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Another Hopeless Disease - Mycoplasma Fermentans (Incognitus Strain)

Write to Karl Loren -- he will answer

This is just another of the hopeless diseases -- with its own name. Each of them has its own invented name. The treatments recommended are never any use -- they all lead, eventually, to death or the psychiatrist's pills, which, also, lead to death.

Three is a cure.  It does not lie in drugs.

Click here to return to the page on many different hopeless diseases, then read the fully developed article on fibromyalgia. Your solution is there, whether you believe it or not.]

Karl Loren


Source

Mycoplasma Overview

SHASTA CFIDS

For years we in the CFS/FMS/MCS community hav*e been watching the reports of Gulf War Illness (GWI) knowing, instinctively, that we all had something in common. Not only do we all have common symptoms, but we may also be infected with common pathogenic organisms. That pathogen is a Mycoplasma. Various pathogenic strains have been identified including the fermentans (incognitus), penetrans, genitalium, hominis, and pneumoniae. And, we may be infected with several of these strains at one time. Following is a simple overview of the information I have gathered about this Mycoplasma pathogen and how it affects us.

HOW WAS MYCOPLASMA INFECTION IDENTIFIED IN GWS AND CFIDS PATIENTS?
The information trail started with Garth and Nancy Nicolson. Their daughter returned from the Gulf War with an unexplained illness. She was unable to continue her studies at college, and moved back home. Soon after, her parents both became ill with the same symptoms. Medical tests revealed nothing abnormal, but they all continued to worsen. Fortunately for them, however, the Nicolson’s were molecular pathologists with an entire research laboratory at their disposal. The Nicolson’s drew blood and tissue samples from themselves and their daughter, and set the research team, to work.
Garth Nicolson Ph.D. is a professor and former chairman of the Department of Tumor Biology at the University of Texas, M.D. Anderson Cancer Center, Houston, TX. He is also a professor of Internal Medicine, Pathology and Laboratory Medicine at the University of Texas Medical School. He has published over 500 scientific and medical papers, has edited 14 books, he is the current editor of two scientific and medical journals. Dr. Nicolson has been nominated for the Nobel Prize in cell microbiology, is among the 100 most cited researchers in the world, and sits on the board of the American Association of Cancer Research. Nancy Nicolson, Ph.D. is president of the Rhodon Foundation for Biomedical Research. She, also, has published numerous scientific papers and was a professor in the Department of Immunology and Microbiology at Baylor College of Medicine.
What they found was a living Mycoplasma pathogen. In order to find this organism, they had to break open the leukocytes (white blood cells), and perform a specific test called a Polymerase Chain Reaction (PCR) of the DNA of the organism. Nancy also perfected another test, called Gene Tracking, which confirms the PCR results. (1) To gather more information, they then started testing other Gulf War Illness (GWI) patients. What they found was that approximately 50% were positive for the live organism. The Nicolson’s then researched treatment options and found a number of antibiotics that were effective against the organism. (2) After a lengthy course of antibiotics, they recovered. But, the word was out, and requests for testing of GWI patients kept coming in to the lab. They were inundated! As their evidence mounted, they published their data (3) (4) (5) and testified before the President’s Panel on Gulf War Illnesses. (6)
Then the connection was made by the government of the similarities between GWI and CFIDS. (7) By this time, the Nicolson’s lab was already running tests of those with CFIDS---with the same results-- approximately 50% positive! Garth and Nancy Nicolson even wrote an article for the CFIDS Chronicle outlining the diagnosis and treatment of GWI/CFIDS. (8)
But, the politics of medicine and research slowed the gears of progress! Garth and Nancy had to relocate their non-profit lab (The Institute for Molecular Medicine), first to Irvine, CA, then to Huntington Beach, CA. They have had difficulty finding funding for the Mycoplasma research. For their research to continue with CFIDS testing, they need a new grant. In the meantime, they have formed a non-profit organization and take tax deductible donations. Presently, one can become a "Friend of the Institute" and have the various tests done at The Institute for Molecular Biology lab, as well as, participate in the research (see Mycoplasma Resource List for full instructions).
They only recently opened a private laboratory, International Molecular Diagnostics, that can run a variety of tests and does third-party billing of insurance for part of the cost of the tests.

Those of us who have tested positive and have begun treatment with the antibiotics recommended by the Nicolson’s have had tremendous success. Some of these people have been ill with CFS/FMS/MCS for 15-20 years. But, they are feeling better for the first time since becoming ill! Some have even returned to work. Many have completed several months of antibiotics, and several have been taking them continuously for 4-5 years. Since most of us in the CFS/FMS/MCS community have been ill with this organism for a lot longer than the GWI patients do, it may take longer to successfully treat the infection.

WHAT IS MYCOPLASMA?
Mycoplasmas are the smallest and simplest organism known. They are not new. They were discovered over 100 years ago and evolved from bacteria. The "garden variety" mycoplasma is not usually associated with severe diseases. (13) However, sometime over the past 30 years, the organism has been altered to become more lethal. The Mycoplasmas found by the Nicolson’s, in their lab, contain unusual gene sequences that were probably inserted into the Mycoplasma by a specific laboratory procedure. This discovery has led them to conclude that the new forms of mycoplasma were specifically engineered for germ warfare. (9) In it’s laboratory evolution, the Mycoplasmas have became more invasive, more difficult to find, and capable of causing severe diseases in humans. Diseases, like Gulf War Illness, CFS, FMS, MCS, Rheumatoid Arthritis, and AIDS, for instance.

