Acute rheumatic fever

Rheumatic fever is a sequel to group A streptococcal pharyngitis. Although one-third of sufferers give no history of sore throat and have negative cultures, there is usually an antibody response (occasionally, indolent carditis may present late when all evidence of previous streptococcal infection h...

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Bibliographic Details
Published in:The Journal of infection 1998-05, Vol.36 (3), p.249-253
Main Author: Hutchison, S.J.
Format: Article
Language:English
Subjects:
Adolescent
Bacterial diseases
Biological and medical sciences
Child
Female
Human bacterial diseases
Humans
Infectious diseases
Male
Medical sciences
Myocarditis - etiology
Prognosis
Recurrence
Rheumatic Fever - diagnosis
Rheumatic Fever - drug therapy
Rheumatic Fever - pathology
Rheumatic Fever - prevention & control
Rheumatic Heart Disease - diagnosis
Staphylococcal infections, streptococcal infections, pneumococcal infections
Streptococcus pyogenes
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Summary:Rheumatic fever is a sequel to group A streptococcal pharyngitis. Although one-third of sufferers give no history of sore throat and have negative cultures, there is usually an antibody response (occasionally, indolent carditis may present late when all evidence of previous streptococcal infection has cleared). Epidemiological studies, particularly in military institutions, have confirmed the link between streptococcal infection and subsequent rheumatic fever. Perhaps the most convincing evidence of this link is the effectiveness of penicillin in preventing initial and recurrent attacks of rheumatic fever. There is clear evidence that rheumatic fever results from an autoimmune response to epitopes in the organism which are cross-reactive with similar epitopes in human tissues. Rheumatogenic strains of streptococcus, e.g. M5, probably differ from non-rheumatogenic strains by the presence in their M protein molecules of epitopes which cross-react with cardiac and other tissues. In general, patients with rheumatic fever are hyperimmune to all streptococcal products. The strength of antibody response is a major determinant of the attack rate of rheumatic fever following streptococcal infection. Pharyngeal infection with a rheumatogenic strain of streptococcus may produce such a response in a patient previously hypersensitized by repeated streptococcal infections in childhood.
ISSN:0163-4453
1532-2742
DOI:10.1016/S0163-4453(98)93991-3