| Causes of Scleroderma (MAIN MENU) | | | |
| 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) |
| Borrelia Burgdorferi Infection |
| 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 |
| I Tested HIV Positive. What Does This Mean? Does it Mean I Have AIDS? A positive HIV test result means that you are infected with HIV (Human Immunodeficiency Virus), the virus that causes AIDS (Acquired Immune Deficiency Syndrome). Being infected with HIV does not mean that you have AIDS right now. However, if left untreated, HIV infection damages a person's immune system and can progress to AIDS. The Body. |
| 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. |
| Brave new nanoworld may hold key to health. Brain cancer, multiple sclerosis, arthritis, Alzheimer’s, cardiovascular disease, diabetes, and Crohn’s disease have one thing in common: each is related to calcification, a process in which calcium-phosphate deposits appear in parts of the body where they shouldn’t be, with potentially toxic and deadly consequences. Straight.com 12-29-05. |
| Association of Nanobacteria with Dermatological Diseases.When combining all the different analysis results, psoriatics showed positivity for nanobacteria in 11 of 13 patients (85%), patients with lichen ruber planus in 6 of 6 (100%), patients with nummular or other eczema in 6 of 6 patients (100%). The presence of nanobacteria were also observed in a few patients with skin diseases such as scleroderma and lichen sclerosus, pyoderma gangrenosum and Sezary syndrome (a rare malignant T cell lymphoma). These patients were too few to draw a definite conclusion. More studies are needed to elucidate the role on nanobacteria in these diseases. Nanobaclabs, Inc. |
| Nanobacteria A Problem For Space Travellers, Says NASA. Trials were conducted at NASA to observe nanobacteria in a bioreactor chamber which simulates conditions of space travel. In this microgravity environment, nanobacteria were found to multiply five times faster compared to normal gravity on Earth. Nanobacteria were also shown to possibly be an infectious risk for crew members living in close quarters. Science a Go Go. |
| 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 |
| 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) |
| There's no cure, but scleroderma can be managed. We don't know what causes scleroderma. Researchers suspect that there is a genetic link. The theory is that while a specific genetic trait predisposes the individual, scleroderma will only occur after exposure to some environmental agent, such as a particular virus. Post-Bulletin. Mayo Clinic. 06/04/07. (Also see: Causes of Scleroderma: Genetics, and What is Scleroderma?) |
| 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. |
| Parvovirus B19 as Possible Triggering Factor of Endothelial and Fibroblast Alterations in Systemic Sclerosis. The infection of endothelia and fibroblasts by B19, and in particular, the consequent enhanced TNF-alpha expression may be of pathogenetic importance in SSc. Moreover, the vascular deposition of C5b-9 suggests a role for humoral immunity possibly induced by a state of endothelial neoantigenicity evoked by virus-mediated cell injury. C. Ferri. FRI0151 EULAR 2005. |
| Severe Systemic Autoimmune Disease Associated With Epstein-Barr Virus Infection. The authors describe a girl who developed a severe systemic autoimmune disease with severe autoimmune hemolytic anemia, mild autoimmune thrombopenia, antineutrophil antibodies, and fatal autoimmune hepatitis after EBV infection. PubMed. J Pediatr Hematol Oncol. 2004 Dec;26(12):831-833. (Also see: Liver Involvement) |
| Increased prevalence of human parvovirus B19 DNA in systemic sclerosis skin. The increased prevalence of human parvovirus B19 DNA in SSc skin showed the possibility that the virus may be involved in the formation of skin tissue abnormalities in the disease. PubMed. Br J Dermatol. 2004 Jun;150(6):1091-5. |
| Viral infections: their elusive role in regulating susceptibility to autoimmune disease. Viral infections may trigger autoimmune disease. Complicating our understanding of how viral infections promote disease is the realization that viral infections can sometimes prevent auto-aggressive reactions. PubMed. Microbes Infect. 2003 Aug;5(10):911-21. |