The earlier form of Mycoplasma was studied by Dr. Shyh Lo, formerly of Tanox Biosystems, a spin-off biotechnology company from the Baylor College of Medicine, but now affiliated with the Armed Forces Institute of Pathology in Washington D.C. Dr. Lo has been credited with discovering the new pathogenic form of Mycoplasmas, and he currently holds several patents on methods for special handling of the organisms for study and development. (10) In one of his patents (in 1991), Dr. Lo lists the following diseases that are caused by Mycoplasma: HIV infection, AIDS, Aids Related Complex (ARC), Chronic Fatigue Syndrome, Wegener’s Disease, Sarcoidosis, Respiratory Distress Syndrome, Kibuchi’s Disease, Alzheimer’s Disease, and Lupus. (10) In addition, Baseman and Tully have reviewed the literature on the role of Mycoplasmal infections in human disease and have concluded that they are important factors or co-factors in a variety of chronic illnesses. (11)
Unlike bacteria, the Mycoplasma has no cell wall. This enables it to invade tissue cells, incorporating the cell's nutrients, and using the cell to replicate itself (much like a retrovirus). (13) When the Mycoplasma breaks out of the cell, it takes a piece of the host cell membrane with it. When the immune system attacks the Mycoplasma, it also gets "turned on" to attacking the host cell. In this way, an autoimmune condition can begin. Autoimmune conditions associated with Mycoplasmas include arthritis, Fibromyalgia, myositis, thyroid dysfunction (Hashimoto’s or Grave’s Diseases), and adrenal dysfunction, signs and symptoms of Lupus, Multiple Sclerosis, and Lou Gehrig’s Disease. (12)
The Mycoplasma organism has the capacity to invade cells, tissues and blood, producing systemic infections in numerous organ systems. According to Dr. Nicholson, it can penetrate the central and peripheral nervous system. Because it has the ability to damage the immune system by invading the natural killer cells (NK cells) of the lymphocytes, it weakens them, reduces their numbers, and renders them susceptible to viral infections, such as Human Herpes Virus 6 (HHV6), HHV7 or HHV8. (14) (15) (16) It may also explain some of the environmentally sensitive responses that are seen with CFIDS and MCS.
Mycoplasma infection can trigger inflammatory cytokine over-production that is commonly seen in CFS/FMS. With the induction of CD-4+ helper cells of the immune system, an over production of cytokines such as Interleukin-1, Interleukin-6 and Tumor Necrosis Factor-alpha occurs. (15)(16)(17) These elevated cytokines have been implicated in the development of many of the CFS/FMS symptoms, including neurological involvement. (19)(20) They can have specific or nonspecific stimulatory or suppressive effects on lymphocytes, as measured by B and T cell activation. (18) In addition, the Mycoplasma infection has immunomodulating effects, activating the hypothalmic-pituitary-adrenal axis. This can cause a cascade of limbic system symptoms characteristic of CFS/FMS. (19)
The Mycoplasma is a slow-growing, stealth-type organism that can cause the patient to be very ill. It activates the immune system, then can successfully hide from it within the host immune cells. It can then circulate throughout the body and go wherever a white blood cell can go. It can cause infection deep within any or all organs. It can even cross the blood/brain barrier and cause brain and spinal infection. It has also been known to cross the placental barrier to an unborn fetus.
Unless the white blood cell is split open and examined for the evidence of the live organism, it can go undetected for years. Because the organism resides deep within the cells, conventional antibody tests may be relatively useless. (21) The splitting open (fraction) of leukocytes (white blood cells) from a fresh blood sample, with a forensic PCR test is the most accurate way to detect the presence of active infection with a live pathogen. Further gene-tracking techniques perfected by the Nicolson’s are even more accurate. (22)

CONTAGION
Although the researchers have not clearly established how contagious the Mycoplasmas are, they have made some inferences from the data they have collected. The Mycoplasma organism has been found in the blood and body fluids, spinal fluid, bone marrow, urine, and in the lungs, nose and mouth. The Mycoplasma is reported to be able to survive for two hours outside the body. Of those with Gulf War Illness, 50% of their spouses have contracted the disease and 100% of their children. Several babies have also been known to be born with the disease. Some sort of chemical exposure or immune distress (i.e., auto accident, surgery, cancer) appears to pre-date the onset of illness. Of those with CFS, FMS, and MCS, numerous friends and spouses have the illness, as well as close relatives. So, from the anecdotal reports, it would appear that Mycoplasma is contagious after both casual and intimate contact. This means that the organism may possibly be passed to another through sputum (coughing droplets that contain the organism), saliva, sexual secretions, blood, and urine. The disease is also developing in family pets.
If one tests positive for any of the Mycoplasmas, in order to safeguard those with whom you have close contact, it would be prudent to do the following: Wash your hands a lot, never share your food or drink with another, wash eating utensils with extremely hot water, keep your hands away from your face, avoid closed-air spaces where air is re-circulated (i.e., offices, airplanes), and use protective sexual practices.

TREATMENT
If detected early, the diseases associated with invasive mycoplasmal infections are treatable with long cycles of high-dose antibiotics. (23)(24)(25) Followed with long cycles of low dose antibiotics. Since the organism is a slow-growing, intracellular type with a long life cycle, several, long term courses of antibiotics may be necessary. The infection may need to be treated for several months or years. (The disease is treated much as Lyme’s Disease is treated.) If a person is taking antibiotics, the testing will not detect the presence of Mycoplasma in the blood. And, if a person has been taking antibiotics, they must wait for at least two months, after stopping the antibiotics, for the test to be accurate.

As yet, we do not know if antibiotics are a cure for Mycoplasma infections. Mycoplasma fermentans (incognitus) has the ability to enter any cell and alter itself, changing its cellular makeup with every cell division. This may make it impossible for readily available antibiotics to clear the body of this organism. (14) Also, one antibiotic may not be appropriate for all species of Mycoplasma.
What we are hoping for is to cause the organism to be diminished or go dormant until a cure is discovered. To do that, we need to kill as much of the live organisms from our bodies as possible with the antibiotics. Once our white blood cells are free of the infection, then they can become healthier and can, hopefully, do a better job to keep the Mycoplasma under control. This may take several months or years of antibiotic treatment to accomplish. During this time, it is important to not stop taking the antibiotic too early, for a relapse is certain.

IS TREATING MYCOPLASMA INFECTION THE ANSWER TO CURING CFIDS?
The precise nature and cause of CFS/FMS/MCS is not clear at this time. However, recent studies have shown that several microorganisms may be a factor in CFIDS. Clinical PCR testing has been positive for all of the human herpes viruses, particularly Epstein-Barr Virus (EBV) and Human Herpes Viruses-6, 7 & 8 (HHV-6, HHV-7, HHV-8). Most recently, organisms like Human T-lymphotropic virus (HTLV) types I and II, the foamy or Spuma virus, and the Chlamydia pneumoniae bacteria have also been demonstrated. (26)
Perhaps with this evidence, it would appear that CFIDS has many causative organisms? That is a possibility. Researchers studying AIDS have found that Mycoplasma and HHV-6a may be co-factors for causing AIDS. (14) And, it is further speculated that this same HHV-6 virus may be a co-factor in CFIDS and Multiple Sclerosis. Dr.’s Konnie Knox and Donald Carrigan from the Greenfield, Wisconsin Laboratory (see Mycoplasma Resources), offer some of the most sophisticated human herpes assays in the world. They have been doing extensive research into the various forms of human herpes viruses and their effects on the body. Present in about 98% of the population, HHV-6 remains dormant and harmless in healthy people. But, when activated (possibly by the Mycoplasma infection), it can cause a highly dysregulated immune system often resulting in severe immune suppression. This increases an individuals vulnerability to control severe infections (such as Mycoplasma). Perhaps, if HHV-6 were a co-factor of our disease (along with Mycoplasma), it would appear to be best to be tested and treated for both concurrently, if one is found to be positive.
While the researchers sort out the chicken-or-the-egg, one-organism-one disease, multi-factor theories, it seems prudent for us to test for and consider treating the organisms that we can. Especially when, in the case of Mycoplasma, a few simple antibiotics can bring us so much relief! In the case of a positive test for HHV-6, there are several new antivirals, i.e., Zovirax or Labucavir that may be effective.

