use day- to day or even week-to-week comparisons for whether you are improving. The only reliable way to tell is to compare each months chart and see if the symptoms are improving overall. Again frustrating, because you really can't tell if you're improving for at least one full cycle. Unless of course, you're one of those miracle Rocephin cures, which is rare. The rest of us suffer for a month, and then begin comparing each month's date to the previous to see if there is improvement.

Typical uncomplicated recovery. Before starting your antibiotics you might find yourself feeling pretty bad, or at the least, not very good. Once you start though:

Oh my God, I'm gonna Die.

Ugh, I feel horrible.

Feeling bad.

Feeling much better.

Wow! I feel pretty good!

Symptoms gone!

Now Cycle 1 Cycle 2 Cycle 3 Cycle 4

This chart assumes many things, mostly that nothing goes wrong, that the choice of antibiotic and its level are correct from the start, etc..It is intended to be an example of how a typical recovery might feel.

The Lyme Disease Cycle. Is not really 30 days precisely. Rather, in women it tends to match their menstrual cycle in number of days. In men the cycle is usually around 21 day. But again, these vary from person to person. The only way to know for sure is to make a chart of your symptoms and then begin looking for patterns.


There are many different strains of Lyme Disease. Fortunately there
is also a variety of antibiotics. The trick is to find the antibiotics which your stain is susceptible to and that your body will tolerate in high doses. This can be extremely discouraging, to spend weeks or months on a particular antibiotic, only to figure out that it isn't working. This is one reason that Lyme Disease is frequently treated with two different antibiotics at the same time. Another is that doubling up provides a much higher kill rate. If the
first set of antibiotics you try doesn't seem to be doing much, don't be afraid to ask you doctor for a few short trials of some others. Try each one for three days. Remember how you felt each third day. Continue with the one/ones which hit you the hardest.

Cephalosporins - When they work, they work extremely well. This family is effectively an "instant" kill, meaning that it can kill the bacteria regardless of the stage of the its life-cycle. Naturally, like everything else, they're more effective during the reproductive cycle. But, essentially, this class of antibiotics pokes holes in the bacterial cell wall and causes the little buggers to bleed to death.

Penicillins - This class blocks cell wall formation during the reproductive cycle of the bacteria. They are a slow-kill antibiotic, but usually highly effective.

Cyclenes - Generally gum up the DNA of the bacteria. Without functioning DNA, the bacteria can't reproduce or grow.

Advanced Macrolides - Block protein synthesis in the bacteria. Without proteins, the bacteria have a difficult time doing much of anything.

Metronidazole - Does three things: gums up the bacterial DNA,
suffocates the bacteria that may be in anaerobic mode, and breaks their little legs so they can't run and hide (almost literally! The bacteria use their flagellum to escape attacking white blood cells, but without functioning flippers, they become easy targets). One possible problem with this antibiotic, is that it may be a tad too useful. By enabling the immune system to see and catch the bacteria the body is suddenly hit with the realizationthat there is tremendous infection going on. The immune system response can be intense. Possibly a great choice for "mop-up" later in treatment.

Antibiotics dosage and duration.
Typical bacteria have very short cycle times, usually measured in hours or minutes. This means, that an antibiotic that is given at a standard rate to produce an effective 10-20% kill rate can kill a typical infection in just a matter of a few days. With each cycle the antibiotic kills some percentage of whatever bacteria are still left. When the numbers get low enough your body cleans up the stragglers, thus keeping the "percentage of what's left" from becoming one of those "limits that never reach zero" problems that you dreaded back in high school algebra. The Lyme bacteria behaves the same way. With each cycle the standard rate of antibiotics will kill some percentage of whatever is there. Except that the Lyme bacteria has a cycle time measured in weeks! (3-4) It could take years to kill the infection at standard rates! Antibiotics are dosed quite high, and often combined, in order
to achieve the highest kill rate possible without killing the patient (you) in the process. But even forcing a very high kill rate can still take 4-6 months before the levels are brought down far enough for your body to overwhelm the stragglers. The other reason that antibiotic levels are kept very high for Lyme Disease treatment is that the bacteria isn't just in one or two easy-to reach places. It's everywhere. That includes the central nervous system (CNS) and inside cells, joints, etc, etc....Many antibiotics have a difficult time
reaching these places in concentrations high enough to effectively kill the disease in these areas. Don't let your doctor under-dose treatment options and effective dosage rates. Duration, or how long you stay on the high rate of antibiotics is just as important. A typical infection by a typical bacteria is beaten to death for many cycles past when it should have all been dead, just to make sure. Why not the same with Lyme? Currently, you'll be lucky if your doctor agrees to one full cycle symptom-free. Press for one full cycle fever-free. If you manage to stay on antibiotics for anything after that, consider yourself blessed. But 3-4 fever- free cycles, assuming that you're back living a healthy lifestyle and doing what you can to keep your immune system pumped up in top condition, well, that should to it. Time to stop and see if it's really as dead as we all hope it is.

wonderfullife
09-10-2011, 04:14 PM
Overview:
The herxheimer reaction, nicknamed "herx" or otherwise referred to as Jarisch- Herxheimer (J-H) is a phenomena originally observed in the treatment of syphilis, but later found in other illness. In general terms, it is described as a temporary increase of symptoms when anti-syphilitic drugs (antibiotics) are administered. What is known or speculated about Lyme disease herxheimers are based heavily on the reactions seen in syphilis. This is due to the fact both diseases are caused by a bacteria known as a spirochete, the former being Treponema pallidum, the latter Borrelia burgdoferi (B.b). However the herxheimer reactions in Lyme disease are not identical to those seen in syphilis, especially in terms of timing, frequency and duration as noted below.

In Lyme disease it is thought that the cause of herxheimers are the result of endotoxin release, that is toxin(s) within the spirochete that are released as the B.b are killed or broken down. This may be a result of the toxin(s) itself or the body's immune response to such.


Symptoms:

As mentioned, the general description is a temporary increase in symptoms, but also included is the development of new ones. More specifically the most common events include: increased joint or muscle pain, headaches, chills, fever (usually low grade), drop in blood pressure, hives and rash. A multitude of other symptoms have been described.

Worth noting is that hives and rash are sometimes mistaken for an allergic reaction. It is up to one's physician to determine this, but with close observation and the use of medications such as Benedryl often prevents stopping antibiotics prematurely. In more severe cases of J-H a reduction of the dosage or temporarily cessation of the treatment is an alternative.


Timing, Frequency and Duration:

This is individualistic and Herxheimer can occur within days to weeks after the onset of antibiotic therapy. In some patients they occur only once or twice (if at all) and with others continue throughout the course of treatment, usually lessening in severity. They can occur and are more often described in cycles (example: every 4 weeks) and have been reported to last from days to weeks.

It can be very beneficial to document these exacerbations. Some physicians use this as a guideline for treatment. Further it may help differentiate herxheimers from the normal symptoms or progression of Lyme disease.


Treatment:

Herxheimer reactions can be very difficult on patients and affect compliance with therapy so supportive measures should be sought or utilized to lessen discomfort if needed. The use of aspirin, NSAIDs (non steroidal anti inflammatory drugs), pain medication, muscle relaxers, hot baths or others remedies can be appropriate. Of note, some have found Benedryl helpful even in the absence of rash or hives.

The good news is that the herxheimer is thought to indicate that the antibiotics are indeed working and that following each worsening may bring about more improvement. However the lack of herxheimer reaction should not cause anxiety if symptoms are improving.


Other considerations:

Something often overlooked but can present with similar symptoms as a herxheimer is Candida (yeast) infection. Treatment with acidophilus and if needed prescription medications such as Nystatin or Diflucan can be utilized.

Sources of Information:

Lyme Disease 1991 - Patient/Physician Perspectives from the U.S. and Canada The Jarisch-Herxheimer Reaction James H. Katzel M.D.
Managing Lyme Disease (1996) Joseph J Burrascanno M.D.
Principles and Practice of Infectious Diseases 4th Ed . Mandell, Douglas and Bennett
Seronegative chronic relapsing neuroborreliosis. Lawrence C, Lipton RB, Lowy FD, Coyle PK Eur Neurol 1995;35(2):113-117

wonderfullife
09-10-2011, 09:15 PM
Allicin, one of the active principles of freshly crushed garlic homogenates, has a variety of antimicrobial activities. Allicin in its pure form was found to exhibit i) antibacterial activity against a wide range of Gram-negative and Gram-positive bacteria, including multidrug-resistant enterotoxicogenic strains of Escherichia coli; ii) antifungal activity, particularly against Candida albicans; iii) antiparasitic activity, including some major human intestinal protozoan parasites such as Entamoeba histolytica and Giardia lamblia; and iv) antiviral activity. The main antimicrobial effect of allicin is due to its chemical reaction with thiol groups of various enzymes, e.g. alcohol dehydrogenase, thioredoxin reductase, and RNA polymerase, which can
affect essential metabolism of cysteine proteinase activity involved in the virulence of E. histolytica.

wonderfullife
09-10-2011, 09:16 PM
Serology is currently the method of choice for the laboratory diagnosis of Lyme Borreliosis, but it must be interpreted with caution. A total of 954 patients with suspected Lyme borreliosis were evaluated on the basis of clinical and serological data. The seroprevalence of Borrelia burgdorferi antibodies was 4.4 percent (42 of the 954 serum samples). The most frequent clinical manifestation was erythema migrans which occurred in 50 percent of the seropositive patients, followed by neuroborreliosis (16.6 percent) and arthritis (11.9 percent). Carditis was rare. Our findings suggest that for the diagnosis of Lyme borreliosis, serologic tests need to be combined with clinical signs and symptoms.


PMID: 21978712 [PubMed - in process]

wonderfullife
09-10-2011, 09:25 PM
(NaturalNews) In Traditional Chinese Medicine, Lyme disease is treated as toxic fire. These fire toxins are treated with extreme heat clearing herbs. From the western point of view, fire toxins include aggressive entities such as bacterial and viral infections but are not limited to them. They can be amoebic parasites and even just toxins of chemical nature or metal particles. Likewise, from a western point of view, the heat clearing herbs have been proven to have a very effective anti-viral and antibacterial action as well as a "cleansing of the blood" effect on other small particles.

Below is a TCM protocol for Lyme Disease grouped into three parts:

Clearing The Toxic Fire (Killing The Bacterium)

Based on the best of TCM protocols, here is a "clear toxic heat" formula for use as an anti-toxin or "fire quenching agent." These amazing herbs have been successfully used against fire toxins such as malaria, pneumonia, diphtheria, septic angina, typhoid fever and others.

The 6 herbs used in this formula to clear toxic heat are 5:1 extracts of:
Chuan xin lian - Andrographis paniculate (a very effective anti-toxin heat clearing herb with anti-spirochetal action in particular)
Huang Lian - Coptis chinensis (Anti-toxin heat clearing)
Jin Yin Hua - Flos Lonicerae japonicae (Anti-toxin heat clearing)
Da Qing Ye - Folium Isatidis (Anti-toxin heat clearing)
Ban Zhi Lian - Scutellaria barbata; Herba (Anti-toxin heat clearing)
Tu Fu Ling - Smilax glabra; Rhizoma (Anti-spirochetal action)

As part of this protocol it is also important to take 2 grams twice daily of Hu Zhang powder (Natural resveratrol from Knotweed in 5:1 extract). It is positive against Leptospirosis, Treponema denticola (spirochetes in oral flora), Bartonella (Buhner) and many gram neg and gram pos bacteria.

Continually Removing The Toxins From The Joints:

Xu Duan (ChineseTeasel Root) taken with a "Clear Toxic Heat" formula will help drive the spirochetes from the joints into the blood stream (where it can be killed by the heat clearing herbs). Xu Duan Teasel in tincture form is the best way your body can absorb it.

Maximizing Your Immune System With a Strong Defense:

There must also be an effective formula for the immune system that is suitable for long term use. Reishi mushroom and Chinese Astragalus 5:1 (Called Strong Defense) are perfect.

Together all these herbs become the building blocks of a true hard working lyme disease protocol that, although formulated from ancient herbs, becomes "cutting edge" in fighting this toxic fire we call Lyme Disease.

Sources: This protocol is based entirely on author's research and knowledge of Traditional Chinese Medicine.



Learn more: http://www.naturalnews.com/028216_lyme_disease_remedies.html#ixzz1aJnHdGxo

wonderfullife
09-10-2011, 09:35 PM
It is hard to definatly say anything works 100% when dealing with lyme it all depends how long you have had it un treated. Each person is diffrent and the dis-ease is diffrent in each person.

Here are some suggestions:
Chinese medicine,
Oxygen therapy
MMS1 and MMS2
Collidal silver
Bicarb and maple syrup cancer therapy
Yoga and Tai Chi to help to keep one mobile and cope with pain etc.
Diet: organic foods , unflouridated water, Paleo high protein and high fat foods.
Raw milk
Fermented foods live yogurt.
Vitamin D
Vitamin B's
Kefir
Rest
Omega 3's
Vitamin C
Positive Mental attitude affirmations
Clearing negative energies (cleansing your Chakras)
SADS Light therapy
No matter what one does do there will be a herx ( if you are lucky you may not get one) The main thing to remember is do not give up at the first hurdle or the first herx the herx means something is working.

wonderfullife
09-10-2011, 10:16 PM
Abstract
A tick-borne, multisystemic disease, Lyme borreliosis caused by the spirochete Borrelia burgdorferi has grown into a major public health problem during the last 10 years. The primary treatment for chronic Lyme disease is administration of various antibiotics. However, relapse often occurs when antibiotic treatment is discontinued. One possible explanation for this is that B. burgdorferi become resistant to antibiotic treatment, by converting from their vegetative spirochete form into different round bodies and/or into biofilmlike colonies. There is an urgent need to find novel therapeutic agents that can eliminate all these different morphologies of B. burgdorferi. In this study, two herbal extracts, Samento and Banderol, as well as doxycycline (one of the primary antibiotics for Lyme disease treatment) were tested for their in vitro effectiveness on several of the different morphological forms of B. burgdorferi (spirochetes, round bodies, and biofilmlike colonies) using fluorescent, darkfield microscopic, and BacLight viability staining methods. Our results demonstrated that both herbal agents, but not doxycycline, had very significant effects on all forms of B. burgdorferi, especially when used in combination, suggesting that herbal agents could provide an effective therapeutic approach for Lyme disease patients.

Borrelia burgdorferi, the primary causative agent of Lyme disease, is a spirochetal bacterium that can adopt different inactive forms, such as cystic and granular forms (round bodies), as well as colonylike aggregates both in vivo and in vitro, in the presence of unfavorable conditions such as exposure to the antibiotics commonly used for treating Lyme borreliosis.1-4 Unfortunately, when B. burgdorferi is in these inactive forms, conventional antibiotic therapy will not destroy the bacteria.3 Still to date, the frontline treatment for Lyme disease is administration of pharmaceutical antibiotics such as doxycycline, minocycline, clarithromycin, penicillin G, and ceftriaxone.4,5 Many studies have shown that in spite of continued and high-dose antibiotic therapy, chronic Lyme disease is not treated successfully in many cases.6 Also, in the absence of ongoing antibiotic treatment, relapse is common.7,8 This means that even after antibiotic treatment, the host immunity fails to prevent recurrence.8 One possible explanation for this clinical observation is the presence of different morphological forms of B. burgdorferi, which mayprotect it from the antibacterial therapy. Soon after treatment, relapse is observed, most likely because the B. burgdorferi can revert to the spirochetal form. Furthermore, the cost of antibiotic treatment, especially when administered intravenously, is substantial. Antibiotic therapy may also cause multiple undesirable side effects.9 Thus, there is an urgent need for novel, more efficient, and more cost-effective treatment approaches that can efficiently eliminate all forms of B. burgdorferi.
There is an alternative clinical treatment option gaining wide use, called Cowden Condensed Support Program, that utilizes several herbal extracts designed to eliminate microbes in Lyme disease patients. Richard Horowitz, MD, president of the International Lyme and Associated Diseases Educational Foundation (ILADEF), has prescribed this protocol for over 2000 of his patient and reports that it has been effective for more than 70% of them. The two herbal agents from the Cowden Condensed Support Program selected for this study are Samento (a pentacyclic chemotype of Cat's Claw [Uncaria tomentosa] that does not contain tetracyclic oxindole alkaloids), with reported antibacterial and antiviral properties, and Banderol (Otoba sp.), known to have antibacterial, antiprotozoal and anti-inflammatory effects.10-12 Both herbal agents are used during the first two months of Cowden Condensed Support Program, then in rotation with other antimicrobials for the duration of this 6-month protocol.
n this study, we evaluated these natural antimicrobial herbal extracts as well as doxycycline (one of the primary pharmaceutical antibiotics for Lyme disease treatment) for their potential effects on the different forms of B. burgdorferi.

The infectious B31strain of B. burgdorferi used in this study, obtained from American Type Tissue Collection(ATCC# 35210), was culturedin 5% CO2 at 34 oC, in Barbour–Stoener–Kelly H (BSK H) medium supplemented with 6% rabbit serum (Sigma, St. Louis, Missouri) to midlogarithmic stage (2 × 107 cells/ml). Samento and Banderol were obtained from Nutramedix LLC (Jupiter, Florida). Doxycycline was obtained from Sigma. A wide range of concentrations of Samento and Banderol were initially tested to determine the effective concentrations (1:100–1:1000 dilutions). For doxycycline, a concentration 10× higher than the reported minimum bactericidal concentration (250 µg/ml) was used.13 Triplicate test tubes containing BSK H medium, with and without the appropriately diluted antimicrobial agents, were inoculated with a final density of 5 × 106 cells/ml of the test organism.

Direct cell counting methods with Petroff-Hausser counting chambers and morphological studies using fluorescent and darkfield microscopic techniques, as well as LIVE/DEAD BacLight Bacterial Viability Assay (Life Technologies Corp, Carlsbad, California), were utilized to assess the effect of the antimicrobial agents. For statistical analyses, one sample paired T-test was performed using NCSS statistical software (NCSS LLC, Kaysville, Utah).
In the first set of experiments, we tested the in vitro susceptibility of the spirochete and round-body forms of the B. burgdorferi B31 strain to Samento and Banderol extracts for 96 hours, then direct cell counting and darkfield morphological evaluation methods were used to measure the effects of the antimicrobial agents. For both herbal extracts, the dilution of 1:400 most efficiently eliminated both the spirochetal and round-body forms (Figure 1A and 1B). However, when we used the combination of Samento and Banderol extracts, 1:300 dilution showed the most effectiveness, and this concentration was chosen for further study (Figure 1C). As a negative control, 0.25% ethanol treatment was also included in all experiments, because these herbal extracts contain ~25% ethanol to transport the nutrients into the cells and for stability.

In these experiments, we also compared the effect of Samento and Banderol with doxycycline, the most common antibiotic treatment agent for Lyme disease treatment in a 96-hour treatment period. Our results showed that doxycycline (250 µg/ml) was very effective in eliminating the spirochetal form of B. burgdorferi, but it significantly increased the round-body forms. Comparing this doxycycline data with that of the herbal extracts, Banderol and the combination of Samento and Banderol (1:300) were more efficient in eliminating both the spirochetal and round-body forms of B. burgdorferi in vitro (Figures 1A–C).

In the next set of experiments, we evaluated the effect of the different antimicrobial agents on biofilmlike colonies of B. burgdorferi. The cultures were treated as described above for 96 hours and stained with BacLight fluorescent viability stains, which can help visualize the effects of the antimicrobial agents on the bacterial cells (Figure 2). The green fluorescent stain (SYTO 9, with excitation/emission maxima of about 480/500 nm) colors healthy bacteria that have intact membranes, thus staining live cells; and the red dye (propidium iodide with excitation/emission maxima of about 490/635 nm) colors
In the absence of antimicrobial agents, B. burgdorferi is forming biofilmlike colonies (Figure 2A) with mainly live bacterial cells. In the presence of Samento extract (1:300), the colonies were significantly smaller and less organized (Figure 2B), but they did stain with green dye, indicating that live cells remained. In the presence of Banderol extracts, the size of colonies did not show any reduction; however, the cells inside the colonies are >90% dead.

In the presence of both herbal extracts, no sign of any colony formation was observed in the cultures, but we found evidence of a few individual nonmotile but green spirochetes and round bodies. In the presence of doxycycline (250 µg/ml), the average colony size was increased and contained mainly live round-body forms.

In this study, our working hypothesis was that for an efficient therapy, we have to find antimicrobial agents that can eliminate all the forms of B. burgdorferi. During the course of Borrelia infection, the bacteriumcan shift among the different forms, converting from the spirochete form to the others when presented with an unfavorable environment and reverting to the spirochete when the condition is again favorable for growth.1-4 To successfully eradicate B. burgdorferi, antimicrobial agents should eliminate all those forms, including the spirochetes, round bodies, and biofilmlike colonies.
Here we have provided evidence that two natural antimicrobial agents (Samento and Banderol extracts) had significant effect on all three known forms of B. burgdorferi bacteria in vitro. We have also demonstrated that doxycycline, one of the primary antibiotics used in the clinic to treat Lyme disease, only had significant effect on the spirochetal form of B. burgdorferi.5
Our later results might provide some explanation for why relapse is so common after discontinuing antibiotic therapy. For example, some of the recent reports on animal experiments demonstrated that although pharma­ceutical antibiotics are effective in ameliorating disease, the infection may persist even after seemingly effective therapy, which suggested that Borrelia may remain viable even after antibiotic administration.14-15 If those pharmaceutical antibiotics only eliminate one form of this bacterium, the other forms could be the source of the persistent disease.

The other very important fact needs to be considered for an effective treatment for Borrelia infection: this bacterium typically has a life span ranging from several weeks to six to eight months; therefore, it may take six to eight months for even one generation of Borrelia to become exposed to the antimicrobial for elimination.16 Since the herbal extracts like Samento are reported to be nontoxic, they can be safely taken daily for the long period of time necessary to thoroughly eradicate Borrelia from an infected body.17
In summary, our study has provided in vitro research data on a novel treatment approach using herbal antimicrobial agents to efficiently eradicate B. burgdorferi, the Lyme disease bacterium.

http://www.townsendletter.com/July2010/sapi0710.html

tschingu
10-10-2011, 04:45 PM
(NaturalNews) In Traditional Chinese Medicine, Lyme disease is treated as toxic fire. These fire toxins are treated with extreme heat clearing herbs. From the western point of view, fire toxins include aggressive entities such as bacterial and viral infections but are not limited to them. They can be amoebic parasites and even just toxins of chemical nature or metal particles. Likewise, from a western point of view, the heat clearing herbs have been proven to have a very effective anti-viral and antibacterial action as well as a "cleansing of the blood" effect on other small particles.

Below is a TCM protocol for Lyme Disease grouped into three parts:

Clearing The Toxic Fire (Killing The Bacterium)

Based on the best of TCM protocols, here is a "clear toxic heat" formula for use as an anti-toxin or "fire quenching agent." These amazing herbs have been successfully used against fire toxins such as malaria, pneumonia, diphtheria, septic angina, typhoid fever and others.

The 6 herbs used in this formula to clear toxic heat are 5:1 extracts of:
Chuan xin lian - Andrographis paniculate (a very effective anti-toxin heat clearing herb with anti-spirochetal action in particular)
Huang Lian - Coptis chinensis (Anti-toxin heat clearing)
Jin Yin Hua - Flos Lonicerae japonicae (Anti-toxin heat clearing)
Da Qing Ye - Folium Isatidis (Anti-toxin heat clearing)
Ban Zhi Lian - Scutellaria barbata; Herba (Anti-toxin heat clearing)
Tu Fu Ling - Smilax glabra; Rhizoma (Anti-spirochetal action)

As part of this protocol it is also important to take 2 grams twice daily of Hu Zhang powder (Natural resveratrol from Knotweed in 5:1 extract). It is positive against Leptospirosis, Treponema denticola (spirochetes in oral flora), Bartonella (Buhner) and many gram neg and gram pos bacteria.

Continually Removing The Toxins From The Joints:

Xu Duan (ChineseTeasel Root) taken with a "Clear Toxic Heat" formula will help drive the spirochetes from the joints into the blood stream (where it can be killed by the heat clearing herbs). Xu Duan Teasel in tincture form is the best way your body can absorb it.

Maximizing Your Immune System With a Strong Defense:

There must also be an effective formula for the immune system that is suitable for long term use. Reishi mushroom and Chinese Astragalus 5:1 (Called Strong Defense) are perfect.

Together all these herbs become the building blocks of a true hard working lyme disease protocol that, although formulated from ancient herbs, becomes "cutting edge" in fighting this toxic fire we call Lyme Disease.

Sources: This protocol is based entirely on author's research and knowledge of Traditional Chinese Medicine.



Learn more: http://www.naturalnews.com/028216_lyme_disease_remedies.html#ixzz1aJnHdGxo


I myself had amazing healing succes with oriental traditional medicine treating my lyme disease.

