The anterior half of the small intestine of old mice was used for this histopathologic study. All tissues were taken at 7 days after a challenging infection with 200 Trichinella spiralis larvae.
The nonirradiated, immunized mice showed a subacute inflammatory response similar to that known to be characteristic in untreated mice at this period postchallenge. However, the irradiated, immunized mice showed a response that differed in type and/or degree. In those irradiated (450 r) 8 days prior to the challenging infection (15 days prior to necropsy), there was only a minimal response of the type that precedes the acute response, and in degree it was even less than that noted in nonirradiated, nonimmunized mice given only the challenging infection. However, in those irradiated 12 days prior to challenge (19 days prior to necropsy), there was a much more striking subacute response, which compared, except in intensity, with that noted in the nonirradiated, immunized mice. Extensive lymphoid proliferation in the former suggested recovery was underway. These various findings are consistent with the adult-worm counts for comparable groups in classifying the immune status. By both measurements, those irradiated 8 days prior to the challenge had no demonstrable acquired immunity, while those irradiated 12 days prior to challenge had immunity of an intermediate degree (i.e., significantly more than that of the nonimmunized mice, but significantly less than that of the nonirradiated, immunized mice).
On the basis of these and other observations in the irradiated mice, a working hypothesis is presented to explain the irradiation interference with the strong, previously-established immunity. The ultimate effect is an indirect one brought about by damage to the hematopoietic system, which is thereby unable to supply the large numbers of cellular elements needed to initiate and/or maintain an effective inflammatory response in the area of worm elimination. Without an effective response, worms remain despite unaltered preformed antibody titers. If, as seems likely, the inflammatory response is triggered by an antibody-antigen reaction(s), a direct effect(s) would be involved as well, but this has not been demonstrated.
Department of Pathology, Baylor University Medical Center, Dallas, Texas.
Present Address: Parasitology Section, Bureau of Laboratories, New York City Department of Health, 600 West 168 Street, New York 32, New York.