|Gray, S - WASHINGTON STATE UNIV|
|Kim, B - WASHINGTON STATE UNIV|
|Konkel, M - WASHINGTON STATE UNIV|
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 1, 2000
Publication Date: September 1, 2001
Interpretive Summary: Chickens carry the microorganism, Campylobacter, in their intestines. Sometimes this organism will make its way from contaminated retail poultry products to the intestines of human consumers. When this happens, the consumer may contract a severe diarrhea called campylobacteriosis. We have studied some attributes of Campylobacter that contribute to their ability to become part of the population of bacteria normally present in chicken intestines. We discovered that altering certain genes (creating mutations in certain genes) prevented the mutant Campylobacter strains from living in the chicken intestinal tract. However, vaccinating chickens with these mutant strains did not protect birds against intestinal colonization by Campylobacter.
Technical Abstract: We have previously shown that introduction of mutations into the dnaJ and cadF genes of Campylobacter jejuni eliminated the ability of these mutants to colonize the ceca. Presently, we have two additional C. jejuni strains with mutations in two other genes, ciaB and pldA. The objective of the present work was to determine if the ciaB and pldA genes are involved in cecal colonization. A secondary objective was to determine if inoculation of chicks with these strains conferred protection from subsequent challenge with the parental strain. In the first part of two similar experiments we inoculated birds with each of the mutant strains and attempted to recover these from the ceca. We found that none of the strains other than the parent were capable colonizers. In arithmetic terms, the average concentration of the mutants in cecal material was approximately 10 cells per gram of cecal contents. In contrast, the parent strain from which the mutants were derived was present in cecal matter at approximately 100,000,000 cells per gram of cecal contents. In the second part of each experiments we inoculated chicks either intraperitoneally or both orally and i.p. with the mutant strains. Then we challenged the inoculated birds with the parental strain (106 CFU and 104 CFU, respectively). None of the strains, parent or mutant, caused mortality (or observable morbidity), even though the inoculation dose with the mutants was high;108 CFU on day of hatch and 108 CFU given both orally and i.p. on days 3 and day 10. Inoculation with the mutants did not provide protection from subsequent challenge with the parental strain. We conclude that mutations in genes cadF, dnaJ, pldA, and ciaB impair the ability of C. jejuni to colonize the cecum.