Tag: Lyme’s disease

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Cell Wall Deficient Pathogens – L-Forms

Rheumatoid arthritis and other autoimmune diseases are actually the body’s attempt to find and kill human cells that had been colonized by pathogenic bacteria or fungi. At the microscopic level single celled organisms can exist in forms that are as different as the baby tadpole to the fully grown frog. During times of better health of the host the parasitic pathogen can change forms and hide from the better armed immune system within a few infected cells. During times of sickness, when there may be a flair up of the chronic symptoms, the colonies of cell wall deficient microbes multiply within the infected host cells and the host cells divide. Eventually the number of infected cells increase to another level of the pathogens life cycle and the host cells can split open and release pathogens that have the outer wall again which might increase risk of spreading the infection to other hosts.L-forms are referring to a “Life-form” stage of bacterial growth in which the bacterium can lose its outer wall and start growing within the interior of a human cell or other host cell. The following article by Amy Proal goes into extensive detail about the history of research in the field of autoimmune disease and cell wall deficient pathogens. http://bacteriality.com/2007/08/18/history/

Lida Mattman, a pioneer in the field of L-form microbes, is pictured at her microscope. She died at age 96 in 2008.  Obituary: http://www.lymenet.de/literatur/lida_mattman.htm

Sue Massie is a mother who found that Lyme’s disease was a problem for her husband, herself and their 6 children. She shares her family’s medical journey – they all were sick with low grade chronic symptoms. Dr. Mattman is quoted near the bottom of the article regarding the potential risk of infection from physical contact with a human carrier of Lyme’s disease (Borrellia burgdoferi):

“Dr. Mattman believes that touching can spread Lyme disease. The Lyme spirochete can actually occur in tears, and therefore can be transmitted to hands, which contaminates doorknobs, pens, people shaking hands, etc. This appears to be consistent with the observation that whole families often culture positive for Lyme and present with symptoms.” http://www.springboard4health.com/notebook/health_lyme_disease.html

  • A link to the book by Lida H. Mattman, Ph.D in Immunology from Yale University, “Cell Wall Deficient Forms: Stealth Bacteria“: http://www.lymebook.com/cell-wall-deficient-forms-mattman
  • A book review about Lida Mattman’s book, Cell Wall Deficient Forms: Stealth Bacteria:
    From Book News, Inc.
    Mattman (immunology, Nelson Medical Research Institute, Warren, MI) explores pleomorphic forms of bacteria and fungi, which are inconvenient to deal with but allow a much more precise identification of a pathogen and diagnosis of disease. She provides information to help researchers determine the organisms that should be added to the childhood vaccine, especially for boys; the bacterium found in its pleomorphic state in direct smears of synovial fluid of rheumatoid arthritis cases; the chronic disease for which an acid-fast organism is routinely found in smears of 72-h blood cultures in any routine medium; the bacterium that has a life cycle in the human erythrocyte as complex as that of Plasmodium malaria; the common pathogen of which the L form can permanently damage mammalian myocardium; and other microbes. No dates are noted for previous editions. Book News, Inc.®, Portland, OR http://www.personalconsult.com/articles/lymecellwalldeficiency.html
  • Excerpt from the book “The Top Ten Treatments for Lyme Disease” http://www.lymebook.com/marshall-protocol:  “In the past, sarcoidosis patients have received only minimal benefit from antibiotic therapy. But Dr. Marshall discovered that, upon reduction of 1,25-D levels, sarcoidosis patients can actually be cured with antibiotic therapy.”

Coinfections are a frequent problem within autoimmune disease sufferers. Sarcoidosis patients have had a variety of different species of pathogens cultured from blood samples. A weakness in immune strength may leave some people more susceptible to be a host for the types of pathogens that can survive in the L-form and colonize within human or other host cells. The good news is that the same treatment plan helps the human’s immune system to recognize the infected cells and reduce the infection without chemotherapy or other immune suppressing medications.

Benicar is a medication used in the Marshall Protocol, the treatment plan developed by Trevor Marshall, a biomedical engineer who worked on finding treatment for his own case of sarcoidosis.

Benicar acts to block the Angiotensin Receptor on cell surfaces. It may help the host defense by removing the disguise of “self” that the colonized cells may be using to confuse the healthy uninfected white blood cells. The overactivity of white blood cells is the characteristic response of autoimmunity that adds to long term degeneration. Previous medication strategies have been to suppress the overactive response. The use of Benicar every 6 hours maintains a constant inhibition of the Angiotensin Receptor that may help the healthy WBC identify the sick ones. Another benefit of Benicar therapy would be to reduce wasting of magnesium resources by the kidneys.

Excerpt from “The Stealth Pathogen Theory”  http://www.shoptown.com/Dean/ALS2Lyme.htm:

In the case of rheumatoid arthritis, Dr. Hoekstra has found that virtually all the patients he has studied have had significant amounts of a bacteria called Propioni bacterium acnes. “This is the genus and species of the organism we believe is responsible for propagating and perpetuating this disease,” says Dr. Hoekstra. “It is a very common bacteria in an altered state of being–it’s cell wall deficient.”

 The bacteria was first identified and described in 1981 by G.A. Denys at Wayne State University in Detroit, Michigan. “This bacteria is passed transplacentally, from mother to fetus, and this may be responsible for rheumatoid arthritis showing up in generations in a single family,” says Dr. Hoekstra.

 Why this bacteria is prevalent in seemingly all cases of rheumatoid arthritis is not clear; overuse of antibiotics may be a factor encouraging its growth. “The use of antibiotics is one of the most potent ways of inducing cell wall deficiency; bacteria seem to do this as a survival mechanism.”

 In other words, when a bacteria is transformed into a cell wall deficient form, it assumes different characteristics from the whole or native type of microorganism it used to be, Dr. Hoekstra explains. “The organism remains intact except it loses its cell wall and its antigenic characteristics, enabling it to function as a cellular chameleon.” When it loses its antigenic signature, the bacteria is able to mask itself against destruction by the immune system’s antibodies which can no longer recognize it as an antigen (foreign protein).

 Dr. Hoekstra’s mentor, Lida Holmes Mattman, Ph.D., also of Wayne State (now professor emeritus of biology), confirmed the causal role of P. acnes in a laboratory experiment. Dr. Mattman extracted the bacteria from the synovial fluid (which lubricates joints) of human arthritis patients, and injected it into chicken embryos. The chicks then exhibited symptoms of rheumatoid arthritis. When she treated the chicks with antibiotics known to disable P. acnes, the disease disappeared.

Disclaimer: Opinions are my own and the information is provided for educational purposes within the guidelines of fair use. While I am a Registered Dietitian this information is not intended to provide individual health guidance. Please see a health professional for individual health care purposes.