So I am all for it, but I strongly disagree with the advice you are giving.
It is overly simplyfied at it's best.

wonderfullife
14-10-2011, 02:03 AM
I myself had amazing healing succes with oriental traditional medicine treating my lyme disease.

So I am all for it, but I strongly disagree with the advice you are giving.
It is overly simplyfied at it's best.

The advice I have given is what I have done for myself what I am using now and It is not medical advice I have just found it has helped me with my dis-ease.
I wanted an alternative to antibiotics and pharmacy drugs which in some cases cost the earth and do not help the person.
Some may be searching for alternatives and everyone should do their own research and find what works best for them. We are all diffrent.
My father nearly died from this illness so did my mother but they survived.
I very nearly died from it and i survived and that wasn't from the pharmacy industry that saved my life or my father or my mother.
You may feel i have over simplyfied but as i said It worked for me and I am still here to tell the tale.
Yes our minds can heal us positive thoughts can heal us yes that is simple and yes it works.
Every thought we have creates a thing positive and negative thoughts create somthing whether we like it or not. We can create illness in our bodies or we can heal our bodies.
It's not very easy to quieten those pesky gremlins of negative thoughts that give us fear based thoughts but once we go to the jaws of the dragon and face them it becomes a whole lot easier.
I am not promising a cure for anything it's up to each person to find for themselves their own Cure.

"Your body is exactly like a movie projector, and the film running through the projector is all of your thoughts and feelings. Everything you see on the screen of your life is what has been projected from within you, and is what you have put into the film.

By choosing higher thoughts and feelings you can change what you see on the screen at any time. You have complete control of what goes into your film"

wonderfullife
14-10-2011, 02:05 AM
Onset of cutaneous vasculitis and exacerbation of IgA nephropathy after
Bartonella henselae infection.

Cozzani E, Cinotti E, Ameri P, Sofia A, Murialdo G, Parodi A

Clin Exp Dermatol 2011 10 10

Bartonella henselae is the aetiological agent of cat-scratch disease. Recently, there have been reports of other conditions associated with this bacterium, including leucocytoclastic vasculitis, thrombocytopenic purpura, maculopapular and urticarial eruptions, granuloma annulare, erythema nodosum, erythema marginatum and erythema annulare.We report the first case, to our knowledge, of the simultaneous occurrence of cutaneous vasculitis and nephrotic syndrome in a 65-year-old woman with IgA nephropathy after a B. henselae infection transmitted by a cat scratch. The aetiopathogenetic role of B. henselae was hypothesized on the basis of the serological demonstration of acute B. henselae infection, the immunofluorescence findings, and the prompt resolution after azithromycin treatment. Patients reporting cat scratches or bites should undergo accurate clinical examination, routine laboratory examinations, urinalysis and clinical surveillance.

wonderfullife
14-10-2011, 02:18 AM
Kempf F, De Meeûs T, Vaumourin E, Noel V, Taragel'ová V, Plantard O,
Heylen DJ, Eyraud C, Chevillon C, McCoy KD

Infect Genet Evol 2011 09 29

Ixodes ricinus is a European tick that transmits numerous pathogenic agents, including the bacteria that cause Lyme disease (Borrelia burgdorferi sensu lato). This tick has been considered as a classic example of an extreme generalist vector. However, host-associations in such vector species are difficult to determine from field observations alone and recent work suggests that host specificity may be more frequent in ticks than previously thought. The presence of host-associated vector groups can significantly alter the circulation and evolutionary pathway of associated pathogens. In this paper,we explicitly test for host-associated genetic structure in I. ricinus. We analyzed genetic variability at 11 microsatellite markers in a large sample of ticks collected directly from trapped wild animals (birds, rodents, lizards, wild boar and roe deer) at five sites in Western and Central Europe. We found significant levels of genetic structure both among host individuals and among host types within local populations, suggesting that host use is not random in I. ricinus. These results help explain previous patterns of structure found in off-host tick samples, along with epidemiological observations of Lyme disease.

wonderfullife
14-10-2011, 03:13 AM
The Countess of Mar, House of Lords, 11 October 2011:


I can think of no other group that is systematically discriminated against by the medical profession and social services. No other illness than ME has such a big impact on the lives of so many people and yet is given such limited funding for specialist care services and scientific research.

--------------------------------------------------------------------------------

From the Hansard report on proceedings in the House of Lords, 11 October 2011

The Countess of Mar had strong words to say about the treatment of people with ME/CFS in the House of Lords on 11 October 2011 during a debate on the Second Reading of the Health and Social Care Bill:

I intend to concentrate on Clause 8, which deals with the Secretary of State’s duties as regards the protection of public health, and to voice my concerns about the proposals for HealthWatch. Other noble Lords far more qualified than I am have dealt and will deal with the more complex matters. I remind the House that I am chairman of Forward-ME, a loose alliance of CFS/ME charities, and patron of several charities which care for people with ME or are funding research into the illness. I also suffer from the chronic effects resulting from sheep dip poisoning.

As has already been said, I believe that the Secretary of State must take the steps listed in Clause 8, which inserts new Section 2A into the National Health Service Act 2006. It is highly unlikely but possible for him or his successors to ease themselves out of what are recognised to be very important functions because they are not obliged by law to undertake them. I am sure that the noble Earl cannot have failed to notice my frustration when I have been trying to get what I consider to be very reasonable recognition and treatment for people with myalgic encephalomyelitis or CFS/ME-sheep farmers and farm workers who are ill as a result of being exposed to organophosphates, and Gulf War veterans-only to find that no one is ultimately responsible for ensuring that they receive adequate medical treatment. It is the “Not me guv” syndrome. I find it hard to believe that in 20 years of campaigning so little progress has been made.

That is particularly so with members of the CFS/ME community. They were delighted when, in 2002, the Chief Medical Officer arranged for £8.5 million to be ring-fenced in order for specialist centres to be set up regionally for the purposes of diagnosis and treatment of this illness. Some centres were established, but several have gradually disintegrated because the hospital trusts have withdrawn continued funding for appropriate staff. This has left many very sick people without recourse to inpatient treatment in a specialist centre since the ward at Queen’s Hospital in Romford was recently closed, without daycare or, in some cases, without the continuing services of a GP. Perhaps most distressing is the dearth of provision for children who frequently become very ill because they have been pushed too hard in the early stages of their illness by people who do not understand ME.

If Her Majesty’s Government are seeking to improve the lot of NHS patients, it is those who suffer chronic illnesses of currently unknown aetiology, who do not respond to standard drug or other treatments, who most deserve to be protected. I can think of no other group that is systematically discriminated against by the medical profession and social services. No other illness than ME has such a big impact on the lives of so many people and yet is given such limited funding for specialist care services and scientific research.

In desperation, frustration, or perhaps, egged on by periodic dramatic pronouncements from a small group of psychiatrists and eagerly taken up by the media supporting allegations of the spurious nature of this illness, medical practitioners and social workers too frequently resort to incarcerating adults in psychiatric hospitals under Section 3 of the Mental Health Act or, in the case of children, imposing child protection proceedings under the Children Act after accusing their parents of fabricated illness ideation. They are then subjected to treatment which I believe to be excessively harsh. When that fails, the patient is accused of failing to co-operate and is abandoned by the professions.

As the Minister knows, this is not fundamentally a psychiatric condition-there is an enormous amount of international, peer-reviewed research that points towards viral or environmental toxin causation, though it is not surprising that some patients show occasional signs of anxiety or depression as do sufferers from other chronic illnesses such as arthritis or cancer. Are they made to have cognitive behavioural therapy or graded exercises without any medical treatment? Why are the international consensus criteria published in the Journal of Internal Medicine in July 2011, which laid out clearly the criteria for diagnosis of ME, and its predecessor, the Canadian criteria, rejected by NICE and the NHS?

ME is assumed to affect about a quarter of a million people in the UK. Some are mildly affected, some moderately affected and about 25 per cent are believed to be so seriously affected that they are housebound or even bedbound. There is no central register of cases so there is no accurate assessment of its prevalence. I suggest that this disease should be the responsibility of the NHS Commissioning Board to ensure that services are provided. ME would otherwise simply get lost in the sea of other much higher profile conditions such as cancer, diabetes and heart problems, which will dominate the allocation of resources by local commissioning groups.

There is a strong economic argument for ensuring that GPs can recognise and refer ME to clinics that can intervene early and mitigate the severity of the illness. This potentially reduces the levels of social care and welfare support required and, in time, should make huge net savings. A recent study by Simon M Collin et al, The Impact of CFS/ME on Employment and Productivity in the UK, showed that,


“each year 4.424 working age adults with CFS/ME might be referred for specialist assessment, and that this group would already have incurred productivity costs of £102.2 million due to their illness by the time of the assessment”.

The researchers conclude:


“The main implication of our findings is that effects on employment and productivity must be accounted for in estimates of the cost-effectiveness of CFS/ME interventions and service provisions”.

They make the point that many adults are not referred to specialist centres and that this financial estimate is very conservative. Indeed, earlier research by Sheffield Hallam University concluded that the total costs to the nation of CFS/ME exceed £3 billion when account is taken of the costs of healthcare, welfare support and social care in addition to lost earnings.

Simply looking at the economic aspects of the illness, it makes good sense to ensure early diagnosis. Research shows that early intervention by specialist teams will frequently prevent the illness becoming severe. There is clearly a need for joined-up thinking. Clause 12 inserts new Section 3B(3), which requires the Secretary of State to have regard to four key points. I think that I have made the case for ME to be an appropriate case for the board to prescribe services and facilities. It is time that the discrimination against these patients ended, and this Bill could provide just the vehicle.
http://www.meassociation.org.uk/?p=8383

wonderfullife
14-10-2011, 03:35 AM
Serology is currently the method of choice for the laboratory diagnosis of Lyme Borreliosis, but it must be interpreted with caution. A total of 954 patients with suspected Lyme borreliosis were evaluated on the basis of clinical and serological data. The seroprevalence of Borrelia burgdorferi antibodies was 4.4 percent (42 of the 954 serum samples). The most frequent clinical manifestation was erythema migrans which occurred in 50 percent of the seropositive patients, followed by neuroborreliosis (16.6 percent) and arthritis (11.9 percent). Carditis was rare. Our findings suggest that for the diagnosis of Lyme borreliosis, serologic tests need to be combined with clinical signs and symptoms.
http://www.ncbi.nlm.nih.gov/pubmed/21978712

wonderfullife
14-10-2011, 03:37 AM
Thirty-five deer mice, Peromyscus maniculatus, were trapped on Gannet Cluster 2 (GC-2), one of a group of islands numbered by convention in the Gannet Island Archipelago, and examined for ectoparasites. One species each of Acari (Ixodes uriae) and Siphonaptera (Orchopeas leucopus) were recovered. Samples of mice favored males to females (3.41). Twenty-nine percent (10) of the mice were free of ectoparasites. Males were more heavily parasitized than females when both parasites were considered. No ticks were recovered from the female mice, while the males that were parasitized carried adult Ixodes uriae. These 2 ectoparasites parasitizing P. maniculatus, which is a known reservoir host for Lyme disease (Borrelia burgdorferi), may carry B. garinii and their presence would have serious implications for the spread of this human pathogen northward in continental North America.
http://www.bioone.org/doi/abs/10.1645/GE-2548.1

wonderfullife
18-10-2011, 08:03 PM
Ehrlichiosis is a disease caused by several tick-borne bacterial species in the genus Ehrlichia (pronounced err-lick-ee-uh) which were first recognized in 1935. Over the next several decades, since these veterinary pathogens that caused disease in dogs, cattle, sheep, goats, and horses were identified. Currently, three species of Ehrlichia in the United States and one in Japan are known to cause disease in humans; others will likely be recognized in the future as methods of detection improve.

Human Erhlichioses

There are two major types of human ehrlichiosis in the U.S.; human monocytic ehrlichiosis (HME), caused by E. chaffeensis; and human granulocytic ehrlichiosis (HGE), caused by E. phagocytophila. Clinically, they are difficult to differentiate. Symptoms for both include fever, headache, malaise, and muscle aches. Rashes occur more frequently with HME than HGE. Treatment for both are with antibiotics in the tetracycline family, most commonly doxycycline. Fatalities are rare (2-3% of diagnosed cases), but can occur as the result of complications from infection. Complete diagnosis requires serological or molecular tests to differentiate Ehrlichia species, but treatment should begin after clinical diagnosis. Asymptomatic infections probably occur with all Ehrlichia. Improved diagnostic tools and an increased awareness of ehrlichiosis are revealing that these infections are more common than previously suspected.

Equine and Canine Ehrlichiosis

Both horses and dogs are susceptible to Ehrlichia, although the species involved vary (see below for details). In dogs, the clinical signs for different types of ehrlichiosis are similar and difficult to separate clinically. These include fever, epilepsy, incoordination, lethargy, anemia, and bleeding episodes. Asymptomatic infections are probably common. The clinical signs in horses vary more between the two types of ehrlichiosis. Signs of equine granulocytic ehrlichiosis (EGE, E. phagocytophila) include fever, lethargy, anorexia, ataxia and limb edema. Equine monocytic ehrlichiosis (Potomac horse fever, E. risticii) most often manifests as colitis (inflamation of the colon), resulting in diarrhea, colic, loss of appetite, depression, and possibly laminitis.

Biology of Ehrlichia

Ehrlichia are bacteria, related to Rickettsia, and are obligate intracellular parasites, meaning they can not survive outside of a cell. These bacteria have only recently begun to receive much research attention, and there are still many questions about their transmission cycles and reservoir hosts. There are likely to be taxonomic revisions of Ehrlichia and Anaplasma as further research occurs. Many Ehrlichia are tick-borne, although there are some species which use other invertebrates as intermediate hosts, such as snails and helminths. The transmission cycles for some Ehrlichia species have not yet been determined.

Ehrlichia are often differentiated based on the mammalian cell type they infect. Monocytes, granulocytes, and neutrophils are most frequently involved, and the common name of the resulting disease reflects the cell type (e.g. monocytic or granulocytic ehrlichiosis). More than one species of Ehrlichia can cause disease in most vertebrate hosts.

Species of Ehrlichia in the U.S.

Ehrlichia chaffeensis

Disease: humans (HME), rarely monocytic erhlichiosis in dogs.

Vectors: Amblyomma americanum (lone star tick); possibly Dermacentor variabilis (American dog tick)

Distribution: HME has been diagnosed from every state in the U.S. except the Dakotas. It is more common in the southeastern U.S., largely congruent with the distribution of A. americanum.

Reservoir hosts: probably white-tailed deer, rodents and/or dogs.

Ehrlichia phagocytophila

Disease: granulocytic ehrlichiosis in humans (HGE), horses (EGE), dogs, cattle.

Vector: In the eastern U.S., Ixodes scapularis (black-legged tick or deer tick). Elsewhere, other members of the I. ricinus group (I. ricinus, I. pacificus, I. persulcatus).

Distribution: U.S., Europe. In the U.S., it has been reported from areas where I. scapularis and I. pacificus are present, predominately in the northeast, midwest and California. Cases have been identified in Florida, but the level of transmission is unclear.

Reservoir hosts: rodents, possibly deer.

A note on species nomenclature: Initially, the agent of HGE was identified as an Ehrlichia but not named. Later, it was determined that the agent of HGE, E. equii (agent of equine granulocytic ehrlichiosis), and E. phagocytophila (agent of ehrlichiosis in cattle and deer in Europe), were genetically almost identical. The name E. phagocytophila has priority, and all three are now generally considered as E. phagocytophila. Some literature may differentiate between the three, and revision of the group is likely to change some generic and specific names.

Ehrlichia canis

Disease: primarily dogs (canine monocytic ehrlichiosis).

Vectors: Rhipicephalus sanguineus (brown dog tick), possibly A. americanum.

Distribution: worldwide.

Ehrlichia ewingii

Disease: primarily dogs (canine granulocytic ehrlichiosis). Human infection is rare.

Vectors: unknown, but likely to be R. sanguineus or A. americanum.

Distribution: primarily the southcentral states in the United States.

E. risticii

Disease: Horses (Potomac horse fever or equine monocytic ehrlichiosis); has also been isolated from dogs. An equine vaccine is available, but protection is of short duration and booster inoculations are required.

Vector: unknown but not tick-borne. Snails and helminths may be involved as intermediate hosts.

Distribution: much of North America, particular the east coast; Europe. More common along major waterways and in summer.

Other Ehrlichia

Other Ehrlichia have been described and may be agents of disease for livestock and wild animals. The taxonomic status of some of these are unclear and the transmission cycles are largely unknown.

Florida Situation

Typically, there are 1-5 reported cases of human ehrlichiosis in Florida each year. More cases probably occur, but are not severe enough to seek medical attention or are not confirmed by laboratory tests. Veterinary cases are not always reported, but both canine and equine ehrlichiosis also occur in Florida.

In August 2001 an unusual cluster of 4 ehrlichiosis cases in Jefferson county occurred, prompting the county health office to declare a medical alert. The conditions that led to this cluster are unknown, but it is likely to be related to tick populations and tick-human contact. The species of Ehrlichia involved was confirmed in one case, and is probable in the others, as E. chaffeensis.

Several species of ticks which transmit Ehrlichia spp. are present in Florida. These include I. scapularis, A. americanum, and D. variablis.


Prevention and Management

As with any vector-borne pathogen, the primary disease preventative measure is to minimize contact with the vectors. For humans, protective clothing, such as long pants and socks tucked into pants will reduce tick contact; repellents containing DEET are effective against most ticks. Permethrin-based repellents can be sprayed on boots and clothing. For dogs, there are various treatments in sprays, spot-ons and collars (active ingredients include permethrin, fipronil, amitraz). Permethrin and pyrethroid based sprays and spot-ons for horses will reduce tick bites.

For all host species, thorough tick checks and grooming to remove attached ticks will reduce transmission of tick-borne pathogens. Use fine-tipped forceps to remove ticks; grasp the tick near the skin and pull straight back. Do not squeeze the abdomen or apply heat or petroleum products; this may cause the tick to regurgitate into the host!

Tick population reduction is difficult and it is unclear how effective it will be in reducing infection rates. Various methods have been tested, including vegetation management, acaracide treatment, host exclusion, and host treatment. Treatment of hosts, via treated feed or feeding stations that apply acaricide to hosts, are promising methods for population reduction of ticks which feed on deer.

Further Information

Bakken, J. S. and J. S. Dumler. 2001. Proper nomenclature for the HGE agent. Emerging Infectious Diseases 7: 486. http://www.cdc.gov/ncidod/eid/vol7no3/bakken.htm

CDC's Health Topics: http://www.cdc.gov/ncidod/dvrd/ehrlichia/Index.htm

McQuiston, J. H. et al. 1999. The Human ehrlichioses in the United States. Emerging Infectious Diseases 5: 635-642. http://www.cdc.gov/ncidod/eid/ vol5no5/mcquiston.htm

Ticks: http://edis.ifas.ufl.edu/IG088



Footnotes

1.

This document is Fact Sheet ENY-662 (IN191), one of a series of the Entomology and Nematology Department, Florida Cooperative Extension Serivce, Institute of Food and Agricultural Sciences, University of Florida. Date first published: February 2001. Reviewed: August 2006. Please visit the EDIS Web site at http://edis.ifas.ufl.edu.


2.

Cynthia C. Lord and C. Roxanne Rutledge Connelly, Assistant Professors, Florida Medical Entomology Laboratory, Vero Beach, FL; Entomology and Nematology Department, Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida, Gainesville, 32611.


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The Institute of Food and Agricultural Sciences (IFAS) is an Equal Opportunity Institution authorized to provide research, educational information and other services only to individuals and institutions that function with non-discrimination with respect to race, creed, color, religion, age, disability, sex, sexual orientation, marital status, national origin, political opinions or affiliations. For more information on obtaining other extension publications, contact your county Cooperative Extension service.

U.S. Department of Agriculture, Cooperative Extension Service, University of Florida, IFAS, Florida A. & M. University Cooperative Extension Program, and Boards of County Commissioners Cooperating. Millie Ferrer-Chancy, Interim Dean.
http://edis.ifas.ufl.edu/in191

wonderfullife
18-10-2011, 08:06 PM
A type of bacterium known to cause dental decay and skin ulcers may also be linked to bowel cancer, scientists suspect.

Two independent research teams have now found the bug Fusobacterium in colon tumours.

It's not yet clear if the pathogen might cause cancerous changes or whether it is an incidental finding, they told Genome Research journal.

If it is to blame, antibiotics might be able to treat it and prevent cancer.

Bowel cancer is the third most common cancer in the UK after after breast and lung.

Although the exact cause of bowel cancer is unknown, there are certain factors that increase risk, such as a strong family history of the disease and older age.

It may be that Fusobacterium infection can be added to that list, according to the experts, but they say much more work is needed to establish this.

The infection has already been linked with a gut condition called ulcerative colitis which is itself a risk factor for bowel cancer.

Continue reading the main story
Early warning signs and symptoms
A persistent change in normal bowel habit, such as going to the toilet more often and diarrhoea, especially if you are also bleeding from your back passage
Bleeding from the back passage without any reason, particularly over the age of 50
A lump in your tummy or a lump in your back passage felt by your doctor
Unexplained iron deficiency in men or in women after the menopause
Unexplained extreme tiredness

And other cancers are known to be linked with certain bacteria and viruses - for example, HPV and cervical cancer.

The first study, led by Dr Robert Holt from Simon Fraser University in Canada, identified Fusobacterium's hallmark in RNA present in bowel cancer tumours. RNA is genetic material similar to DNA which is involved in transmitting and translating the genetic code.

The other team, led by Dr Matthew Meyerson from the Dana-Farber Cancer Institute in Boston, US, found microbial sequences of DNA indicative of Fusobacterium.

Together, they looked at more than 100 samples of healthy and cancerous bowel tissue.

Sarah Williams, of Cancer Research UK, said the research gave a clue about the environment in which bowel cancer grows, but added: "It's early days and we look forward to the results of more specific, in-depth studies.

"In the meantime, people can reduce their risk of bowel cancer by not smoking, cutting down on alcohol, keeping a healthy weight, being active, reducing the amount of red and processed meat in their diet and eating plenty of fibre."
http://www.bbc.co.uk/news/health-15333364

wonderfullife
20-10-2011, 10:13 PM
Shortly after 6 p.m. on a drizzling, dreary November day in 2010, two men dressed in green surgical scrubs opened the door of the Iceman's chamber in the South Tyrol Museum of Archaeology in Bolzano, Italy. They slid the frozen body onto a stainless steel gurney. One of the men was a young scientist named Marco Samadelli. Normally, it was his job to keep the famous Neolithic mummy frozen under the precise conditions that had preserved it for 5,300 years, following an attack that had left the Iceman dead, high on a nearby mountain. On this day, however, Samadelli had raised the temperature in the museum's tiny laboratory room to 18°C—64°F.

With Samadelli was a local pathologist with a trim mustache named Eduard Egarter Vigl, known informally as the Iceman's "family doctor." While Egarter Vigl poked and prodded the body with knowing, sometimes brusque familiarity, a handful of other scientists and doctors gathered around in the cramped space, preparing to do the unthinkable: defrost the Iceman. The next day, in a burst of hurried surgical interventions as urgent as any operation on a living person, they would perform the first full-scale autopsy on the thawed body, hoping to shed new light on the mystery of who the Iceman really was and how he had died such a violent death.

Egarter Vigl and Samadelli carefully transferred the body to a custom-made box lined with sterilized aluminum foil. In its frozen state, the Iceman's deep caramel skin had a dignified luster, reminiscent of a medieval figure painted in egg tempera. With the agonized reach of his rigid left arm and the crucifixate tilt of his crossed feet, the defrosting mummy struck a pose that wouldn't look out of place in a 14th-century altarpiece. Within moments, beads of water, like anxious sweat, began to form on his body. One droplet trickled down his chin with the slow inevitability of a tear.

This was not the first time that the Iceman had been subject to intense scientific scrutiny. After Austrian authorities first recovered the mummy in 1991, scientists in Innsbruck cut a large gash across his lower torso as part of their initial investigation, along with other incisions in his back, at the top of the skull, and on his legs. It was later determined that the shallow conch of gray rock where he had been found was on the Italian side of the border with Austria, so the body and the artifacts surrounding it were relocated to Bolzano. Over the years, numerous less invasive explorations of the remains were conducted there, including x-ray and CT scan imaging studies and an analysis of the mummy's mitochondrial DNA. The most astonishing revelation came in 2001, when a local radiologist named Paul Gostner noticed a detail that had been overlooked in the images: an arrowhead buried in the Iceman's left shoulder, indicating that he had been shot from behind. Later work by Gostner and his colleagues with more powerful CT imaging devices revealed that the arrow had pierced a major artery in the thoracic cavity, causing a hemorrhage that would have been almost immediately fatal. The oldest accidentally preserved human ever found was the victim of a brutally efficient murder.

