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Necrotic enteritis (NE) is a widespread avian disease caused by Clostridium. Infection can decrease broiler performance due to affected gut health. At present, the primary control measure against this infection is the use of in-feed prophylactic antibiotics. We hypothesized that the context in which C. perfringens is first recognized by the innate immune system would impact its downstream capacity to cause necrotic enteritis. The aim of this study was to test this hypothesis.
One-day-old Ross 708 birds (n=108) were allocated in 3 treatments: saline control and C. perfringens (heat-killed) injection with or without β-glucan (1 mg). Intra-abdominal inoculations were performed on all chickens at day 1 of age. We used a natural-exposure infection model to induce NE. Predisposing factors included housing conditions with access to litter, changes in feed composition, coccidial exposure, and a feed withdrawal stress. A Coccivac-B52 vaccine was used as a consistent source of live Eimeria oocysts, and was administered at 15X the recommended dose through oral gavage on day 13. Finally, feed was withdrawn for 24 h on day 18 as an additional stressor that encouraged NE development through changes in nutrient availability and disruption of commensal microbial communities. Six birds per treatment were sampled on each of days 17, 21, and 40. Blood was collected, and birds were euthanized to collect bursa of Fabricius, spleen, liver, and small intestine. Cecal contents were collected for subsequent determination of C. perfringens abundance. Ileum was collected for morphological analysis. The remaining small intestine was examined for NE lesions.
Natural infection model produced subclinical NE. Gross necrotic lesions were found in all treatment groups on days 17, 21, and 40. A majority (85.2%) of sampled animals showed NE specific lesions, and values were limited to low severity scores (1 and 2). Mild clinical manifestations, including diarrhea and bloody feces, were identified during week 3 after the coccidiosis vaccine challenge. No mortalities were observed in response to NE. Day-1 immune priming produced classic acute inflammatory response. Examination of leukocyte recruitment kinetics and activation showed a peak response 12 h after intra-abdominal stimulations. Thus, we selected this time point to confirm activation of the acute inflammatory response following intra-abdominal inoculation with CP and β-glucan. Examination of organ weights during the 40-day production period showed a significant selective reduction in organ weight among CP birds. Inclusion on β-glucan during intra-abdominal immune priming on day 1 prevented this reduction. Inclusion of β-glucan during early-life immune priming improved ileal morphology and prevented reduction in feed efficiency. On day 21 CP+β-glucan primed birds showed significantly higher villus width compared to saline and CP alone groups.
We found that early-life exposure to C. perfringens in the presence of β-glucans improved ileal morphology, prevented immune organ weight decline, and maintained feed efficiency upon subsequent C. perfringens infection. Thus, our findings showcase the potential of β-glucans to reduce the negative impact of NE in poultry. Our results suggest enhanced resilience to C. perfringens which may be relevant in industrial settings. In particular, these findings suggest added benefits of β-glucan inclusion in developing poultry NE vaccines.