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Old 08-09-2011, 08:00 PM   #21
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Default Lyme deppression and suicide

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
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Old 08-09-2011, 08:02 PM   #22
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Default ADHD or is it Lyme?

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.
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Old 08-09-2011, 08:04 PM   #23
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Default Lyme Rage

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
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Old 08-09-2011, 08:07 PM   #24
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Default U.S. admit Lyme is a bio weapon

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
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Old 08-09-2011, 08:09 PM   #25
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Default Lyme disease and teeth

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
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Old 08-09-2011, 08:11 PM   #26
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Default Ground zero for Lyme is in the mouth

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/
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Old 08-09-2011, 08:12 PM   #27
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Default UK Lyme petition

Here is a UK Lyme petition

http://www.ipetitions.com/petition/uklymepetition/
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Old 08-09-2011, 08:16 PM   #28
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Default Gulf War syndrome

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
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Old 08-09-2011, 08:18 PM   #29
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Default Lyme Blog

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/
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Old 08-09-2011, 08:21 PM   #30
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Default Voices from the shadows

http://voicesfromtheshadowsfilm.co.uk/2011/trailer/
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Old 08-09-2011, 08:24 PM   #31
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Default Dr Chris Steele's son has Lyme T.V Dr

"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
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Old 08-09-2011, 08:25 PM   #32
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Default Pierrick Fédrigo 3 times winner tour de France

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/
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Old 08-09-2011, 08:27 PM   #33
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Default Stroke and Lyme

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
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Old 08-09-2011, 08:30 PM   #34
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Default Persisting atypical and cystic forms of BB

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
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Old 08-09-2011, 08:32 PM   #35
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Default Spirochetes Unwound

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
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Old 08-09-2011, 08:33 PM   #36
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Default Lyme Arthrities

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
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Old 08-09-2011, 08:36 PM   #37
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Default Dr who has realised the effects of Lyme

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
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Old 08-09-2011, 08:42 PM   #38
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Default A Dr who had to go to 35 Drs b4 diagnoses

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Old 08-09-2011, 08:44 PM   #39
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Old 08-09-2011, 08:45 PM   #40
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