Production of Group A Streptococcal Cervical Lymphadenitis in Mice. ∗,†

Abstract

The fact that hemolytic streptococcal infections are implicated in the causation of rheumatic fever is well documented (1-3). Further, there is much evidence to suggest that rheumatic fever occurs as a result of an inappropriate immune response on the part of the host to the streptococcus or its products (4,5). Nevertheless, the pathogenesis of rheumatic fever remains obscure, its elucidation being seriously handicapped by the lack of a suitable experimental analog. The development, therefore, of an affection in experimental animals, bearing sufficient resemblance to rheumatic fever in man to satisfy the most stringent criteria, might well constitute a significant advance toward definition of the mechanism by which the human disease arises. One avenue of attack on this problem is represented by the attempt to simulate in experimental animals a sequence of events comprable to that which is assigned importance in human rheumatic fever; namely, repeated infections of the upper respiratory tract with group A streptococci (6). In order to pursue this particular investigate approach, it is essential to develop a method by which group A streptococcal infection can be achieved via the upper respiratory route in an experimental animal.

The present paper describes the successful production of group A cervical lymphadenitis in mice by means of a modification of the intranasal technic described by Sonkin (7). In addition, the pathogenesis of the infection is delineated on the basis of systematic histologic observations.

Methods. Swiss mice of the Webster strain, weighing between 15 and 20 g, were injected intraperitoneally with 0.3 ml of a 2.5% solution of chloral hydrate, and then allowed to inhale ether until deeply anesthetized.