Abstract

The acquisition of immunity against Trichinzella spiralis through recovery from a prior infection with the homologous parasite has been demonstrated in the rat (1), the guinea pig (2), the pig (3), and the monkey (4). Most investigators are agreed that the acquired immunity is directed largely against the intestinal phase of the parasite, although the precise mechanism of the immunity is still obscure. Some believe the immune response is made chiefly or entirely by the tissues of the intestinal wall itself, and that the tissues of the remainder of the body have comparatively little or nothing to do with the immune process. An increased secretion of mucus and increased intestinal peristalsis are presented by those supporting this view as the chief factors operative in the immunity. These workers generally have failed to demonstrate either the passive transfer of immunity with the serum or the development of an inflammatory reaction in the intestinal wall of the immune host, and much of their contention is based upon these negative observations (5). Other investigators, however, consider that a generalized immune response must be made to the parasite before an animal can acquire a substantial degree of immunity, although they feel that this response may, and probably does, act upon the parasite only in strategically disposed sites, of which the intestine is one. In the present paper, the results are offered from a study of acquired immunity to trichiniasis in the albino mouse. Strangely, the mouse has been but little employed in experimental trichiniasis. One of the few reports in which this animal has been used is that by the author and Kaplan of some years ago in which it was shown that rabbit antiserum rich in the specific antibody conferred to mice a partial immunity against trichiniasis (6). It is now shown that mice become actively immune to Trichinella spiralis as a result either of prior infection with the parasite or of vaccination with its antigens. The results are offered with a view to throwing some further light upon the mechanism of immunity in this disease.

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