Other scientists filled in biographical details. Analysis of chemical traces in his bones and teeth indicated that Ötzi, as he is also called, grew up northeast of Bolzano, possibly in the Isarco River Valley, and spent his adulthood in the Venosta Valley. Pollen found in his body placed his final hours in the springtime, and his last hike probably along a path up the Senales Valley toward an alpine pass just west of the Similaun Glacier. Close examination of his hand revealed a partially healed injury, suggestive of a defensive wound from an earlier fight. DNA analysis of food remnants found in his intestines—his stomach appeared to be empty—indicated that sometime before he met his demise, he had eaten red meat and some sort of wheat. Putting these facts together, scientists theorized that adversaries had an altercation with the Iceman in the valley south of the pass, chased him, and caught up with him on the mountain, where the body was discovered more than 5,000 years later.

It was a good story that fit the evidence—until Gostner took a closer look at the Iceman's guts. Though he had retired, the radiologist kept studying the CT scans at home as a kind of hobby, and in 2009 he became convinced that scientists had mistaken the Iceman's empty colon for his stomach, which had been pushed up under his rib cage and appeared to Gostner to be full. If he was right, it meant the Iceman had eaten a large, and presumably leisurely, meal minutes before his death—not the sort of thing someone being chased by armed enemies would likely do.

"Gostner came over and told us he thought the stomach was full," said Albert Zink, director of the EURAC Institute for Mummies and the Iceman in Bolzano, who oversaw the autopsy last November. "And we thought, OK, then we have to go inside and sample the stomach." After further thought, Zink and his colleagues drew up a more ambitious plan: a head-to-toe investigation involving seven separate teams of surgeons, pathologists, microbiologists, and technicians. Perhaps most remarkable, this choreographed intervention would be accomplished without making any new incisions in the Iceman's body. Instead, the scientists would enter the body through the "Austrian windows"—their name for the overenthusiastic cuts made by the initial investigators.

"This will happen once," Zink said, "and then never again for many, many years."

"This is the brain," announced neurosurgeon Andreas Schwarz, as he maneuvered a neurological endoscope into the top of the Iceman's head. Like the other scientists in the room, Schwarz was wearing 3-D glasses, and as he inched the instrument deeper inside the skull, a blurry 3-D image appeared on a computer monitor. It was a little after 1 p.m., and by that point the Iceman had already undergone six hours of poking, probing, gouging, and sample gathering. The surgical teams had taken snippets of muscle and lung. They had bored a hole in his pelvis to collect bone tissue for DNA analysis. They had rummaged around his thorax, trying to get close to the arrowhead and the tissue around it. They had even plucked some of his pubic hair. His skin had lost its luster and had a dull, leathery look, like a chicken wing left in the freezer too long.

Now they were peeking inside his brain to see if a mysterious shadow on a previous CT image might be an internal clot, or hematoma, at the rear of the skull, indicating a blow to the head. But the operation was not going smoothly. Schwarz's endoscope kept bumping into ice crystals that blurred the camera lens. After an hour, the neurosurgery team finished up, not entirely sure whether they had obtained a viable sample.

The initial attempts to explore the stomach were also frustrating. Peter Malfertheiner, of the Otto-von-Guericke University of Magdeburg, tried to insinuate an endoscope down the Iceman's throat into the stomach, but five millennia of atrophy and mummification blocked the way. Egarter Vigl stepped in with a less delicate approach. Using the large Austrian window at the lower end of the torso, he stuck a gloved hand into the Iceman's gut. He pulled out two large chunks of undigested food, then switched to a kitchen spoon and scooped several more ounces from the Iceman's very full stomach.

By the end of the day, the laboratory freezer brimmed with 149 biological samples—"enough for about 50 papers," quipped one of the biologists. As soon as the autopsy concluded, Samadelli lowered the temperature in the laboratory below freezing. The next morning he and Egarter Vigl spruced up the body with a fine spray of sterilized water, which froze on contact. Then they slid the Iceman back into his high-tech igloo and closed the door.

The autopsy had taken about nine hours; analysis of the material gleaned will take years. The first revelations were disclosed in June, when Zink and his colleagues presented some of their initial findings at a scientific meeting. Thanks to the DNA in a tiny speck of pelvic bone culled during the autopsy, the Iceman has joined the company of renowned biologists James D. Watson and J. Craig Venter as one of a handful of humans whose genomes have been sequenced in exquisite detail.

The genetic results add both information and intrigue. From his genes, we now know that the Iceman had brown hair and brown eyes and that he was probably lactose intolerant and thus could not digest milk—somewhat ironic, given theories that he was a shepherd. Not surprisingly, he is more related to people living in southern Europe today than to those in North Africa or the Middle East, with close connections to geographically isolated modern populations in Sardinia, Sicily, and the Iberian Peninsula. The DNA analysis also revealed several genetic variants that placed the Iceman at high risk for hardening of the arteries. ("If he hadn't been shot," Zink remarked, "he probably would have died of a heart attack or stroke in ten years.") Perhaps most surprising, researchers found the genetic footprint of bacteria known as Borrelia burgdorferi in his DNA—making the Iceman the earliest known human infected by the bug that causes Lyme disease.

The autopsy results have also rewritten the story of the Iceman's final moments. The neuroscientists determined that blood had indeed accumulated at the back of the Iceman's brain, suggesting some sort of trauma—either from falling on his face from the force of the arrow, Zink speculated, or perhaps from a coup de grâce administered by his assailant. DNA analysis of the final meal is ongoing, but one thing is already clear: It was greasy. Initial tests indicate the presence of fatty, baconlike meat of a kind of wild goat called an alpine ibex. "He really must have had a heavy meal at the end," Zink said—a fact that undermines the notion that he was fleeing in fear. Instead, it appears he was resting in a spot protected from the wind, tranquilly digesting his meal, unaware of the danger he was in.

And of course, unaware of the intense attention awaiting him far in the future. The Iceman might be the most exposed and invaded person who ever walked the planet. "There were moments yesterday," Zink said in a soft, almost surprised voice, "when you felt sorry for him. He was so … explored. All his secrets—inside him, outside him, all around him—were open to exploration." He paused and added, "Only the arrowhead remains inside him, as if he's saying, This is my last secret."
http://ngm.nationalgeographic.com/2011/11/iceman-autopsy/hall-text

I find this hard to believe that they were able to find bb in a 5000 year old body and yet they cannot find it in living humans now.

wonderfullife
20-10-2011, 10:26 PM
The bacteria that live in and on us might be responsible for whether we are healthy or unhealthy, and even whether we are fat or thin, writes Ed Yong.

I was born just under 30 years ago. That moment, just before I emerged into the world, was the last time in my life that I would be completely sterile.

Inside the womb, it was just me and mum - a universe of two. But outside, there was a world of bacteria and other microbes, and as soon I entered that world, they became part of me. They colonised my skin. They set up shop in my guts. And these passengers are an essential part of my life.

These hitchhikers, and the genes they carry, are known as the microbiome. We all have them, and they are legion.

There are 100 trillion of them - more than the number of people who have ever lived. Walt Whitman was right when he said: "I am large - I contain multitudes."

Their cells outnumber mine by 10 to one. Their genes outnumber mine by 100 to one. To the nearest approximation, I am microbes
So who am I? Ed Yong, a human defined by my body and my genome? Or am I a vehicle for bacteria? Am I one individual or an entire universe?

I think it is the latter. These bacteria are not just passive passengers - they affect my life, my health, even my mind. They are like a hidden organ, as essential to me as my intestines or my stomach, but rather than a single mass, this is an organ made of millions of swarming cells.

It is also an organ with many jobs. The bacteria allow me to harvest energy from my food, by breaking down substances that I otherwise could not. They manufacture nutrients that I cannot make myself. They suppress the growth of harmful bacteria that would otherwise make me ill. They educate my immune system, teaching it to treat them as me and not attack them.

To all intents and purposes, my microbiome is me. They are my partners in life. My story is theirs and to understand me, you need to understand them.

My microbiome consists of thousands of species, and they come in many different communities. Yet my microbiome is distinct from yours. There is some overlap, but no two people have quite the same collection. Think about different cities like London and Tokyo. They contain residents of different cultures, occupations and backgrounds, all mingled together in different ways to produce communities with different characters.

And that is what our microbiomes are like - their membership is influenced by all the events of our lives, right from our first day. I was born naturally, so my first bacteria come from my mum.

It amuses me to think that mum's first birthday present to me was a slathering of vaginal microbes. Not quite the Xbox I had in mind, but unquestionably more useful. If I was born via C-section, I would have ended up with a different set of colonisers, from my mum's skin and from the hospital environment.
This is a big moment, because these pioneers dictated which species arrive later. The ones I got from Mum wielded lots of genes for breaking down milk proteins - clearly, that is a useful ability to have if you are eating nothing but milk for many months.

Breast milk does not just feed baby. It contains special sugar molecules that nourish baby's first bacteria. These molecules may even have evolved as part of breast milk, to selectively feed the right bacteria in a baby's bowels.

When I moved on to solids, my menu became more diverse, and so did my microbiome. It started to include many more species. That is because gut bacteria help to break down our food and each type uses its own cutlery set - the genetic equivalent of steak knives or soup spoons. So gut bacteria are our partners in digestion.

However, because our food today is largely uncontaminated and heavily processed, we risk having a more simplified microbiome. Eating too much food has the same effect. When we flood our guts with calories, as we often do in developed countries, some species of bacteria bloom at the expense of others. This is why obese people have a less diverse microbiome than lean people.

Antibiotics could do the same thing. I received dozens of courses of antibiotics as a child, many of which were for viral infections like colds, which antibiotics do nothing for. Antibiotics kill bacteria, the ones we want as well as those we do not. These grow back, but there is some evidence that they never fully recover.

So in many ways, because of the events in my life, Planet Ed is a less diverse place than it might have been a century ago. The various cities on my body are becoming a bit gentrified. And that might be a problem.

A diverse microbiome is not just about digesting food. It influences my immune system. It crowds out harmful bacteria. It could influence our risk of bowel diseases, allergies, asthma, obesity, diabetes, and infections.

It is important to understand this. I said earlier about my bacteria that to understand me, you need to understand them. Perhaps in the future, we will be able to solve certain medical problems by influencing our hidden legions. That is already starting to happen.

An American doctor, Alexander Khoruts, has treated people with crippling gut infections by - and brace yourselves if you are a bit squeamish - basically giving people poo transplants.

He has taken the gut bacteria of a healthy person and put them inside a sick person. No-one quite knows why it works, but it seems to. This is really early science, but it heralds a future where we may be able to more deliberately manipulate our gut passengers to improve our health. If I go to a doctor, maybe she will check my gut type as well as my blood type.

It is also important to understand that the microbiome is not a group of tenants, who I happen to accommodate. They are not pets. These bacteria have a surprising and perhaps unsettling degree of control over my fate.
If you take sterile mice and give them the microbiome of fat mice, they too become fat. Why? Because these bacteria were extracting more energy from the animals' food, and manipulating the animals' biochemistry so that it stored fat rather than burning it.

The microbiome could also affect our brain. We know that sterile mice, which do not have any microbiome at all, behave differently from normal ones. They are more active, less anxious and less risk-averse.

And you can change all of that if you transplant a microbiome into them at an early age. One group of scientists even managed to change the behaviour of normal mice by feeding them with one specific species of bacterium - it changed the levels of signalling chemicals in their brains, and reduced behaviours that are analogous to stress, anxiety or depression.

No-one really knows how this works in mice, let alone whether it applies to humans. But it does seem that the microbiome has some sort of impact on our behaviour, even if we do not quite know the details yet.

Our knowledge about the microbiome is still in its infancy. Scientists are discovering more and more all the time.

But for the moment, it is clear that I at least would have a diminished understanding of my own life if I failed to consider the teeming millions that share it with me. My microbiome does not just live inside me - it is me.

In many ways, I am like a superorganism - an alliance between the genes of several different species, only one of which is human.
http://www.bbc.co.uk/news/magazine-15356016

wonderfullife
20-10-2011, 11:35 PM
Despite improvements in prevention, diagnosis and treatment, Lyme borreliosis (LB) is still the most common arthropod-borne disease in temperate regions of the northern hemisphere, with risk of infection associated with occupation (e.g. forestry work) and certain outdoor recreational activities (e.g. mushroom collecting). In Europe, LB is caused by infection with one or more pathogenic European genospecies of the spirochaete Borrelia burgdorferi sensu lato, mainly transmitted by the tick Ixodes ricinus. Recent surveys show that the overall prevalence of LB may be stabilising, but its geographical distribution is increasing. In addition, much remains to be discovered about the factors affecting genospecific prevalence, transmission and virulence, although avoidance of tick bite still appears to be the most efficient preventive measure. Uniform, European-wide surveillance programmes (particularly on a local scale) and standardisation of diagnostic tests and treatments are still urgently needed, especially in the light of climate change scenarios and land-use and socio-economic changes. Improved epidemiological knowledge will also aid development of more accurate risk prediction models for LB. Studies on the effects of biodiversity loss and ecosystem changes on LB emergence may identify new paradigms for the prevention and control of LB and other tick-borne diseases.

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Introduction

Lyme disease (or Lyme borreliosis, LB) is a multisystemic inflammatory disorder caused by an immune response to the pathogenic genomic species of Borrelia burgdorferi sensu lato (sl), which are transmitted by the hard ticks of the Ixodes ricinus species complex [1,2]. Despite substantial efforts to improve surveillance and control of LB in recent decades, it is still the most prevalent arthropod-borne disease in the temperate regions of the northern hemisphere [1], with approximately 65,500 patients annually in Europe (including notified cases and qualified estimates per country from 1987 to 2006, although the years covered vary) [3]. In the last few decades, the incidence of LB has been increasing in some countries and areas of Europe, but not in others. However, the effect of improvements in diagnosis and reporting of the disease on such statistics is unknown (see [3] for a review). Less controversial is the fact that the geographical distribution of LB is still expanding, especially towards higher altitudes and latitudes ([3] and references therein). Moreover, LB is likely to become an increasingly relevant health risk in the near future due to complex interactions between diverse environmental and socio-economic factors, which will affect various aspects of disease ecology and epidemiology, as outlined below.

The importance of LB has led to a surge in research effort, on all aspects of LB biology, ecology and epidemiology. The purpose of this review is to summarise the most recent findings (especially those of the last five years) and indicate where there is still controversy and lack of knowledge.

Transmission, epidemiology and clinical symptoms

Ecology and disease transmission
The ecology of LB is based on interactions between the pathogenic agent (B. burgdorferi sl), the vector (Ixodes ticks) and vertebrate reservoir hosts.

The B. burgdorferi sl complex currently comprises at least 18 genospecies [2]. In Europe, several of these are pathogenic to humans: B. afzelii, B. garinii, B. burgdorferi sensu stricto (ss), B. bavariensis (previously B. garinii OspA serotype 4) and B. spielmanii, while the pathogenicity of others such as B. lusitaniae, B. valaisiana, and B. bissetii is still uncertain [4]. In ticks, B. afzelii and B. garinii are the most common European circulating genospecies, followed by B. burgdorferi ss and B. valaisiana [5], whereas B. lusitaniae has a more focal distribution, especially in the Mediterranean basin [6]. Several genospecies may also be present simultaneously in a vector [5]. Although all pathogenic genospecies may cause erythema migrans (a red rash or patch on the skin), different genospecies are also associated with other clinical manifestations of the disease: B. burgdorferi ss is most often associated with arthritis and neuroborreliosis, B. garinii with neuroborreliosis, and B. afzelii with the chronic skin condition acrodermatitis chronica atrophicans [7].

The distribution and prevalence of various genospecies is known to vary on a local and regional scale, both temporally and spatially [5,8] with a higher biodiversity of genospecies between 4 °W and 20 °E, where there is a higher prevalence of ticks infected with Borrelia [8]. In addition, there is an uneven geographical distribution of LB manifestations across Europe: in Norway, for example, 71% of LB cases have neuroborreliosis, while in Germany, 85% of cases have erythema migrans [9]. Borrelia genospecies are also associated with particular reservoir hosts: for example, B. afzelii and B. bavariensis tend to be associated with rodents, B. valaisiana and most B. garinii serotypes with birds [4], B. lusitaniae with lizards and B. spielmanii with dormice [10]. On the basis of the sequence of housekeeping genes, it has been shown that the genetic structuring of Borrelia genospecies is dependent on the migration pattern of host populations [11], so that genospecies that are associated with birds are dispersed further than those associated with mammals. Borrelia can also be classified according to outer surface protein (Osp) sequences (there are 21 OspC major groups) and recent research suggests that these genotypes are ecologically and epidemiologically diverse [12,13]. However, despite its relevance to development of preventive measures and treatment, knowledge of the distribution and symptoms associated with each genospecies and genotype is still far from complete, and the genetics of Borrelia transmission and virulence are starting to be unravelled [10,14].

The bridge vectors (vectors that feed on more than one host species) that transmit B. burgdorferi to humans in Europe are primarily the tick I. ricinus and, less frequently, I. persulcatus. Ticks have three life stages: larva, nymph and adult, each lasting one to two years. Hard ticks seek hosts by ‘questing’ or climbing up grass stems or onto the edge of leaves, and extending their forelegs in response to thermal and chemical cues. They then drop or crawl onto hosts that pass or brush their forelegs. Larvae, nymphs and female adult ticks take one blood meal, lasting several days, from a vertebrate host (while adult males mate with feeding adult females). Between meals, the larvae and nymphs remain in leaf litter until moulting is complete, while adult females lay a batch of eggs in the litter then die). Borrelia may be acquired by a tick from feeding on an infected host or when feeding very close to an infected tick on the same, even uninfected, host (transmission by co-feeding) or from the site where an infected tick has recently finished its blood meal, (transmission by localised extended co-feeding) [10]. Once infected, competent tick species retain the pathogen even between moults, effectively transmitting the pathogen to the next feeding stage and/or to a host.

The most recent meta-analysis of surveillance data indicates that the overall mean prevalence of Borrelia infection in ticks in Europe is 13.7% (range: 0–49.1) although the prevalence is higher in adults (18.6%) than in nymphs (10.1%); Central Europe (Austria, Czech Republic , Germany, Switzerland, Slovenia and Slovakia) has by far the highest rates (in nymphs, >11%; in adults, >20%) [5]. In fact, peak prevalence has recently been confirmed between 5 °E and 25 °E longitude [8].

The capacity of ticks to transmit Borrelia to various hosts is influenced by a series of factors, including those intrinsic to ticks (e.g. questing behaviour, diapause duration, host preference, mating strategy [15] and tick density [16]), as well as extrinsic biotic and abiotic factors (e.g. climatic conditions, vegetation type and management, and host behaviour, abundance, susceptibility, tick burden and reservoir competence [17-20]). It has been shown that ticks infected with Borrelia may actually have an increased host-finding capability [21]. The tick–host interaction is particularly important for Borrelia infection dynamics, since the feeding tick secretes salivary vasoactive mediators and immunomodulators that facilitate the transmission of the pathogen from the tick to the host and vice versa [22]. Transmission efficiency can also vary in relation to Borrelia genospecies and duration of host infectivity [23,24].

Tick nymphs are mainly responsible for transmitting Borrelia to humans and quest most actively from spring to autumn in microenvironments with more than 85% relative humidity, such as in deciduous or mixed woodland with high ecotonal indices [17,25], as well as in suburban and urban environments [26] and roadsides [27]. For humans, exposure risk in a known tick-infested site can be as high as one infected tick per person per hour of exposure, or 0.25 infected ticks per 100 metres walking distance [21]. Transmission does not usually occur within the first 24 hours of the blood meal [28], so immediate removal of ticks is a highly recommended preventive measure (see below).

In Europe, confirmed competent reservoir hosts (i.e. tick hosts that can be infected with Borrelia and transmit this agent to uninfected ticks) include many common species of small and medium-sized rodent (mice, rats, squirrels, hares and rabbits), as well as several bird species (especially passerines), reptiles and insectivores [10,29]. Conversely, many large wild and domesticated vertebrates (e.g. deer and sheep) are considered non-competent reservoirs (i.e. ticks feeding on them do not acquire Borrelia; however, ticks may transmit Borrelia to each other when feeding very close together on these non-competent hosts). Host specificity is the result of the resistance or sensitivity of Borrelia genospecies to the serum complement of various host species, which leads to the survival or death of the pathogen, respectively [30]. Importantly, non-competent reservoir hosts, such as deer, may also serve as crucial maintenance hosts for feeding ticks of all stages [10]. The presence and density of these hosts is associated with the density of ticks, but their effect on tick-borne infection dynamics is complex [31]. The presence of non-competent reservoir hosts can decrease the transmission potential of Borrelia, reducing the prevalence in the vector and subsequent disease risk to humans (a dilution effect [32,33]). Ogden and Tsao [34] have shown that any host that feeds enough ticks to reduce the overall infection prevalence in nymphs, by diverting them away from competent host species, would be likely to increase the tick population density by improving the chances of successful tick feeding. However, the overall effects of changes in biodiversity on LB emergence have yet to be thoroughly investigated [35].

Epidemiology
Although LB is not a particularly new emerging disease, an accurate description of LB epidemiology in Europe is still not possible because few countries have made this disease mandatorily notifiable [3,9,36]. Unfortunately, there appears to be no plan to continuously monitor LB at the European level [37]; instead this is recommended only ‘Where the epidemiological situation in a Member State so warrants ...’, although such situations are not defined [38]. Therefore, surveillance statistics in Europe are based on non-standardised case criteria and uncoordinated systems of data collection [39,40]. Moreover, these data are inaccurate because patients with erythema migrans and other clinically diagnosed cases may be under-reported, the geographical distribution of referrals for testing is unknown, the criteria for serological diagnoses are not standardised, seropositivity due to past infection may be included, and data from remote regions may be lacking [41,42]. In addition, patients may be infected by one or two (rarely three) pathogenic B. burgdorferi genospecies and heterogeneity in symptoms caused by these various agents complicates surveillance [43].

A summary of the currently available epidemiological data is available in [3]. Epidemiological studies indicate the mean annual number of LB notified cases (including qualified estimates) in Europe is more than 65,400 (incidence rates per country range from less than one per 100,000 population to about 350 per 100,000 population). In Europe, LB occurs between 35 °N and 60 °N, and generally below 1,300 metres above sea level. However, there is strong heterogeneity in spatial distribution: the level of antibodies to B. burgdorferi sl is highest in residents of northern and central countries and lowest in those in the southern countries. In addition, at a local level, there is a focal pattern of distribution related to suitable tick habitat, including some hotspots where more than 100 cases per 100,000 population per year are recorded (e.g. parts of Slovenia, Germany and Austria, the Baltic coastline of southern Sweden, and some Estonian and Finnish islands).

LB risk is specifically linked to tick abundance and exposure. Therefore, although higher risk is no longer considered to be correlated with residency in rural areas, higher LB risk is associated with occupation (e.g. forestry work and farming) and especially with certain leisure activities (e.g. hunting, mushroom collecting and berry picking) and age (with two groups mainly affected: children aged 5–14 years and adults aged 50–64 years).

Since infection is correlated with tick abundance and exposure (and, therefore, tick activity), diagnosis of acute LB peaks in June and July in many northern and central countries of Europe, while a second smaller peak may occur in southern countries in late summer or early autumn; however, both erythema migrans and chronic forms of the disease can be diagnosed throughout the year [3]. Although the number of LB cases seems to be increasing in some areas, such trends are extremely heterogeneous and/or remain to be confirmed [3].

Clinical symptoms
The clinical presentation of LB ranges from acute to chronic illness, with wide variation attributed to the different Borrelia genospecies and/or genotypes implicated in the infection (as described above and in [44]), although the exact mechanisms maintaining chronic symptoms have yet to be confirmed. Diagnosis is primarily clinical and takes into account the risk of tick bite. Clinical case definitions for use in Europe – although not official European Union case definitions – are available in [45].

Briefly, several days or weeks after a tick bite, if Borrelia infection occurs, in 60–80% of cases this will be characterised by erythema migrans (the rash or patch on the skin about 10 cm across that may expand peripherally as a palpable band, and may or may not be itchy) [46], although early infection may be completely asymptomatic. Other early symptoms include influenza-like symptoms, fever, fatigue, headaches and muscle or joint pain. Several weeks or months after infection through a tick bite (with or without a previous history of erythema migrans), neuroborreliosis (noted in 10–20% of symptomatic patients) in the form of meningoradiculitis, meningitis or meningoencephalitis [47], Lyme arthritis or Borrelia lymphocytoma may occur [45]. Less frequently, multiple erythemata, or carditis are diagnosed [45,48]. Months or even years after Borrelia infection, acrodermatitis chronica atrophicans, lymphocytoma, chronic arthritis (fairly rare in Europe), encephalomyelitis or chronic neuroborreliosis (very rare in Europe) may be observed [45].