CONCLUSION
Infection with a Mycoplasma organism appears to cause most of the signs and symptoms of CFS/FMS/MCS. It can also account for most of the dysregulation of the immune system and the abnormal immune tests. It seems prudent to be tested for this organism, and if positive, to be treated with the recommended antibiotics. Many of us have been ill for 10-20 years and have spent thousands of dollars on treatments that did nothing. Wouldn’t it be a Godsend to have a treatment that worked?

The treatment course is long term and often difficult for many. And, while we may not become completely well, there is preliminary evidence that many of us who are taking the antibiotics are improving! It has certainly been a horrible disease for the Gulf War Veterans to contract, but for us, the fact that they did has saved many lives in the CFS/FMS/MCS community!

REFERENCES

1. Nicolson, N.L. and Nicolson, G.L., The Isolation, Purification and Analysis of Specific Gene-containing Nucleoproteins and Nucleoprotein Complexes, Methods of Molecular Genetics, 5:281-298 (1994)
2. Nicolson, Garth L., Antibiotics Recommended When Indicated for Treatment of Gulf War Illness/CFIDS, (1996)
3. Nicolson, G.L., and Nicolson, N.L., Chronic Illness of Operation Desert Storm: The Presence of Stealth Microorganisms in Gulf War Veteran’s Blood Suggests that Biological Warfare May Have Been Used In Desert Storm, Extraordinary Science, (1995)
4. Nicolson, G.L., Hyman, E., Korenyi-Both, A., Lopez, D.A., Nicolson, N.L., Rea, W., and Urnovitz, H., Progress on Persian Gulf War Illness-Reality and Hypotheses, International Journal of Occupational Medicine and Toxicology, Vol. 4, No.3, pp. 365-370, (1995)
5. Nicolson, G.L., and Nicolson, N.L., Diagnosis and Treatment of Mycoplasmal Infections in Persian Gulf War Illness—CFIDS Patients, International Journal of Occupational Medical Immunology and Toxicology, 5: 69-78 and 83-86, (1996)
6. Nicolson, Garth L & Nicolson, Nancy L., Mycoplasma Infections In Gulf War Illness: Results of a Preliminary Study on the Prevalence of Mycoplasmal Infections in Desert Storm Veterans with Chronic Fatigue and other Symptoms, Presented to the President’s Panel on Gulf War Syndrome, Washington, DC, August 14-16, (1995)
7. Schmidt, P., Blanck, R.M., Gulf War Syndrome and CFS, The CFIDS Chronicle, 8:25-27 (1995)
8. Nicolson, G.L. and Nicolson, N.L., Mycoplasma Infections-Diagnosis and Treatment of Gulf War Illness/CFIDS, CFIDS Chronicle, 9 (3): 66-69, (1996)
9. Nicolson, Garth L., Ph.D. and Nicolson, Nancy L., Ph.D., Summary Of Persian Gulf War Illness Pilot Study On Mycoplasmal Infections In Veterans and Family Members, 1997
10. Lo, Shyh-Ching, Patent # 5215914: Adherent and Invasive Mycoplasma, Patent # 5534413: Adherent and Invasive Mycoplasma, Patent # 5242820: Pathogenic Mycoplasma, Patent #5532134: Mycoplasma Diagnostic Assay, IBM Patent Server Database
11. Baseman, J. and Tully, J, Mycoplasmas: Sophisticated, Reemerging, and Burdened by their Notoriety, Emerging Infectious Diseases, 1997; 3:21-32
12. Nicolson, Garth L. Chronic Infections In CFS, FMS and Gulf War Illness, 1997
13. "Archives of Pathological Laboratory Medicine", May, (1993)
14. Montagnier, L., HIV, Cofactors and AIDS, Abstract from the International Conference on AIDS, June 6-11 (1993)
15. Rawadi, G., Roman-Roman, S, et.al., Effects of Mycoplasma fermentans on the Myelomonocytic Lineage: Different Molecular Entities with Cytokine-inducing and Cytocidal Potential, Journal of Immunology, Jan. 15 (1996)
16. Gallily, R., Salman, M., Tarshis, M., Rottem, S., Mycoplasma fermentans (incognitus strain) Induces TNF alpha and IL-1 Production by Human Monocytes and Murine Macrophages, Immunological Letters, 34(1):27-30 Sept. (1992)
17. Brenner, T., Yamin, A., Abramsky, O., and Gallily, R., Stimulation of Tumor Necrosis Factor-alpha Production by Mycoplasma and Inhibition by Dexamethasone in Cultured Astrocytes, Brain Research, 608(2):273-79 Apr. 16 (1993)
18. Haier, Joerg, M.D., Nasralla, Marwan, and Nicolson, Garth L., Mycoplasmal Infections in Blood from Patients with Chronic Fatigue Syndrome, Fibromyalgia Syndrome or Gulf War Illness, Abstract from the International CFS Congress, Sydney, Australia, 1998
19. Brenner, T., Yamin, A., and Gallily, R., Mycoplasma Triggering of Nitric Oxide Production by Central Nervous System Glial Cells and its Inhibition by Glucocorticoids, Brain Research, 641(1):51-56 Mar. 28 (1994)
20. Weidenfeld, J., Wohlman, A., and Gallily, R., Neuroreport 6(6):910-12 Apr. 19 (1995)
21. Komaroff, A. L., Bell D.S., Cheney, P.R., Lo, S.C., Absence of Antibody to Mycoplasma fermentans in patients with Chronic Fatigue Syndrome, Clinical Infectious Disease, 17(6):1074-75 Dec. (1993)
22. Nicolson, G.L., and Nicolson, N.L., The Eight Myths of Operation Desert Storm and Gulf War Syndrome, Medicine, Conflict & Survival (1997)Hannan, P.C., Antibiotic Susceptibility of Mycoplasma fermentans Strains From Various Sources and the Development of Resistance to Aminoglycosides in Vitro, Journal of Medical Microbiology, Jun. 42(6):421-28 Jun (1995)
23. Poulin, S.A., Perkins, R.E., Kundsin, R.B., AIDS-Associated Mycoplasmas and Antibiotic Susceptibilities, Abstract of American Society of Microbiology Meeting, (1993) (abstract no. G-21)
24. Poulin, S.A., Perkins, R.E., Kundsin, R.B., Antibiotic Susceptibilities of AIDS-Associated Mycoplasmas, Journal of Clinical Microbiology, Apr. 32(4):1101-03 Apr (1994)
25. Vojdani, Ari, Immunology of Chronic Fatigue Syndrome, pp.36-42 (1997)

