Incidence and associated risk factors of necrotic enteritis in Belgian layer pullet flocks.

Necrotic enteritis (NE) caused by Clostridium perfringens is commonly reported in broilers. Recently, increased NE prevalence in layer breeds was reported in the Indian subcontinent. NE is also frequently observed by veterinary practitioners in Europe, mainly during the pullet rearing phase. In this study, data from layer pullet flocks in Belgium over a 5-year period (2013-2017) were used to assess the incidence of NE and identify potential risk factors for NE in layer pullets. NE was observed in 26% of the layer pullet flocks receiving veterinary intervention. This accounts for an overall estimated NE incidence of 12.3% in Belgian layer pullet flocks. Occurrence of NE was significantly associated with coccidiosis, with flocks being diagnosed with coccidiosis being two-fold more likely to develop NE. Additionally, birds kept in aviary houses were less prone to NE than flocks reared in floor systems or enriched cages. At necropsy, necrotic lesions in the small intestine were comparable to NE in broilers. A single strain of C. perfringens was isolated from the necrotic lesions of three different birds from the same flock; however, no NetB could be detected.

Host intestinal biomarker identification in a gut leakage model in broilers.

Intestinal health problems are a major issue in the poultry industry. Quantifiable easy-to-measure biomarkers for intestinal health would be of great value to monitor subclinical intestinal entities that cause performance problems and to evaluate control methods for intestinal health. The aim of the study was to identify host protein biomarkers for intestinal inflammation and intestinal barrier damage. Proteomic analysis was conducted on ileal and colonic content samples of broilers under an experimental gut damage and inflammation model. Effects of the challenge treatment resulted in a worse gut condition based on macroscopic gut appearance (p < 0.0001). Also microscopic changes such as shortening of the villi and increased crypt depth (p < 0.0001) as well as higher infiltration of T-lymphocytes (p < 0.0001) were seen in the duodenal tissue of challenged animals. Several candidate proteins associated with inflammation, serum leakage and/or tissue damage were identified with an increased abundance in intestinal content of challenged animals (p < 0.05). Conversely, brush border enzymes were less abundant in intestinal content of challenged animals (p < 0.05). These candidate biomarkers have potential to be used in the field for detection of gut barrier failure in broilers.

Elevated faecal ovotransferrin concentrations are indicative for intestinal barrier failure in broiler chickens.

Intestinal health is critically important for the welfare and performance of poultry. Enteric diseases that cause gut barrier failure result in high economic losses. Up till now there is no reliable faecal marker to measure gut barrier failure under field conditions. Therefore, the aim of the present study was to identify a faecal protein marker for diminished intestinal barrier function due to enteric diseases in broilers. To assess this, experimental necrotic enteritis and coccidiosis in broilers were used as models for gut barrier failure. Ovotransferrin was identified as a marker for gut barrier failure using a proteomics approach on samples from chickens with necrotic enteritis. These results were confirmed via ELISA on samples derived from both necrotic enteritis and coccidiosis trials, where faecal ovotransferrin levels were significantly correlated with the severity of gut barrier failure caused by either coccidiosis or necrotic enteritis. This indicates that faecal ovotransferrin quantification may represent a valuable tool to measure gut barrier failure caused by enteric pathogens.

Timing of predisposing factors is important in necrotic enteritis models.

Since the ban of antimicrobial growth promotors, the importance of necrotic enteritis in broilers increases. Reliable and reproducible infection models are required for pathogenesis studies and product screening. Two major predisposing factors in necrotic enteritis models are fishmeal supplementation to feed and Eimeria infection. However, many unsolved issues regarding these predisposing factors still exist. Therefore, the influence of timepoint of fishmeal administration (onset on day 8 or day 18), timing of coccidiosis challenge (day 15 or day 19) and strain of coccidiosis challenge (field strain vs. commercial vaccine) on the induction of necrotic enteritis lesions was investigated. The birds were inoculated with Clostridium perfringens three times per day for four consecutive days (day 17 until day 20) and were scored for the presence of necrotic enteritis on days 22, 23, 24, 25 and 26. Supplementation of the diet with fishmeal from day 8 onwards increased the likelihood of necrotic enteritis compared to supplementation from day 18 onwards. Birds challenged on day 19 with coccidiosis were more likely to have necrotic enteritis on scoring days 23 and 24 compared to birds challenged on day 15. Differences on other scoring days were less pronounced. Finally, the strain of coccidiosis challenge had little influence on the induction of necrotic enteritis. Findings of this study can help researchers to set up successful necrotic enteritis infection models.

Passive immunization against Histomonas meleagridis does not protect turkeys from an experimental infection.

Histomonosis or blackhead is a disease of gallinaceous birds, caused by the protozoan Histomonas meleagridis. As recent regulatory action has removed almost all drugs against this disease from the European market, the development of new prophylactics has become crucial. Identification of the protective immune mechanism would facilitate the choice and development of a vaccination strategy to prevent histomonosis. In this study, turkeys were either actively or passively immunized and were then challenged to assess the role of antibody-mediated immunity in the protection form this disease. Active immunization was performed either by experimental infection and treatment or by intramuscular injection with lysed H. meleagridis. Passive immunization was attempted by intraperitoneal administration of pooled, concentrated, neutralizing antisera from immunized donor animals to naive turkeys. A significantly higher IgG response was observed after infection and treatment than after intramuscular injection, which in turn was higher than the responses of placebo and control birds. While active immunization of turkeys by intramuscular injection of dead H. meleagridis antigens appeared not to be protective against histomonosis, immunization by infection and treatment did induce protection. However, no significant level of protection could be observed in the passively immunized birds. These results suggest that serum antibodies to H. meleagridis may not be a key component in the protection against this parasite. It is, however, possible that the concentration of antibodies at the mucosal site is insufficient. Therefore, further investigation on mucosal immune responses is necessary.