Clostridium perfringens (CP) is the etiological agent of necrotic enteritis (NE) in broiler chickens which is responsible for massive economic loss in poultry industry in response to voluntary reduction and withdrawal of antibiotic growth promoters. Large variations exist in the CP isolates in inducing intestine NE lesions. However, limited information is available on CP isolate genetics in inducing NE with other predisposing factors. This study investigated the ability of five CP isolates from different sources to influence NE pathogenesis by using an Eimeria maxima (EM) co-infection NE model: Str.13 (from soil), LLY_N11 (healthy chicken intestine), SM101 (food poisoning), Del1 (netB+tpeL-) and LLY_Tpel17 (netB+tpeL+) (NE-afflicted chickens). The 2-week-old broiler chickens were pre-infected with EM (5x103 oocysts) followed by CP infection (around 1x109 colony-forming-unites per chicken). The group of LLY_Tpel17 isolate with EM coinfection had 25% mortality. No mortality was observed in the groups infected with EM alone, all CP alone or dual infections of EM/other CP isolates. In this model of EM/CP co-infections, the relative percentages of body weight gain showed statistically significant decreases in all EM/CP groups except EM/SM101 group, when compared with the sham control group. Mild gut lesions were observed in chickens infected with EM/Str.13 or EM/SM101 groups. However, evident lesions were observed in three groups of EM/LLY_N11, EM/Del1, EM/LLY_Tpel17, all of which possess essential NE pathogenesis locus in genomes. Our studies indicate that LLY_Tpel17 is highly virulent to induce severe gut lesion, and would be a good CP challenge strain for studies in investigating pathogenesis and evaluating the protection efficacy for antibiotics alternative approaches

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