 


Source

Mycoplasma quotes
Mycoplasma

"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 have chronic invasive infections involving certain uncommon mycoplasmas, such as Mycoplasma fermentans (incognitus strain). "--Dr Nicolson

"Mycoplasma fermentans (incognitus) has been tested on the Texas Department of Corrections prisoners in the late 1980s prior to the Gulf War. It was tested on death row inmates as well as other inmates in Huntsville, Texas. The guards then contracted it from the inmates, and the guards then gave it to their families and community. This mycoplasma vaccine testing was funded by the U.S. Army, and today there is an outbreak of 350 people in the Huntsville area with a strange disease resembling GWS."--Dr Nicolson

"Researchers  Dr. Garth Nicolson and his wife Nancy have found a tiny bacterial microbe (a "mycoplasma")  in the blood of nearly half the ill vets with GWI.  Amazingly, this infectious agent has a piece of HIV (the AIDS virus)  attached to it.  This microbe could never have occured naturally. On the contrary, the composition of the microbe suggests  a man-made and genetically-engineered biological warfare agent."--Dr Cantwell MD

"As soon as homosexuals signed up as guinea pigs for government-sponsored hepatitis B vaccine experiments, they began to die with a strange virus of unknown origin. The hepatitis B experiments began in Manhattan in the fall of 1978; the first few cases of AIDS (all young gays from Manhattan) were reported to the CDC in 1979. Scientists have also failed to explain how a brand new herpes virus was also introduced exclusively into gays, along with HIV, in the late 1970s. This herpes virus is now believed to be the cause of Kaposi's sarcoma, the so-called "gay cancer" of AIDS. Before AIDS, Kaposi's sarcoma was never seen in healthy young men. Identified a decade after HIV, in 1994, this KS virus is closely related to a primate cancer-causing herpes virus extensively studied and transferred in animal laboratories in the decade before AIDS. Also downplayed to the public is a new microbe (Mycoplasma penetrans), also of unknown origin, that was introduced into homosexuals, along with HIV and the new herpes virus. Thus, not one but three new infectious agents were inexplicably transferred into the gay population at the start of the epidemic (HIV, the herpes KS virus, and M.penetrans)."--Alan Cantwell MD

"The Geneva convention prohibits the development and testing of biological weapons, otherwise known as germ warfare agents, and similar provisions are specified in the Nuremberg Codes. Nonetheless, some mycoplasmas have been engineered and/or laboratory modified for use as biological/germ warfare agents. In 1970, the Department of Defense made an appropriations request for 10 million dollars into a 5 year study to develop immune system ravaging micro-organisms for germ warfare." George Hylak on Mycoplasma http://members.aol.com/ghylak/health.htm

        "He wrote back and made a statement that the modified mycoplasma (M. fermentans incognitus) "...was found especially near TDCJ institutions." TDCJ is the acronym for the Texas Department of Criminal Justice. It had previously been known as the Texas Department of Corrections (TDC)
        Dr. Watson is the head of the Human Genome Project and was a co-discoverer of DNA. It seemed pretty strange to me that someone of that magnitude would be running around the Texas prisons. I was told at the time Dr. Watson was here there were experimental flu vaccines being administered to inmates. Bill Langlois, producer of Channel 11 in Houston, has also verified that Dr. Watson was at the Texas Department of Corrections during that time. Sally stated she had not found anything looking at the 1980's Board Agendas and Minutes. I asked if she had looked further back than the 80's and she said "No".
        One of the experiments involved the use of M. pneumoniae. It is one of the most virulent types of mycoplasmas. Another experiment involved the mixing of viruses and mycoplasmas. The experiment of viruses and mycoplasmas was the hypothesis I made in 1997. However, the researchers who experimented on the inmates knew the effect of viruses and mycoplasmas as far back as 1976; twenty-one years earlier.
        This pathogen had been released in our community with complete lack of regard for the inmates, the guards who worked at the prisons, the guards' families they came home to and the community at large. No one was informed. The experiments using M. pneumoniae lasted 10 years. The other had a time duration of "indefinite" with each overlapping one another.
        When I studied Lyme Disease in 1997 I found the same antibiotic treatment was used to treat Lyme as is used to treat mycoplasmal infections. My son was diagnosed with parvovirus B19 not Lyme Disease, but he responded to the antibiotic. This didn't make sense until I found that ticks carry mycoplasmas."--Candace Brown


Source

 

AIDS

AIDS – Acquired Immunodeficiency Syndrome is perhaps the most feared disease on the planet. Usually fatal, it slowly destroys the immune system until the individual is vulnerable to a wide variety of diseases that rarely affect non-infected persons. Those diseases may affect brain, lungs, eyes, or other organs, as do pneumocystis carinii pneumonia and Karposi sarcoma. People with AIDS also can experience debilitating weight loss, diarrhoea, weakness and depression.

AIDS is the most controversial disease of our time. Because the condition initially infected homosexuals, bisexuals and intravenous drug users, governmental attitudes and policies have been slow to respond to this growing epidemic. There has also been a great deal of controversy surrounding treatment methods.

AIDS has given birth to an entire industry involving specialist physicians and drug therapies (Altman 1998). It is estimated that the United States Public Health Service’s annual AIDS research budget was over $1.5 billion in 1994 (Division PHS Budget 1994). Burroughs Wellcome, the manufacturers of AZT, the most commonly used drug to inhibit the replication of HIV, reports sales in excess of $379 million of AZT during the 1992-1993 fiscal year.  These early figures indicate that this has been a boom industry for those associated with the manufacture of AZT and other drug related companies servicing this market.

The World Health Organization (WHO) estimates that since the initial discovery associated with HIV/AIDS, out of approximately 30.6 million people around the world who were infected with HIV, approximately 11.7 million had died from AIDS by mid 1997. It is estimated that 860,000 adults and children are living with HIV/AIDS in North America alone. (UNAIDS/WHO report : ‘Global HIV/AIDS Epidemic’ November 27, 1997).

Mycoplasma fermentans (incognitus) and AIDS

Medical literature states that Mycoplasma fermentans has been recognized as an infectious pathogen in humans, and is associated with an acute fatal disease in previously healthy patients without AIDS (Armed Forces Institute of Pathology). Mycoplasma incognitus has now also been linked with AIDS (Nicolson 1998).

