UUSIA AJATUKSIA BORRELIOOSIN SYISTÄ, LEVIÄMISESTÄ JNE.

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Lähettäjä: Soijuv Lähetetty: 17.8.2004 10:53



New Ideas About The Cause, Spread and Therapy of Lyme Disease



Dr. James Howenstine

http://www.rumormillnews.com/cgibin/for ... read=51356

Townsend Letter for Doctors and Patients, July 2004

Lyme Disease was initially regarded as an uncommon illness caused by the spirochete Borrelia burgdorferi (Bb). The disease transmission was thought to be solely by the bite from a tick infected with this spirochete. The Bb spirochete is able to burrow into tendons, muscle cells, ligaments, and directly into organs. A classic bulls-eye rash is often visible in the early stage of the illness. Later in the illness the disease can afflict the heart, nervous system, joints and other organs. It is now realized that the disease can mimic amyotrophic 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, chronic pain and many other conditions.

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. A factor contributing to making Bb so dangerous is that it can survive and spread without having a cell wall (cell wall-deficient CWD). Many valuable antibiotics kill bacteria by breaking down the cell wall. These antibiotics often prove ineffective against Bb.

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). Dr. Robert Rowen knows a family where the mother?s infection spread to 5 of her 6 children1 all of whom recovered with appropriate therapy. It is difficult to believe that these children were all bitten by ticks and seems more plausible that person to person spread within the family caused this problem. Dr. Mattman states ?I?m convinced Lyme disease is transmissible from person to person.? In 1995 Dr. Mattman obtained positive cultures for Bb from 43 of 47 persons with chronic illness. Only 1 of 23 control patients had a positive Bb culture. Dr. Mattman has subsequently recovered Bb spirochetes form 8 out of 8 cases of Parkinson?s Disease, 41 cases of multiple sclerosis, 21 cases of amyotrophic lateral sclerosis and all tested cases of Alzheimer?s Disease. The complete recovery of several patients with terminal amyotrophic lateral sclerosis after appropriate therapy shows the great importance of establishing the diagnosis of Lyme Disease.

Some very important information has recently become available about the spread and magnitude of the problem with Lyme Disease. The severity of the Lyme illness is related to the spirochete load in the patient. Few spirochetes produce mild and asymptomatic infection. A study from Switzerland in 1998 pointed out that only 12.5% of patients testing positive for Bb had developed symptoms. A German boy developed Lyme arthritis 5 years after his tick bite. Often mycoplasmal infections remain without symptoms until the victim suffers a traumatic event (stress, injury, accident, etc.). These stressing events enable the mycoplasma to begin consumption of cholesterol and symptoms may begin to present. The mechanism of this deterioration is thought to be suppression of the immune system secondary to stress.

Many patients with LD have concomitant infections with other parasites (Ehrlichia in white blood cells and Babesia in red blood cells). Some patients have all 3 parasites. Each requires a different therapy with Babesia being particularly difficult to eradicate. Recently, Artemisinin appears effective in Babesia infections. All co-infections must be eliminated to obtain a successful result.

Dr. Joanne Whitaker relates that nearly every patient with Parkinson?s Disease (PD) has tested positive for Bb. Dr. Luis Romero reports that 3 patients with PD are 99% better after TOA-free cat?s claw (Uncaria tomentosa) therapy. When Dr. Mattman cultures 25 patients with fibromyalgia all subjects had positive cultures of the CWD Bb, which causes LD. She relates that Bb can be found in tears and could thus easily appear on the hands where touching could spread LD. Several families are now documented where nearly every family member is infected. How sick the individual patient becomes probably relates to their initial spirochete dose, immune system, detoxification capability and stress levels.

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. One physician has cared for 5000 children with LD: 240 of these children were born with the disease. Dr. Charles Ray Jones, the leading pediatric specialist on Lyme Disease, has found 12 breastfed children who have developed LD. Miscarriage, premature births, stillbirths, birth defects, and transplacental infection of the fetus have all been reported. Studies at the University of Vienna have found Bb in urine and breast milk of LD mothers.

Researchers at the University of Wisconsin have reported that dairy cattle can be infected with Bb, hence milk could be contaminated. Bb can also be transmitted to lab animals by oral intake such as food.

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.

Lyme Disease is the fastest growing epidemic in the world. LD is grossly under-reported so there may be far more than the 200,000 cases reported annually in the US. Drs. 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.

Dr. Joanne Whitaker, a Lyme disease victim from childhood, has developed a reliable test for the presence of Lyme disease. This test looks for the Bb organism, not antibodies, and is able to identify the cell wall deficient (CWD) form of the spirochete as well as the actual Bb organism. The test is called Q-RIBb which stands for quantitative rapid identification of Bb. Dr. Lida Mattman has confirmed that Dr. Whitaker?s test is sensitive because there has been a 100% correlation between a positive culture of Bb by Dr. Mattman?s lab and a positive Q-RIBb test from Dr. Whitaker?s Laboratory.