Microbial or serological confirmation of Borrelia infection is needed for all manifestations of the disease except for typical early skin lesions [49]. The diagnosis of some chronic forms of LB is currently controversial [50], and it has also been suggested that the overdiagnosis and overtreatment of LB may be an important problem [51].

Diagnostic methods

Direct detection of B. burgdorferi sl
Although the diagnosis of LB is primarily based on the most obvious clinical sign, erythema migrans, diagnosis of other forms of LB require confirmation by means of a diagnostic test [52]. A wide range of methods have been developed for the direct detection of B. burgdorferi sl in clinical tissue specimens, including microscopic examination, detection of B. burgdorferi-specific proteins or nucleic acids, and cultivation. Although culture is the most commonly used method of direct detection, success rate depends on sample type. While mean recovery rates of Borrelia from skin biopsies of patients with erythema migrans and acrodermatitis chronica atrophicans are up to 70% [43], those for cerebrospinal fluid (CSF) are much lower. Future diagnostic methods may include PCR-based molecular techniques that can rapidly confirm clinical diagnosis of LB, and identify Borrelia genospecies in tissue specimens or cultured isolates [53]. However, even molecular methods have not yet been standardised since protocols and gene targets vary between laboratories and more clinical validations are needed [53]. Importantly, a negative PCR result does not necessarily indicate the absence of Borrelia [54]; therefore, the use of a PCR-based assay to confirm diagnosis of LB in the absence of serological evidence of Borrelia infection is not currently recommended.

Indirect diagnosis of B. burgdorferi sl
The complexity of the antigenic composition of B. burgdorferi sl and the temporal appearance of antibodies to different antigens at successive time intervals after Borrelia infection means the development of a serological test with high sensitivity and specificity is a challenge. The most commonly used serological methods for the detection of antibodies to B. burgdorferi sl include indirect immunofluorescent antibody assay (IFA) and an enzyme-linked immunosorbent assay (ELISA) [54]. Nevertheless, specific antibodies are often not detectable in the early stage of infection with the use of currently available test methods.

In more than 50% of cases, diagnosis of LB can be made on the basis of an expanding erythema (confirmed after a one-week follow-up). In the absence of erythema migrans at least one other clinical manifestation must be noted and confirmed using serological diagnosis of Borrelia in blood or CSF. According to the most recent German Society for Hygiene and Microbiology (Deutsche Gesellschaft für Hygiene und Mikrobiologie, DGHM) guidelines [43], serological diagnosis for patients in Europe should follow a two-step procedure: (i) ELISA and if reactive, followed by (ii) an immunoblot, if possible using recombinant antigens (p100, p58, p41i, VlsE, OspC, DbpA), including those expressed primarily in vivo (VlsE and DbpA), instead of whole-cell lysate antigen blots. OspC and VlsE are the most sensitive antigens for IgM antibody detection [54]. European standardisation of these diagnostic tests and new markers for detecting active infections are urgently required [55].

Treatment

Surprisingly, our review found that there is no European consensus on treatment and that economic considerations and national guidelines on avoidance of drug resistance also impact the current treatment of choice (no comparative costs are available). Treatment of the vast majority of LB cases is based on antibiotics, with drug type, dose, route (oral or intravenous) and duration varying with stage of the disease, as well as with symptoms. Treatment regimes and recommendations are summarised from the regularly updated European Union Concerted Action on Lyme Borreliosis (EUCALB) website [1] and [49], where doses can also be found. See also [49,51,56] for recent reviews on evaluation of treatments.

In general, in almost all LB cases, the disease is resolved with short courses of antibiotics [51,57], although longer courses are recommended for relapses or more serious and/or chronic forms. Some authors advocate that all symptomatic LB cases should be treated in order to avoid progression to later stages of the disease, and suggest that the earlier treatment begins, the less likely it is that more severe forms will follow [58]. However, overtreatment is considered a problem by others [51], although thus far, drug resistance has been noted only in vitro [59]. On the other hand, few data are available on the risk of long-term effects of non-treatment in asymptomatic LB patients [60]. Several studies have now shown that a few so-called chronic or ‘post-LB’ forms of the disease do not respond to antibiotics, although the reason for this is subject to some debate [50,51,61].

The main risks involved in treatment appear to be inappropriate patient management following inaccurate diagnosis. As mentioned above, both over- and underdiagnosis of LB is suspected.

Prevention

It has been suggested that individual or community measures to reduce the probability of tick bites and LB infection could be extremely effective preventive methods [62-64]. For example, in order to decrease the risk of tick bites and Borrelia transmission, people living in or visiting tick-infested areas are advised to avoid tick habitats, to wear long, light-coloured trousers (tucking them into socks) and to use insect repellent that contains permethrin (on clothes) or N,N-Diethyl-meta-toluamide (DEET) (on clothes or directly on skin). After visiting or working in such areas, a shower is recommended and a thorough check for ticks should be done, including careful inspection of the neck, armpits and groin. Tick bites can also be avoided by carefully inspecting and removing ticks from pets [65]. Any attached ticks should be removed immediately with tweezers if available, by seizing and pulling steadily on the mouthparts, without twisting [66] and the attachment site disinfected. Since ticks do not have a high probability of transmitting Borrelia until 12–24 hours after beginning to feed, immediate removal of ticks is one of the most effective ways of avoiding Borrelia infection. The site should be monitored for 30 days after the bite for signs of erythema migrans (there are many websites that clearly illustrate these procedures, e.g. [67]).

There is currently no vaccine available on the European market. Thus far, the development of a vaccine for humans against B. burgdorferi sl infection has concentrated on the highly immunogenic outer surface proteins of this pathogen. Although an OspA-based vaccine was developed and licensed in 1998, it was withdrawn from the market in 2002 for economic reasons, as well as doubts as to its long-term efficacy (it was also not recommended for children under the age of 15 years or for people with arthritis). The future of vaccines of this type is uncertain; vaccine research continues, with the aim of generating protection against all pathogenic genospecies of B. burgdorferi sl [68]. New approaches include transmission-blocking vaccines, which act on proteins produced by ticks that appear to improve the transmission of the Borrelia spirochaetes from vector to host [69]. Factors critical to an effective and accepted vaccine will probably include the following: a detailed knowledge of the host–parasite cycle on a local, regional and European scale and of the distribution and prevalence of Borrelia genospecies; a better understanding of the symptoms associated with infection with each genospecies; and standardised serological confirmation of all suspected LB cases, including genospecies identification. Further studies on the role of surface lipoproteins of B. burgdorferi sl are also urgently needed [70]. In addition, enhancement of the epidemiological surveillance of LB, both of the disease itself and the abiotic and biotic factors that affect it, would improve risk assessment and aid prevention immeasureably [71].

Current geographical distribution of LB

LB occurs across Europe, with a distribution closely matching that of the vector I. ricinus. This tick species can be infected with Borrelia throughout its wide latitudinal range, from northern Turkey and the Atlas Mountains of Tunisia to northern Sweden [8,72,73]. Infected tick density also decreases with increasing altitude, although the ticks are now found at up to 1,300 metres [74,75]. Consequently, the incidence of LB decreases from the endemic areas of central Europe to the southern and northern limits [3,8]. However, studies on a local scale often reveal a higher incidence than previously recorded at a regional scale [16], so that monitoring LB locally may be important for treating and preventing the disease.

Factors triggering changes in LB incidence

The changes in capacity of I. ricinus to transmit B. burgdorferi sl in Europe could be due to changes in elements of the transmission process [40,76], such as: transmission coefficient (due to genetic changes in pathogen, vector and/or host [10]); survival rates of ticks (as a result of favourable abiotic changes [72]); increased tick abundance (resulting from increased availability of reservoir hosts and/or habitat [77]); increased exposure of humans to tick bites (due to an increase in outdoor activities [76]). Theoretical studies indicate that complex interactions between these factors will probably yield wide spatio-temporal fluctuations in the relative abundance of different Borrelia genospecies and LB incidence [23].

Global climate change inducing higher minimum temperatures (night-time and winter) and earlier springs are likely to affect many aspects of tick phenology [78], such as their local distribution, density and survival rates. For example, as a result of climate change, ticks have already spread into higher latitudes and altitudes in many European countries [72,75,78], while tick abundance is mainly affected by host abundance and habitat structure [25,79]. Regional studies with reliable long-term surveillance data show that an increase in tick abundance has also resulted in an increased incidence of LB, and that this increase is correlated with climatic factors [77]. However, climate change may not contribute to an overall increase in LB, since there may be an extended and more intense LB transmission season in some areas, while the risk of LB could decrease, at least temporarily, in locations with repeated droughts or severe floods, as shown in [80].

Instead, climate-related changes in land use and socio-economic influences on human behaviour are more likely to have a strong impact on the distribution and abundance of ticks and Borrelia infection risk (as noted for tick-borne encephalitis; [81]), especially in highly disturbed ecosystems, such as managed forests, peri-agricultural and urban and peri-urban sites [79]. A concomitant increase in the density of wild and domestic vertebrates, paralleled with expansion of suitable habitats for competent reservoir hosts, is expected to increase tick density, B. burgdorferi circulation and hence LB incidence [22,35,40,78,82]. The specific and combined contributions of all environmental and socio-economic factors to the observed pattern and predicted future impact of several tick-borne diseases in Europe were assessed within the Framework 6 Integrated Project Emerging Diseases in a changing European eNvironment (EDEN) [83].

Assessing the risk of infection

The complex multi-strain multi-host interactions associated with B. burgdorferi sl infection make it difficult to determine the risk of infection to humans [29,84,85]. While risk assessment may be based on well-planned surveillance of tick and Borrelia genospecies distribution and abundance [86,87] and/or serological surveillance of Borrelia infection in humans [88-90], it has been also been suggested that high-risk biotopes should be identified [91]. Spatial models have been developed to identify high-risk areas based on environmental and climatic features [92]. A model based on the long-term trends of habitat suitability for I. ricinus in Europe shows that the distribution of such habitats has remained relatively stable, although parts of Europe show increasing (Ireland, and parts of the United Kingdom, France, Spain, Portugal and Italy) or a decreasing (Balkans, countries in the central parts of Europe and southern Scandinavia) suitability [80]. On a smaller spatio-temporal scale, the risk of exposure to Borrelia-infected ticks in the Italian Alps was predicted with a model based on bootstrap aggregation of tree-based classifiers within a geographic information system (GIS) [93]. The resulting map of the probability of encountering a questing I. ricinus nymph infected with B. burgdorferi sl has provided an important risk assessment tool for local human health authorities and policymakers.

Although the above methods can be used for risk and human exposure assessments, they cannot be used for addressing these as dynamic processes during a growing or declining epidemic. A detailed R0 (basic reproduction number) map would be an easy-to-interpret overview of LB risk following the introduction of B. burgdorferi sl into an area and could be suitable for following an LB epidemic (R0 being a measure of the risk of establishment of a disease in a certain area or population, defined as the expected number of new infections induced by a typical infectious individual during the full infectious period in a susceptible population [94]). For tick-borne pathogens, R0 can now be estimated using a next-generation matrix method [95], based on accurate biological conditions. However, Rosà and Pugliese [96] found that the effect of host densities on the R0 of tick-borne infections depends strongly on the regulation of tick populations. Since there is currently very little information on which factors affect natural tick populations, more complete, long-term field data are still needed before accurate R0 maps can be produced.

Conclusion

In Europe, the annual number LB cases is increasing in some areas, and tick vectors are expanding their range, to higher altitudes and latitudes, suggesting that LB will remain an important health concern in the coming decades, especially in light of economic, land use and climate change predictions. In addition, the effect of the resulting biodiversity loss and ecosystem changes on LB emergence should be an important focus of investigation, especially to identify new paradigms for the prevention and control of LB and other tick-borne diseases. It emerges from our review that standardised diagnoses are crucial to treating and combatting LB in Europe, as are European-wide reporting systems and datasets concerning all aspects of the molecular ecology and epidemiology of LB [10]. Preventive measures aimed at minimising tick-bite risk are promoted as one of the best ways to avoid Borrelia infection. Many authors agree that a concerted effort to improve surveillance is essential for monitoring this disease [9,36,49,55] and we consider that more complete eco-epidemiological knowledge is also needed to develop accurate risk prediction models.

Acknowledgements
We thank the Autonomous Province of Trento for funding research on wildlife disease at the Fondazione Edmund Mach. The preparation of the manuscript was also funded by the European Centre for Disease Control (ECDC public tender OJ/2007/04/13 – PROC/2007/003: Assessment of magnitude and importance of vector-borne diseases in Europe. Contract number ECDC.63).
http://www.eurosurveillance.org/View...rticleId=19906

wonderfullife
22-10-2011, 07:42 PM
http://www.bbc.co.uk/iplayer/episode/b016c128/Landward_2011_2012_Episode_17/

Try and watch b4 taken off internet.

Tick slot starts at 22.09

wonderfullife
22-10-2011, 08:43 PM
One might wonder how anything so tiny could cause controversy so huge.
The deer tick may be barely visible to the naked eye — about the size of a sesame seed — but the bug can carry with it Lyme disease and a boatload of misery and controversy.
This month, that host of ills is front and centre as York Region politicians and municipalities lend their voice to concerns over the disease, health officials scour local forests for signs of it, and medical experts from around the world converge in Toronto to discuss how it can be beat.
Lyme disease is an illness caused by the Borrelia burgdorferi bacteria spread through the bite of an infected black-legged tick. Symptoms can include a bull’s-eye rash, fatigue, fever, headache, muscle and joint pain and swollen lymph nodes.
Quick treatment with antibiotics is critical for recovery, but some say that debates over testing and diagnosis have left many Canadians misdiagnosed, chronically ill and paying for treatment outside the country to try to recover their lost health.
Jessica Taliana became active in the fight for better ways to deal with the disease after both her children became infected.
The Woodbridge resident told a York Region Council of Health and Community Services meeting this week that Lyme is spreading seven times faster than AIDS and West Nile put together.
“You have a province full of angry, upset people who feel helpless, hopeless and abandoned by their own health care.”
Not everyone shares those views, though.
Ministry of Health records show relative stable numbers in Ontario, about 100 cases per year over the past four years. Spokesman Andrew Morrison said infected ticks are much more common in the United States, compared to the relatively limited areas in southern and eastern Ontario locations where it can be found, along the north shores of Lake Erie, Lake Ontario, plus the St. Lawrence River.
But Jim Wilson, with the Canadian Lyme Disease Foundation, suggests the numbers are much higher, but hidden because of Canada’s reliance on faulty testing.
Dr. Daniel Cameron, past president of the International Lyme and Associated Diseases Society, says the incidence of Lyme is growing in Canada, especially in Ontario, spreading via migrating songbirds which carry on average 1.5 deer ticks on every bird crossing the U.S. border.
The U.S.-based society holds its annual conference in Toronto next week, the first time in Canada.
“Lyme is a political disease,” said Rosanna Magnotta, whose husband Gabe passed away after suffering from Lyme for years.
Mr. Magnotta, owner of Magnotta Winery in Vaughan, went undiagnosed under Canada’s two-stage blood test until the infection was too entrenched in his body to be overcome, she says.
A sold-out fundraiser in Mr. Magnotta’s memory held in Richmond Hill Sept. 30 raised nearly $6,000 for the cause.
At the same time, a petition by MPP Brian Bailey, calling for better testing, training of doctors and public awareness, is garnering support, endorsed this week by Newmarket and Richmond Hill councils.
Vaughan, Markham, Aurora and East Gwillimbury have also lent their support to the petition, as have several federal politicians including Frank Klees and Julian Fantino, according to Richmond Hill’s Josephine Vaccaro-Chang, one of the fundraiser organizers.
It is not certain exactly how prevalent Lyme is in York Region. This month, the region is scheduled to begin tick sampling in two York Region forests.
A flannel cloth will be dragged through vegetation and leaf litter and black-legged ticks will be submitted to the federal lab for Lyme disease testing.
York’s medical officer of health, Dr. Karim Kurji, says some of the concerns among Lyme activists may be valid. Not all doctors are well-educated on Lyme and the tests may not be picking up all the strains, he says.
Between 2005 and 2011, 14 cases were reported in the region, none contracted here, he said. However those numbers reflect only those cases reported to public health, he said, and don’t include those diagnosed with different tests outside of the country.
But Dr. Kurji would not comment on Canada’s testing protocol. “That is not the area where we are the experts,” he said, adding the Centre for Disease Control in Atlanta and Canadian Public Health Laboratory Network support current testing.
“It is quite a controversial field,” he said.
The region is doing its best to raise awareness, he said, and he understands the concerns of those who were not diagnosed in time.
“They did not receive antibiotics they needed and suffered badly or their families suffered badly. We are sympathetic to that.”
.

http://www.yorkregion.com/community/article/1230282--tiny-lyme-tick-provokes-huge-controversy

wonderfullife
22-10-2011, 09:11 PM
http://goanimate.com/movie/0XCA4kvs8vk4?utm_source=facebook

Worth a watch

wonderfullife
27-10-2011, 09:47 PM
Patients with Lyme disease often report dissatisfaction with how their case has been (mis)handled by medical professionals and the medical establishment in general. Many have called on celebrities with Lyme disease to use their exposure to raise Lyme awareness and force changes in how the disease is diagnosed and treated. There are many famous people rumored to have Lyme disease, or to have overcome the condition, as well as a handful who have openly admitted to having been seriously affected by the infection with the spirochaetal Lyme disease bacteria. Writers with Lyme disease

A number of authors have gone on record stating that they suffered (or continue to suffer) from Lyme disease, perhaps because the cognitive effects of Lyme have such a profound result on a writer’s ability to continue working. Maintaining a handle on intricate plot development and the finer points of your protagonist’s character clearly suffer immensely when neuroborreliosis has confounded your short-term memory and your concentration is non-existent. Rebecca Wells, author of The Divine Secrets of the Ya-Ya Sisterhood is one such author, who faced diagnoses of dystonia, epilepsy, and was even encouraged to simply take antidepressants to clear up her symptoms.

Perhaps the most vocal of Lyme disease advocates who are also authors is Amy Tan, author of The Joy Luck Club and The Bonesetter’s Daughter, amongst other books. Tan is still affected by the condition after contracting the infection in 1999. Details of her experience with Lyme disease are given on the author’s website (AmyTan.net) and included flu-like illness, numbness and tingling in the extremities, neck stiffness, insomnia, rapidly vacillating blood sugar levels, and fourteen brain lesions in her frontal and parietal lobes. A New York Times Bestselling writer, Tan possibly explains the cognitive effects of Lyme disease better than most: “By day, my memory was held together with friable threads, my concentration was as easy to disperse as blown dust…”. Such Lyme disease symptoms will be familiar to many patients.
Another writer having suffered with Lyme disease is the Pullitzer Prize-winning Alice Walker, author of The Color Purple. Walker has documented her struggle with Lyme disease in an essay entitled ‘The Same River Twice: Honoring the Difficult’, written and published in 1996. At the time Alice Walker became symptomatic with Lyme disease she was filming The Color Purple and the problems she experienced had a profound effect on her relationship (which eventually broke down) as well as her ability to work. Walker has become something of a Lyme disease advocate since her experience, despite having been effectively cured of the condition with appropriate treatment.

Singers and Actors with Lyme Disease

Daryl Hall, of Hall and Oates fame, is possibly the most famous singer having suffered from Lyme disease. Hall was diagnosed in 2006 after becoming extremely ill whilst on stage and actually stumbling off stage with a fever of 102 degrees. The rest of the duo’s July tour was cancelled as Hall returned to New York for treatment. As Hall was treated promptly with antibiotics he appears to have no lasting effects from the illness, a familiar story with many celebrities who are lucky enough to be able to afford extensive and speedy health-care in contrast to many with chronic Lyme disease.

Neneh Cherry is another celebrity affected by Lyme disease; the singer contracted the infection around 1990 and Lyme disease prevented her from doing much work until 1992 during a slow convalescence from the infection.
Meadow Soprano faced a number of terrifying scenarios in the HBO series The Sopranos, but the actor who played her, Jamie-Lynn Sigler described her ordeal with Lyme disease in her memoir ‘Wise Girl’. Sigler contracted Lyme disease when she was nineteen and filming the series in Hamburg, Sussex County, at the height of the cult TV show’s popularity. Initial symptoms included tingling in her feet which rapidly progressed to paralysis of her legs. She spent five days in Long Island’s North Shore Hospital while doctors desperately tried to diagnose her condition, eventually treating her with appropriate antibiotics. Sigler apparently suffers no ill-effects as a result of her terrifying experience but has said that “It was such a life-altering experience… I realized it could all be taken away in a moment.“

Richard Gere is another casualty of Lyme disease, although he also appears to be cured of the disease with no chronic effects. Gere was diagnosed with Lyme disease as he was about to start filming ‘Autumn in New York’ with Winona Ryder. The infection laid him low for a week but the actor was quickly diagnosed and treated. Talking to friends about the experience Gere allegedly said “This is one scary disease. I felt as though every ounce of strength had gone from my body. Within hours I could barely lift my head from the pillow.”
Archer Wins Gold after Lyme Paralysis

Archery champion Mel Clarke has had a rough ride during her career, with an extremely debilitating case of Lyme disease almost proving fatal as she attended the World Archery Championships in America in 2003. Clarke, ranked second in the world at the time, quickly became ill during competition and within minutes was unconscious and rushed to hospital. The then 23yr-old was connected to a life-support machine in hospital with doctors fearing for her life. Unconscious for nearly two weeks, Clarke awoke to find herself on a ventilator and being tube-fed.

The world champion archer already suffered from reflex sympathetic dystrophy (an arthritic condition) and was left paralysed from the waist down and blind in one eye after her battle with Lyme disease. Despite these considerable obstacles, and doctors telling her that she would never shoot an arrow again, Mel Clarke is now one of Britains’ top Paralympians with six Paralympic world records to add to her ten national able-bodied records.
Other Famous Lyme Disease Patients

Other celebrities with Lyme disease include Brooke Landau, freelance reporter and producer most famous for her work on the Today Show. Landau gave an interview to NBC because she “wanted to talk to others because I would not have been sick for 7 years if the insurance companies didn’t make money off of sick people.” Landau had a congenital heart defect, a possible reason why she was so badly affected by Lyme disease which can cause Lyme carditis.
Perhaps the most famous person to have revealed their brush with ticks is George W. Bush. Medical records released by the White House showed that the former president was successfully treated for early localized Lyme disease after his doctors spotted the Lyme disease rash, erythema migrans. The president’s love of mountain-biking is likely the cause of his exposure to ticks and some have blamed the infamous malpropisms and linguistic oddities uttered by George W. Bush on the cognitive effects of Lyme disease. The seeming simplicity of Bush’s Lyme disease case meant that the former president did nothing to aid other Lyme disease patients during his time in office and one wonders what would have happened had he experienced symptoms of chronic Lyme disease. Actress Parker Posey, and bushcraft expert Ray Mears are other famous people with Lyme disease stories who are doing more to highlight the condition; hopefully their media exposure can help bring about positive change.
http://lymediseaseguide.org/celebrities-with-lyme-disease

wonderfullife
27-10-2011, 09:52 PM
Lyme disease symptoms in animals are often very similar to adult symptoms of Lyme disease or Lyme disease symptoms in children. The difficulty detecting symptoms in animals however is that they cannot directly communicate how they are feeling, meaning that you have to be alert to subtle changes in your companion animals’ behaviour, especially if you think that they may have been exposed to Lyme disease infection. Lyme disease has been reported in dogs, cats, horses, cows, and goats and symptoms frequently include fever, lameness, joint soreness, listlessness and fatigue, loss of appetite, and swollen glands. Where infection spreads it can result in problems with the heart, liver, kidneys, eyes, and nervous system, with younger animals often at risk of acute issues such as kidney failure. Chronic Lyme disease symptoms in animals may include unexplained weight loss, laminitis, spontaneous abortions, and poor fertility, particularly in horses and cows. Some of those caring for animals such as horses and dogs have also noted changes in mood and temperament following Lyme disease, which may be a symptom in itself or could stem from chronic pain from Lyme arthritis, or general fatigue and malaise. Just as in humans with Lyme disease, the symptoms in animals are likely to be intermittent and variable, making it difficult to judge whether they are all part of the same condition or are a reaction to long walks, other infection, environmental conditions, nutritional deficiencies, or other medical issue. The initial signs of Lyme disease may also be difficult to detect with any rash often concealed by an animal’s coat, and signs of fatigue frequently dismissed as a simple reaction to a long country walk or being away from home on a camping trip, for example.