Shih Ching-Lo of the Armed Forces Institute of Pathology has stated that ‘Mycoplasma fermentans can cause death on its own’. Despite this mycobacterium’s link to AIDS and its invasive nature, most people are not aware of how it affects the body.

Mycoplasma fermentans has been described as a ‘co-factor’ in the progression of AIDS (Nicolson 1998). Growing evidence identifies Mycoplasma’s as an opportunistic pathogen and possibly a co-factor in many other chronic disease processes. M. fermentans was shown to be associated with lesions in the kidneys of HIV-positive patients, and was detected in 40% of HIV positive homosexual men, but in less than 1% of the general population.

Luc Montagnier, the founder of the HIV virus reports that Mycoplasma infections accelerate the progression of HIV disease by stimulating the replication of HIV-1 through selective activation of CD4+ T-lymphocytes. When a cell lysate of human Mycoplasma was added to cultured lymphocytes infected with HIV, significant enhancement of HIV replication was observed. This organism has the ability to produce systemic infections, manifesting itself in numerous organ systems. He further states that this Mycoplasma is highly invasive, and can activate, either directly or indirectly, CD4 lymphocytes and render them susceptible to viral infections.

Nicolson reports that Mycoplasma fermentans produces systemic infections in AIDS patients and in previously healthy non-AIDS patients, manifesting itself as a flu-like illness. It also enhances the cytopathic effect of HIV, producing fatal wasting illnesses (Human Pathology, May 1993). This report made the first association between Mycoplasma fermentans infection and AIDS-like illness in HIV-negative patients.

Mycoplasma fermentans (incognitus strain) can generate toxic oxygenated products that damage the host cell. This damage, probably to the cell membrane, allows the Mycoplasma access to the interior of the cell. Once inside the cell wall, the Mycoplasma can alter the cell structure, possibly incorporating itself into the cell during division. If this occurs, the original cell has been altered, and the Mycoplasma continues to proliferate.

Nicolson (1998) has demonstrated that Mycoplasma fermentans:

  • co-factor of HIV in AIDS patients

  • pathogen in rheumatoid and other forms of arthritis, damaging connective tissues (tendons and ligaments) in the joints

  • cytocidal (killing) effect on white blood cells, promoting a suppression of the immune system. This effect can kill the body's first line of defence in fighting disease

  • retains the ability to induce a lethal toxicity in white blood cells, further destroying the immune system

  • inflames the uterine tubes, leading to further infections and problems, which may include painful or irregular menses

  • infects the kidneys, leading to nephropathy (kidney damage), affecting the body's ability to filter liquid waste, and thus increasing the body's toxin levels

  • triggers the production of necrosis factors and nitric oxide in the CNS, which may lead to a decrease in nerve impulse and spinal cord transmission and accelerate degenerative tissue damage

  • exerts strong immune suppressive properties

  • cause fatal respiratory disease within respiratory epithelial cells

  • produces ‘wasting syndrome’ and can cause fatal systemic infection, manifesting a physical appearance similar to that of late stage AIDS patients

  • cause liver infection, mimicking chronic alcoholism and cirrhosis

  • transferred transplacental and may cause chorioamnionitis

  • infect the peritoneal lining, causing peritonitis

In addition to the above documented tissue damage and diseases, Mycoplasma fermentans has been found to activate female hormones. Many female sufferers of Gulf War Syndrome and Mycoplasma fermentans infections begin to show physical signs of false pregnancy, or pseudocyesis. Nicolson reports that the body reacts as if conception has taken place and begins to gain weight to support a foetus. The weight gain and torso swelling persists since there is no birth to signal the body to stop producing the necessary amount of hormones. Thus the woman may constantly appear pregnant, and there have also been reports of women passing placental-like masses.

Mycoplasma fermentans has the ability to infect the entire body. Detection is difficult unless DNA detection using Polymerase Chain Reaction (PCR) laboratory testing is used. Furthermore, Mycoplasma fermentans passes intra-cellular, invading different types of tissue. This means that it can be migrate through cells selectively, damaging cells as it goes.

HIV and its co-factors (viruses and bacteria accompanying HIV) impair the cellular walls of all structures including blood vessels, nerve cells and soft tissue structures. This damage can result in blockages of both small and large blood vessels. Obstructions reduce further the flow to the limbs, brain, heart and other vital structures. In fact, transient ischemic attacks, strokes and heart attacks have been recorded in extremely high numbers amongst patients in advanced stages of AIDS Neubauer 1988). Daily transient ischemic attacks increase as AIDS progresses, resulting in mental impairment, loss of muscle control, decreased memory, and reduced independence.

The drug Doxycycline has been demonstrated to be effective in the overall management of Mycoplasma fermentans. It has the ability to enter the cell and is considered effective against fighting this organism. The antibiotics are not a cure but a treatment. As Montagnier states, ‘the presence of this organism (Mycoplasma fermentans) can greatly increase the number of target cells, and raise the level of virus (HIV) replication too high to be controlled by the immune system. Eradication of the Mycoplasma will not be possible by antibiotic treatment alone, since it undergoes an intracellular phase’ (International Conference on AIDS, 6-11 June 1993). Mycoplasma fermentans has the ability to enter any cell and alter itself, changing its cellular makeup with every cell division. This makes it almost impossible for readily available antibiotics to clear the body of this organism.

Hyperbaric Oxygenation and AIDS

Mycoplasma has been identified as a ‘co-factor’ and has a synergistic effect increasing the hold of HIV. Further immune suppression accelerates the host effect and promotes further secondary opportunistic effects including circulatory AIDS disturbances.

'Hyperbaric Oxygenation has been demonstrated to be effective in the management of HIV/ AIDS. HBOT can force oxygen into all body fluids, by-passing the red blood cells, which are the regular oxygen carriers (Jain 1995). This by-pass overcomes the continuing complications associated with oxygen starvation in the tissues (hypoxia). HBOT helps reduce the severity of secondary complications arising from opportunistic infections' (Jain 1995).

In previous sections we have discussed the benefits of Hyperbaric Oxygenation associated with patients who have suffered strokes, TIAs and peripheral vascular disease. Neubauer also reports that the mechanism of HBOT may benefit AIDS patients. Reillo in AIDS Under Pressure (1997) reports numerous patients with fully developed AIDS that have benefited from HBOT.

Dr Kief, treated a number of AIDS patients in the 1980s with ‘hyperbaric ozone blood washings’. He reported improvement of many associated symptoms including thrush, fungal infections, gastrointestinal problems and chronic low energy (Kief 1993).