Case Reports Illustrating the Critical Importance of
Establishing the Diagnosis of Lyme Disease.

Case 1: Larry Powers, a former Mr. America in 1962, became ill with the symptoms of Parkinson?s Disease in 1990. Sinemet therapy was taken for eight years but he gradually became worse. He became confined to a wheel chair and required help with eating. After learning that Lyme Disease might be causing his symptoms of PD he started taking TOA-free cat?s claw (Uncaria tomentosa). Within three weeks he was out of his wheelchair and fishing for 100 pound tarpon.

Case 2: Tom Coffey at age 34 developed diplopia, severe hypertension uncontrolled by drugs, and impaired balance. A diagnosis of amyotrophic lateral sclerosis was made. Surgery was performed to correct the diplopia. By June 2001 he was unable to swallow saliva and feeding tube nutrition was begun. His weight had fallen by 100 pounds. Nutritional support from the tube feedings produced slow resolution of the swallowing problem. Consultation with a Lyme expert uncovered the history of a bulls-eye rash after a tick bite. Therapy with Rocephin led to complete recovery.

Case 3: A young male college student developed such sever cognitive difficulties he was forced to drop out of school. A Q-RIBb test was positive for LD and he resumed a normal life after receiving 4 months of antibiotic therapy.

What Causes Neurone Death in Amyotrophic Lateral Sclerosis (ALS)?

One of the most insidious mimics for Lyme Disease is ALS. The neurotoxins released by the Bb organism are capable of causing neurologic dysfunction in the central nervous system that produces symptoms typical of amyotrophic lateral sclerosis. The pathological hallmark of ALS is motor neurone degeneration and death.

Research performed by Dr. Harold Clark and Dr. Garth Nicholson and coordinated by Donald W. Scott2 has resulted in a breakthrough in our understanding of amyotrophic lateral sclerosis.

Mycoplasma was discovered in 1898. These are living particles of bacterial nucleic acid which do not have a cell wall. In 1971 Rottem et al.3 learned that most species of mycoplasma were absolutely dependent for their growth on the consumption of pre-formed sterols including cholesterol obtained from animal and human host cells. These mycoplasmas live harmlessly in host cells until they are stimulated to activity by a stressing traumatic event (bullet wound, bad fall, injury from accident etc.). The growth of the mycoplasma consumes the cell?s cholesterol resulting in death of the affected cell. Mycoplasmas have been identified in ALS using high resolution blood morphology. In the November 9, 2001 issue of Science Dr. Daniel Mauch4 et al. revealed that the glial cells surrounding the motor neurone sully the extra cholesterol needed to repair and replace aging synapses. If the repair does not properly occur, the motor neurone cells proceed to die form overwork. Glial cells are also heavily involved in gathering, processing and storing glutamate. Elevations in glutamate have been found in brain tissue in ALS.

A mycoplasma species, probably fermentans, which was harmlessly sequestered in a glial cell, becomes aroused by some traumatic stressful event. This mycoplasma then consumes the glial cholesterol which makes up 40% of the glial cell membrane, causing rupture and death of the glial dell. The death of these glial cells releases large amounts of glutamate which becomes elevated in brain tissue. Within the neurone some of the excess glutamate accesses a urea molecule. The urea molecule gives up an ammonia ion which converts a glutamate molecule into less dangerous glutamine. This leaves the former urea molecule as a cyanate ion which damages the motor neurone?s mitochondria. One of the consequences of the damaged mitochondria is a decrease in the energy output available to the neurone. This produces the severe weakness and fatigue seen in patients with chronic fatigue syndrome. If the mitochondrial injury is severe the neurone dies. The death of motor neurone stops message delivery to muscle tissue ? a universal finding in ALS.

This avid consumption of cholesterol may also contribute to the endocrine dysfunction seen in ALS because it decreases the amount of cholesterol available to produce estrogen, testosterone, progesterone, hydrocortisone, and aldosterone. Patients with ALS, fibromyalgia, and chronic fatigue syndrome often have hypothalamic dysfunction which may result in adrenal insufficiency, hypothyroidism, and gonadal failure.

Lyme disease frequently exhibits neurologic abnormalities because the Bb neurotoxins are drawn to the fatty tissue found in the brain and peripheral nerves. As a consequence sudden deafness, Bells palsy, Parkinson?s Disease, Multiple Sclerosis, reflex sympathetic dystrophy, peripheral neuritis, and chronic pain may appear.