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Multiple Sclerosis

It is important to remember that MS is only one part of a person and not the person.

MS does not represent them, it is not their identity, they are as normal as the next person.  

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Are Bacteria the Root Cause of MS and Other "Auto-Immune" Disorders?

There is mounting evidence that some, maybe all, cases of MS are caused by a "pathogen complex"; an initial infection that opens the door to an opportunistic invasion by bacteria, viruses, yeasts/molds; and the toxins they produce; which wreaks havoc on the host immune system triggering an inflammatory response, sickness and long term damage. Reports of auto-immune disorders that respond to antibiotic therapy abound; these include MS, ALS, RA, PD, IBD, and more. The mix of invaders could be quite unique to each patient and, thus, so would be the necessary weapons to affect a cure. "Standard" diagnostics and "standard" treatments would be virtually useless because there would be no "standard" disease.

 

Much of current MS research focuses on the inflammatory process and how this can be suppressed. Little research is focused on what is causing the inflammation in the first place. The immune system has been labeled the "bad boy" of the disease process and although research continues on viruses as a possible cause, bacteria have been essentially ruled out. A review of the historical literature reveals that this may be premature. Not only do bacteria exist with extremely sophisticated mechanisms to evade detection from standard tests, but the toxins they produce can be equally damaging to the infected host and trigger a major inflammatory immune response.

 

A Little History                                                                                                                                                                                            

Back in the early 1900's MS was generally understood to be a bacterial infection caused by a spirochete (a spiral shaped bacteria). This bacteria was identified by microscopy with silver staining and patients were treated with arsenic and other remedies of the day. (Remember, this was before antibiotics were discovered.) The two World Wars destroyed much of the European scientific data and interest shifted to the study of viruses following the escalating epidemics of polio in Europe and in the United States in mid-century.

 

The Trouble with Mainstream Thinking - A Scientific Parallel

(Don't Confuse Me with the Facts; I've Already Made Up My Mind)

 

In 1984 a young Australian GP, Dr. Barry Marshall, working with pathologist Robin Warren, found Helicobacter pylori in 77 percent of his patients with deodenal ulcers. At the time, mainstream medicine insisted that bacteria could not live within the hostile environment of the stomach and blamed ulcers on stress, smoking, spicy foods - everything BUT bacteria. So Dr. Marshall infected himself with H.pylori, developed stomach ulcers, treated himself with antibiotics and cured the ulcers to prove his point. Even then his work was largely ignored. It took nearly a decade for doctors to take his findings seriously and for patients in western countries to finally get the right treatment for their illness. In the meantime, ulcer patients received a host of unnecessary drugs and surgeries for the symptoms of their stomach ulcers, to the tune of billions of dollars in treatments, without ever affecting the root cause. Twenty years later, Dr. Marshall received a Pulizer Prize in recognition of his work.

 

The Case for Mycobacteria                                                                                                                                                                       

Recently another Australian, Dr. Thomas Borody, has reported similar findings in the treatment of Crohn's Disease, another inflammatory condition of unknown cause. Dr. Borody has proposed that Crohn's disease is caused by the bacteria, Mycobacterium avium paratuberculosis. The microbe is a member of the family of bacteria that cause diseases such as tuberculosis and leprosy. Over the past 20 years he has conducted a series of studies showing not only the presence of these bacteria in Crohn's patients, but that all tend to respond to a combination of certain specific antibiotics.

 

Researchers in New York have recently reported that the leprosy bacteria, Mycobacterium leprae, is the direct cause of nerve demylenation in leprosy. "The nerve damage, a hallmark of leprosy previously thought to be a byproduct of the immune system's response to the leprosy bacteria, now seems to be a direct result of the leprosy bug attaching itself to specialized nerve cells called Schwann cells, ..." M. leprae is known to cause debilitating neurological injury in humans but the clinical manifestation occurs years after a slow infectious process. (Sound familiar?) They also discovered that the bacteria sequesters itself in the regenerating non-myelinated nerve cells and waits "for a chance to attack again once they multiply and escape from these cells."

 

The Case for Spirochetes                                                                                                                                                                        

Spirochetes as a species are not a new phenomenon; they have been found in the mid-gut of termites preserved in 20 million year old amber and over time they have evolved very sophisticated survival techniques. They are pleomorphic which means that they can quickly shift from their normal spiral shape to "cysts" and "granules" to survive unfavourable conditions; they can even shed their cell wall ("L-forms", "cell wall deficient" or "cell wall divergent") and coat themselves with fibrin to avoid detection by the host's immune system. This makes them extremely difficult to detect in standard lab tests. Since many antibiotics target the cell wall to detect and kill bacteria, those drugs are thus rendered completely useless as a treatment. Spirochetes prefer to infect the brain, the joints and the heart although they can and will infect any organ of the host. Infection is usually caused by an insect bite and is frequently accompanied by multiple co-infections by other bacteria and/or viruses via the carrier insect.

