Abstract
Although a mass of evidence exists which supports the etiologic relationship between group A streptococcal infections and the pathogenesis of human disease (6, 36, 49, 103, 112), our knowledge of the mechanisms involved in the initiation of the tissue lesions characteristic of the sequelae of streptococcal infection in man is far from complete. The hallmarks of the poststreptococcal sequelae in humans are the development of rheumatic fever, arthritis, glomerulonephritis, chorea and other less defined clinical manifestations. Lasegue’s dictum (68) that “acute rheumatism licks the joints but bites the heart” still characterizes the significance of cardiac and joint involvement as “major” manifestations, which are related to their importance as diagnostic criteria, but do not necessarily refer to their importance in the severity of the process, its activity, or prognosis.
Keywords
- Rheumatoid Arthritis
- Migration Inhibitory Factor
- Synovial Tissue
- Rheumatic Fever
- Streptococcal Infection
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Ginsburg, I., Zor, U., Floman, Y. (1977). Experimental Models of Streptococcal Arthritis: Pathogenetic Role of Streptococcal Products and Prostaglandins and Their Modification by Anti-Inflammatory Agents. In: Glynn, L.E., Schlumberger, H.D. (eds) Experimental Models of Chronic Inflammatory Diseases. Bayer-Symposium, vol 6. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66573-8_22
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