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Infections (General)

Early research authored by dermatologist, Alan Cantwell M.D., whose histologic examination of scleroderma skin biopsies revealed acid-fast bacterial forms, and also contemporary research implicating various microbes and the suggested mechanisms by which these may contribute to the development and progression of the various forms of scleroderma.

Microbiome dysbiosis is associated with disease duration and increased inflammatory gene expression in systemic sclerosis skin. Arthritis Research & Therapy 6th February, 2019; 21:49

Using advanced Integrated Metagenomic Sequencing Analysis (IMSA), researchers at the Geisel School of Medicine at Dartmouth, Hanover, NH, studied the skin biopsies of 23 systemic scleroderma (SSc) patients to examine the relationship between host genetic expression and the dermal microbiome. Findings included significant microbiome dysbiosis in diseased skin lesions, exhibiting either more or less of certain types of bacteria that were otherwise found in healthy biopsy samples. Conclusions drawn from this study demonstrate a correlation between disease duration and increased inflammatory gene expression in the presence of dermal microbiome dysbiosis.

Commentary in Scleroderma News, dated February 19th, 2019: Systemic Sclerosis Patients Have Deregulated Levels of Skin Microorganisms, Study Shows.

Systemic sclerosis is associated with specific alterations in gastrointestinal microbiota in two independent cohorts. BMJ Open Gastro 2017; 4:e000134.

Norwegian (Oslo) and American (UCLA) university researchers collaborated in a controlled-study to examine gastrointestinal bacterial composition in order to determine if geographical and ethnic variations in lower gastrointestinal tract dysbiosis bears any relationship to systemic scleroderma (SSc) pathogenesis. Their findings suggest that SSc patients had higher levels of inflammation-causing bacteria in the gut than bacteria that are believed to afford protection against inflammation and that this finding was more evident in North American study participants, which the authors believe may be due to diet and genetic variations.

To read more: Science News commentary, published on May 12th, 2017.

Acid-Fast Bacteria as a Possible Cause of Scleroderma. Dermatologica 136: 141-150 (1968)

Report abstract (1966) describing the finding of mycobacteria-like acid-fast bacteria found in the skin biopsies of several scleroderma patients. Although the organisms were small in number and difficult to culture, similar to the difficulties of culturing the causative organisms of tuberculosis or the systemic skin disease, leprosy, A. R. Cantwell Jr M.D., etal, concluded that clues regarding the pathogenesis of scleroderma should not be ignored and called for further study of his findings to prove or disprove an infectious etiology .

Acid-Fast Bacteria in Scleroderma and Morphea. Arch Dermatol. 1971;104(1):21-25. doi:10.1001/archderm.1971.04000190023004

Skin biopsies of ten systemic and limited scleroderma patients were culture-positive in 7 out of 10 tissue sections for acid-fast, gram-positive, pleomorphic bacteria, confirming earlier findings in 1947 by Wuerthele-Caspé. Additionally, rare acid-fast organisms were detected in Fite-Faraco stained tissue sections from four scleroderma and two morphea patients. Study authors, Cantwell and Kelso, call for  consideration of this type of microbe as a cause of scleroderma, until the microbe’s pathogenicity is clarified.

Nodular Scleroderma and Pleomorphic Acid-Fast Bacteria. Arch Dermatol. 1980;116(11):1283-1290. doi:10.1001/archderm.1980.01640350073020

Report of rare acid-fast bacteria and less rare non-acid-fast coccoid forms, compatible with Staphylococcus epidermidis, found in nodule biopsies of nodular scleroderma, an uncommon form of the disease, presenting with multiple, raised dermal nodules. This study reconfirms earlier findings by researchers, Cantwell, Kelso and Rowe, who conclude that these microbial morphologic forms may be related to “cell-wall-deficient L forms” or unusual mycobacterial growth forms, and call for further study to elucidate on the possible role bacteria may play in scleroderma pathogenesis.

Histologic observations of pleomorphic, variably acid-fast bacteria in scleroderma, morphea, and lichen sclerosus et atrophicus. Int J Dermatol. 1984 Jan-Feb;23(1):45-52.

1984 study supporting a decades-long held hypothesis of the association of pleomorphic, variably acid-fast coccoid form mycobacteria with scleroderma. Dermatologist and medical researcher, Dr. Alan Cantwell Jr. confirms these skin tissue findings in biopsies taken from six systemic scleroderma, ten limited scleroderma, and four lichen sclerosus et atrophicus patients samples, describing the microbes’ location and speculating as to the type of microbe that may be implicated, based on microscopic observation.

Infectious disease as aetiological factor in the pathogenesis of systemic sclerosis. Neth J Med. 2010 Nov;68(11):348-53.

A 2010 review of the knowledge-base of infectious risk factors in systemic sclerosis and the possible mechanisms by which exposures to infections might induce pathologic processes, published in the Netherlands Journal of Medicine.

The role of infections in the immunopathogensis of systemic sclerosis–evidence from serological studies. Ann N Y Acad Sci. 2009 Sep;1173:627-32. doi: 10.1111/j.1749-6632.2009.04808.x.

Study demonstrating the higher prevalence of toxoplasmosis, cytomegalovirus and hepatitis B virus in 80 European systemic scleroderma patients as compared with 296 healthy control subjects, implying that infectious agents may be implicated in disease pathogenesis and expression, as reported in the Annals of the New York Academy of Sciences.

The prevalence of infectious agents in patients with systemic sclerosis.  Turk J Med Sci. 2015;45(6):1192-7.

Study finds a higher rate of infections are associated with systemic scleroderma (SSc), including H. pylori, cytomegalovirus, Epstein-Barr Virus, and parvovirus B19 in serological samples of 30 Turkish SSc patients as opposed to an equal number of healthy control subjects.









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