| Causes of Scleroderma (MAIN MENU) |
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| Causes of Scleroderma: Infection |
| This page was written by Shelley Ensz and has not yet medically edited. |
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| Overview |
| Researchers have long suspected an infection component may be involved as the trigger of some cases of scleroderma and there is an ongoing study about persistent infection as a possible cause of scleroderma. |
| Infection and Rheumatic Diseases (General) |
| Research Could Result in New Treatments for Autoimmune Disorders and Common Infections. University of Missouri-Kansas City researcher has discovered how the pathogen Staphylococcus aureus (S. aureus) disables an essential component of the human immune system. S. aureus (also called "Staph infection) is a leading cause of community acquired and hospital-related infections. Kansas City InfoZine. 03/19/07. |
| Scientists Find Previously Unknown Receptors On Adult Stem Cells. Scientists have discovered that marrow stem cells, undifferentiated cells that eventually give rise to the blood cells that fight infection, possess receptors that recognize bacteria and viruses. The findings could have important implications for treating autoimmune diseases. Medical News Today. 06/23/06. (Also see: Stem Cell Transplants) |
| Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease. Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistance. Clinical Microbiology Reviews, January 2006. |
| Infections and autoimmunity--good or bad? Microbial infections can act as environmental triggers inducing or promoting autoimmunity resulting in clinical manifestations of autoimmune disease in genetically predisposed individuals. Increasing evidence suggests the opposite outcome, which is the prevention or amelioration of autoimmune processes following microbial encounters. These latter observations support conceptually the "hygiene hypothesis," suggesting that cleaner living conditions will lead to enhanced incidence of autoimmune disorders, asthma, and allergies. PubMed. J Immunol. 2005 Jun 15;174(12):7481-6. |
| Induction, exacerbation and inhibition of allergic and autoimmune diseases by infection. Epidemiological and experimental data suggest that infections or the exposure to non-pathogenic bacteria protect individuals from developing some autoimmune and atopic disorders. However, there is also solid evidence suggesting that infections can exacerbate or even directly cause autoimmune and allergic disorders. PubMed. Trends Immunol. 2005 May;26(5):260-7. |
| Amplification of autoimmune disease by infection. Reports of infection with certain chronic persistent microbes (herpesviruses or Chlamydiae) in human autoimmune diseases are consistent with the hypothesis that these microbes are reactivated in the setting of immunodeficiency and often target the site of autoimmune inflammation. We suggest that patients with autoimmune disorders receiving immunosuppressing drugs should benefit from preventive antiviral therapy. PubMed. Arthritis Res Ther. 2005;7(2):74-84. |
| The role of infections in the pathogenesis of autoimmune diseases. The etiology of autoimmune diseases remains largely unknown but candidate etiologic factors include genetic abnormalities and infections. PubMed. Curr Drug Targets Inflamm Allergy. 2005 Feb;4(1):99-103. |
| Hepatitis C virus, Sjogren's syndrome and B-cell lymphoma: linking infection, autoimmunity and cancer. Viruses have been proposed as possible etiologic or triggering agents of systemic autoimmune diseases (SADs), with hepatitis C virus (HCV) being one of the viruses most frequently associated with autoimmune features and with systemic autoimmune diseases such as mixed cryoglobulinemia or Sjogren's Syndrome. Moreover, the association between HCV infection and hematologic malignancies, mainly non-Hodgkin's lymphoma (NHL), is supported by several studies. PubMed. Autoimmun Rev. 2005 Jan;4(1):8-15. (Also see: Liver Involvement, Cancer and Scleroderma, and Sjogren's Syndrome) |
| Bactrial Infections |
| Lack of Evidence for Bacterial Infections in Skin in Patients With Systemic Sclerosis (SSc). The data presented here do not support the contention that persistent bacterial infections play an important role in the pathogenesis of SSc. M.D. Mayes. Am J Med Sci. 2009 Apr;337(4):233-5. |
| "Study of Persistent Infection in Systemic Sclerosis Skin and Vessels", Maureen D. Mayes, M.D., at Wayne State University and the University of Texas at Houston. This project examines persistent bacterial infection of the skin or small blood vessels as a potential cause of scleroderma. Results could lead to treatments that target the bacterial infection. 10-21-01 to 10-21-04 |
| Borrelia Burgdorferi Infection |
| Borrelia-associated early-onset morphea: A particular type of scleroderma in childhood and adolescence with high titer antinuclear antibodies? Results of a cohort analysis and presentation of three cases. We observed a statistically highly significant association between morphea, serologic evidence of Borrelia infection, and high-titer antinuclear antibodies when disease onset was in childhood or adolescence. J. C. Prinz. Journal of the American Academcy of Dermatology. Volume 60, Issue 2, Pages 248-255 (February 2009). (Also see: Morphea) |