Where Lyme disease is suspected in an animal it is important to seek medical attention and assessment as soon as possible in order to begin treatment. Antibiotic treatment for Lyme disease in animals is usually very effective, especially when started promptly, and most animals recover and experience no long-term adverse effects. Where treatment is delayed there may be more severe damage which is more difficult to repair and may need other medications or treatments to control, such as anti-inflammatory drugs or dialysis.
Lyme Disease Symptoms in Animals – Prevention

Lyme disease prevention is obviously preferable to having to have your animals suffer Lyme disease infection and require treatment. In areas endemic for Lyme disease it is wise to restrict outdoor exposure to ticks for all family members, including any animals in the house. This can mean putting up deer fences, clearing shrubbery and leaf piles around the house, keeping grass short, and avoiding areas of dense vegetation when out walking or camping. Prodigious use of tick-repellents is also wise, with permethrin very effective for tick control. Discussing tick control products with your veterinarian will help in making decisions to safeguard your pets’ health and that of the rest of the family who may be exposed to ticks brought into the home on the coats of pets. Although Lyme disease is not contagious it may be transmitted to several family members from just one tick that is brought into the house.

Vigilance is of utmost importance, with both dogs and cats best checked daily for the presence of ticks. Brushing the animals’ fur over a light colored surface can help to identify any ticks that may be brushed off in order to destroy them safely. Ticks are most commonly found on the head and neck of an animals along with the ears, toes, armpits, and groin where ticks can hide and feed unobserved. Ticks are very small however and may be disguised against an animal’s fur. Where a tick feeds for a number of days it is likely to become more visible as it swells to the size of a small grape. An engorged tick is more likely to have been in place for a longer time and to have spread Borrelia bacteria and Lyme disease. Monitoring for symptoms in any animal from whom a tick has been removed is of paramount importance although Lyme disease symptoms in animals may take several weeks or months to appear.
http://lymediseaseguide.org/lyme-disease-symptoms-in-animals

wonderfullife
28-10-2011, 02:30 PM
Swedish researchers have discovered a new tick-borne illness that can cause blood clots in the legs and lungs, with three cases having been reported in Sweden.

•Swedish researchers in 'depression gene' find (28 Sep 11)
•Sweden hit by rise in tick-borne encephalitis (27 Aug 11)
•Superbugs on the rise in Sweden (1 Jun 10)
A total of eight cases of the disease have been reported so far, with patients in Germany, Switzerland, and the Czech Republic also having been infected.

All of those affected by the disease suffer from a weakened immune system, the Dagens Nyheter (DN) newspaper reported.

The illness, which researchers call “neo disease” after the bacteria which causes it, Candidatus Neoehrlichia mikurensis, also brings about flu-like symptoms with long-lasting high fevers, coughing, and aches.

The disease can be treated with antibiotics.

The first case was discovered in the summer of 2009 after a 77-year-old man from Gothenburg came down with a high fever and lost consciousness.

During his treatment, doctors discovered blood clots in his leg and lungs. The man's fever returned several times and doctors eventually found traces of an unknown bacteria in his blood.

The disease, which is transmitted by ticks, had never before been reported in Sweden and it was unclear what caused the disease in humans.

The two additional Swedes who have become ill due to the bacteria are in their sixties and seventies.

It remains unclear why the disease causes blood clots, but researchers have a number of theories in mind.

“When the body can't deal with an infection in the blood, it traps the infection in a blood clot,” Christine Wennerås, a professor at Sahlgrenska University Hospital in Gothenburg, told the newspaper.

According to researchers, ten percent of ticks in southern Sweden carry the bacteria.
http://www.thelocal.se/36944/20111025/#

wonderfullife
28-10-2011, 02:42 PM
Borrelia burgdorferi, a tick-borne bacterial pathogen, causes a disseminated infection involving multiple organs known as Lyme disease.
Surface proteins can directly participate in microbial virulence by facilitating pathogen dissemination via interaction with host factors. Here we show that a fraction of the B. burgdorferi chromosomal gene-product BB0337, annotated as enolase or phosphopyruvate dehydratase, is associated with spirochete outer membrane and is surface-exposed. B. burgdorferi enolase, either in a recombinant form or as a membrane-bound native antigen, displays enzymatic activities intrinsic to the glycolytic pathway. However, the protein also interacts with host plasminogen potentially leading to its activation and resulting in B. burgdorferi-induced fibrinolysis. As expected, enolase displayed consistent expression in vivo, however, with a variable temporal and spatial expression during spirochete infection in mice and ticks. Despite an extracellular exposure of the antigen and a potential role in host-pathogen interaction, active immunization of mice with recombinant enolase failed to evoke protective immunity against subsequent B. burgdorferi infection. In contrast, enolase immunization of murine hosts significantly reduced the acquisition of spirochetes by feeding ticks suggesting that the protein could have a stage-specific role in B. burgdorferi survival in feeding vector. Strategies to interfere with the function of surface enolase could contribute to the development of novel preventive measures to interrupt the spirochete infection cycle and reduce incidences of Lyme disease.


PMID: 22025510 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22025510

wonderfullife
28-10-2011, 03:01 PM
Assessment of the microbial diversity residing in arthropod vectors of medical importance is crucial for monitoring endemic infections, for
surveillance of newly emerging zoonotic pathogens, and for unraveling the associated bacteria within its host. The tick Ixodes ricinus is recognized as the primary European vector of disease-causing bacteria in humans. Despite I. ricinus being of great public health relevance, its microbial communities remain largely unexplored to date. Here we
evaluate the pathogen-load and the microbiome in single adult I. ricinus by using 454- and Illumina-based metagenomic approaches. Genomic DNA-derived sequences were taxonomically profiled using a computational approach based on the BWA algorithm, allowing for the identification of known tick-borne pathogens at the strain level and the putative tick
core microbiome. Additionally, we assessed and compared the bacterial taxonomic profile in nymphal and adult I. ricinus pools collected from wo disti nct geographic regions in Northern Italy by means of V6-16S rRNA amplicon pyrosequencing and community based ecological analysis.

A total of 108 genera belonging to representatives of all bacterial phyla were detected and a rapid qualitative assessment for pathogenic bacteria, such as Borrelia, Rickettsia and Candidatus Neoehrlichia, and for other bacteria with mutualistic relationship or undetermined function, such as Wolbachia and Rickettsiella, was possible. Interestingly, the ecological analysis revealed that the bacterial community structure differed between the examined geographic regions and tick life stages. This finding suggests that the environmental context (abiotic and biotic factors) and host-selection behaviors affect their microbiome. Our data provide the most complete picture to date of the bacterial communities present within I. ricinus under natural conditions by using high-throughput sequencing technologies. This study further
demonstrates a novel detection strategy for the microbiomes of arthropod vectors in the context of epidemiological and ecological studies.

wonderfullife
28-10-2011, 03:13 PM
There has been a sharp increase in the number of reported cases of tick-borne encephalitis (TBE) in Sweden this year, according to the Swedish Institute for Communicable Disease Control (Smittskyddsinstitutet).

What increase is due to unclear, but the weather and the availability of deer and rodents are important factors.

So far this year 144 cases of the disease have been reported, marking a significant increase. In August alone, 66 cases had been uncovered as of the 24th of the month, compared with 25 to 48 cases during the corresponding period between 2007 and 2010.

However it remains a mystery as to why the numbers are so high in comparison with other years.

Areas most affected are around Stockholm and Lake Mälaren, where experts point to the growing numbers and increased resilience of ticks as well as weather conditions this year, although it is still hard to pinpoint one specific reason.

Marika Hjerteblomsten Qvist, epidemiologist at SMI told Svenska Dagbladet,
”Ticks can handle cold and snowy winters quite well, but during that time there are fewer deer, so there is no direct connection.”

The weather is also relevant to how many people were camping in the countryside, which also affects the risk of being affected.

Encephalitis, is an inflammation of the brain, caused often by a virus carried in the saliva of ticks.

"Most people who get TBE don’t even notice it. They may only have flu-like symptoms, but only about one percent of the ticks carry the virus, and even if you get bitten by one, it is not certain that you will get ill,” added Hjerteblomsten Qvist.

http://www.thelocal.se/35800/20110827/

wonderfullife
07-11-2011, 04:25 PM
Study Shows Lyme Disease More Prevalent Than Reported

By PETER BRANNEN

As the Island boards of health begin to engage in a five-year effort to battle tick-borne illnesses on the Vineyard, early field work from a group of medical students on the Island points to serious deficiencies in reporting tick diseases to state public health officials, especially for Lyme disease.

For two weeks ending last Friday, a team of rural health scholars, nursing and pharmacy students from the University of Massachusetts conducted 945 surveys on ferries, at the high school, at ESL classes and at local churches about tick-borne illness. The work complemented hours of interviews with Island health care workers and pharmacists also conducted by the students. The work is supported by a $250,000 grant from the Martha’s Vineyard Hospital.

Results presented last Friday at the regional high school show early statistical evidence of high rates of Lyme disease here.

Researchers report that in 2010 Island pharmacies filled an estimated 1,200 prescriptions for doxycycline, the antibiotic of choice for treating Lyme disease. Of those prescriptions, pharmacists estimated that 90 per cent, or 1,080 of the prescriptions were for new cases of Lyme. By contrast the Centers for Disease Control recorded 25 officially-reported cases of Lyme disease in Dukes County.

“We know that the number less than 30 is not right,” said Tisbury health commissioner and study coordinator Michael Loberg. “The state knows it’s not right, the physician prescribing community knows it’s not right. We don’t need to capture every patient; we just need to get a good representative number because we’d like to show that our interventions can change that number, and capturing only 30 patients isn’t going to give us the database we need.”

The medical students agree, saying future funding for the study and prevention of tick-borne illnesses on the Island depends on a baseline of accurate data.

“There was no one who thought that incidence reporting was anything other than very important,” said Mr. Loberg. “But I think that everyone also realizes just how beleaguered everyone is in the health care delivery space.”

To relieve some of the paperwork-intensive burden of reporting, the medical students recommend that the Island establish a dedicated tick-borne health care worker to assist providers with reporting and act as a conduit between the state Department of Public Health and the Island. Mr. Loberg is hopeful that state public health grant money may be available to support such a position.

“The good news is the state worked well with the students and I think everyone is going to be pulling in the same direction to fix this,” he said. “I’m quite hopeful.”

Researchers also underscored the importance of prophylactic treatment for tick-borne illnesses. It is now believed that taking 200 milligrams of doxycycline within 72 hours of receiving a deer tick bite can significantly reduce the chance of contracting Lyme disease. The researchers also suggested the Island consider pressing for regulatory changes that would allow pharmacists to dispense the treatment without a prescription, much like the Plan B emerg ency contraceptive pill. Survey results show that the approach has the support of Island pharmacists, even though it would require a complex legislative process.



“We’re not saying it’s easy to do, we’re not even saying it’s the right thing to do, but the students are saying that it should be looked at and I think the committee generally agrees,” Mr. Loberg said.

The medical students also found there was ample room for better education about tick-borne illnesses in the community, particularly among high-risk workers like landscapers and construction workers and also for tourists and casual visitors. While most survey respondents could identify Lyme as a tick-borne illness, many were largely ignorant of other diseases such as babesiosis and anaplasmosis. Public service announcements at local movie theatres before screenings, and education programs in the public schools were among the recommendations.

The boards of health are preparing to make a set of recommendations to the Island selectmen next year, and Mr. Loberg said the work of the medical students puts them in a good position to do so.

“I felt that in terms of the quantity of the work that they did, the thousand questionnaires that were filled out, the fact that they were able to reach out to the at-risk communities, they greatly exceeded my expectations,” he said. “But the quality of what they did even exceeded that. They’ve come up with actionable recommendations for us to consider. It doesn’t mean that we will choose to go forward with all of them but they have talked to people in the community and come back with some ideas. That’s exactly what we wanted them to do. I think they reflected very well on the University of Massachusetts.”
http://www.mvgazette.com/article.php?32750

wonderfullife
07-11-2011, 04:27 PM
The letters from the doctors all start the same way: It was a pleasure to meet this man, Bruce Shilton, a strong upstanding member of the community, criminal lawyer for 24 years, judge on the Ontario Court of Justice for six. Whatever Mr. Shilton’s health problems are, the doctors say, they will get to the bottom of it.
And they never do.
Mr. Shilton is no longer working as a criminal lawyer, no longer sitting on the bench. He is sitting, instead, at his kitchen table in Oak Ridges, rifling through a stack of letters from medical specialists, letters that offered him hope but led to dead ends.
Like many who have fallen into this Lyme disease abyss, Mr. Shilton spends most of his time sorting through medical paperwork, trying to track down a solution to the medical mystery that derailed his life 10 years ago.
TIRED OF ANONYMITY
And he is tired of doing so in anonymity. Reluctantly, this judge — who used to command attention in the courtroom — now hopes to command attention for a controversial disease and its victims who may not have the same resources and respect he has, who are sometimes viewed as hypochondriacs or kooks.
Mr. Shilton is neither. He did not know much about Lyme disease back in 1998 when he first started to get sick, but he did know a lot about the law.
A certified specialist in criminal law, he had written books, was active in legal education, sat on the Federation of Law Societies of Canada travelling panel and was appointed to the Ontario Court of Justice, posted to the Newmarket courthouse.
When he wasn’t working he was busy playing oldtimers hockey, coaching, walking the golf course two or three times a week and raising three children. He almost never got sick.
That suddenly changed.
“I remember cutting grass at the cottage and I almost collapsed. It was really strange.”
He was beset with an “unplugged feeling,” unable to focus or eat, like the worst flu ever. He figured he’d picked up some kind of bug while working at the Don Jail. But it didn’t go away.
Over the years, a host of other symptoms emerged: migraines, fatigue, painful joints, recurring sinus infections, lower back pain, abdominal discomfort and visual problems.
COULD NO LONGER WORK
He’d moved from his home near Hwy. 7 to north Richmond Hill to be near the Newmarket courts, but gradually found he could no longer make it to work. In 2004, he took a month off and never went back.
He became a “house hermit,” he says, bouncing from one specialist to the other, about 25 in all, undergoing hundreds of tests including the ELISA test for Lyme disease, but they all came back negative.
Mr. Shilton knew that Lyme disease is an illness that spreads through the bite of an infected tick, is associated with a bull’s eye rash and is best treated quickly with antibiotics.
What he found out too late is that not everyone notices a tick bite; or has the trademark rash; that the ELISA, Canada’s primary test for the infection, is notoriously unreliable; and a short round with antibiotics, if you are lucky enough to get it, does not always work.
In 2007, one of the doctors went out on a limb and sent Mr. Shilton’s blood to California for a different kind of Lyme test, the Western Blot, one that is believed to be more accurate but not the first line of testing in Canada.
“I remember asking him, ‘is it good news or bad news?’ and he told me it was both. Good news because we know what it is, bad because it’s not easy to treat.”
Not much has changed since the day he learned he has Lyme and he thinks that’s because it was not discovered early enough.
At 54, his life has come to a grinding halt.
“I have basically led the cloistered life of a chronically fatigued person. My symptoms are numerous and I have for all intents and purposes become housebound.”
The thing that drives him nuts is the certainty that all this could have been prevented — for him and thousands like him — if the health system would just get off the fence and start taking the disease more seriously, as seriously as it does, say, West Nile that gets a big media blitz every summer.
He is calling for a task force or independent review of testing and treatment protocols and ultimately, a tick-borne disease clinic.
‘WE ARE LYME LEPERS’
“We are the lyme lepers of this generation,” he says. “They ignore our requests for treatment thinking we are a bunch of whining hypochrondriacs ... Patients are left with nothing except chronic illness and ultimately a slow death when the disease finally shuts down an organ or two.”
He considers what happened to Gabe Magnotta, Vaughan’s Magnotta Winery owner who lost his life after battling the disease more than a year ago. He wonders “what will it take to get those in control of the health system to sit up and take notice? ...How is it that no politician is willing to step into the fire?”
It’s why he’s decided to speak out. After such a busy life, there isn’t much else to do.
“It’s pretty sad,” he says. “Boredom is brutal, when you go from my old life to this ...
“Judges are treated pretty well. You walk into the courthouse, you’re treated well. You get used to that. And then all of a sudden nobody knows who you are anymore. You’ve got nowhere to go, nothing to do. Your circle of life shrinks.”
His kitchen cupboard is filled with bottles of supplements and potions he hopes will get him back on his feet again. There’s something called a rife machine, an experimental frequency device. He is being treated by a specialist in New York, a Dr. Maureen McShane who contracted the disease herself in Quebec and now treats Lyme patients in a way that no Canadian doctor does, or dares to.
He thinks it is helping and he feels fortunate he can afford the treatment when so many others, unidentified and untreated, struggle in silence.
He admits it is unusual. Judges do not usually comment on government issues, especially in a critical way, but he believes it’s his duty to speak for those who can’t.
“Maybe they’ll think ‘oh, maybe these people are not so crazy after all’.”
http://www.yorkregion.com/feature/article/1233175--i-m-housebound-my-life-has-shrunk-judge

wonderfullife
18-11-2011, 05:33 PM
In many cases it is not the patient's disability that determines the disease state but rather the presence or absence of natural immune factors or antibodies. THE PROBLEM IS ANTIBODIES ARE NOT A DIRECT MEASUREMENT OF ACTIVE INFECTION EITHER.

How could this have happened?

Part of the problem was the newly emerging science and technology of antibody serology testing known as ELISA tests. (Enzyme Linked Immuno Sera Assays)

ELISA tests look for an enzymatic color change that indicates the presence or absence of Lyme antibodies in a patient's serum.

If you still see a color change when a patient's serum is diluted with 512 parts water then it is said a patient has a dilution titer of 1:512

NOTE - higher titer numbers do not have any correlation to how sick a patient is feeling! In fact a high number indicates the presence of lots of immunity. A patient with a high titer is better able to fight the infection than someone who is producing low numbers of antibody or has a borderline or even negative titer.

Not only was it clear that ELISA tests were quick and easy to develop, but they were cheap and easy to administer. The convenience of ELISA tests was a powerful enticement to both doctors and patients. Let's face it 10 CCs of blood is more convenient than having several brain, skin, bladder or heart, biopsies that would cost thousands of dollars!

The problem was that from the very beginning it was assumed and generally accepted that these tests were a better diagnostic tool than patient evaluations based on symptoms and a response to treatment.

It was erroneously accepted that the absence of antibodies in the blood meant no infection was present anywhere in the patient's body.

Even more disturbing was the incorrect assumption that the drop in antibody levels during treatment indicated a microbiological cure. Thus, many studies concluded that patients were cured if they eventually tested negative for Lyme antibodies.

Both assumptions were and continue to be incorrect!

It certainly looks good on paper for a doctor if he can tell a patient that based on the test that they are negative for Lyme disease, but in reality the more accurate statement is that the patient is simply negative for the presence of those antibodies for which that particular test is sensitive for! But absence of antibodies does not mean the patient cannot have active infection.

ELISA TESTS CAN VARY GREATLY FROM LAB TO LAb. Since each lab holds there own patent on their own test, they are all competing to say they have the best test. It is a competitive business, and certain buzz words like specificity, sensitivity, efficacy, and accuracy are used to try and out sell one competitor's lab test over another.

This gives rise to many methods of testing efficacy, which are implemented by competing labs to be able to say that their test is better than the competition's tests. This is usually based on predetermined laboratory standards.

Unfortunately, laboratory methods of determining an ELISA test's efficacy and accuracy does not directly correlate to accuracy of determining infection in a human being.

If a laboratory tests its ELISA test on 100 test tubes of an identical known sample, and simultaneously on 100 test tubes of distilled water (the control group), and it picks up 99 of the 100 samples and only one of the control samples the lab can claim their test is 99% accurate. It had a 1% rate of false negatives and a 1% rate of false positives. (The lab chooses what dilution titer it accepts as positive. For one lab it maybe 1:256 for others it is as high as 1:1024)

A 99% sensitivity sounds great and most doctors and lay people would say if they heard this data that this ELISA test is 99% effective, and accurate.

But these tests cannot tell you if a patient who is infected but makes no antibodies (seronegative patients) has active Lyme disease. Also there is evidance that in humans with high titers the tests can still be as high as 55% inaccurate!

What if I told you that some manufacturer's tests are only sensitive to only one of the antibodies we produce to the Lyme bacteria, and it is an antibody that is rarely elevated in late Lyme?

What if I told you this test only had moderate sensitivity and requires highly positive serum to have a reagent color change?

Now what if I told you that out of over 100 different Lyme ELISA tests by different labs that they were all slightly different?

And now what would you think if I told you each lab that holds a patent on its ELISA test want to make a profit on the test so they present their data in a way to make their test to appear to look better than the competition?

Now what would you say if I told you that many medical institutions are actually corporations that own patents on these Lyme tests, and that the reputations of those institutions, and the researchers that developed them are all on the line if their test is found to be fallible?

What are the consequences to the reputations of these institutions if patient who say they are still sick after treatment are denied treatment because of these fallible tests?

What if a patient becomes disabled or dies?
The admission that the Lyme bacteria is alive and sequestered in some seronegative patients is not welcome news to the developers of these tests. But rather than do the type of autopsy and tissue studies to truly compare their tests, the manufacturers have chosen to manufacture PATIENT STUDIES THAT DON'T COMPARE THEIR TESTS TO TISSUE STUDIES BUT INSTEAD TO OTHER EQUALLY BAD SERUM TESTS.
If a carpenter only has a yard stick 29 inches long, and he only tests its precision with another yardstick 29 inches long it will always appear that his yardstick is accurate!

So how do the lab's claims to the efficacy of these tests actually stand up in the real world for the diagnosis of Lyme disease?

Hundreds of labs and ELISA tests were evaluated by an independent sources, and were found several times to be less that 65% accurate. (This was based on triple-paired identical positive serum samples that were sent to 516 labs across the US) In some cases some labs were far below this average.

So without even arguing that some Lyme patient's blood can be antibody negative despite an active infection, even in the patient whose blood is highly positive, that patient still runs as much as a 45% chance or higher of still testing negative with an ELISA test.

So a patient can be antibody negative and still have infection, but they can also have loads of antibody and still test negative simply by virtue of the lab's inability to deliver consistently accurate results
http://www.avonhistory.org/bug/blot1.htm#n2

wonderfullife
26-11-2011, 09:18 PM
A 10-year-old boy was referred to the New England Eye Center because of severe bifrontal headache associated with blurry vision, vomiting and horizontal double vision for 2 weeks. The patient was currently being treated with doxycycline 100 mg by mouth twice a day, which was started 2 weeks prior to presentation for a tick bite noted on his genitalia. The patient had no other significant medical or ocular history.

Examination

On examination, the patient’s best corrected visual acuity was 20/15 in both eyes. Pupils were 5 mm and only slightly reactive to light. Extraocular motility was full. By Maddox rod, 14 ∆D of esotropia was noted in primary and left lateral gaze, with 12 ∆D of esotropia noted in right lateral gaze. Anterior segment examination of both eyes was unremarkable. Posterior segment examination was remarkable for blurred optic nerve head margins bilaterally. A peripapillary splinter hemorrhage was found superonasal to the right disc (Figures 1a and 1b).

What is your diagnosis?

Bilateral disc edema

The differential diagnosis of bilateral disc edema in a pediatric patient includes processes that may increase intracranial pressure, including mass lesions such as glioma, meningitis, dural venous thrombosis and pseudotumor cerebri.

The clinical history of severe headaches associated with nausea and vomiting in our patient suggests meningeal inflammation. Potential etiologies for subacute meningitis include viral (enterovirus), which is more common in the summer months, as well as Lyme, which is a tick-borne bacterial illness.

Dural venous thrombosis may occur in conjunction with a complicated middle ear infection (acute otitis media with mastoiditis) or sinusitis with intracranial extension. The visual symptoms tend to progress more rapidly in this subset of patients as intracranial pressure can rise quickly, and cerebral edema may also occur.

Infratentorial tumors such as pilocytic astrocytoma, medulloblastoma and ependymoma are more common in the pediatric population and may be associated with optic nerve head edema. These tumors may create a rise in intracranial pressure by direct compression of the ventricles, communication of the ventricles, or compression of the veins that drain the cerebrospinal fluid (CSF). Inflammatory and tumor cells may also clog the arachnoid villi directly. Choroidal plexus papilloma may increase CSF production and thus raise intracranial pressure.

Pseudotumor cerebri is a diagnosis of exclusion, and although the prototypical patient is an obese young woman, it has also been described in pediatric patients. In children, there is no gender predilection. Several known associations have been described, including the use of medications such as doxycycline, tetracycline, minocycline, vitamin A and recombinant growth hormone. Both the use and withdrawal of steroids have also been implicated in pseudotumor cerebri.

Diagnosis and management

Visual field testing (HVF 30-2) showed mildly enlarged blind spots bilaterally (Figure 2). Optical coherence tomography revealed elevated nerve fiber layer thicknesses of 290 µm and 260 µm in the right and left eyes, respectively (Figure 3). MRI of the brain revealed normal optic nerves without enhancement, and magnetic resonance venography was negative for dural venous sinus thrombosis. A lumbar puncture was performed. The opening pressure was 35 cm H20, and CSF analysis showed 3 WBCs/mm3 with 89% lymphocytes and a negative Lyme PCR. Serum testing for Lyme was positive for both IgM and IgG titers.

