REVELATIONS OF PERSONAL RESEARCH
Since I had a positive test for a new stealth pathogen named Mycoplasma fermentans incognitus five years ago, I have been curious as to how, why, and when I contracted it. Having been on antibiotics for four years, I am nearly well!!! Could this pathogen have been the cause for CFIDS in my case? I believe so. My research into this new pathogen has led me to some interesting revelations.
Recent research has lead me to conclude that our disease is relatively new and emerging along with many others like Lupus, Multiple Sclerosis, Reactive Arthritis, Post Viral Syndrome, Lyme Disease, etc.
My research has led me to the term "STEALTH PATHOGEN". A stealth pathogen is one that can cause infection by invading the cells, thus hiding from the body’s immune system. Since the organism hides inside the cells, laboratory tests to determine their presence is difficult. Usual antibody tests are worthless. The only way to diagnose the problem is by culture and/or PCR. Often special body fluids or tissue samples are necessary (i.e., cerebral spinal fluid, synovial or joint fluid, bone marrow, glandular biopsies, muscle biopsies, etc.) The disease process develops slowly and the progress is marked with remissions and exacerbations.
Along with Mycoplasma, other pathogens may fall into this group. Most of these are the cell wall deficient forms (also called L-forms or spheroblasts) of common bacteria that can cause a serious disease state. Lida Mattman, Ph.D. of Wayne State University, writes about these pathogens in her book entitled Cell Wall Deficient Forms: Stealth Pathogens. She explains that ordinary bacteria and fungi are capable of mutating to a form that lacks a cell wall. When mutated to this state, they are more invasive (entering cells) and more pathogenic. She explains that the majority of unexplained negative lab cultures concern infection with these cell wall deficient variants of common bacteria.
In my research, I have also been interested in the autoimmune aspect of our disease (and others). This is easily explained if one understands how cell wall deficient organisms operate. Once they enter a cell they incorporate the cells energy source and food as their own. They are hidden from the body’s immune system at this time. While in the cell, they then multiply. They leave the dead cell in search of another. In leaving they take a piece of the cells membrane with it. During the brief time out of the cell, the immune system recognizes both the pathogen and the body’s own cell membrane and sets up a defense against them both. After the pathogen enters another cell, it is not affected by the immune system, but the reaction against the cell membrane sets into motion an attack on other cells of that type. Hence, we often have auto antibodies against our own tissues like thyroid, heart, muscles, joints, etc, which complicates the clinical course of the disease.
In comparing the diseases caused by these "stealth pathogens", I found many correlation's with CFS. There are many overlapping symptoms, many of he same abnormal laboratory tests, and if they are treated with the appropriate antibiotic—the same recovery rate. Another comparison is that they all "emerged" into the medical world at about the same time period—the past 20 years (i.e., Lupus, Multiple Sclerosis, Lyme, Fibromyalgia, Gulf War Syndrome).

DISTURBING THOUGHTS
Suspicion by a noted researcher Garth Nicolson, Ph.D. (originally of the M D Anderson Cancer Research Center in Texas and lately of the Institute for Molecular Medicine in Huntington Beach, CA) that the Mycoplasma fermentans incognitus was bioengineered in order to make it more virulent and useful for germ warfare was another revelation I was unable to handle, at first. Dr. Nicolson explained that he identified an alteration in the molecular structure of the Mycoplasmas he had found in Gulf War Veterans who were ill. The Mycoplasmas were found to have had an envelope gene from an HIV organism inserted into its nucleus (GP 120). This would make the organism more invasive and harder to treat. He explained that this insertion does not occur naturally, but can be "forced" using specialized laboratory techniques. (A mutation caused within a laboratory setting.)
While germ warfare is certainly not a subject that is pleasant or easy to think about, we cannot afford to bury our heads in the sand, either.

Now that Dr. William Reeves has openly admitted that funds, earmarked by Congress for the study of CFIDS, were misappropriated by the CDC, the next question is WHY? Why has the CDC and NIH not funded any studies of suspected pathogens? Why was the diversion of funds used for psychological studies as the only explanation of CFIDS? Is there a hidden agenda? Could the diversion of CFIDS research funds be part of a larger governmental "cover-up" pertaining to germs engineered for war? Is there a connection between the testing of potential wargerms (such as Mycoplasmas &/or other intracellular "stealth pathogens") on civilian populations and CFIDS?

Research done by a fellow sufferers, Sean and Leslee Dudley from the Mycoplasma Registry, led me to the possible connection between Mycoplasma and CFIDS. They led me to a researcher by the name of Shyh-Ching Lo. Lo originally filed a patent on Mycoplasma, with the US Patent Office in 1986. His laboratory research has taken him to Texas and to Maryland. Studies continued until 1996 when four patents were finally granted. The patents involved discovery of two Mycoplasmas with unique morphological and pathobiological properties. It explained that these Mycoplasmas did not appear to be related to any other species of human or animal Mycoplasma. These novel Mycoplasmas were called Mycoplasma penetrans and Mycoplasma fermentans incognitus.

HOW DID SHYH-CHING LO KNOW THIS IN 1986???????
(Especially since the name Chronic Fatigue Syndrome
had not even been coined until 1988!!!)

These Unique Mycoplasmas were deposited with the American Type Culture Collection in Rockville, MD (Otherwise known as the DOD depository for biological warfare.)

In addition I think that it is very interesting that Dr. Lo used one main method—the Polymerase Chain Reaction (PCR) to detect the organisms studied in his patents. He did not utilize antibody tests. His patents explain the pathogen's ability to reside within human tissue cells and evade the detection of the immune system. However, when he corroborated in a CFIDS study with Anthony Komaroff, MD, David Bell, MD and Paul Cheney, MD (three noted CFIDS researchers), it was concluded that CFIDS patients DID NOT have Mycoplasmal infections based on an antibody test. [Absence of Antibody to Mycoplasma fermentans in patients with Chronic Fatigue Syndrome, Clinical Infectious Disease, 17(6): 1074-75 Dec, 1993.] Were the CFIDS doctors bamboozled? Those three independent labs that are reporting high positive results know that antibody tests are worthless on these strains of Mycoplasma because they are intracellular. Perhaps that is precisely why Lo corroborated with the CFIDS researchers——to falsely confirm that Mycoplasmas were not present in CFS patients so they would look elsewhere for a cause. Consequently, the results of the CFIDS/Lo corroborated study have left it difficult to convince the CFIDS researchers to look for Mycoplasmas in their patients. They refuse to believe, as valid, the high percentage of positives (by PCR) that those three different independent labs are reporting. (Reported: Institute for Molecular Medicine=75%, University of California-Irvine=70%, Immunosciences Lab=55%.)

CONCLUSION
How can we be so sure that CFIDS is not infectious if the government does not fund independent researchers to investigate any pathogenic organisms that might be present?
Many of us with CFIDS, especially after reading the historical chronicle Osler’s Web by Hillary Johnson, are beginning to suspect a "cover-up" by the CDC, DOD and NIH regarding the CFS epidemic.
After 25 years since the first reported epidemic, we still don’t know much about CFIDS. Questions remain. What causes it? How is it transmitted? What tests can diagnose it? Who is at risk? How can it be treated? How can it be cured? How can it be prevented? How many people have it? How large is the public health threat it poses. Why does it continue to spread? How can it be stopped? Why does it occur in clusters within households and workplaces? Can the disease be passed from a woman to her unborn child? Can it be transmitted through breast milk? Can it be transmitted to or from household pets? Should persons with CFIDS avoid donating blood, blood products, or organs? These are just some of the questions we should demand an answer to from our government.