Most investigators are agreed that observed differences in the frequency of the myocardial Aschoff body in rheumatic heart disease are the result of the transient nature of the lesion. Aschoff1 recognized this relation, and others2 have observed the disappearance of the Aschoff body after the disappearance of symptoms of rheumatic fever.
More recently, Gross and Ehrlich3 have described the development of the Aschoff body and have attempted to correlate the changes with the clinical course of the disease. They found that the lesion was common in cases in which the infection showed "clinical or anatomical evidence of activity" but infrequent when the disease pursued a chronic course.
At the present time the Aschoff body is almost universally accepted as evidence of existing rheumatic disease, but the terms active infection and activity are ill defined. Active infection has been assumed to occur with changes varying from leukocytosis or