The patient was started on intravenous ceftriaxone 2 gm IV daily and acetazolamide 250 mg by mouth daily. At 10-week follow-up, his symptoms had fully resolved, vision was stable at 20/15 in both eyes, and his esodeviation had diminished to 4 ∆D. The papilledema had also improved, with a decrease in average nerve fiber layer thicknesses to 180 µm and 160 µm by OCT in the right and left eyes, respectively. He was discharged with a peripherally inserted central catheter to complete a 4-week course of IV ceftriaxone.

Discussion

Lyme disease is reported to occur in seven out of 100,000 children, with Lyme neuroborreliosis occurring in 30% of these cases. The most common manifestation of Lyme neuroborreliosis is facial nerve palsy, which is present in about half of Lyme cases that have nervous system involvement. Neuro-ophthalmic manifestations such as ocular motor palsies, particularly abducens nerve palsies, papilledema and optic neuritis can occur with Lyme disease involving the central nervous system.

Approximately 2% of children with Lyme disease develop chronic basilar meningitis. MRI with gadolinium may reveal enhancement of the meninges at the base of the temporal lobes. The onset of meningitic symptoms is often insidious and may be difficult to distinguish from viral or aseptic meningitis such as that from enterovirus. Formation of a post-meningitic obstructive hydrocephalus has been proposed to be a contributing mechanism to the development of papilledema in these individuals diagnosed with Lyme meningitis. Inflammatory cells and necrotic debris may impair CSF reabsorption through the arachnoid villi.

Treatment of Lyme meningitis should focus on eliminating the infectious agent and minimizing the resultant inflammatory response. Ceftriaxone and penicillin G are frequently used parenteral therapeutic agents for Lyme meningitis, with typical courses lasting 4 weeks in duration. The adjunctive use of corticosteroids and acetazolamide is controversial, with no firm treatment guidelines. Patients are followed clinically, and if progression is observed, steroids and acetazolamide may be used to alleviate the elevated intracranial pressure. Ventriculoperitoneal or lumboperitoneal neurosurgical shunting is reserved for severe vision loss or intractable progression
http://www.osnsupersite.com/view.aspx?rid=89679

wonderfullife
26-11-2011, 09:24 PM
4. Lyme disease

A systemic infection caused by a tick bite

Symptoms: Shortness of breath; chest or rib soreness; abdominal cramping, nausea, and vomiting; bull's-eye rash at bite site; neck stiffness; twitching of face or eyelids
Mimics: Mononucleosis, flu, chronic fatigue syndrome, fibromyalgia, depression, meningitis

Tests: If no rash is visible, a two-step blood antibody test is recommended: the ELISA or IFA

5. Multiple sclerosis

A progressive autoimmune disease that attacks the central nervous system

Symptoms: Muscle spasms, lack of coordination, balance problems, blurred vision, cognitive impairment

Mimics: Viral infection, lupus, Alzheimer's, bipolar disorder

Tests: Blood tests to rule out other disorders, a lumbar puncture, and an MRI, which may show the brain and spinal cord damage and lesions characteristic of multiple sclerosis
http://www.aarp.org/health/conditions-treatments/info-06-2011/commonly-misdiagnosed-illnesses.3.html

wonderfullife
26-11-2011, 09:30 PM
The biologist Lynn Margulis died on November 22 at the age of 73. I adapted the following essay about her from my 1996 book The End of Science.


Lynn Margulis was among the most creative challengers of mainstream Darwinian thinking of the late 20th century. She challenged what she called “ultra-Darwinian orthodoxy” with several ideas. The first, and most successful, is the concept of symbiosis. Darwin and his heirs had always emphasized the role that competition between individuals and species played in evolution. In the 1960′s, however, Margulis began arguing that symbiosis had been an equally important factor–and perhaps more important–in the evolution of life. One of the greatest mysteries in evolution concerns the evolution of prokaryotes, cells that lack a nucleus and are the simplest of all organisms, into eukaryotes, cells that have nuclei. All multi-cellular organisms, including humans, consist of eukaryotic cells.
Margulis proposed that eukaryotes may have emerged when one prokaryote absorbed another, smaller one, which became the nucleus. She suggested that such cells be considered not as individual organisms but as “composites.” After Margulis provided examples of symbiotic relationships among living microorganisms, she gradually won support for her views on the role of symbiosis in early evolution. She did not stop there, however. Like Stephen Jay Gould and Niles Eldredge, authors of the punctuated equilibrium hypothesis, she argued that conventional Darwinian mechanisms could not account for the stops and starts observed in the fossil record. Symbiosis, she suggested, could explain why species appear so suddenly and why they persist so long without changing.

Margulis’s emphasis on symbiosis led naturally to a much more radical idea: Gaia. The concept and term (Gaia was the Greek goddess of the earth) were originally proposed in 1972 by James Lovelock, a British chemist and inventor. Gaia comes in many guises, but the basic idea is that the biota, the sum of all life on earth, is locked in a symbiotic relationship with the environment–the atmosphere, the seas and other aspects of the earth’s surface. In fact, the biota chemically regulates the environment in such a way as to promote its own survival. Margulis was immediately taken with Gaia, and she joined Lovelock in promulgating the idea.

I met Margulis in May 1994 in the first-class lounge of New York’s Pennsylvania Station, where she was waiting for a train. She resembled an aging tomboy: she had short hair and ruddy skin, and she wore a striped, short-sleeve shirt and khaki pants. She dutifully played the radical, at first. She ridiculed the suggestion of Ernst Mayr, Richard Dawkins and other ultra-Darwinians that evolutionary biology might be nearing completion, in terms of not requiring any major additions or revisions. “They’re finished,” Margulis declared, “but that’s just a small blip in the 20th century history of biology rather than a full-fledged and valid science.”

She emphasized that she had no problem with the basic premise of Darwinism. “Evolution no doubts occurs, and it’s been seen to occur, and it’s occurring now. Everyone who’s scientific-minded agrees with that. The question is, how does it occur? And that’s where everyone parts company.” Ultra-Darwinians, by focusing on the gene as the unit of selection, had failed to explain how speciation occurs. Only a much broader theory that incorporates symbiosis and higher-level selection could account for the diversity of the fossil record and of life today, according to Margulis.

Symbiosis, she added, also allows a kind of Lamarckianism, or inheritance of acquired characteristics. Through symbiosis, one organism can genetically absorb or infiltrate another and thereby become more fit. For example, if a translucent fungus absorbs an alga that can perform photosynthesis, the fungus may acquire the capability of photosynthesis too and pass it to its offspring. Margulis noted that Lamarck has been unfairly cast as the goat of evolutionary biology. “We have this British-French business. Darwin’s all right and Lamarck is bad. It’s really terrible.” Margulis acknowledged that symbiogenesis, the creation of new species through symbiosis, is not really an original idea. The concept was first proposed early in this century by the Russian biologist Marachovsky. Similar ideas were set forth in the 1920′s by Ivan Emmanual Wallin in a book called Symbioticism and Origins of Species. “An absolutely beautiful, wonderful book that was totally ignored,” Margulis declared.
Before meeting Margulis, I had read a draft of a book she was writing with her son, Dorian Sagan, called What Is Life? The book was an amalgam of philosophy, science and lyric tributes to “life: the eternal enigma.” It argued, in effect, for a new holistic approach to biology, in which the animist beliefs of the ancients are fused with the mechanistic views of post-Newton, post-Darwin science. Margulis conceded that the book was aimed less at advancing testable, scientific assertions than at encouraging a new philosophical outlook among biologists. But the only difference between her and biologists like Dawkins, she insisted, is that she admitted her philosophical outlook instead of pretending that she didn’t have one. “Scientists are no cleaner with respect to being untouched by culture than anyone else.”

Did that mean that she did not believe science can achieve absolute truth? Margulis pondered the question a moment. She noted that science derives its power and persuasiveness from the fact that its assertions can be checked against the real world–unlike the assertions of religion, art and other modes of knowledge. “But I don’t think that’s the same as saying there’s absolute truth. I don’t think there’s absolute truth, and if there is, I don’t think any person has it.”
Then, perhaps realizing how close she was edging toward postmodernism, Margulis took pains to steer herself back toward the scientific mainstream. She resented depictions of her as a scientific feminist, who was trying to replace masculine concepts of nature with feminine ones. She conceded that, in comparison to such concepts as “survival of the fittest” and “nature red in tooth and claw,” her symbiosis views might seem feminine. “There is that cultural overtone, but I consider that just a complete distortion.”

She rejected the notion–often associated with Gaia–that the earth is in some sense a living organism. “The earth is obviously not a live organism,” Margulis said, “because no single living organism cycles its waste. That’s so anthropomorphic, so misleading.” Lovelock encouraged this metaphor, she claimed, because he thought it would aid the cause of environmentalism, and because it suited his own quasi-spiritual leanings. “He says it’s an okay metaphor because it’s better than the old one. I think it’s bad because it’s just getting the scientists mad at you, because you’re encouraging irrationality.”

Both Gould and Dawkins have ridiculed Gaia as pseudo-science, poetry posing as a theory. But Margulis is, in at least one sense, much more hard-nosed, more of a positivist, than they are. Gould and Dawkins each resorted to speculation about extraterrestrial life in order to buttress his view of life on earth. Margulis scoffed at these tactics. Any proposals concerning the existence of life elsewhere in the universe–or its Darwinian or non-Darwinian nature–are sheer speculation, she said. “You have no constraints on the answer to that, whether it’s a frequent or infrequent thing. So I don’t see how people can have strong opinions on that. Let me put it this way: opinions aren’t science. There’s no scientific basis! It’s just opinion!”

She remembered that in the early 1970′s she had received a call from the director Steven Spielberg, who was in the process of writing the movie ET. Spielberg asked Margulis if she thought it was likely or even possible that an extraterrestrial would have two hands, each with five fingers. “I said, ‘You’re making a movie! Just make it fun! What the hell do you care! Don’t try to confuse yourself that it’s science!’”

Toward the end of our interview, I asked Margulis if she minded always being referred to as a provocateur or gadfly, or someone who was “fruitfully wrong,” as one scientist put it. She pressed her lips together, brooding over the question. “It’s kind of dismissive, not serious,” she replied. “I mean, you wouldn’t do this to a serious scientist, would you?” She stared at me, and I finally realized her question was not rhetorical; she really wanted an answer. I agreed that the descriptions seemed somewhat condescending.
“Yeah, that’s right,” she mused. Such criticism did not bother her, she insisted. “Anyone who makes this kind of ad hominem criticism exposes himself, doesn’t he? I mean, if their argument is just based on provocative adjectives about me rather than the substance of the issue, then…” Her voice trailed off. Like other mavericks I have met, Margulis could not help but yearn, now and then, to be a respected member of the status quo, whose work merely confirmed the prevailing paradigm. But without courageous rebels like her, science would never achieve any progress.
http://blogs.scientificamerican.com/cross-check/2011/11/24/r-i-p-lynn-margulis-biological-rebel/

wonderfullife
26-11-2011, 09:37 PM
The job of Patient Advocate came upon me uninvited. I did not apply for this job, nor did I have any qualifications for it. I am a sculptor, not a doctor or a researcher. My daughter became sick with a mysterious fatigue illness and I was the obvious person to fill the job. Learning the job of a PA unfolds over time and there is no instruction manual. Certain ideas and thoughts can be transferred from former jobs and former lives, but much has to be learned from scratch. It is helpful in doing the PA job if you have a lot of time and a lot of money, as the solution to this disease takes a great deal of both. It would also be helpful to have an education in bio-chemistry, of which I have none. The most important qualification that a Patient Advocate needs is persistence and discipline. A PA also needs to remain objective and detached, even under the most extreme conditions. Every Patient Advocate has a patient. My patient is my daughter. The objective of this particular Patient Advocate is to make his daughter better. How to set about it is another matter, and turns out to be a complex and sustained set of illusive problems. While most doctors look at a broad and confusing set of symptoms and try to attach treatments to an entire cohort of partially differentiated patients, the PA’s problem is slightly different. The Patient Advocate, by job definition, is obliged to help one person - in this case, his daughter - his patient. Thus the PA is looking at one narrow and confusing set of symptoms, which makes his problem slightly easier.
Six presentations were given at the Mt. Sinai ME/CFS Research and Treatment Center conference on Sunday November 20, 2011. Here is a lecture delivered by Dr. Kenny De Meirleir, who practices medicine in Brussels. Dr. De Meirleir has worked with ME/CFS patients for many years and is seen as one of the foremost ME/CFS Clinician/Researchers. Dr. De Meirleir spoke for a half-hour on the compassionate use of GcMAF in this patient population. Dr. De Meirleir will be associated with this new ME/CFS Center at Mt. Sinai- as a clinical consultant.
http://cfspatientadvocate.blogspot.com/2011/11/mt-sinai-mecfs-conference-de-meirleir.html

wonderfullife
01-12-2011, 11:36 PM
I first started getting symptoms in July 2007. I was at Wimbledon playing and woke up one day with a lump in the side of my neck. I got some tests done as they didn’t know what it was and they weren’t too sure what they were looking for. Nothing came out of the test.

As the next few days followed I got more symptoms, which included inflamed glands, puffiness in my face and neck, a rash all over my body, extreme tiredness, headaches, body aches, swollen hands and feet.

Each day I would have something new and the doctors weren’t sure what was going on.

I think I saw four different doctors at Wimbledon. I had blood tests done and they didn’t show anything too definitive but it was thought it could have been rubella. Once I returned home it was decided that was the diagnosis.

I took about six weeks off and thought I started to feel OK. I was still puffy looking all over like I had gained weight but my weight hadn’t changed. No one could tell me not to start playing again so I practiced a little and then went to the US to play one lead-up tournament before the US Open and then the US Open.

I was nowhere near prepared enough and lost badly and then at the US Open I lost in the first round. Worse still, I was absolutely exhausted after the first four games of my first-round match.

I stayed in New York to practice with my coach for another week as he was coaching some other players too. We decided I needed to get fit again and lose the puffiness look I had going on. We practiced on court for about 1 to 1.5 hours a day and then cardio on the bike each day. It wasn’t very high intensity but I really found it difficult.

After training like this for five or six days, I started getting chest pains during dinner and periodically it would hurt to breathe. I tried to not think much of it and continued to go out with my friends but as the night went on it got worse and worse.

I went to hospital at about 3 am for tests and they couldn’t really find anything. I thankfully had the help of one of the trainers from the WTA with me and we left the hospital at about 8 am and went back to another one around 11 am as my pain was getting worse. By this stage I was also feeling nauseous.

I had more tests done and the doctors still couldn’t find anything. I spent the next day in my hotel room and didn’t go anywhere and felt somewhat OK so I decided to fly home to my training base in Tampa, Florida.

On the flight home I started getting a shocking headache and by the time we landed my head was pounding. I went to a friend’s place as I felt terrible and as that afternoon went on the pain got worse and worse.

I went home that evening and tried to go to sleep but by 6 am I couldn’t stand the pain any more and called my friend back to get her to come get me and take me to hospital.

Once arriving there they did a couple of tests and told me I had sinusitis so they sent me home with some painkillers and that was that. It turned out I was allergic to what they gave me so that made me sick and I knew the pain I had was not sinusitis.

I spoke to one of the WTA doctors on the phone that afternoon and she told me to go back to hospital and get more tests done. By about midnight the doctors came in to tell me I had viral meningitis and I had to stay in hospital.

I had a spinal tap to relieve some of the pressure and pain I was getting and stayed in hospital for the next three days. From that point I went back home and got the post-tap headache, which they said I would get and for the next seven or eight days laid in bed or on my couch and slept as much as possible. Whenever I sat or stood up I would get a pounding headache but as long as I was horizontal I was OK.

It was a horrible week and I didn’t leave my apartment for the whole time.

Thankfully the same friend who took me to hospital lived close by and would bring me food and go shopping for me as I couldn’t leave. My dad was then able to come over from Australia and he spent the next few weeks with me. Once I was able to walk around without getting headaches I went to see an infectious disease specialist in Tampa as it was decided what was happening to me was all part of the same thing and we had to work it out.

After a couple of weeks of seeing this doctor and having several different tests and visits to him he diagnosed me with Lyme disease. I had never heard of it and didn’t know what it was. He explained to me it is extremely hard to diagnose and you have to base it on symptoms as well as what the tests come back with and he was sure that’s what I had.

I went on two weeks of oral antibiotics followed by four weeks of intravenous antibiotics twice a day, four days a week followed by another two weeks of oral antibiotics.

I was told to not do any exercise during this time and really try to do as little as possible. I pulled out of all the remaining tournaments for the year and based myself in Tampa during this time. After this period it was decided I was probably well enough to fly home to Australia but was told I still had to take it easy.

I eventually started back doing very easy exercise and followed the WTA trainer’s and doctor’s advice very closely as they said I could relapse if I did too much too soon as my immune system was still working so hard to keep me healthy.

My exercise program started with a 20-minute walk every other day and keeping my heart rate under 120. That was nearly impossible, so I did this for a week then started walking every day then bumped it up to two 30-minute sessions and then I could gradually keep increasing the volume as long as I kept feeling healthy.

I started tennis practice in late February/March and trained until my first tournament at the end of April. I was worried the travel and jetlag was going to be too much so I went to the States much earlier then I would normally to acclimatise myself to the time change and weather conditions and made sure I didn’t start training there too hard too fast.

From this point I played two Challenger tournaments and then took two weeks off, played a WTA event in Rome, took another week off and then played the French Open.

There were some days leading up to the French that I felt really tired and unwell so whenever this happened I took the day off and really monitored my health and how I was feeling before I would train anymore. By July I really felt quite good and continued my playing schedule and haven’t looked back since.

On realising how dangerous Lyme can be I’m really glad I followed what the specialists told me and really took it slow to get back to normal. I think the thing that helped me a lot is that I was in the USA when I was eventually diagnosed. It is nearly impossible to know when I contracted it as I travelled through a number of European countries before falling ill in London. From there I went to Australia where Lyme isn’t recognised and then back to the States.

Since getting back to full health I have never felt any symptoms come back or relapsed in any way.
http://samstosur.com/2011/12/01/my-battle-with-lyme-disease/

wonderfullife
04-12-2011, 08:01 PM
Lyme Disease In Dogs, A Real Problem! - YouTube

wonderfullife
08-12-2011, 09:16 PM
A new tick-born disease is starting to make its way around the world. Set to rival Lyme disease, which results from a tick bite, this so-far unnamed disease mimics DVT (deep vein thrombosis), a life-threatening condition usually associated with long-haul flights.
Nine cases of the new disease have been identified, including three in the Swedish city of Gothenburg. All of the people affected had the bacterium, Neoehrlichia mikurensis, in their blood. The bacterium, identified on the Japanese island of Mikura in 2004, is found in ticks and rodents.
http://www.wddty.com/scientists-discover-a-new-lyme-disease-from-tick-bites.html

wonderfullife
08-12-2011, 09:22 PM
Seabirds act as natural reservoirs to Lyme borreliosis spirochetes and may play a significant role in the global circulation of these pathogens. While Borrelia burgdorferi sensu lato (Bbsl) has been shown to occur in ticks collected from certain locations in the North Pacific, little is known about interspecific differences in exposure within the seabird communities of this region. We examined the prevalence of anti-Bbsl antibodies in 805 individuals of nine seabird species breeding across the North Pacific. Seroprevalence varied strongly among species and locations. Murres (Uria spp.) showed the highest antibody prevalence and may play a major role in facilitating Bbsl circulation at a worldwide scale. Other species showed little or no signs of exposure, despite being present in multispecific colonies with seropositive birds. Complex dynamics may be operating in this wide scale, natural host–parasite system, possibly mediated by the host immune system and host specialization of the tick vector.

http://www.liebertonline.com/doi/abs/10.1089/vbz.2010.0267

wonderfullife
08-12-2011, 09:26 PM
Researchers at the University of Gothenburg's Sahlgrenska Academy have discovered a brand new tick-borne infection. Since the discovery, eight cases have been described around the world, three of them in the Gothenburg area, Sweden.
In July 2009 a 77-year-old man from western Sweden was out kayaking when he went down with acute diarrhea, fever and temporary loss of consciousness. He was taken to hospital where it was found that he was also suffering with deep vein thrombosis (DVT). Following treatment with antibiotics, he was discharged some days later with an anticoagulant to thin his blood. However, the man -- who had an impaired immune system -- went down with a fever again.

Brand new infection

Over the following months the 77-year-old was admitted as an emergency case on several occasions, but despite repeated attempts to find a microbe, and repeated doses of antibiotics, the fever returned. Finally the patient's blood underwent special analysis to look for bacterial DNA -- and that produced results. The findings matched a bacterium in an online gene bank and the results were a sensation: the man had contracted a brand new infection in humans which had never been described in the world before.

Never before seen in Sweden

The man's blood contained DNA that derived with 100% certainty from the bacterium Neoehrlichia mikurensis. This bacterium was identified for the first time in Japan in 2004 in rats and ticks but had never before been seen in Sweden in ticks, rodents or humans.

Christine Wennerås, a doctor and researcher at the Department of Infectious Diseases and the Department of Haematology and Coagulation at the University of Gothenburg's Sahlgrenska Academy, has been studying the case since it first came to light. Last year she was able, for the first time, to describe the newly discovered disease in a scientific article published in the Journal of Clinical Microbiology.

"Since our discovery the bacterium has been reported in eight cases around the world, three of them in Gothenburg," says Wennerås.
Causes DVT

All three of the Gothenburg cases involved patients with an impaired immune system, all of whom became ill during the summer months when ticks are most active.

"The nasty thing about this infection is that it causes DVT, at least in people with an impaired immune system," says Wennerås. "This can be life-threatening. Fortunately, the infection can be treated successfully with antibiotics.

Spreads from mammals

"If the newly discovered bacterium is similar to those we already know, it has presumably spread from wild mammals to people via ticks, and it is unlikely that it can be passed on from person to person."

The mikurensis in the bacterium's name comes from the Japanese island of Mikura, where it was first discovered.
http://www.sciencedaily.com/releases/2011/12/111206131404.htm

wonderfullife
11-12-2011, 03:14 PM
While Vermont sportsmen spend November and December hunting deer, Lyndon State College biology professor Alan Giese is busy hunting deer ticks. He tromps through the woods armed with a white flannel sheet, waving it like a flag over brush so the fabric picks up specimens.

It may not sound scientific, but Giese is surveying five locations along the Connecticut River for deer ticks, potential carriers of Lyme disease, for what he hopes will become Vermont’s first systematic tick-population study. He wants to assign hard data to a trend that scientists and public health officials have observed for years: the spread of deer ticks — and Lyme disease — throughout Vermont.

Giese and a student research assistant started their work last spring. They had planned to be done by now, but, thanks to an unusually warm autumn, the research project and its blood-sucking subjects have stayed active longer than normal this year.

“We expected them to shut down in mid-November, and they haven’t,” Giese says, noting that fall is peak season for adult-stage deer ticks. Giese warns that ticks won’t go underground until night temperatures drop below freezing — and stay there. Meterologists are forecasting warm weather for much of the next week.

A decade ago, Lyme was virtually unheard of in Vermont. In 2000, the state Department of Health recorded just 40 cases, two-thirds of them likely contracted out of state. Yet by 2009, there were 408 confirmed and probable cases, with three-quarters of them determined to have originated in Vermont.

After several years of climbing Lyme rates, 2010 saw a slight dip, to 356 cases, and health officials cautiously hoped that better prevention was causing the disease rates to plateau.

Instead, 2011 is shaping up to be the worst year yet: As of last week, there were more than 500 confirmed and probable cases, according to Erica Berl, an epidemiologist with the Vermont Department of Health.

“It had seemed like things were leveling off, so it’s a little concerning that things are going up again,” says Berl. “But one year does not a trend make. We don’t know if it will continue.”

Better detection and diagnosis are probably responsible for some of this year’s increase, Berl says, but there’s no question that deer ticks — and Lyme — are spreading north.

What’s responsible for the uptick? Several scientists point to Vermont’s healthy deer population, which has surged with the reforestation of agricultural land. When a female deer tick feeds on the protein-rich blood of a deer, it yields more eggs than from the blood of other animals, explains state entomologist Jon Turmel.

Turmel suspects the higher incidence of Lyme in 2011 is due to last winter’s heavy snowfall — snow cover has an insulating effect for ticks — and relatively mild temperatures.

“Last year we got a good snow cover before it got really cold,” Turmel says. “And we didn’t have those two weeks in January where it got to 20 below. So I think they overwintered well.”

Another theory attributes the spread of Lyme to global warming. Turmel is skeptical of that explanation, but Giese says it makes logical sense.

“Our winters are less severe,” Giese says. “They start later and end earlier, giving ticks a longer season to do their thing, more time to find a host.”

With his research assistant, Giese has been sweeping for ticks at sites in Ascutney, Thetford, Newbury, Barnet and Lancaster, N.H. His preliminary results confirm that deer ticks are slowly marching northward. At southern survey sites such as Thetford, Giese says a single 100-meter transect could pick up literally hundreds of deer ticks. In far northern Lancaster, that same sweep yielded a maximum of two ticks — sometimes none at all.

