The Incidence and Pathogenesis of Myocarditis in Rabbits After Group a Streptococcal Pharyngeal Infections

Abstract

Rabbits subjected to single pharyngeal infections with group A streptococci developed cardiac lesions characterized by myofiber necrosis and a non-granulocytic cellular reaction with histiocytes, lymphocytes, and Anitschkow myocytes. The histopathologic changes were demonstrable in some animals within 24 hours of inoculation, apparently were maximal 72 hours after induction of infection (at which time they were seen in the hearts of all nine rabbits studied), and thereafter healed in the course of the following 2 weeks. The extent of involvement was variable, and with healing the necrotic areas were replaced by fibrous tissue. When intradermal infections with the same organisms were produced in rabbits, cardiac lesions, indistinguishable from those observed in the pharyngeally infected group, appeared in a much smaller number of animals. The hearts of five of six rabbits sacrificed a month or more following the last of a series of streptococcal pharyngeal infections exhibited lesions characterized chiefly by fibrosis, although mononuclear cellular infiltrations were also noted. In these repetitively infected animals the presence of occasional multinucleated giant cells and a few small foci of calcification were features not encountered in the single infection group. In a second series of rabbits sacrificed 3 days after the last of three pharyngeal infections with different strains of streptococci, acute as well as more chronic changes were observed. In none of the lesions in rabbits subjected to single or multiple streptococcal infections were bacteria demonstrable, either in histologic sections or in cultures of myocardial tissue. A large number of control animals was studied concomitantly, and in only one instance was a lesion, considered comparable to those described in the streptococcal series, encountered. The implications of these findings, particularly in terms of the non-suppurative sequelae of streptococcal infections in man, are discussed.

Host-Parasite Factors in Group a Streptococcal Infections

“…The histopathologic studies on tissue from rabbits given one and/or two spaced injections of erythrogenic toxin are of interest; these changes indicate the ability of such toxins to produce significant damage in various tissues of the host including the mitral valve; there is neither an indication of specificity for this structure within the heart nor a suggestion that the lesions resemble those observed in any sequelae of Group A streptococcal infections. Morpho-logically, more significant lesions have been observed by others (42)(43)(44). It is significant to note, however, that the results of these investigations were obtained in rabbits with living streptococci multiplying in an in vivo environment.…”

The Analysis of Streptococcal Infections

“…3. Murphy and Swift (14) and others (15) have shown that repeated streptococcal infections of rabbits will cause focal cardiac lesions. Kirschner and I-Iowie (16) confirmed these reports, and found a correlation between the incidence and severity of the heart lesions, and the intensity of rise of the anfistreptolysin O titer of the serum.…”

Joys and Surprises of a Career Studying Eukaryotic Gene Expression

“…We had learned from reading animal anatomy books in the medical school library that rabbits have submucosal patches of lymphocytes in the pharynx: "tonsils" (2). In fact, some of the repeatedly infected rabbits did develop reactive nodules in the ventricular heart muscle that somewhat resembled Aschoff bodies, characteristic of rheumatic fever according to our pathologist collaborator, Prof. Wilbur Thomas (3).…”

“…Animal cells were known, of course, to have an envelope surrounding the nucleus, the location of chromosomes and DNA. By autoradiography, 3 H-labeled ribonucleosides were seen to be incorporated first into RNA in the nucleus, whereas basophilic dyes that stained RNA showed that the vast majority of RNA was actually cytoplasmic. Moreover, it took some hours for 3 H-labeled ribonucleosides to label the cytoplasm heavily.…”