ENHANCEMENT OF SALMONELLOSIS AND EMERGENCE OF SECONDARY INFECTION IN MICE EXPOSED TO COLD

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Abstract
Miraglia, GennaroJ. (Bryn Mawr College, Bryn Mawr, Pa.)and L. Joe Berry. Enhancement of salmonellosis and emergence of secondary infection in mice exposed to cold. J. Bacteriol.84:1173–1180. 1962.—Theld50dose for mice ofSalmonella typhimurium, strain RIA, is 4.1 × 105for animals individually housed without bedding and maintained at 25 C. It is 3.8 × 103for animals similarly housed but kept at 5 C. An intravenous injection of 0.1 ml of Proferrin 2 hr prior to infection with RIA lowers theld50to 4.9 × 103and to 4.0 × 101for mice kept, respectively, at 25 and at 5 C. Low environmental temperature and “blockade” of the reticuloendothelial system (RES) lower the resistance of mice to about the same degree, but low temperature and RES impairment together lower resistance as if each were acting independently. No effect of cold could be detected in mice infected with the highly virulent SR-11 strain ofS. typhimurium, since all animals died after infection with only a few cells. Mice that were natural carriers of salmonellae, as judged by fecal discharge, were highly resistant to challenge and responded to cold in a manner similar to normal mice infected with RIA. Strain RIA could be isolated from the tissues of infected animals with greater frequency and persisted longer in mice maintained at 5 C than those at 25 C. Staphylococci were isolated from livers of animals that survived salmonella infection for 14 days at 5 C, and the incidence of staphylococci was proportional to the number of salmonellae injected. At 25 C, only a small percentage of mice had staphylococci in tissues and these occurred independent of the infectious dose of salmonellae. These observations were made on normal mice infected with RIA and on carrier mice infected with SR-11.