“It seems like ticks have sort of exploded,” Giese says. “Five to eight years ago, you hardly ever saw them, and suddenly — boom — they are everywhere.”

Giese also turned up “tantalizing circumstantial evidence” consistent with a study done in Maine that suggests deer ticks are more prevalent in areas with invasive shrubs such as honeysuckle and buckthorn. If nothing else, Giese hopes that might open a new front in Vermont’s war on invasive species.

“If we couldn’t motivate people to get rid of invasives by other means, we’ll scare the hell out of them with Lyme disease,” he says. “Get out the machetes and hack the stuff down!”

Lyme disease is transmitted by bites from deer ticks, officially known as,black-legged ticks, infected with the bacteria Borrelia burgdorferi. The first U.S. case was documented in Lyme, Conn., in 1975; the disease has since spread from Maine to Virginia, and as far west as California. Vermont diagnosed “sporadic” cases of Lyme in the 1980s, says Berl, the state epidemiologist. But it wasn’t until 2006 that the state started to witness a sudden, dramatic increase (see sidebar).

Most infections stem from ticks in the nymph stage because they are small enough — no bigger than a poppy seed — to go unnoticed until they are engorged with blood, 24 to 48 hours after latching onto a host. No solid data exist on the percentage of deer ticks infected with Lyme, but the state health department estimates it’s around 20 percent in Vermont.

Symptoms of early-stage Lyme disease begin days or weeks after infection and are similar to the flu: chills, fever, headache and muscle pain. If left untreated, Lyme can lead to long-term brain and neurological problems, such as memory disorders, nerve damage, numbness, and sleep and vision problems. Not all infections come with Lyme’s signature “bull’s-eye” rash, which can make diagnosis more challenging.

Turmel, the state entomologist, says the state lacks the funds to conduct comprehensive tick monitoring along the lines of what Giese is doing, but it has conducted numerous passive surveys. For three years, officials from the Vermont Department of Forest, Parks and Recreation camped out at 30 deer check-in stations around the state on opening weekend of rifle season and plucked ticks off deer. From 2002 to 2004, the state Department of Health and Agency of Natural Resources asked veterinary clinics to report ticks removed from dogs. All year round, the general public sends tick samples to Turmel and his colleagues for identification.

While commending those efforts, Giese says tick surveillance in Vermont has historically been “spotty,” making it hard to compare data sets. Giese hopes his research will produce more concrete science on how ticks and Lyme are migrating across the state.
http://www.7dvt.com/2011ticks-lyme-disease-vermont

wonderfullife
11-12-2011, 03:17 PM
Chelsey, 11, had been asked to write a letter to Santa in French for a class. The only thing she wanted for Christmas, she wrote, was to get better.

“She didn’t ask for any toys. She just wants to get better. It’s enough to break your heart,” Rector said.

Chelsey has Lyme disease, which she contracted when she was just two years old after being bit by a tick in Ontario. She lives with intense pain daily and barely has energy to do things she once loved to do. Just waking up and getting out of bed in the morning is an ordeal. Her short-term memory is shot – she sometimes forgets where she’s going and has to have a helper with her at school and her grades are starting to drop because of her health. She pops more pills in the run of a day than an addict.

“Sometimes it seems like all I do is take pills,” said Chelsey with a sigh, adding that at least they’ve managed to juggle her medications so she doesn’t have to take them at school. “People stare at me, when I take the medicine at school.”

But she’s still not getting better, says her mom, and they’ve recently added two more medications to her daily routine. The new pills are so strong that Chelsey needs blood work every few weeks to test her liver function because the medication could cause damage to it.

“It’s a risk we’re willing to take at this point,” Rector says.

Chelsey has to fight to keep her weight up – she just hit 80 pounds, a major achievement, since it dropped to 58 pounds at one point – and has no appetite for her favourite foods.

It’s reached the point, Rector says, that Chelsey’s doctor has decided to send her to see an expert on Lyme disease in children based in Connecticut. It’s hoped they’ll be able to secure an appointment before the spring.

That’s going to be pricey for the family, who already shells out between $800 and $1,000 a month for Chelsey’s various medications.

Her insurance will only cover prescriptions and won’t pay for the vitamins and supplements she needs and they have told the family that they will not pay travel costs to the U.S. or for any hospitalization Chelsey may need while there.

It’s possible, Rector said, that Chelsey may have to do an IV therapy, which could be as intensive as a 24-hour-a-day, seven-day-a-week regime.

“I don’t know where we’ll get the money to go, but we have to,” Rector said. “I’ll find somebody, somewhere, to fix her. I have to. That’s my child.”

The only thing she has going for her right now it her age, her mother adds.

“The doctor told us to be glad she’s so young,” Rector said, her voice breaking. “She has her youth on her side. Her heart beats between 140 and 160 beats per minute at rest, and has ever since she was bitten. If she’s older, there would’ve been more wear and tear on her heart.”

Chelsey, who has been living with the disease for nine years now, has reached the point where she’s considered to have chronic Lyme disease – and that means that there may be little hope for a cure in her case.

“They’re saying that once you reach the chronic level, you can get treated, go in remission, and every once in a while it could flare up. It could be 30 years down the road or three years,” Rector said.

But still, the family hasn’t given up hope for a Christmas miracle.

“We’re hoping against hope she doesn’t go into remission and that she’s cured,” Rector said.

http://www.ngnews.ca/News/Local/2011-12-05/article-2826047/Girl-with-Lyme-disease-needs-more-intense-treatment/

wonderfullife
11-12-2011, 03:22 PM
In Central Park, more than 1,000 trees in the red oak family were spangling the scenery with the colors of autumn. But this year, they were failing to do something else they generally do in the harvest season: produce acorns.

“I remember going into areas and you’d get the crunch of acorns under your feet,” said Neil Calvanese, vice president for operations at the Central Park Conservancy. “And this year, you kind of have to search around for them.”

It is a phenomenon happening not only in New York but also throughout the Northeast. While last fall set a recorded high for acorn production, at roughly 250 pounds per tree, this year is seeing a recorded low, with a typical tree shedding less than half a pound of its seeds, said Mark Ashton, a forest ecologist at Yale University. On average, oaks produce about 25 to 30 pounds of acorns a year.

“Scarlet oak, black oak, true red oak,” Dr. Ashton said. “These are the ones that dominate our forest, and these are the ones that aren’t producing acorns this year.”

Coming on the heels of an acorn glut, the dearth this year will probably have a cascade of effects on the forest ecosystem, culling the populations of squirrels, field mice and ground-nesting birds. And because the now-overgrown field mouse population will crash, legions of ticks — some infected with Lyme disease — will be aggressively pursuing new hosts, like humans.

“We expect 2012 to be the worst year for Lyme disease risk ever,” said Richard S. Ostfeld, a disease ecologist at the Cary Institute of Ecosystem Studies in Millbrook, N.Y. “We are already planning educational materials.”

It will probably turn into a big year for animals’ being killed on highways as well. Deer, in search of alternative sources of food, will leave the cover of the oak trees and wander out closer to roads.

“I would expect that traffic collisions are going to be higher in a year like this year,” Dr. Ostfeld said.

While scientists do not fully understand why this year has produced the lowest acorn crop in 20 years of monitoring, there is nothing unusual about large fluctuations in the annual number of acorns. Fingers are not being pointed at global warming.

Oak trees “produce huge, abundant amounts one year and not in other years,” Dr. Ashton said. “I don’t think it’s bad — the whole system fluctuates like this.”

One theory for why oak trees vary their acorn yield is the so-called predator satiation hypothesis. Under this theory, during bumper years, the trees litter the forest floor with seeds so completely that squirrels, jays, deer and bears cannot possibly eat them all. Then, in off years, the trees ramp down production to keep the predator populations from growing too large to be satiated.

But the variability of weather in New York and New England could also be playing a role in the shortage this year.

“A lot of it has to do with the initial spring,” Dr. Ashton said. Acorn production is high when “everything converges on a perfect spring.”

It takes a red oak 18 months to grow an acorn. The tree is pollinated in the spring of one year, and its acorns drop in the fall of the next year. The rainy spring of 2010 could have dampened the wind-driven transfer of pollen from one tree to another, resulting in the acorn dearth this year.

While acorn fluctuation is normal, what is unusual this year is the abundance followed by the steep drop. “In a sense, it’s just another trough,” Dr. Ostfeld said. “But this is the most extreme pair of years that we’ve seen.”

Dr. Ostfeld describes acorns as an engine that drives the forest ecosystem. “When that engine is cooking along,” he said, “you get these heavy knock-on effects.”

The population of field mice, for instance, exploded this summer. While that was good for the mice, it was bad news for low-nesting birds like the wood thrush, whose nests are susceptible to rodent predation. In addition, the large numbers of mice caused an increase in the tick population.

On the other hand, Dr. Ostfeld said, “when you get a failure of the engine, things just change radically.”

Now the field mouse population is expected to crash — about 90 percent have died off in similar glut-dearth acorn sequences in the past. And the outlook is not good for the low-nesting birds, which face an increased threat from hawks and owls.

“The adult wood thrush will take it on the beak by the one-two punch,” Dr. Ostfeld said.

But in the middle of New York City, Central Park will be buffered from the ecosystem effects of the acorn engine.

“It’s a very managed environment,” said Arthur Elmes, the tree data coordinator for the Central Park Conservancy. “It’s nothing that won’t be corrected in years to come.”


This article has been revised to reflect the following correction:

Correction: December 7, 2011



An article on Saturday about a dearth of acorns in the Northeast this fall described incorrectly the wood thrush, an animal in the forest ecosystem that faces an increased threat as a result. Wood thrushes, which nest in shrubs and branches a few feet off the ground, are considered low-nesting birds; they are not ground-nesting birds.

http://www.nytimes.com/2011/12/03/nyregion/boom-and-bust-in-acorns-will-affect-many-creatures-including-humans.html?_r=1

wonderfullife
11-12-2011, 03:25 PM
SANDYSTON -- The woman carefully ran her fingers through the thick black hair around the bear's neck, not because she was afraid of disturbing the bear -- it was dead -- but because her real prey could easily get away in the animal's fur.

Christine Zolnick spent the first day of New Jersey's bear hunting season Monday at a bear check station on the Flatbrook-Roy Wildlife Management Area collecting the small parasitic insects that thrive on most warm-blooded animals.

In particular, Zolnick was looking for ticks and especially deer ticks, which transmit Lyme disease.

While much is known about the tick's life cycle and most of its host animals, including the white-tail deer that lend the insect its name, Zolnick said there is little data on how big a role bears may play.

As warm-blooded animals in the woods, bears could be assumed to be target animals since ticks must have blood to progress through the stages of life, and the female adult tick needs blood to nourish her eggs.

Zolnick is a doctoral student at Fordham University and is doing research on host animal communities and their influence on tick-borne diseases.

Her vector ecology lab in Westchester County, N.Y., has collected tick samples from deer in New York and Connecticut for some time, but she said, "I was curious as to what influence bears might have on these insects."

A fellow doctoral candidate at Fordham, Amanda Makkay, had volunteered to work at the Flatbrook-Roy station during the bear hunt, so Zolnick took the opportunity to collect samples from the bears brought in by hunters.

And most hunters were glad to agree to Zolnick checking for the insects.

"Oh, that one is covered with ticks," said one hunter, who then asked a couple of other hunters to check out the back of his clothing for any ticks that might have jumped across to him.

This first stage was simply to collect a sampling of ticks, along with data as to where the bear was shot.

"So far, I'm pretty sure all these animals have them," Zolnick said late Monday afternoon. "And it looks like they're mostly deer ticks."

The second stage will be to put the insects under the microscope to verify the species, then plan out what, if anything, further needs to be done.

She said there doesn't appear to be anything written on whether bears can develop Lyme disease, and said the adult ticks have already fed twice in their life cycle, "so it would be hard to tell where they got any pathogens."

While Lyme disease is connected with deer ticks, the insects in early stages of their life spend time on birds and smaller mammals such as white-footed mice, before molting into the adults, which move on to larger mammals, such as dogs, deer and humans.

"I really don't feel comfortable drawing any conclusions yet," Zolnick said, "We have to see what's on there, then see if it's worth going further."


http://www.njherald.com/story/16224650/researcher-uses-bear-hunt-to-study-ticks

wonderfullife
11-12-2011, 03:30 PM
Richard Scroggins served 15 months in Iraq as a mechanic with the U.S. Army, but it was a field in Wisconsin that left him in a hospital bed for weeks.


Scroggins left the army in 2010 and joined the reserves, and he was training at Fort McCoy in Wisconsin this summer when, unbeknownst to him, he was bitten by a tick.

"I felt fine when I got back," he said.

But soon after he would spend more than a month in and out of the hospital before being diagnosed with Lyme disease.

After a number of misdiagnoses - including meningitis - and failed antibiotics, one of the doctors noticed rashes common to the disease.

Luckily the symptoms hadn't progressed too far, so he's expected to have a full recovery.

His wife, Brittany, was able to work only one day total during those weeks while she was caring for her husband and going to the hospital.

"I almost lost my job because I had to call in so many times," she said. "They've started working me back in with some hours."

Richard Scroggins, who works as a supervisor with a construction company, is also back at work, but nearly two months with no income coming in has left the family in a rough spot.

"We haven't really caught up yet," he said. "The little savings we had is gone because we had to pay for rent, utilities, gas and insurance."

To make matters worse, before he left for the military training he got a speeding ticket in Krebs. He missed the court date because he was in the hospital, and his license was suspended. He ended up getting arrested for driving with a suspended license and had to pay bail and then go to Krebs and prove that he was hospitalized.

Although all the charges were dropped and his license reinstated - after a fee was paid - the speeding ticket ended up costing about $900, he said.

"Everything just snowballed," Brittany Scroggins said. "I'm so thankful that The Salvation Army has been there to help us."

In addition to the utility assistance the family received earlier, the holiday assistance will help provide some gifts for their two children: Nathan, 5, and Harley, 6.

"It's going to be real nice to still have a good Christmas with the kids," she said.

--------------------------------------------------------------------------------

About the Neediest Families Fund Drive
The Neediest Families Fund Drive was established in 1928 to help Tulsa's poorest families find some peace and comfort for the holidays and the coming year.

This year's goal is to raise $300,000 by Christmas Eve.

In 2010, the fund collected $339,277.

Each Sunday, Wednesday and Thursday through the holiday season, the Tulsa World will spotlight families chosen by The Salvation Army to receive assistance through this year's fund.

None of the money raised is used for administrative costs, and cash is not given directly to the families.

Instead, The Salvation Army issues vouchers for specific needs.

To help families such as the one featured today, send a check or money order to the Neediest Families Fund Drive, in care of the Tulsa World, P.O. Box 21920, Tulsa, OK 74121-1920.

Donations are tax-deductible, and donors can be anonymous.

Original Print Headline: Disease forces family to put lives on hold

http://www.tulsaworld.com/news/article.aspx?subjectid=429&articleid=20111208_11_A13_CUTLIN646987

wonderfullife
11-12-2011, 03:38 PM
This is quite a useful tool if anyone is intrested:

http://app.symptomgrapher.com/login

wonderfullife
20-12-2011, 05:05 PM
If one has been infected with Lyme or if you have Chronic Lyme do not forget to treat your pets and livestock because you can pass on Lyme to animals and they can pass it on to you therefore a viscous cycle.

MMS is very good at dealing with Lyme in humans and animals

http://mms4life.wordpress.com/mms-protocolactivation/mms-methods-and-pets-animals/

wonderfullife
25-01-2012, 06:26 PM
Ticks that can transmit Lyme disease may be more prevalent in the UK than realised, say researchers who have found out how many dogs harbour them.

Experts have suspected for some time that the UK has a growing problem with these tiny pests - rates of the disease have been creeping up in recent years.

In 2010 there were 953 reported cases in England and Wales.

Now, after doing random checks on over 3,500 dogs, Bristol University experts suspects the problem is even bigger.

Of the 3,534 pet dogs inspected at veterinary clinics in the UK between March and October 2009, 14.9% had ticks.

Continue reading the main story

Start Quote
Without considerably better surveillance and routine diagnostic testing, Lyme disease is only likely to become more prevalent”
End Quote
Faith Smith

Lead researcher

Of these, 2.3% turned out to be infected.

The expected prevalence of infected ticks on dogs is 0.5% or 481 infected ticks per 100,000 dogs.

This suggests that the prevalence of this Borrelia infection in the UK tick population is considerably higher than previously thought, the researchers report in the journal Comparative Immunology, Microbiology and Infectious Diseases.

Faith Smith, who led the research, said: "Lyme disease appears to be a rapidly growing problem in the UK with important health and economic impacts in terms of loss of working hours and potential decrease in tourism to tick hotspots.

"Without considerably better surveillance and routine diagnostic testing, Lyme disease is only likely to become more prevalent.

"In particular, future warmer winters might well extend the period over which ticks are active seasonally, while growing wild reservoir host populations, such as deer, will allow the tick population to expand."

Easy to miss

A bite from an infected tick can take between two days and four weeks to show and anyone who has been bitten should look for a "bulls eye" type red rash appearing around the bite.

You may also experience flu-like symptoms, such as tiredness, headaches and muscle or joint pain.

Untreated, Lyme disease can spread to the brain, heart, and joints and in extreme can cause nerve damage, paralysis and blindness.

Ticks are very small - about the size of a poppy seed - and can easily be overlooked.

Most ticks do not carry the infection, but they should be removed promptly if found.

They can be removed with tweezers or special tick hooks, pulling gently upwards away from the skin.

People who develop a rash or other symptoms after a tick bite should consult their GP.

A spokeswoman from the Health Protection Agency said it was important that people realise the risks and remain "tick aware".

"They are out there in woodland areas." She said it was best to keep to footpaths and avoid long grass where possible when out walking and to cover up the skin.

Also, brush off clothes and pet's coats before returning indoors to remove any unattached ticks that might later seek a feed.
More on This Story
http://www.bbc.co.uk/news/health-16706942

Not the best advice in the world but at least Lyme is being noticed in the MSM

wonderfullife
25-01-2012, 07:14 PM
http://www.tbe-info.com/upload/medialibrary/Reported_Cases.pdf

wonderfullife
12-02-2012, 06:56 PM
Here, he shares his latest insights into Lyme disease, including its causes, confounding factors that can make proper diagnosis elusive, and how to get around them, along with his own treatment protocol.

By Dr. Mercola


Some experts feel that almost everyone has been exposed to Lyme disease and may have it in one way, shape or form.

Whether that's true or not is up for debate, but clearly there are those who have it and are severely disabled by it.

Dr. Klinghardt—who is one of my earliest mentors in natural health and always on the leading edge—has actually suffered with Lyme disease himself, and as a result, he's passionate about finding effective natural treatments for Lyme.

The Ongoing Discovery of Lyme Disease


It's now been fairly well-established that chronic infection is an underlying factor in most chronic illnesses. Diseases such as Parkinson's, multiple sclerosis and chronic fatigue are all turning out to be expressions of chronic infections.


"Right at the center of that is the ongoing discovery of Lyme disease," Dr. Klinghardt says.

Lyme disease has recently received a new definition. It now refers to illnesses transferred by insects, as opposed to simply a tick-borne disease. Mosquitoes can carry Lyme disease and many other serious infections, as can spiders, fleas and mites.


"Today I take a very different approach to Lyme disease," Dr. Klinghardt says. "I look at it as nature mingling with our genes. They are trying to incorporate their genome into our genome… Most of the time it goes wrong but sometimes it goes well. This is like the point I want to make upfront; that I take this more evolutionary view of it.

… We know that Lyme spirochetes were around for a long time but something happened maybe 30-40 years ago, where the creatures became more aggressive, more penetrating, and more illness-producing than they were before. Some of us suspect it's a man-made element. Some of us suspect that the global warming may play a role in it.

I personally suspect that the exposure to electromagnetic fields in the home and the microwaves from cell phone radiation are driving the virulence of many of the microbes that are naturally in us, and makes them aggressive and illness producing. There is probably evidence for all sides of the discussion."

Why Lyme Disease is So Tough to Diagnose…


Lyme disease is notoriously difficult to diagnose using conventional tests. And there's great variation in the presentation of the disease as well, depending on where you contracted it, and whether or not you have any other coexisting infections. There is a group of seven or eight microbes that are the most common. The worst ones are Babesia microti and the different forms of Bartonella.


"Underneath that, there's often an infection with Mycoplasma. We still don't know if it's really transferred with the same bite or if the people had it all along and become symptomatic when the immune system is suppressed by the spirochetes," Dr. Klinghardt says.

Other than the co-infections, there is what I call the "opportunistic infections." The combined effect of the initial infection is an immune suppressive effect, and then the patient becomes vulnerable to all sorts of other things. The most common things people contract early on in the course if the illness are different forms of parasites, such as protozoa; Babesia itself being one of them.

There is Giardia, amoebas, Trichomonas, malaria, and different forms of infections that aren't labeled yet. There is a new one, called FL1953. Stephen Frye discovered that. It's a protozoan organism that's causing severe fatigue and illness in chronically ill people. It's almost always present in a patient with Lyme disease.

And then we find a lot of worms in people. They may be microscopic and they may be macroscopic. That means they may be visible in the stool or they may not be visible."

Common Presentations of Lyme Disease


The most simple presentation is the orthopedic forms of Lyme disease as they're typically more superficial, affecting the larger joints. Interestingly, Dr. Klinghardt injects ozone into the joint in these cases, which he claims is:


"100 percent effective if the Lyme disease or… whatever the microbe is, lives in the joint and is confined to the joint space. Simply putting ozone in the joint will kill the spirochetes, and often with one, sometimes two treatments, make the joint completely pain free. That's one form of the expression of Lyme."

When the microbes and the associated immune reactions are situated in the connective tissue, the infection presents as a "vague, dispersed pain," which oftentimes ends up being labeled as fibromyalgia by conventional doctors. The immunological expression of Lyme covers a wide variety of immune system disorders, typically with some aspect of autoimmunity.


"I did my thesis in 1976 on autoimmune diseases and how the autonomic nervous system interacts with the immune system," Dr. Klinghardt says. "We found then that the determining factor of the outcome of an autoimmune disease was the presence of microbes that were catastrophically unresponsive to antibiotics.

Any autoimmune disease, including rheumatoid arthritis, we suspect has an underlying level of Lyme disease that needs to be treated appropriately before the patient has a chance to recover from the illness."

The gastroenterological presentation, where you have constant stomach problems, constipation, recurring stomach ulcers and/or indigestion, is very common, especially with the Babesia infection. This is sometimes the direct outcome of pancreatitis or hepatitis, but it can also be due to parasites acquired after contracting Lyme disease. In these cases, aggressive treatment of the parasites typically resolves the problem.


"The most startling form of the expression of Lyme disease is a wide variety of neurological illnesses," Dr. Klinghardt says.

"That is what we specialize in… We see a lot of cases with multiple sclerosis (MS)… ALS… [and] everything in between: the chronic fatigued patients, the patient with vague, undistinguishable neurological symptoms, the feeling of buzzing in the head, buzzing on the skin, crawling under the skin…"

How to Diagnose Lyme Disease


Insomnia is one of the key symptoms in many cases of Lyme disease, along with neurological symptoms such as headaches and a wide variety of pain syndromes. But you cannot diagnose Lyme disease on symptoms alone, because they're so varied.

Testing is required, but even that is not a sure-shot…

Most commercial tests designed to detect chronic infections are based on measuring your immune reaction—the presence of antibodies—to the invading microbe. However, one of the primary cells that get infected with Lyme spirochetes are the white blood cells themselves, which is a bit of a game-changer… because if your white blood cells are infected, they lose the ability to produce antibodies.

Hence it is relatively common to get a negative test result…

Dr. Klinghardt refers to this as "the Lyme paradox," because in order to diagnose Lyme disease properly with one of the accepted commercial tests, you have to first treat the Lyme disease, in order for your white blood cells to be able to mount an appropriate immune response. Only then can a lab test be used to detect the presence of Lyme disease.


"An exception to that are the test based on direct microscopy, where you're not depending on the immune responses for the patient," he explains.

However, this too has its drawbacks and difficulties. For example, the FISH test for Babesia is done on blood. But Babesia lives in the central nervous system, joints, and connective tissue. It doesn't live in your blood stream, at least not in significant amounts, so it can easily be missed when looking at blood.

To get around the many testing conundrums surrounding Lyme, whenever he suspects Lyme, Dr. Klinghardt treats his patients for Lyme disease for at least six to eight weeks, followed by a Western blot test, which measures immune response. The treatment is initially based on the clinical symptoms presented, along with a form of muscle testing he developed, called autonomic response testing (ART), which incorporates both classical neurological testing and kinesiology.


