Pathogenesis of Trichinous Myocarditis

Abstract

Several authors have recognized and described the histopathology of the parenchymatous lesions and accompanying myocarditis which are seen in the hearts of human cases of trichinosis dying in the fourth to eighth week of the disease. The importance of these lesions in the production of the circulatory failure, which is the cause of death in these cases, has been emphasized. 1 All who have had opportunity to study such material have noted the absence of encysted larvae in the heart muscle even though the skeletal muscles showed at the same time very many encysting and encysted organisms. Almost all of those who have searched sections prepared from such hearts have failed to find larvae present at all. Only Zenker 2 and Frothingham 3 saw them in the human heart, but Graham, 4 working with rats, described lesions similar to those in human cases and in addition found embryos associated with the inflammatory foci. This complete absence of encysted forms with but meager evidence even of the presence of larvae, has led to uncertainty as to the pathogenesis. Simmonds 5 concluded that the myocarditis was due to a toxin produced by the trichinae and brought to the heart in the circulating blood.

In the present study, series of white rats were fed, in approximately known numbers, the larvae digested (McCoy 6 ) from trichinous meat. Animals were killed at appropriate intervals and both fresh, teased preparations and stained sections were made from their tissues. The myocardium showed alterative and exudative lesions in all respects comparable to those found in human hearts. Trichina embryos were found in these foci as early as 5 days after feeding and for some time thereafter.