| Dermatological aspects of Lyme borreliosis. The relationship between infection with B. burgdorferi and other dermatoses, especially morphea, lichen sclerosus, and interstitial granulomatous dermatitis is still debated. (PubMed) Med Mal Infect. 2007 Jul-Aug;37(7-8):540-7. |
| Acute exacerbation of systemic scleroderma in Borrelia burgdorferi infection. Laboratory tests showed an infection with B. burgdorferi sensu lato that was successfully treated with intravenous ceftriaxone, an antibiotic recommended for Lyme borreliosis. This case suggests that Lyme disease should be considered in atypical cases of skin sclerosis in patients predisposed to the development of systemic scleroderma. PubMed. J Eur Acad Dermatol Venereol. 2005 Jan;19(1):93-6. |
| Human Immunodeficiency Virus (HIV) and AIDS |
| An uncommon cause of scleroderma. The greatest paradox is the occurrence of certain autoimmune disorders in the setting of HIV. To the best of our knowledge, the association of HIV with scleroderma has not previously been reported. PubMed. Scand J Rheumatol. 2005 May-Jun;34(3):242-5. |
| Nanobacteria (NB) or "Nanoparticles" |
| This is a very new field of research which is highly controversial. |
| A few researchers suspect that nanobacteria may be a cause of scleroderma or some of its symptoms, such as calcinosis. |
| This is a very new field of research which is highly controversial, however it has recently attracted the attention of researchers at the Mayo Clinic and NASA. Nanobacteria have been found in kidney stones, Alzheimer's disease, heart disease, prostatitis, and some cancers. |
A lot of the controversy surrounding nanobacteria has to do with its very name, in that some researchers do not believe that it represents a life form and thus cannot properly be named "bacteria", because the research on its purported nucleic acid has not been completed yet. Thus, some believe that "nanoparticles" would be a better description for it. |
| Detection of nanobacteria-like material from calcified cardiac valves with rheumatic heart disease. The nanobacteria-like material has been isolated and cultured from calcified cardiac valves with rheumatic heart disease, and its characteristics are similar to those of Se90. Hu YR. (PubMed) Cardiovasc Pathol. 2009 Sep 9. |
| Purported nanobacteria in human blood as calcium carbonate nanoparticles. Nanobacteria-like particles obtained from human blood are able to withstand high doses of gamma-irradiation up to 30 kGy, and no bacterial DNA is found by performing broad-range PCR amplifications. Martel J, (PubMed) Proc Natl Acad Sci U S A. 2008 Apr 8;105(14):5549-54. |
| Persistent Infection in Systemic Sclerosis |
| Parvoviral infection of endothelial cells and stromal fibroblasts: a possible pathogenetic role in scleroderma. Parasitism of endothelia and fibroblasts by B19 (parvovirus B19) with resultant enhanced TNF-alpha expression may be of pathogenetic importance in SSc even in the absence of demonstrable viremia. Treatment strategies include anti-viral therapy, including in the context of intravenous gamma-globulin and anti-TNF therapy. PubMed. J Cutan Pathol. 2004 Jan;31(1):43-50. |
| "Study of Persistent Infection in Systemic Sclerosis Skin and Vessels", Maureen D. Mayes, M.D., at Wayne State University and the University of Texas at Houston. This project examines persistent bacterial infection of the skin or small blood vessels as a potential cause of scleroderma. Results could lead to treatments that target the bacterial infection. 10-21-01 to 10-21-04. (Also see: Clinical Trials and Open Enrollments) |
| Viral Infection |
| Human Parvovirus B19 (B19V) Infection in Systemic Sclerosis (SSc) Patients. Our previous reports suggested a possible association between parvovirus B19 (B19V) infection and SSc, based on higher prevalence of B19V DNA in SSc patients in respect to controls. The recent study outlines some differences in the rate of persistence of B19V DNA, in the simultaneous persistence of 2 genotypes and in the pattern of viral expression among SSc patients and controls. Krystyna Zakrzewska. Intervirology. Vol. 52, No. 5, 2009. |
| Epstein–Barr virus in autoimmune diseases. The Epstein–Barr virus (EBV) is a plausible candidate for playing a role in the pathophysiology of some autoimmune diseases. É Toussirot. (ScienceDirect) Best Practice & Research Clinical Rheumatology Vol 22, Issue 5, Octr 2008, Pp 883-896. (Also see: Autoimmunity) |
| Epstein Barr Virus (EBV)-Associated Primary CNS Lymphomas (PCNSLs) in Elderly Patients on Immunosuppressive Medications. These cases serve as a diagnostic alert for neuropathologists and suggest that increased testing of PCNSLs for EBV by immunohistochemistry or in situ hybridization may be warranted in any patient on any immunosuppressive medication, but particularly the elderly. Kleinschmidt-DeMasters, B.K. MD. Journal of Neuropathology & Experimental Neurology. November 2008. (Also see: Immunosuppressants) |
| Cytomegalovirus-associated cutaneous vasculopathy (CMV) and scleroderma sans inclusion body change. Viruses have long been held to be of pathogenetic importance in the evolution of autoimmune connective tissue disease. The role of tumor necrosis factor alpha blockers in scleroderma cases temporally associated with CMV infection requires further evaluation. PubMed. Hum Pathol. 2006 Nov 2. |