"It's not related to the applied kinesiology system that's quite distinct," Dr. Klinghardt explains. "It... may look similar… [but] we're looking for very specific reflexes that are connected to very specific illnesses. We arrive at a tentative diagnosis through history taking, through looking at skin signs; palpating the tissues; testing the normal neurological reflexes; orthopedic tests, and then we add the muscle testing as an additional tool."

Tests and Lab Recommendations


Dr. Klinghardt exclusively uses the IGeneX Lab in Palo Alto for his blood tests, and Fry Labs in Arizona for direct microscopy testing.


"I don't have a financial investment in it, but it's the gold standard in our field," he says. "They use two different antigens. The commercial labs and hospitals and so forth, they use one antigen and are notorious in under-diagnosing Lyme disease. We recommend to rather not test it than get a false negative, which will sometimes lead the patient 20 years on the wrong track. With the other co-infections, the detection rate drops way down.

… We do the FISH test [for Borrelia] at IGeneX Lab. It's a direct microscopy test which has more false negatives than the western blot.

… The leading test for Bartonella that we use is Fry Labs in Arizona. Steven Fry, who does a wonderful direct microscopy test, often comes back positive with the diagnosis of hemobartonella. Hemo means simply blood – Bartonella in the blood. Remember, he's testing the blood where the Bartonella typically does not live. It lives in the nervous system. So if you find it in the blood in small amounts it generally is an indicator that there is a high amount in other tissues in the body."

An indirect test is the CD57 test. "CD-57" is a specific group of natural killer cells that are particularly damaged by the Lyme spirochetes. Therefore, if your numbers drop to a certain level, it is an indirect indicator that you may have Lyme disease, because the only known infection to suppress CD57 is that of Borrelia burgdorferi.

Normally, your CD57 value should be over 100. If it's lower than that, you're infected with Borrelia. If it's below 60, you probably have both Borrelia and Mycoplasma, and, most likely, some other co-infections.

Dr. Klinghardt's Treatment Approach


Dr. Klinghardt takes microwave radiation and electromagnetic fields very seriously, as it can have a profound impact on Lyme disease.


"One of my primary treatments for Lyme disease is to put people in protective clothing that shields them from incoming microwaves," he says. "We shield the bedside. We turn off the wireless internet at home. We put shielding paint on the houses. That has been a more successful strategy to treating Lyme disease and to get people neurologically well than any of the antibiotics or any of the antimicrobial compounds."

He's convinced that the increased virulence we're now seeing is related to the dramatic increase in electromagnetic fields and microwave radiation from cell phones, cell towers, and all manner of wireless technologies. Therefore, EMF and microwave radiation mitigation are part of the standard protocol, as any subsequent treatment of Lyme disease will not be as effective unless these external factors are addressed.

Below is a summarized outline of Dr. Klinghardt's treatment for Lyme disease. For more information and details, please listen to the interview in its entirety, or read through the transcript.
1.First, external factors that act upon the body 24/7 are evaluated.

This includes electrosmog, EMF, microwave radiation from wireless technologies, and molds. To test for the presence of mold, he uses the ERMI score, which is a semi-quantitative assessment of how much mold is in your home. The score should not exceed 2. However, most of his patients score between 15 and 20. For more information on mold, Dr. Klinghardt recommends www.SurvivingMold.com.
2.Once external influencing factors have been determined, they're remediated and mitigated. (For mold remediation, please refer to this previous article.)

To mitigate microwave radiation, Dr. Klinghardt recommends shielding your home with a graphite paint called Y Shield outside, and use special silver-coated cloth for your curtains. These measures will compromise your ability to receive cell phone calls, so depending on your situation, you may opt to shield just your bedroom, or shield your entire home and just use a landline.

All cordless telephones are removed, and patients are instructed to turn off all the fuses at night, until they have recovered from Lyme disease.
3.Next, the emotional component of the disease is addressed using Energy Psychology tools, including psychokinesiology (PK) which is similar to the Emotional Freedom Technique (EFT), but more refined and advanced...
4.Dr. Klinghardt begins the treatment for Lyme disease by addressing parasites, followed by "the Klinghardt antimicrobial cocktail," which addresses the Lyme spirochetes, Babesia, and Bartonella. For more details and complete recipes to all his treatment cocktails, see www.KlinghardtAcademy.com or send an email to [email protected] Some of the ingredients in his formula include: wormwood (artemisinin)—which has been found to be extremely effective for malaria—combined with phospholipids; vitamin C, and specific herbs.

Lastly, viruses are addressed using a tincture of Native American herbs called Viressence, by BioPure.
5.Additional lifestyle factors are also addressed, including diet and vitamin supplementation.

A Word on Antibiotics


Conventional Lyme treatment hinges on long-term use of antibiotics. While this treatment can indeed be effective, there are many reasons to opt for alternatives such as those detailed by Dr. Klinghardt, as antibiotics will disrupt your gut flora, thereby exposing you to a whole host of other pathologies.

More Information


In Dr. Klinghardt's experience, the International Lyme and Associated Disease Society (ILADS) is by far the best and most responsible group, so to learn more about Lyme disease, see www.ILADS.org.


"Depending on where you live in the U.S., consider the treatment that is offered to you through a Lyme literate physician. Most of them have been through the training at ILADS and I do recommend that," Dr. Klinghardt says.

"But there is a level beyond that, which I'm hoping I'm introducing here. If you just do antibiotics, okay, you just do antibiotics. But if you think more holistically and do the things that I recommend, then you no longer will need to resort to antibiotics because you cover your system on so many other fronts. And with that you're not only treating Lyme disease but you're preventing cancer, diabetes, Alzheimer's disease—you're preventing pretty much all the other things that we didn't know were associated with Lyme.

So by treating the mold, by getting electrosmog under control, by treating the infections, by treating insulin resistance, we are preparing the patient for a much happier, healthier, longer, and more productive life, which is of course what I'm hoping for…"

Again, Dr. Klinghardt provides free access to all his recipes on his web site, so to learn more about his treatment, please see www.KlinghardtAcademy.com.

wonderfullife
08-03-2012, 09:02 PM
If one suffers from deppression the cause could be mold and if one has Lyme well this a recipe for disaster.
http://www.survivingmold.com/
Understanding the Illness

"Things didn't used to be so difficult to accomplish. It didn't used to be impossible to make it through a day at work. Now you find it almost impossible to get through a load of laundry. You are so tired all of the time. You are just hoping your disability is approved so you can live.

Maybe you were a star athlete at school and at the top of your class. Now you just try to make it through your classes and survive the massive headache that hits by second period. That's if you can handle the nausea and vomiting that starts, or the diarrhea that is inevitable. Just trying to stay awake and focus on your studies at school becomes the goal of your entire day -not to mention remember what you are learning. Gone are the days of zipping through your classes and getting to ball practice after school. You can't even breathe well enough at school to make it through the day. Dreams of being a part of that state championship athletic team have been destroyed.

This is what happens to people who are injured by Dangerous Buildings - those that are filled with toxins that your body cannot process because of your genes. This is a real illness and wreaks havoc on your body. Your body's response to the poisons causes such inflammation throughout the major systems of your body that life as you knew it has changed forever.

Of course while all of this is happening in your body, you probably still look ok. You get told all of the time that you don't look sick. But you sure do feel sick.

Maybe you have been to countless doctors and had countless tests, only to be told everything is normal or that you have allergies. Or even worse, that you look fine, so your complaints must be in your head. You are told you are just depressed and that you have a phychological problem.


There is Hope!

We want you to know you are not alone. You are not crazy. And this illness is not all in your head.

It is a real illness that has destroyed lives. But, there is hope!

The first step is finding out what the problem is. And you have come to the right place for that. The best part is, once you or your doctor determine what is going on in your body by getting the right laboratory testing, investigating the relevant patient history and understanding symptoms experienced, there is a proven treatment method that has worked for so many.

People get their lives back and are armed with the knowledge they need to know to keep their bodies safe.

Do not give up, and know that there is help available for you."

wonderfullife
08-03-2012, 09:27 PM
"Just when I thought my health situation couldn’t get any more complicated…

Oh! Hello, mycotoxicosis. How long have you been sitting there?

One of the many things Lyme Disease does is suppress, distract, and otherwise incapacitate a normal, functioning immune system. Lyme patients have to be especially careful about mold.

A healthy body can easily deal with common household molds (e.g. most varieties of Stachybotrys, Aspergillus, and Penicillium). But individuals with compromised immune systems apparently cannot. Our bodies don’t recognize and kill the mold. The liver can and will process it, but it’ll ultimately just keep recirculating through the intestine with our bile and back into our bloodstream.

So you get a situation where you just kind of have this normally harmless mold hanging out inside you, going about its business. I mean, the human body is a damp, warm, dark area, right? Mold is a fat kid munching cake in there as long as nothing comes along, recognizes a problem, and tries to kill it.

But the arrangement doesn’t work quite as well for the immune-compromised host. See, most mold is toxic to some degree or another, and when your body has become a climate-controlled mold assisted living community, every single microgram of metabolic byproduct from that mold ends up in your already overwrought body. And it isn’t strictly good for you. In fact, it will make you sick on top of your original sick. And that exacerbates your original illness. And you are screwed. Forever.

This is why Lyme doctors tend to be very concerned about their patients’ degree of mold exposure. And this is what my doctor brought up last week when we discussed the fact that I’ve hit a plateau in my treatment results and I don’t seem to be getting better as easily as we expected. We did some tests to confirm, and this does indeed seem to be an issue.

At present I live in my parents’ basement (yep, like those guys you make fun of on the internet). After I had to stop working full time and could no longer afford to live on my own, my parents offered me either a room in their basement or one on the first floor. I figured I’d be less of a bother downstairs, and there was also more room for crap I refused to throw out, so that’s what I chose. Turns out, that was probably the exact wrong decision. You know what happens in basements, right? Mold. Whole communities of mold. Mold debutante balls, mold city councils, mold jamborees, and, if the basement floods, mold pool parties. Also, field trips to Carrie’s lungs, apparently.

When I first read about Lyme and mold I was a little concerned. I knew it was a possible complication, so I tested the air in my basement room. Basically, you lay out a petri dish pre-treated with some kind of potato starch mold food. Leave it undisturbed in the room for an hour, then store it for 5-7 days somewhere dark at room temperature. If there’s mold after the incubation period you can send it in to a lab to analyze and report what you have and how much of it.

My room came back showing lowish-to-borderline levels of common household molds. I figured I could relax. The levels weren’t high. There was no black mold.

I did not realize the extent to which many Lyme patients are unable to handle even modest amounts of common household mold. Especially in living spaces, where they (being, you know, sick) might lie in bed for the majority of the day.

I’m feeling overwhelmed by this development. And stressed out. I wonder how much time I’ve lost being almost willfully oblivious to this problem. I wonder why there always seems to be One. More. Thing. to tackle, those ever-moving goalposts taunting me while I desperately try to just be a healthy, functioning person. I’m glad I know what I have to do, but it’s hard to be grateful, exactly.

Stay tuned for the game plan. Because there is one, and that’s the bright side here."
http://www.lygerlyger.com/2011/06/lyme-and-mold-the-pbj-of-misery/

wonderfullife
08-03-2012, 10:26 PM
Dr. Dietrich Klinghardt, MD, PhD is well known for his successful treatment of neurological illness and chronic pain with Integrative Medicine.

Here, he shares his latest insights into Lyme disease, including its causes, confounding factors that can make proper diagnosis elusive, and how to get around them, along with his own treatment protocol.

Some experts feel that almost everyone has been exposed to Lyme disease and may have it in one way, shape or form.

Whether that's true or not is up for debate, but clearly there are those who have it and are severely disabled by it.

Dr. Klinghardt—who is one of my earliest mentors in natural health and always on the leading edge—has actually suffered with Lyme disease himself, and as a result, he's passionate about finding effective natural treatments for Lyme.

The Ongoing Discovery of Lyme Disease


It's now been fairly well-established that chronic infection is an underlying factor in most chronic illnesses. Diseases such as Parkinson's, multiple sclerosis and chronic fatigue are all turning out to be expressions of chronic infections.


"Right at the center of that is the ongoing discovery of Lyme disease," Dr. Klinghardt says.

Lyme disease has recently received a new definition. It now refers to illnesses transferred by insects, as opposed to simply a tick-borne disease. Mosquitoes can carry Lyme disease and many other serious infections, as can spiders, fleas and mites.


"Today I take a very different approach to Lyme disease," Dr. Klinghardt says. "I look at it as nature mingling with our genes. They are trying to incorporate their genome into our genome… Most of the time it goes wrong but sometimes it goes well. This is like the point I want to make upfront; that I take this more evolutionary view of it.

… We know that Lyme spirochetes were around for a long time but something happened
maybe 30-40 years ago, where the creatures became more aggressive, more penetrating, and more illness-producing than they were before. Some of us suspect it's a man-made element. Some of us suspect that the global warming may play a role in it.

I personally suspect that the exposure to electromagnetic fields in the home and the microwaves from cell phone radiation are driving the virulence of many of the microbes that are naturally in us, and makes them aggressive and illness producing. There is probably evidence for all sides of the discussion."

Why Lyme Disease is So Tough to Diagnose…


Lyme disease is notoriously difficult to diagnose using conventional tests. And there's great variation in the presentation of the disease as well, depending on where you contracted it, and whether or not you have any other coexisting infections. There is a group of seven or eight microbes that are the most common. The worst ones are Babesia microti and the different forms of Bartonella.


"Underneath that, there's often an infection with Mycoplasma. We still don't know if it's really transferred with the same bite or if the people had it all along and become symptomatic when the immune system is suppressed by the spirochetes," Dr. Klinghardt says.

Other than the co-infections, there is what I call the "opportunistic infections." The combined effect of the initial
infection is an immune suppressive effect, and then the patient becomes vulnerable to all sorts of other things. The most common things people contract early on in the course if the illness are different forms of parasites, such as protozoa; Babesia itself being one of them.

There is Giardia, amoebas, Trichomonas, malaria, and different forms of infections that aren't labeled yet. There is a new one, called FL1953. Stephen Frye discovered that. It's a protozoan organism that's causing severe fatigue and illness in chronically ill people. It's almost always present in a patient with Lyme disease.

And then we find a lot of worms in people. They may be microscopic and they may be macroscopic. That means they may be visible in the stool or they may not be visible."

Common Presentations of Lyme Disease


The most simple presentation is the orthopedic forms of Lyme disease as they're typically more superficial, affecting the larger joints. Interestingly, Dr. Klinghardt injects ozone into the joint in these cases, which he claims is:


"100 percent effective if the Lyme disease or… whatever the microbe is, lives in the joint and is confined to the joint space. Simply putting ozone in the joint will kill the spirochetes, and often with one, sometimes two treatments, make the joint completely pain free. That's one form of the expression of Lyme."

When the microbes and the associated immune reactions are situated in the connective tissue, the infection presents as a "vague, dispersed pain," which oftentimes ends up being labeled as fibromyalgia by conventional doctors. The immunological expression of Lyme covers a wide variety of immune system disorders, typically with some aspect of autoimmunity.


"I did my thesis in 1976 on autoimmune diseases and how the autonomic nervous system interacts with the immune system
Dr. Klinghardt says. "We found then that the determining factor of the outcome of an autoimmune disease was the presence of microbes that were catastrophically unresponsive to antibiotics.

Any autoimmune disease, including rheumatoid arthritis, we suspect has an underlying level of Lyme disease that needs to be treated appropriately before the patient has a chance to recover from the illness."

The gastroenterological presentation, where you have constant stomach problems, constipation, recurring stomach ulcers and/or indigestion, is very common, especially with the Babesia infection. This is sometimes the direct outcome of pancreatitis or hepatitis, but it can also be due to parasites acquired after contracting Lyme disease. In these cases, aggressive treatment of the parasites typically resolves the problem.


"The most startling form of the expression of Lyme disease is a wide variety of neurological illnesses," Dr. Klinghardt says.

"That is what we specialize in… We see a lot of cases with multiple sclerosis (MS)… ALS… [and] everything in between: the chronic fatigued patients, the patient with vague, undistinguishable neurological symptoms, the feeling of buzzing in the head, buzzing on the skin, crawling under the skin…"

How to Diagnose Lyme Disease


Insomnia is one of the key symptoms in many cases of Lyme disease, along with neurological symptoms such as headaches and a wide variety of pain syndromes. But you cannot diagnose Lyme disease on symptoms alone, because they're so varied.

Testing is required, but even that is not a sure-shot…

Most commercial tests designed to detect chronic infections are based on measuring your immune reaction—the presence of antibodies—to the invading microbe. However , one of the primary cells that get infected with Lyme spirochetes are the white blood cells themselves, which is a bit of a game-changer… because if your white blood cells are infected, they lose the ability to produce antibodies.

Hence it is relatively common to get a negative test result…

Dr. Klinghardt refers to this as "the Lyme paradox," because in order to diagnose Lyme disease properly with one of the accepted commercial tests, you have to first treat the Lyme disease, in order for your white blood cells to be able to mount an appropriate immune response. Only then can a lab test be used to detect the presence of Lyme disease.


"An exception to that are the test based on direct microscopy, where you're not depending on the immune responses for the patient," he explains.

However, this too has its drawbacks and difficulties. For example, the FISH test for Babesia is done on blood. But Babesia lives in the central nervous system, joints, and connective tissue. It doesn't live in your blood stream, at least not in significant amounts, so it can easily be missed when looking at blood.

To get around the many testing conundrums surrounding Lyme, whenever he suspects Lyme, Dr. Klinghardt treats his patients for Lyme disease for at least six to eight weeks, followed by a Western blot test, which measures immune response. The treatment is initially based on the clinical symptoms presented, along with a form of muscle testing he developed, called autonomic response testing (ART), which incorporates both classical neurological testing
and kinesiology.


"It's not related to the applied kinesiology system that's quite distinct," Dr. Klinghardt explains. "It... may look similar… [but] we're looking for very specific reflexes that are connected to very specific illnesses. We arrive at a tentative diagnosis through history taking, through looking at skin signs; palpating the tissues; testing the normal neurological reflexes; orthopedic tests, and then we add the muscle testing as an additional tool."

Tests and Lab Recommendations


Dr. Klinghardt exclusively uses the IGeneX Lab in Palo Alto for his blood tests, and Fry Labs in Arizona for direct microscopy testing.


"I don't have a financial investment in it, but it's the gold standard in our field," he says. "They use two different antigens. The commercial labs and hospitals and so forth, they use one antigen and are notorious in under-diagnosing Lyme disease. We recommend to rather not test it than get a false negative, which will sometimes lead the patient 20 years on the wrong track. With the other co-infections, the detection rate drops way down.

… We do the FISH test [for Borrelia] at IGeneX Lab. It's a direct microscopy test which has more false negatives than the western blot.

… The leading test for Bartonella that we use is Fry Labs in Arizona. Steven Fry, who does a wonderful direct microscopy test, often comes back positive with the diagnosis of hemobartonella. Hemo means simply blood – Bartonella in the blood. Remember, he's testing the blood where the Bartonella typically does not live. It lives in the nervous system. So if you find it in the blood in small amounts it generally is an indicator that there is a high amount in other tissues in the body."

An indirect test is the CD57 test. "CD-57" is a specific group of natural killer cells that are particularly damaged by the Lyme spirochetes. Therefore, if your numbers drop to a certain level, it is an indirect indicator that you may have Lyme disease, because the only known infection to suppress CD57 is that of Borrelia burgdorferi.

Normally, your CD57 value should be over 100. If it's lower than that, you're infected with Borrelia. If it's below 60, you probably have both Borrelia and Mycoplasma, and, most likely, some other co-infections.


Dr. Klinghardt's Treatment Approach


Dr. Klinghardt takes microwave radiation and electromagnetic fields very seriously, as it can have a profound impact on Lyme disease.


"One of my primary treatments for Lyme disease is to put people in protective clothing that shields them from incoming microwaves," he says. "We shield the bedside. We turn off the wireless internet at home. We put shielding paint on the houses. That has been a more successful strategy to treating Lyme disease and to get people neurologically well than any of the antibiotics or any of the antimicrobial compounds."

He's convinced that the increased virulence we're now seeing is related to the dramatic increase in electromagnetic fields and microwave radiation from cell phones, cell towers, and all manner of wireless technologies. Therefore, EMF and microwave radiation mitigation are part of the standard protocol, as any subsequent treatment of Lyme disease will not be as effective unless these external factors are addressed.

Below is a summarized outline of Dr. Klinghardt's treatment for Lyme disease. For more information and details, please listen to the interview in its entirety, or read through the transcript.
1.First, external factors that act upon the body 24/7 are evaluated.

This includes electrosmog, EMF, microwave radiation from wireless technologies, and molds. To test for the presence of mold, he uses the ERMI score, which is a semi-quantitative assessment of how much mold is in your home. The score should not exceed 2. However, most of his patients score between 15 and 20. For more information on mold, Dr. Klinghardt recommends www.SurvivingMold.com.
2.Once external influencing factors have been determined, they're remediated and mitigated. (For mold remediation, please refer to this previous article.)

To mitigate microwave radiation, Dr. Klinghardt recommends shielding your home with a graphite paint called Y Shield outside, and use special silver-coated cloth for your curtains. These measures will compromise your ability to receive cell phone calls, so depending on your situation, you may opt to shield just your bedroom, or shield your entire home and just use a landline.

All cordless telephones are removed, and patients are instructed to turn off all the fuses at night, until they have recovered from Lyme disease.
3.Next, the emotional component of the disease is addressed using Energy Psychology tools, including psychokinesiology (PK) which is similar to the Emotional Freedom Technique (EFT), but more refined and advanced...
4.Dr. Klinghardt begins the treatment for Lyme disease by addressing parasites, followed by "the Klinghardt antimicrobial cocktail," which addresses the Lyme spirochetes, Babesia, and Bartonella. For more details and complete recipes to all his treatment cocktails, see www.KlinghardtAcademy.com or send an email to [email protected] Some of the ingredients in his formula include: wormwood (artemisinin)—which has been found to be extremely effective for malaria—combined with phospholipids; vitamin C, and specific herbs.

Lastly, viruses are addressed using a tincture of Native American herbs called Viressence, by BioPure.
5.Additional lifestyle factors are also addressed, including diet and vitamin supplementation.

A Word on Antibiotics


Conventional Lyme treatment hinges on long-term use of antibiotics. While this treatment can indeed be effective, there are many reasons to opt for alternatives such as those detailed by Dr. Klinghardt, as antibiotics will disrupt your gut flora, thereby exposing you to a whole host of other pathologies.

More Information


In Dr. Klinghardt's experience, the International Lyme and Associated Disease Society (ILADS) is by far the best and most responsible group, so to learn more about Lyme disease, see www.ILADS.org.


"Depending on where you live in the U.S., consider the treatment that is offered to you through a Lyme literate physician. Most of them have been through the training at ILADS and I do recommend that," Dr. Klinghardt says.

"But there is a level beyond that, which I'm hoping I'm introducing here. If you just do antibiotics, okay, you just do antibiotics. But if you think more holistically and do the things that I recommend, then you no longer will need to resort to antibiotics because you cover your system on so many other fronts. And with that you're not only treating Lyme disease but you're preventing cancer, diabetes, Alzheimer's disease—you're preventing pretty much all the other things that we didn't know were associated with Lyme.

So by treating the mold, by getting electrosmog under control, by treating the infections, by treating insulin resistance, we are preparing the patient for a much happier, healthier, longer, and more productive life, which is of course what I'm hoping for…"

Again, Dr. Klinghardt provides free access to all his recipes on his web site, so to learn more about his treatment, please see www.KlinghardtAcademy.com.




Source: Video Transcript

Related Links:

Dr. Klinghardt's Treatment of Lyme Disease (2009)


http://articles.mercola.com/sites/articles/archive/2012/02/05/dr-dietrich-klinghardt-on-lyme-disease.aspx?e_cid=20120205_SNL_Art_1

wonderfullife
08-03-2012, 10:40 PM
By Daily Express reporter


BRITAIN faces a shock rise in diseases caused by ticks this spring – thanks to an EU ruling.




Biting ticks thrive in bracken, which has spread following a dry winter and an EU ban on Asulam, a herbicide used to control it.

Now TV survivalist Ray Mears is leading a campaign to warn countryside users about it.

Asulam was banned by the EU on December 31 because of fears over its effects on certain crops.

Ticks get attached to skin by crawling up trouser legs or under clothes. In 2010, cases of a flu-like illness called Lyme disease from ticks rose 24 per cent to 1,361.

BADA-UK – the Borreliosis and Associated Diseases Awareness charity – is holding a Tick Bite Prevention Week in March.

It advises ramblers to tuck their trousers into their socks and to wear waxed or smooth materials.

Ray Mears, patron of BADA-UK, said: “The control of bracken is vital to the survival of ­numerous species of flora and fauna, as well as reducing tick populations.”








The control of bracken is vital to the survival of ­numerous species of flora and fauna, as well as reducing tick populations







Ray Mears patron of BADA-UK