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Old 31-12-2009, 11:44 AM   #1
multiverse
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Exclamation Lyme Disease Alert! (Please take time to read)

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=XnRrd.../index.htm</a>Here'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: "" 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/lymed..._campaign=lyme) has this interesting information:
Quote:
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:...gl=us&ie=UTF-8

And here is an interesting book that theorizes about the disease's origins:. The Amazon description of the book says,
Quote:
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!
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Old 21-02-2010, 11:56 AM   #2
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Default ADD or Lyme disease?

This article outlines how Lyme disease can be mis-diagnosed as Attention Deficit Disorder:
http://www.samento.com.ec/sciencelib...ymediseas.html
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Old 21-02-2010, 07:39 PM   #3
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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.


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Old 22-02-2010, 10:01 PM   #4
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Default Cover up?

Quote:
Originally Posted by hoverfly View Post
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?
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Old 22-02-2010, 10:06 PM   #5
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Default Lyme-literate doctors

Quote:
Originally Posted by hoverfly View Post


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!
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Old 08-09-2011, 07:09 PM   #6
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Quote:
Originally Posted by hoverfly View Post
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
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Old 08-09-2011, 07:23 PM   #7
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Quote:
Originally Posted by multiverse View Post
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
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Old 08-09-2011, 07:26 PM   #8
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Default M.S or Lyme?

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/
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Old 08-09-2011, 07:27 PM   #9
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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/
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Old 08-09-2011, 07:29 PM   #10
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Default Why can't Doctors treat chronic Lyme?

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/
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Old 08-09-2011, 07:31 PM   #11
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Default What you can do about Lyme

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/
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Old 08-09-2011, 07:32 PM   #12
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Default Jesse Ventura and Lyme

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Old 08-09-2011, 07:33 PM   #13
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Default Lyme borreliosis

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
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Old 08-09-2011, 07:39 PM   #14
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Default Celebraties with Lyme

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Old 08-09-2011, 07:46 PM   #15
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Default Cat Scratch fever and Bartonellosis

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.
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Old 08-09-2011, 07:48 PM   #16
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Default Lyme Aggression

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.
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Old 08-09-2011, 07:51 PM   #17
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Default Lyme and sudden infant death

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
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Old 08-09-2011, 07:52 PM   #18
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Default The complexities of Lyme disease

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
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Old 08-09-2011, 07:54 PM   #19
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Default Lyme disease or Dyslexia ?

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
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Old 08-09-2011, 07:55 PM   #20
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Default Lyme and Thyroid

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/
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