Experimental Campylobacter jejuni Infection of Adult Mice

Abstract

HA-ICR adult mice were studied to develop an animal model for Campylobacter jejuni enteritis in humans. Fecal and ileal cultures made by selective and nonselective methods showed that C. jejuni and related organisms are not bowel commensals. Intragastric feeding of 108 CFU of three different strains of C. jejuni produced infection in 100% of the animals, and infection rates were dose dependent. Pretreatment with antibiotics or opiates was not necessary to induce infection. Fresh isolates and strains passed on artificial media yielded similar infection rates. Infected mice did not show signs of illness, but transient bacteremia within 10 min of oral infection was observed in nearly 100%. The small intestine was the principal target organ, with epithelial inflammation seen 48 h after infection. Control mice offour species had undetectable serum immunoglobulin G antibody specific for the infecting strain, but infected mice showed peak titers at 1 week with rapid decline. Immunoglobulin M titers rose minimally, and immunoglobulin A titers did not rise. Infected mice uniformly became chronic asymptomatic excretors, shedding 104 to 106 CFU/g of feces; a minority were biliary carriers. Intestine carriage was most pronounced in the stomach and proximal small intestine. Because this experimental infection led to bacteremia, transient pathological changes, and immunoglobulin G titer rises, this model may be useful for evaluating the effects of prophylactic and therapeutic interventions.

Systemic spread of Campylobacter jejuni after intravenous infections

“…Our results, in agreement with previous observations [5,6,8,12], indicate that granulocytes contribute to the clearance of C. jejuni from the bloodstream and these 'infected' granulocytes are eliminated from the bloodstream by the liver. Bacteria, surviving phagocytosis by granulocytes and Kupffer's cells, were shed into the intestine via bile duct, because bacteria were found also in the gall-bladder in high numbers and in the feces.…”

“…(i.e. crossing the gastrointestinal barrier) begins with invasion of the intestine, followed by systemic spread and colonization of internal organs [6,8,9], and reappearance in the gut (as shown in this study). For this purpose, mice were infected intravenously in order to investigate the systemic interactions between host and Campylobacter jejuni, after intestinal translocation.…”

“…There have been several reports, both from clinical and experimental observations that C. jejuni spreads from the intestine and colonizes internal organs [6,8,9]. In this study an animal model for i.v.…”

CheY‐mediated modulation of Campylobacter jejuni virulence

“…Campylobacter spp. are unable to cause diarrhoea when fed to mice, but can effectively colonize the mucous layer of the gastrointestinal tract (Blaser et al, 1983;Lee et al, 1986). The ferret model was used to measure the ability of the strains to cause diarrhoeal disease (Doig et al, 1996).…”

Phagocytosis of entericCampylobacterby human and murine granulocytes

“…These experiments outlined the role of phagocytes in the clearance of C. jejuni from systemic sites. Other investigators emphasized the role of the humoral immune response mechanisms against Campylobacter infections [4,5]. On the other hand, in vitro experiments also demonstrated the phagocytosis of C. jejuni by mononuclear cells and macrophages [6,7].…”