Infection with Bacteria as The Cause of Scleroderma

by Alan Cantwell, Jr., M.D. © 2000

Ask most doctors what causes scleroderma and they will tell you the cause is unknown. Furthermore, they will claim that no infectious agent has ever been shown in scleroderma. However, for more than 50 years scientific evidence has been accumulating in the medical journals showing that bacteria are indeed associated with scleroderma, and with closely allied diseases, such as lupus and rheumatoid arthritis.

In the past decade many chronic diseases once believed to be non-infectious are now thought to be caused by viruses, bacteria, or by tiny mycoplasma-like organisms which have characteristics of both bacteria and viruses. Even certain forms of cancer are now considered infectious.

Stomach ulcers were definitely thought to be non-infectious for most of the last century, and physicians and microbiologists insisted bacteria could not grow in the acid environment of the stomach. The ultimate proof that certain bacteria could cause stomach ulcer disease was obtained when a physician-researcher drank a culture of the ulcer-producing bacteria and produced the disease in himself.

It is unthinkable (but true) that decades of research showing organisms in scleroderma and arthritis would be ignored by the medical establishment. Especially now that antibiotics appear to have a beneficial effect in these diseases, it is imperative for physicians to be aware of this research and to stop pretending it does not exist.

Before reviewing the case for bacteria in scleroderma and RA, it is important to acknowledge the role of mycoplasma-like organisms in these diseases. For most of the twentieth century, medical science has regarded these bacteria-like and virus-like microbes as laboratory curiosities of little import. But mycoplasmas can invade cells and even the cell nucleus, thereby promoting chronic infection difficult to eradicate.

Mycoplasma (also known as cell-wall deficient bacteria) are derived from bacteria which have shed all or part of their cell wall. Many chronic diseases may prove to be due to infectious bacteria which transform into the mycoplasma state in order to better adapt to the body. In recent years, mycoplasmas have been discovered in such diverse diseases as Gulf War Illness, AIDS, and certain forms of cancer.

Mycoplasmas may all look and act similarly when in the cell-wall deficient phase - and if a particular mycoplasma becomes stuck in this phase and does not revert back to its original "parent" bacteria, it is impossible to determine the exact bacterial origin of the mysoplasma in question.

Mycoplasma are notoriously difficult to detect and to culture. Thus, they frequently go unrecognized in disease states. Mycoplasma research is still in its infancy, and most experts in the field are microbiologists, rather than practicing medical doctors. Nevertheless, there is a wealth of research implicating mycoplasmas in human disease. The best book on this subject is Cell Wall Deficient Forms: Stealth Pathogens, by mycoplasma expert and Professor Emeritus Lida Holmes Mattman of the Department of Biology at Wayne State University in Detroit.

The Road Back Foundation advocates the use of antibiotic therapy for scleroderma and RA, based on the mycoplasma research first undertaken in the 1940s by Thomas McPherson Brown, M.D., and his microbiologist co-worker Harold W. Clark, Ph.D., currently the Director of the Mycoplasma Research Institute of Beverly Hills, Florida.

The scientific evidence linking mycoplasma to these diseases is simply explained in Dr. Brown's book, The Road Back: Rheumatoid Arthritis, Its Cause and Treatment, [now out of print] and in Clark's Why Arthritis?: Searching for the Cause and the Cure of Rheumatoid Disease. Medical writer Henry Scammell has also authored two books based on Brown's research: The New Arthritis Breakthrough, and Scleroderma: The Proven Therapy That Can Save Your Life.

Fig. 1: A clump of acid-fast, rod-shaped bacteria in the dermis portion of the skin of scleroderma. Fite-Faraco (acid-fast) stain, magnified 1000 times. The first report of "acid-fast" bacteria (similar to the kind of microbes that cause tuberculosis) in scleroderma was published by Virginia Wuerthele-Caspe Livingston, M.D. in 1947. These unusual microbes were discovered in skin scrapings from a woman with ulcerations of the fingers. In later collaboration with pathologists, dermatologists, and microbiologists, she further characterized the peculiar and multi-shaped (pleomorphic) bacteria she consistently isolated from scleroderma cases. Her scleroderma research progressed into microbiologic studies showing similar-appearing acid-fast bacteria in various forms of cancer. Until her death in 1990 at the age of 84, Livingston constantly studied and published her findings on the various aspects of the 'sclero-bacillus' she isolated from scleroderma and the 'cancer microbes' associated with cancer. Despite the furor and controversy that her papers elicited from the cancer establishment, she never wavered in her belief that microbes were at the root of 'autoimmune' and cancerous diseases.

Livingston wrote two books about her lifelong research: Cancer: A New Breakthrough (1972), and The Conquest of Cancer (1984). Her major scientific publications (including the original scleroderma papers) and confirmatory papers by other leading scientists are collected and reprinted in Livingston's The Microbiology of Cancer, available from the Livingston-Wheeler Foundation in San Diego, California.

In 1953, Livingston's finding of bacteria in scleroderma was confirmed by scientists at the Pasteur Institute in Brussels. Additional confirmation was published in 1966 in the Archives of Dermatology, when my own research (co-authored with professors of dermatology and microbiology) showed acid-fast bacteria in the skin biopsy samples from scleroderma cases. During the 1970s and 80s nine additional papers also confirmed the presence of cell-wall deficient, mycoplasma-like microbes in the skin of scleroderma, as well as in multiple diseased organs at autopsy in a fatal case of scleroderma. Like Livingston's bacteria, the organisms we cultured from various patients were pleomorphic. In some fatal cases, the organisms cultured near death were similar to acid-fast mycobacteria associated with tuberculosis, whereas in milder cases the microbes were identified as staphlococci or corynebacteria. Using a tissue stain designed by Lida Mattman to detect acid-fast bacteria and cell-wall deficient bacteria (mycoplasma), bacteria were identified in the skin biopsy material from all cases.

