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Streptococci and Rheumatic Fever

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Microorganisms and Autoimmune Diseases

Part of the book series: Infectious Agents and Pathogenesis ((IAPA))

Abstract

Rheumatic fever occurs as a delayed sequel to group A streptococcal infection. The disease is usually manifested as an inflammation of the joints or heart, but symptoms of chorea, subcutaneous nodules, or erythema marginatum may be present. The importance of rheumatic fever is due to the involvement of the heart in the disease, which can be fatal in the acute stage or can lead to chronic rheumatic heart disease with scarring and deformity of the heart valves. Although rheumatic fever has declined in decades past, the current resurgence of the disease has kept us aware of its presence. The pathogenesis of the disease is related to the host immune response made simultaneously against the streptococci and the heart and host tissues. During the past decade, progress has been made in our understanding of rheumatic fever as an autoimmune disease. Figure 1 highlights the components of the disease. The target antigens in the heart, including cardiac myosin, have been identified, and the streptococcal M protein epitopes recognized by antimyosin antibodies in acute rheumatic fever have been determined. The class I M protein epitope was found on group A streptococcal M protein serotypes that were associated with acute rheumatic fever outbreaks. Antibodies against the streptococcal group A carbohydrate antigen were shown to persist in valvulitis, and antistreptococcal antibodies have been shown to recognize epitopes on the heart-cell surface or valve endothelium.

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Cunningham, M.W. (1996). Streptococci and Rheumatic Fever. In: Friedman, H., Rose, N.R., Bendinelli, M. (eds) Microorganisms and Autoimmune Diseases. Infectious Agents and Pathogenesis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0347-3_2

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