Experimental Campylobacter jejuni infection in Macaca nemestrina

Abstract

Experimental infection of four specific-pathogen-free Macaca nemestrina monkeys (aged 3.5 and 4.5 months) with Campylobacterjejuni 81-176 caused acute diarrheal illness, characterized by fluid diarrhea, bloody stools, and fecal leukocytes, which lasted for approximately 7 to 11 days. Histologic examination of intestinal biopsies showed acute colitis characterized by infiltration of the mucosa with neutrophils and lymphocytes, and cryptitis. There were no histologic changes in the small intestine. Excretion of C. jejuni was demonstrated for 2 to 4 weeks postchallenge. Plasma antibodies to C. jejuni group antigen were elevated after challenge. Only mild diarrhea occurred after rechallenge with the same strain or with a heterologous C. jejuni strain (79-168) followed by further elevation in specific immunoglobulins A, M, and G. Four 1-year-old juvenile M. nemestrina monkeys which had experienced multiple infections with Campylobacter spp. did not exhibit illness when challenged with C. jejuni 81-176. All had elevated immunoglobulin A, M, and G plasma antibodies prior to challenge, and these humoral antibody levels were indicative of the immunity to challenge. The results demonstrate that C. jejuni infection in M. nemestrina caused colitis with clinical and pathologic results similar to those found in humans and indicate that prior infection protects against subsequent challenge.

Phagocytosis of entericCampylobacterby human and murine granulocytes

“…The effect is even greater when both complement and immune serum are present. This is in agreement with the previously published in vivo investigations [8,14]. Opsonization also increased stimulation of PMNs, as shown in animal models [8].…”

An environmentally regulated pilus‐like appendage involved inCampylobacterpathogenesis

“…and an isogenic pspA mutant to cause disease in a modification of the ferret disease model ( Table 5). The wild-type strain causes a moderate to severe diarrhoea in this model, with green mucoid stools, often with occult or frank blood, consistent with symptoms observed when 81-176 was fed to humans (Black et a/., 1988) or primates (Russell et a/. , 1989).…”

Four decades of leading‐edge research in the reproductive and developmental sciences: The Infant Primate Research Laboratory at the University of Washington National Primate Research Center

“…Studies in the IPRL investigating the prevalence of Campylobacter infection indicated that 70% of infants housed in the lab were infected by at least one strain of Campylobacter by 18 months of age [Russell et al, 1988]. A prospective study of Campylobacter infection was conducted on four infants (3 1 /2 to 4 1 /2 months old) that were specific pathogen free for both Campylobacter and Shigella [Russell et al, 1989]. These infants were experimentally infected with two Campylobacter jejuni serotypes that were obtained from outbreaks of human C. jejuni infections [Blaser et al, 1979;Glass et al, 1983].…”