Purpose: In this study, we hypothesize that intestinal diseases aggravate C. jejuni colonization in live birds.
Methods: Broilers were challenged with parasite Eimeria maxima at 14 days of age. The birds were then challenged with Clostridium perfringens five days later to induce NE. After additional four days, small intestinal tissues were collected for histopathology and molecular assessments.
Results: We found that E. maxima induced intestinal inflammation shown as mass immune cell infiltration into lamina propria, swelling and shortening villi, and crypt elongation compared to unchallenged birds. Interestingly, subsequent C. perfringens challenge exacerbated intestinal inflammation with additional severe histopathology shown as bleeding, peeled villus epithelial line, blunted villi, and muscularis externa fibroblast nucleus disarray. Molecular biology examination by real time PCR revealed that coccidiosis induced elevated inflammatory mediators Infγ and Il23 mRNA accumulation. NE further elevated inflammatory mediators Il1β and Tnfα mRNA expression. Importantly, coccidiosis and NE increased C. jejuni 16S RNA accumulation by 11- and 51-folds, respectively, compared to uninfected birds. Altogether, these results suggest that NE aggravates coccidiosis-induced intestinal inflammation and both intestinal diseases increase intestinal C. jejuni colonization, which potentiates carcass contamination and campylobacteriosis incidences.
Significance: We found that chicken flocks suffering from intestinal diseases pose a higher risk of C. jejuni contamination, hence the preventing and treatment of chicken intestinal diseases will benefit not only reducing foodborne disease incidences but also improving chicken productivity.