Systemic infection induced by Campylobacter jejuni: Development of a mouse model and elucidation of molecular mechanisms

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Terhorst, Samantha
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Qijing Zhang
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Veterinary Microbiology and Preventive Medicine
Our faculty promote the understanding of causes of infectious disease in animals and the mechanisms by which diseases develop at the organismal, cellular and molecular levels. Veterinary microbiology also includes research on the interaction of pathogenic and symbiotic microbes with their hosts and the host response to infection.
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Campylobacter jejuni clone SA has emerged as the predominant cause of Campylobacter-associated ovine abortion in the U.S., and this clone is highly pathogenic in pregnant sheep and guinea pigs. To induce abortion, orally ingested Campylobacter must be able to translocate across the intestinal epithelium and spread systemically. To understand the pathogenic mechanisms and immune protection of C. jejuni-induced abortion, it is necessary to develop a cost-effective animal model to evaluate systemic infection induced by this pathogenic clone. In this study, two different breeds of female mice (BALB/c and CD-1) were orally inoculated with C. jejuni IA3902, a clinical clone SA isolate whose complete genome sequence has been determined, to evaluate the induction of bacteremia and hepatic infection. Our results revealed that CD-1 mice were more susceptible than BALB/c mice to infection by IA3902. In CD-1 mice, C. jejuni IA3902 induced bacteremia and hepatic infection within 1 hour after oral inoculation, and bacteremia peaked at 8 and/or 12 hours after inoculation. Compared with IA3902, the magnitude and duration of bacteremia and hepatic infection induced by C. jejuni strains NCTC 11168 and 81-176 were significantly less prominent, indicating that IA3902 is more virulent than the other strains tested with regard to systemic spread. Mutagenesis in IA3902 showed that the loss of the capsule (ÄkpsS) completely prevented the organism from causing bacteremia and hepatic infection, while the loss of pVir plasmid did not affect systemic spread. These findings indicate that the CD-1 mouse model is suitable for examining critical steps of Campylobacter pathogenesis and identify the capsule as a key virulence factor of this pathogenic organism to induce bacteremia.

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Sun Jan 01 00:00:00 UTC 2012