Neubauer (1998) reports on a 29-year old male with AIDS related circulatory problems. The man suffered a sudden cerebral haemorrhage secondary to an HIV infection of the brain. The cerebral attack left him with left-sided paralysis and an inability to walk without a walker. Hyperbaric Oxygenation was commenced daily for one hour at 2 ATA. He also received physical therapy on an outpatient basis. After two weeks he began to regain use of his left leg. During this period he reported that he was not experiencing the levels of debilitating fatigue associated with his AIDS. He also gained ten pounds during the initial several weeks of HBOT due to his increased appetite. After one month, the patient had greater control of his previously paralysed lower limb and could now open and close and move his left arm and hand. Continued HBOT has enabled him to return to independent activities with improved mobility.

One of the secondary effects of circulatory compromise is evidenced with Kaposi’s sarcoma. Kaposi’s sarcoma has been linked to one of the many human herpes viruses as recorded by Moore and Chang. This opportunistic infection attacks blood vessels causing purplish lesions both externally and internally with multiple associated secondary complications. Normally treated with chemotherapy and radiation, these lesions have been reported to benefit from HBOT. Reillo (1998) has documented the benefits of HBOT with Kaposi’s sarcoma.

Pneumocystis carinii pneumonia is another secondary infection responsible for killing a significant number of AIDS patients. Despite preventative drug treatments, this secondary infection is also devastating, dramatically affecting AIDS sufferers. Reillo has found that patients with AIDS who use HBOT in conjunction with medication have the best results for minimizing secondary complications.

  • 'Hyperbaric Oxygenation when administered as an on-going treatment prolongs both the quantity and quality of life of the patients suffering AIDS. HBOT alleviates the blood vessel problems directly associated with HIV and herpes infections. HBOT is safe, enhances the effectiveness of drug therapies, reduces adverse side effects and shortens the length of time associated with secondary infections. Hyperbaric Medicine clearly has a supportive role in the management of chronic illness, including AIDS' (Reillo 1999).

 


Source

   Mycoplasma    
 
 
 

SCIENTIFIC FACTS VERSUS FICTION
ABOUT MYCOPLASMA
Aristo Vojdani, Ph.D., M.T.

INTRODUCTION

Members of the genus Mycoplasma are the smallest organisms lacking cell walls that are capable of self-replication and cause various diseases in humans, animals, and plants. 

Seven different species of mycoplasma have been associated with various infections in humans.  The earliest reports of mycoplasma infectious agents in humans appeared in the 1930s, 1940s and finally, in the early 1960s.  The definite relationship between Mycoplasma pneumoniae and the primary atypical pneumoniae was established.

Mycoplasma pneumoniae
Today, M.pneumoniae remains an important cause of pneumonia and other airway disorders such as tracheobronchitis and pharyngitis.  This organism is also associated with extrapulmonary manifestations such as hematopoietic, joint, central nervous system, liver, pancreas and cardiovascular syndromes.

Mycoplasma genitalium
M.genitalium
was originally isolated from urethral specimens of two men with nongonococcal urethritis.  This organism could be involved in pelvic inflammatory disease.  A DNA probe hybridization assay has indicated that M.genitalium was present in urogenital specimens collected from 60% of male homosexual patients with recurrent or persistent nongonococcal urethritis and 22% of heterosexual men with recurrent urethritis, compared with 9% of men without urethritis.

Ureaplasma urealyticum
Ureaplasma urealyticum
is considered to be a commensal organism in the lower genital tract of sexually-active women and has been found at a colonization rate of 40 to 80%.  In some colonized pregnant women, ureaplasmas have been considered to be a cause of chorioamnionitis and premature delivery.  They are frequently transmitted from mothers to their infants, and this may cause various diseases which includes pneumonia, persistent pulmonary hypertension, chronic infection of the central nervous system and bronchopulmonary dysplasia.

Mycoplasma fermentans, M. pirum, M. hominis, and M.penetrans
Mycoplasma fermentans
, M. pirum, M. hominis, and M. penetrans have been proposed as human pathogens and possible cofactors in HIV infection.  These organisms may contribute to the variation in the time from infection with HIV to the development of AIDS symptoms.

Mycoplasma fermentans (incognitus)
Mycoplasma fermentans
is considered to be a commensal in the human mucosal tissues and has often been found in saliva and oropharyngeal of 45% of healthy adults.  Also, M. fermentans organisms have been isolated from the human urogenital tract and are suspected of invading host tissues from a site of mucosal colonization.

Although mycoplasmas are recognized primarily as extracellular parasites or pathogens of mucosal surfaces, recent evidence suggests that certain species may invade the host cells.

The molecular and cellular bases for the invasion of  M. fermentans from mucosal cells to the bloodstream and its colonization of blood remain unknown.

Also, it remains unclear whether M. fermentans infection of white blood cells is transient, intermittent or persistent.  It is not clear how these stages influence any disease progression.  The invasion of host blood cells by M. fermentans is due to inhibition of phagocytosis by a variety of mechanisms, including antiphagocytic proteins such as proteases, phospholipases and by oxygen radicals produced by mycoplasmas.

Mycoplasma fermentans is capable of fusing with lymphocytes and changing their immunological characteristics.

Mycoplasma fermentans cells are able to fuse with Tlymphocytes and change their characteristic of cytokine production.  By electron microscopy we have been able to show that M. fermentans can indeed fuse with CD4 (Molt-3) cells and induce production of proinflammatory cytokines such as IL-6 and tumor necrosis factor alpha.

Prevalence of M. fermentans in patients with Chronic Fatigue Syndrome (CFS) and comparison with healthy subjects

Using PCR and genetic probes, we were able to demonstrate that between 30 and 35% of CFS patients and 4 to 8% of healthy controls do carry the Mycoplasma fermentans genome in their peripheral blood mononuclear cells.

While PCR and genetic probes are rapid and sensitive methods for detecting M. fermentans in clinical specimens, the clinical significance of this organism in Chronic Fatigue Syndrome should be determined by further research studies.

We emphasize that M. fermentans is not the etiologic agent for Chronic Fatigue Syndrome.  It may serve as a cofactor in the induction of cytokines and other immune abnormalities found in CFS.  These abnormalities may compromise the immune system, allowing other agents, whether they be biological, chemical, or both, to exert an effect resulting in symptomatology shown in CFIDS.  Therefore, if the genome of this bacteria is detected in the blood cells of patients with chronic illnesses, treatment with antibiotics may be the logical step for its elimination from the blood.