 

Lida H. Mattman, Ph.D., Pulizer Prize nominee and author of the textbook, "CELL WALL DEFICIENT FORMS, Stealth Pathogens," presents photographic plates of  L-colony and typical spirochetes in blood cultures of MS patients. Dr. Mattman is convinced that MS is a spirochetal disease and that it is just a matter of time for mainstream science to accept the facts uncovered by researchers such as herself who study pleomorphic pathogens. The preface of her textbook states:

 

"Pleomorphic forms are the first growth in culture, and usually predominate as the pathogen flourishes in vivo. They were observed in clinical specimens in the laboratories of Louis Pasteur and Robert Koch and recognized as pathogenic. So why have they been ignored for many decades? In classrooms, two errors have been perpetuated: (1) students are taught to fix smears with heat [due to their high lipid content, cell wall deficient (CWD) forms melt into globs when heated], and (2) only the Gram stain is on the desks of microbiology students. The Gram stain should always be accompanied by Acridine Orange, which shows that otherwise unidentified material contains nucleic acids and, therefore, is cellular. Pleomorphism is an unfortunate phenomenon from the diagnostic point of view. Bacteria and fungi have lost their name tags. However, the greater efficiency in solving diagnostic mysteries compensates for the great inconvenience in identification. (...)"

 

Spirochetal cysts have been reported by the Department of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway, in 10 out of 10 CSF specimens of MS patients; some of these cysts were cultured back to their classic spirochete form.

 

A 2006 study of thirty blood samples from Alzheimer's patients found that all thirty samples tested positive for Borrelia burgdorferi, the spirochete responsible for Lyme Disease which is a recent manifestation very similar in symptoms to MS, RA and other "auto-immune" disorders. In other research, the outer surface protein of B. burgdorferi has been shown to induce amyloid-like fibrils in vitro; morphological changes similar to those observed in Alzheimer's disease have been induced by exposing mammalian glial and neuronal cells to B. burgdorferi spirochetes.

 

Recent DNA research has tracked the lineage of B. burgdorferi bacteria to Ice Age Europe, blasting previous medical dogma which had labelled B. burgdorferi and its current manifestation, Lyme Disease, as a relatively new pathogen unique to North America.

 

Lyme Disease has supplanted syphilis, another in the family of spirochetes which if untreated can cause severe neurological damage and death, as the new "Great Imitator" because of its wide ranging and difficult to diagnose symptoms. Lyme Disease is frequently accompanied by co-infections from such pathogens as Babesia, Erlichia, Bartonella and Mycoplasma.

 

The Case for Boosting, Not Suppressing, the Immune System

Several studies have revealed that Natural Killer Cells (NK Cells) are severely depleted in patients suffering from auto-immune disorders. Scientists have been at a loss to explain the significance of this. One recent study of a drug used to treat rejection of organ transplants, thought to be of benefit to MS patients because of its ability to suppress the growth of T-cell lymphocytes (the suspected cause of MS inflammation and damage), revealed that the drug did not suppress T-Cells but instead boosted NK Cell activity. Further, the longer the treatment, the more the NK Cells expanded, and the better the MS patient outcome.

 

What's Clogging Up the System?                                                                                                                                                             

Several other independent studies have discovered that fibrinogen is a key component in "auto-immune" dysfunction. The higher the fibrinogen count, the more sluggish the circulation and the worse the patient responds to any given treatment. From a logic standpoint, it just stands to reason that in order for any treatment to work, it first must get to the site of the problem. If circulation is blocked, oxygen, nutrients and medicinal treatments cannot reach the cells and toxins will not be flushed from the system.

 

What If ...                                                                                                                                                                                                      

What if the real cause of MS and other "auto-immune" diseases is an extremely variable mix of pathogens which invade host cells, overburdening and exhausting the immune system, depleting cellular oxygen and nutrients, and producing toxins which clog circulation and poison the host. It is well understood that antibiotics and antiviral's, although powerful tools as a first line of defence in acute infection, are losing their effectiveness; pathogens are becoming more and more resistant to pharmaceuticals with each passing year. A healthy and robust immune system is the ultimate answer.

 

Whether it be a spirochete, a mycobacterium, a virus or, more likely, a complicated mix of varying pathogens unique to each sufferer of an "auto-immune" disease, the facts are rapidly piling up which point to an external cause for MS and like illnesses. If so, current attempts to halt progression of disability by suppressing the immune system are fraught with peril. If pathogens are the cause of disease and disability we must hunt them down with better diagnostics. We must protect and enhance the immune system, improve circulation, clear the body of toxic substances produced by such pathogens and support the body with proper nutrition and rehabilitative physiotherapy.

 

 

Author - K Schneider (USA) - Nov 2008

 

 

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