Skip to main content
ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #100219
Title: ROLE OF THE CIAB, AND PLA23 CAMPYLOBACTER GENES ON VIRULENCE, INTESTINAL COLONIZATION, AND ORGAN INVASION, WHEN GIVEN IN OVO OR DAY-OF-HATCH

Author
item Ziprin, Richard
item KONKEL, M - WASHINGTON STATE UNIV.
item Hume, Michael
item Stanker, Larry
item Young, Colin

Submitted to: Poultry Science Association Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 8/7/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Campylobacter jejuni is a commensal of the chicken intestinal tract. We have previously shown that introduction of mutations into the dnaJ and cadF genes eliminated the ability of these mutants to colonize the ceca. The objective of the present work was to make additional determinations of the Campylobacter genes involved in cecal colonization and organ invasion. A secondary objective was to determine if the mutants were avirulent when given to chicks either in ovo or orally on day-of-hatch. Chicks were treated either by direct injection of the embryo in ovo or by intraperitoneal injection on day-of-hatch. Chicks were treated with either the parental Campylobacter strain, F38011, or with the mutants. The in ovo challenge dose was 10**4 CFUs and the intraperitoneal challenge dose was 10**8. Liver samples and cecal contents were examined for the presence of Campylobacter when the chicks were 14 days old. Campylobacter jejuni were recovered from the ceca of all birds challenged with the parental strain, regardless of challenge route. Livers of birds challenged in ovo with the parental strain often contained Campylobacter. In contrast, the ciaB strain colonized the ceca but not the liver, and the pla23 strain was a poor colonizer of both liver and cecum. None of the strains, parent or mutant, caused mortality (or observable morbidity) on intraperitoneal challenge even though the doses were high. We conclude that mutations in cadF, dnaJ and pla23 impair the ability of Campylobacter to colonize the cecum or infect the liver. In contrast, ciaB retains an ability to colonize the cecum though it was seldom recovered from liver. By determining the role of these genes in colonization we hope to find some means to prevent Campylobacter from establishing in the gastrointestinal