Mycoplasmafermentans in Persian Gulf War veterans

Due to the similarity of symptoms in patients of Gulf War Syndrome and Chronic Fatigue Syndrome, we applied the PCR and genetic probe methodologies to the blood samples of the soldiers and found a similar percentage (32%) to be positive for the M. fermentans genome.  Since the percent detection of M. fermentans genome in Persian Gulf War Syndrome is similar to that of Chronic Fatigue, we believe that M. fermentans is a cofactor and not the major cause of illness in the soldiers of the Persian Gulf War.

Claims that HIV genome was inserted in mycoplasma fermentans are unfounded.

In one study, it was suggested that pathogenic mycoplasma genomes were genetically manipulated, and part of the HIV genome was inserted into M. fermentans causing a large number of disease cases among veterans.  To prove or disprove this claim, we attempted to amplify various regions of the HIV genome by using primers specific for different regions of the HIV genome in the PCR assay.  We also utilized the extremely sensitive method of Southern Blot analysis with probes specific for the HIV genome.  Using both methodologies we found no portion of the HIV genome among DNA samples of Gulf War veterans who were infected with mycoplasma.  In all cases, we found that only the M. fermentans-specific probe reacted with the DNA samples and the specific probe of HIV did not react.  The results of this experiment  clearly indicate that the above claim regarding insertion of the HIV genome into M. fermentans is scientifically unfounded.

Mycoplasma and rheumatoid arthritis

  • The occurrence of various mycoplasma and ureaplasma species in joint tissues of patients with rheumatoid arthritis and other human arthritides can no longer be ignored.
     
  • M. fermentans was suggested more than 20 years ago as a cause of rheumatoid arthritis (RA) on the basis of isolation from synovial fluids of a few patients.  Recently, with PCR methodology, the M. fermentans genome was found in 40% of synovial biopsy specimens and in 21% of joints of patients with rheumatoid arthritis respectively.  This genome was also found in 20% of patients with spondyloarthropathy and psoriatic arthritis and in 13% of patients with unclassified arthritis.
     
  • M. fermentans was not detected in any specimens from patients with reactive arthritis, chronic juvenile arthritis, osteoarthritis or gouty arthritis.

Minocycline in rheumatoid arthritis

In two recently-published independent randomized trials, rheumatoid arthritis patients were treated with 100 mg of oral minocycline twice daily or a placebo for a period of 26 weeks.  In the minocycline group, more minocycline-treated patients than placebo showed greater than 75% improvement in swollen joint count, tender joint count and in clinical parameters such as serum C-reactive protein (CRP) level and erythrocyte sedimentation rate (ESR).  In these studies, the intergroup differences were statistically significant for these findings and the mean changes over time revealed continual improvement in the minocycline-treated patients during the entire period of both studies.

This and other presently-available data on minocycline therapy in rheumatoid arthritis suggest that such treatment may be considered along with disease-modifying anti-rheumatic drugs such as methotrexate, sulfasalazine, gold salts and hydroxychloroquine.  However, additional clinical research is necessary to document the long-term efficacy of minocycline in the decreased progression of joint destruction.  We believe that such long-term study about the efficacy of minocycline should be conducted on patients who are positive for mycoplasma and chlamydia genome (since we detect the chlamydia trachomatis genome in blood and joint fluid of 20% of patients with rheumatoid arthritis) and not by random selection of arthritis patients.  Such selection or comparison between mycoplasma- and chlamydia-positive patients with mycoplasma- and chlamydia-negative individuals may further increase the clinical efficacy of minocycline or doxycycline in future double-blind placebo studies.

The eradication of the pathogenic mycoplasmas from blood and various tissue sites requires an intact functional immune system, which most patients with chronic illnesses do not possess.  Therefore, immune enhancement strategies along with prolonged drug therapy may help to eliminate mycoplasma from the human body.

Drs. Baseman and Tully, in Emerging Infectious Diseases, Volume3, January-March, 1997, concluded that "the available data and proposed hypotheses that correlate mycoplasmas with disease pathogenesis range from definitive, provocative and titillating to inconclusive, confusing and heretical.  Controversy seems to be a recurrent companion of mycoplasmas, yet good science and open-mindedness should overcome the legacy that has burdened them for decades."

Importance of measuring IgG and IgM antibodies against mycoplasma fermentans

We have developed a specific ELISA assay for measurement of antibodies against mycoplasma fermentans and compared the results to the presence of DNA in the blood.  We found that only in about 60% of cases where M. fermentans was positive, antibodies to M. fermentans antigens were elevated significantly.  In the other 40% in which the genome was positive, IgG and IgM antibodies were not detected.  This may be due to the nature of the M. fermentans cell invasion, the inhibition of phagocytosis, and the lack of immune response to this organism in these individuals.

On the contrary, in about 20% of cases, the M. fermentans genome was absent but antibodies of IgG and IgM isotype were detected in their blood.

The absence of M. fermentans DNA from blood cells and the simultaneous presence of antibodies to this mycoplasma in the serum of the same patients suggests chronic infection of other tissues or cells with Mycoplasma fermentans.  Another possibility is that these antibodies are cross-reactive in their nature.  This means that antibodies produced against collagen, cartilage, and thyroid in some patients with autoimmune disease may cross-react with mycoplasma antigens and give false positive results.  For this reason, we measured antibodies against synthesized peptides corresponding to M. fermentans and were able to reduce the degree of cross-reactivity.

Gold standard for detection of mycoplasmas

  • The polymerase chain reaction (PCR) for detection of mycoplasma genomes is still the gold standard.
     
  • However, confirmation of PCR should be done by southern blot and molecular probes in order to decrease the rate of false positivity and improve false negativity.
     
  • Antibodies (IgG, IgM and IgA) against peptide-specific mycoplasma should be performed simultaneously.
     
  • As no diagnostic tool is 100% accurate, we suggest that PCR, molecular probe, and IgG, IgM, and IgA antibodies should all be performed to gain the most accurate result.

If you need further information or you wish to add to our scientific knowledge, feel free to contact us.

It is certain that physicians’ access to this revolutionary technology
will lead to early diagnosis of infectious diseases
and improvement in patient care.

 

 
   
 
 

 


Source

  NEURONTIN AND BRAIN INJURY TREATMENT
By Gail Kansky and Mike Reynolds

Dr. Jay W. Seastrunk is a psychiatrist who has worked with brain injuries for the past 30 years. With a practice in Duncansville, Texas, and a satellite office in Dana Point, California, Dr. Seastrunk has been treating all types of focal brain injuries he believes he's found in patients with CFIDS and multiple chemical sensitivity diseases.

