TY - JOUR
T1 - The virtual disappearance of rheumatic fever in the United States
T2 - Lessons in the rise and fall of disease
AU - Gordis, L.
N1 - Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1985
Y1 - 1985
N2 - Although the group A streptococcus is the critical etiologic agent of rheumatic fever, the disease may well be multifactorial in origin. While improved medical care and the use of penicillin and other antibiotics have contributed significantly to the decline of rheumatic fever in the United States, the decline antedated the availability of antibiotics, and in addition the changes in rheumatic fever in the United States cannot be fully accounted for solely by medical care and antibiotic use. The difficulty is that we lack adequate information regarding other possible cofactors. Studies of such factors are not feasible in the United States today in view of the very low incidence of the disease, but such etiologic investigations could be initiated and conducted in developing countries. From the clinical standpoint, the low risk of rheumatic fever today suggests that perhaps we should reassess present policies regarding our hunt for the streptococcus and our determination to eradicate it. However, any relaxation of our currently recommended approaches to streptococcal infections should be undertaken with great caution, since we do not understand the reasons for the decline and consequently cannot fully anticipate the possible results of any relaxation in policy. In any case, such a relaxation would be high inappropriate for developing countries in which the risks of rheumatic fever and rheumatic heart disease remain so high. Finally, there is an urgent need for additional research both on the biology of the streptococcus and the pathogenic mechanisms involved in the development of rheumatic fever as well as on other factors that may interact with the streptococcus and influence the risk of disease. Such research may not only be valuable in improving the health of populations that are at high risk for rheumatic fever in developing countries, but may also shed light on the pathogenesis of other non-suppurative sequelae of infectious diseases.
AB - Although the group A streptococcus is the critical etiologic agent of rheumatic fever, the disease may well be multifactorial in origin. While improved medical care and the use of penicillin and other antibiotics have contributed significantly to the decline of rheumatic fever in the United States, the decline antedated the availability of antibiotics, and in addition the changes in rheumatic fever in the United States cannot be fully accounted for solely by medical care and antibiotic use. The difficulty is that we lack adequate information regarding other possible cofactors. Studies of such factors are not feasible in the United States today in view of the very low incidence of the disease, but such etiologic investigations could be initiated and conducted in developing countries. From the clinical standpoint, the low risk of rheumatic fever today suggests that perhaps we should reassess present policies regarding our hunt for the streptococcus and our determination to eradicate it. However, any relaxation of our currently recommended approaches to streptococcal infections should be undertaken with great caution, since we do not understand the reasons for the decline and consequently cannot fully anticipate the possible results of any relaxation in policy. In any case, such a relaxation would be high inappropriate for developing countries in which the risks of rheumatic fever and rheumatic heart disease remain so high. Finally, there is an urgent need for additional research both on the biology of the streptococcus and the pathogenic mechanisms involved in the development of rheumatic fever as well as on other factors that may interact with the streptococcus and influence the risk of disease. Such research may not only be valuable in improving the health of populations that are at high risk for rheumatic fever in developing countries, but may also shed light on the pathogenesis of other non-suppurative sequelae of infectious diseases.
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U2 - 10.1161/01.CIR.72.6.1155
DO - 10.1161/01.CIR.72.6.1155
M3 - Article
C2 - 4064266
AN - SCOPUS:0022373367
SN - 0009-7322
VL - 72
SP - 1155
EP - 1162
JO - Circulation
JF - Circulation
IS - 6
ER -