The leading concept of R.’s development is streptococcus theory, confirmed not only by theoretical research, but also by more than twenty years of rheumatology.
The development of P. is usually preceded by angina (see) or acute respiratory disease caused by group A p-hemo-lytic streptococcus (see Streptococci), which is indirectly confirmed by the discovery of P. in the majority of patients. in the serum of high titers of various anti-streptococcal antibodies: antistreptolysin-0 (ASL-O), antistreptogyaluronic nidase (ASG), antistreptokinase (ASK), antideoxyribonuclease B (anti-DNA B). The importance of streptococcal infection in the development of P. is also confirmed by the fact that the disease can be prevented by thorough treatment of angina and inflammatory diseases of the nasopharynx. The link between R. and streptococcal infection is also justified by epidemiological studies conducted in boarding schools, military schools and barracks for military personnel. Epidemiological studies also show that one of the conditions for the emergence of primary P is the severity of streptococcal infection and the long-term carriage of streptococcus with inadequate treatment of angina. According to Baum (J. Baum, 1979), the titers of anti-streptococcal antibodies are higher in those patients whose P. developed after angina.
А. S. Labinskaya (1975) found the presence of streptococcus in the yawn during the first 2 weeks of the disease in 100% of primary and 90% of patients with recurrent rheumatism. According to E.P. Ponomaryova (1971), release from streptococcus is faster in primary than in recurrent R., but in both cases, prolonged administration of penicillin and bicillin is necessary.
To date, the existence of “rheumatogenic” strains of streptococcus has been discussed. According to Stollerman (G. N. Stollerman, 1975), strains of streptococcus devoid of lipoproteinase (“turbidity factor”) are considered “rheumatogenic”. It suggests that the development of carditis, polyarthritis, chorea, and other clinical manifestations of R is due to different “rheumatogenic” strains of streptococcus. This point of view is contradicted by the data of E.P. Ponomaryova (1971) and A.S. Labinskaya et al. (1972), who showed that 15-20 serotides of streptococcus are detected in the yawning of patients with R. in the active phase of the disease, which may also be present in clinically healthy individuals and patients with other streptococcal infections. However, the problem of “rheumato genetic” strains of streptococcus still attracts attention due to the known fact of the development of epidemic angines, after which the incidence of rheumatism is 10 times higher than after sporadic. According to A. S. Labinskaya and V. V. D. Belyakov (1978), the formation of “rheumatogenic potential” of streptococcus occurs in the course of the epidemic process in so-called closed teams. The development of R. after streptococcal infection is, however, not due to a special strain of the microbe with “rheumatogenic” properties, but rather to the massiveness of the infection and the duration of the streptococcal helminth – important factors in the development of an anti-strep-gococcal immune response, without which R. cannot develop, as well as without infection itself.
The role of streptococcal infection in the development of recurrent rheumatism is peculiar. In this case, according to Stollerman (1964), there is a longer duration of streptococcus in the nasopharynx and greater sensitivity to infection with a new serotype of streptococcus, but without the development of an adequate anti-streptococcal immune response (anti-streptococcal antibody titers are usually low), which has led to the search for other etiological factors, such as viruses. G. D. Zalessky and his colleagues attach importance to viruses of the Coxsackie A13 type (so called rheumatism virus), and V. P. Kaznacheev – virus-streptococcal association.
Recently, the question of the role of streptococcus (see L-shaped bacteria) in the development of P., mainly return forms, has been actively developed. The discovery of antibodies to L-forms of streptococcus mainly in patients with prolonged, continuous and recurrent course of R. gives reason to think about the role of these transformed streptococcus in the progression of R. In the opinion of V. Timakov and G. Ya. D. Belyakov (1978) et al., the formation of L-forms of streptococcus leads to its long-term preservation in the patient’s body, and their reversal (i.e., reverse transformation) into the original species promotes relapses of R., which can develop without infection with a new serotype of streptococcus, as a result of activation of a persistent streptococcus infection in the body.