Dr. Seastrunk believes that people who have experienced brain injuries, including PWCs, can be helped by Neurontin (gabapentin). The drug, originally developed by the Japanese, helps stabilize injured brain cells and helps to stop them from misfiring. Neurontin is a synthetic amino acid that is similar to L-Lucine but does not work the same as L-Lucine or GABA. However, because its molecular structure is so much alike, it uses the same transport system as L-Lucine to absorb the drug into the blood and then the brain.

Dr. Seastrunk finds the majority of his patients have a history of head trauma, but focal brain injuries can also be inherited. Brain focal injuries can be caused by toxic conditions as well as infections, high fevers, and illnesses such as MS and ALS. Various tests are used that can include Magnetic Resonance Imaging (MRI), that are usually normal. Functional MRIs are used to measure blood flow and a Magnetic Resonance Spectroscopy (MRS) identifies chemicals in the brain. This last test is one that, by combining it with special computer software, shows chemicals such as lactate that is elevated when one has an immune dysfunction. N-acetyl-apart (NAA) is a marker that shows the presence of neurons. In CFIDS, the left frontal lobe is usually the more severely affected, although sometimes there are nerve endings from the left frontal lobe that cross over to the right frontal lobe.

 In MCS, combined with CFIDS, a liver spectroscopy can show an increase in glutamine, a toxic by-product. The creatine is often markedly abnormal. Dr. Seastrunk has a questionnaire that he calls an organic evaluator that, when answered by PWCs, shows a 95% rate of demonstrable brain pathology. The left frontal lobe is responsible for retrieving and restoring memories, understanding, and word finding while the right frontal lobe has cognitive dysfunctions that include mood swings and sleep abnormalities. Kindling is a process that happens when exposure to small amounts of a chemical or a toxic exposure causes the brain injury to fire. Dr. Seastrunk believes that chemicals trigger the nasal nerve cells that go to the brain and begin this firing process. He does not believe that detoxification will help since the chemicals are not actually in the brain. Women outnumber men with these illnesses because they are more sensitive to smells and that can trigger a focal brain injury. Both stress and sleep deprivation activate a focal brain injury. Thus, Dr. Seastrunk believes that you don't have to treat the immune system if the brain is treated. The brain will correct the immune abnormalities once treated correctly.

Parke-Davis, the company that purchased gabapentin, has seen dosages that range from 3,000 to 6,000 mg per day while, even at 10,000, the drug is not toxic. Dr. Seastrunk has never found anyone to be allergic to Neurontin in the hundreds of patients he has treated. It does not cross-react with other medications. Magnesium, however, will block Neurontin.

Neurontin is taken "in as evenly spaced intervals as possible. It is not wise...to take it only in the a.m. and then repeat in the p.m.," says Dr. Seastrunk. Side effects will occur when people first take the drug but usually pass aAer two to four weeks. However, we have heard from PWCs who claim they have side effects after being on the medication for months. One side-effect seen initially, is feeling drunk, while another is feeling excessively irritable. Some have felt their balance affected after being on the drug long-term and one PWC broke a hip while on the drug one year and, the next year, broke an ankle. Dr. Seastrunk tries to move the dose up to 3200 mg as quickly as possible, beginning at 100 to 400 mg dosages. At 3200 mg, he checks the blood level to see how much the blood is absorbing. While there are no therapeutic levels established for Neurontin, he looks for blood levels to be S to 18. Usually, benefits will increase up to 3200 mg and then level off. If one increases the dose too fast or is taking too much, he or she will feel drunk. Doses are often increased every two to three days, and two years is often the time taken for a full effect.

Migraines can sometimes occur with Neurontin. Increasing the dose can sometimes stop them. If not, Depakote (1,500 to 2,000 mg/day) or Parlodel (2.5 mg before meals) is prescribed. Dr. Seastrunk feels that a significant number of his patients show improvement but are still sick because they have something that is continuing to injure their brains. Often, this turns out to be Mycoplasma incognitus fermentens or Chlamydia pneumonia. About 15-20% of his PWCs have returned to normal health while the rest show a significant improvement, he claims. Some of these patients were bed-bound for years.

Brain injuries are also treated with SSRIs (ser-atonin reuptake inhibitors) such as EfTexor or Zoloft. Klonopin can help but can be habit-form-ing. Dr. Seastrunk says, "The antidepressant Effexor is often added ...for those who tolerate it, Effexor can be a tremendous boost toward healing." 

Neurontin is expensive, at about $400.00 monthly. If you have no drug card or state insurance and earn less than $16,000 annually as an individual, the company will provide you with any amount of Neurontin for just $3.00 monthly. If you have no insurance but make more than $16,000, the company will charge $45.00 monthly. 

Weight gain is often found by patients taking Neurontin. Dr. Seastrunk says this "is usually due to fluid retention or increased absorption of food and may be treated accordingly." Sometimes a PWCs initial reaction is to develop all their early symptoms in the first week. Dr. Seastrunk usually hospitalizes patients when he first begins the drug therapy. Those beginning the antibiotic therapy for additional microbes in combinations are advised to go very slowly. The antimicrobial therapy can take a few years. All these treatments are still considered experimental. Patients reactions vary from feeling initially drunk to being incredibly irritable. Yet some have claimed they have had no side effects at all. 

Three groups of patients have been found: 

    1) 10-15% respond quickly and have little psychological trouble 

    2) 60-70% respond but take longer 

    3) 5% do not respond at all, while 5-10% won't comply with the regimen

     "Close contact between the doctor and the patient" is needed for the first three months, emphasizes Dr. Seastrunk, "to fine tune the dosage."

If you are not sure you have a Focal Point Injury, members may send a SASE for a copy of Dr. Seastrunk's questionnaire, called "The Organic Evaluator." Requests should be addressed to the National CFIDS Foundation, 103 Aletha Rd., Needham, MA 02492. Neurontin is one of the drugs mentioned in Dr. Jay Goldstein's Treatment Protocol for Physicians, which is also available under the materials column.

 Dr. Seastrunk has become very interested in Chlamydia pneumoniae and Mycoplasma fermen-tans (incognitus) and, during a lecture, said, "We see a certain portion of people who have this illness and focal brain dysfunction and they get better, but they continue to have sickness...we begin to look at Mycoplasma incognitus and Chlamydia pneumonia. Chlamydia pneumonia ...could be an explanation of the vascular problems that we see on MRI...they've got these things that look like MS that are vascular...it suggests that there's something actively ongoing that may be infectious that's continuing to injure the brain, and we need to kill that organism to stop the continuing injury."

(Sources for this article was material provided by the office of Dr. Jay Seastrunk and personal communication with PWCs.) 

 

The National CFIDS Foundation * 103 Aletha Rd, Needham Ma 02492 * (781) 449-3535 Fax (781) 449-8606





 

 


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