Following the lead of Livingston, my scleroderma research progressed to similar studies of lupus erythematosus (another autoimmune disease) and certain forms of cancer. These studies all showed that pleomorphic bacteria, most likely in a mycoplasma state of growth within the diseased tissue, could be cultured and identified from these diseases. The results of these studies performed over a quarter-century are contained in my book, The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. In addition, abstracts of most of these Cantwell papers can be retrieved online at the PubMed website sponsored by the National Library of Medicine ( http://www.ncbi.nlm.gov/PubMed ).

The scleroderma research of Livingston and her colleagues that began in the 1940s is undoubtedly related to current research implicating mycoplasmas in human disease. Her papers published in the 1950s clearly show pleomorphic microbes consistent with what are now known s mycoplasmas or cell wall deficient bacteria.

For the first half-century Livingston's microbiology of scleroderma and cancer has been clearly outside the mainstream of medical thought. Although ignored by the medical establishment, her discoveries have never been disproven.

Despite all this, there is a wealth of research pointing to bacteria as the cause of scleroderma. Ignoring this research is indeed [unfortunate], particularly when it is again fashionable to talk about infectious agents in cancer, and at a time when antibiotics seem to be of value in treating diseases like scleroderma and RA.

Fig. 2: Purple-red coccoid (round) forms in the dermis between the collagen bundles of scleroderma. Giemsa stain, magnified 1000 times. Both photos reprinted from Cantwell and Rowe: Nodular scleroderma and pleomorphic acid-fast bacteria, Archives of Dermatology, 1980 (see bibliography.)

Dr. Cantwell is a retired dermatologist. mail address: PO Box 29532, Los Angeles, CA 90029. Email: alanrcan@aol.com

Selected Bibliography:

Brown TM, Scammell H: The Road Back, Rheumatoid Arthritis - Its Cause and Treatment. M. Evans and Co., Inc., New York, 1988.

Delmotte N, vander Meiren L: Recherches bacteriologiques et histologique concernant la sclerodermie. Dermatologica 107:177-182, 1953 (Basel).

Cantwell AR Jr., Wilson JR: Scleroderma with ulceration secondary to atypical mycobacteria. Archives of Dermatology 94: 663-664, 1966.

Cantwell AR Jr., Craggs E, Wilson JW, et al: Acid-fast bacteria as a possible cause of scleroderma. Dermatologica 136: 141-150, 1968 (Basel).

Cantwell AR Jr., Kelso DW: Acid-fast bacteria in scleroderma and morphea. Archives of Dermatology 104: 21-25, 1971.

Cantwell AR Jr., Kelso DW: Hypodermitis sclerodermaformis and unusual acid-fast bacteria. Archives of Dermatology 115: 449-452, 1979.

Cantwell AR Jr., Kelso DW: Autopsy findings of non-acid-fast bacteria in scleroderma. Dermatologica 160: 90-99, 1980 (Basel).

Cantwell AR Jr., Rowe L, Kelso DW: Nodular scleroderma and pleomorphic acid-fast bacteria. Archives of Dermatology 116: 1283-1290, 1980.

Cantwell AR Jr.: Histologic observations of coccoid forms suggestive of cell wall deficient bacteria in cutaneous and systemic lupus erythematosus. International Journal of Dermatology 21: 526-537, 1982.

Cantwell AR Jr.: Histologic observations of pleomorphic, variably acid-fast bacteria in scleroderma, morphea, and lichen sclerosis et atrophicus. International Journal of Dermatology 23" 45-52, 1984.

Cantwell AR Jr.: Pleomorphic, variably acid-fast bacteria in an adult patient with disabling pansclerotic morphea. Archives of Dermatology 120: 656-661, 1984.

Cantwell AR Jr., Cove JK: Variably acid-fast bacteria in a necropsied case of lupus erythematosus with acute myocardial infarction. Cutis 33: 560-567, 1984.

Cantwell AR Jr.: The Cancer Microbe: The Hidden Killer in Cancer, AIDS, and Other Immune Diseases. Aries Rising Press, Los Angeles, 1990.

Clark HW: Why Arthritis? Searching for the Cause and the Cure of Rheumatoid Arthritis. Axelrod Publishing of Tampa Bay, Inc., Tampa Bay, FL, 1997.

Livingston Wuerthele-Caspe V, Brodkin E, Mermod C: Etiology of scleroderma. Preliminary clinical report. Journal of the Medical Society of New Jersey 44: 256-259, 1947.

Livingston Wuerthele-Caspe V, Alexander-Jackson E, Anderson JA, et al: Cultural properties and pathogenicity of certain microorganisms obtained from various proliferative and neoplastic diseases. American Journal of Medical Science 220: 638-648, 1950.

Livingston VWC: Cancer: A New Breakthrough. Nash Publishing Corp., Los Angeles, 1972.

Livingston-Wheeler V: The Micro-biology of Cancer (Compendium). Livingston-Wheeler Medical Clinic Publication, San Diego, 1977.

Livingston-Wheeler V, Addeo EG: The Conquest of Cancer. Franklin Watts, New York, 1984.

Mattman LH: Cell Wall Deficient Forms: Stealth Pathogens (ed 2). CRC Press, Boca Raton, FL, 1993.

Scammell H: The New Arthritis Breakthrough. M. Evans & Co., Inc., New York, 1998.

Scammell H: Scleroderma: The Proven Therapy That Can Save Your Life. M. Evans & Co., Inc., New York, 1998.