In view of the well known multiplicity of bacteria isolated from endocarditic lesions, workers in this field have always more or less distinctly felt that the essential question in the pathogenesis of endocarditis is one of bacterial localization. Under what conditions will bacteria localize on the endocardium? While early experimental investigators (Wyssokowitsch, 1 Ribbert 2 ) succeeded in producing an endocarditis by combining the bacterial infection with a gross trauma to the heart-valves, observations on experimental endocarditis without such trauma (Lissauer, 3 Saltykow 4 ) have been rare until recently. Birkhaug 5 produced a subcutaneous lesion with a streptococcus infected agar focus, and obtained endocarditis with regularity by intravenous reinfections with the same organism. He interprets these results in the sense of an etiological specificity of the organism employed. Siegmund 6 produced experimental endocarditis by daily intravenous injections of rapidly increasing doses of B. coli or staphylococcus. Siegmund 6 and Dietrich 7 conclude that a peculiar state of immunity, associated with an altered capacity of the endocardium to react, is the essential condition for bacterial localization on the endocardium.

In the course of observations on infectious disease processes in horse serum sensitized guinea pigs we found, that on single intraperitoneal injection of salmonella or Staphylococcus aureus, sensitized guinea pigs developed with considerable regularity an endocardial lesion, which was only occasionally met with in non-sensitized controls. The lesion consists of nodular monocytic proliferations—“proliferative endocarditis”. Desensitization previous to the infection practically prevented the above nodular reaction of the endocard, desensitization after the infection was without detectable influence.

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A Retrospective Survey of Endocardial Proliferative Lesions in Rats

Studies on the Pathogenesis of Endocarditis.