Abstract:
Although numerous epidemiological and clinical studies have shown a definite relationship between a previous infection with strains of Group A streptococci and the appearance
of sequelae (rheumatic fever, arthritis, nephritis), the mechanisms which lead to their
development are still not fully understood. Since man is the only animal species which
suffers from natural infections with Group A streptococci, and since it is agreed that
viable streptococci cannot usually be isolated from the lesions characteristic of the
chronic complications, Koch’s postulate can at best incriminate these micro-organisms
only in the etiology of the acute infections but not in their subsequent complications.
Despite many attempts to duplicate rheumatic fever, arthritis and acute glomerulonephritis in laboratory animals including higher apes, as a rule, the tissue lesions which
developed in some of the animals bore little resemblance to the human lesions, and no
true duplication of a disease syndrome similar to that seen in human beings has been
reported.
Two major theories have been proposed by various investigators to explain the nature
of poststreptococcal complications. One theory proposes that the toxic effects of
some streptococcal products (streptolysins O and S, erythrogenic toxin, proteinase,
cell-wall mucopeptide-polysaccharide complex) are responsible for the initiation of the
chronic lesions in the heart, joint and kidney characteristic of poststreptococcal diseases.
The second theory suggests that the immunopathological phenomena (immune complex
disease, cross-reactive immunity, delayed hypersensitivity) which develop in certain pa-
tients who have become sensitized to one or more of the streptococcal products are responsible for the initiation of the disease in man.
These two hypotheses are not, of course, mutually exclusive. Although no unified
theory has been advanced which adequately explains the nature of the various post-
streptococcal complications, a combination of both views may fit many, if not all, the
features characteristic of these sequelae. Some theories on the pathogenesis of human
poststreptococcal diseases and on the mechanisms of tissue injury induced by Group A
streptococci have been recently reviewed (Taranta and Uhr, 1971; Ginsburg, 19720, b).
The purpose of this paper is to describe some of the mechanisms by which Group A
streptococci localize and persist in mammalian tissues and to relate the experimental
models to the pathogenesis of poststreptococcal sequelae in man.