In consequence of the withdrawal of products that assisted animal production, such as antimicrobial growth promoters, once-controlled enteric diseases have returned and new multifactorial diseases causing gut disorders of unknown origin have emerged in broilers. One of these widespread syndromes causing intestinal health problems in broilers is in the field referred to as "dysbacteriosis". During the present study, the histopathology of the intestinal tract of broilers affected with dysbacteriosis was analysed. Commercial broilers were given a macroscopic dysbacteriosis score by experienced veterinarians during necropsy. Samples from the duodenum and caecum were taken from each broiler for histopathological analysis. An increase in the macroscopic dysbacteriosis score coincided with increased villus atrophy, a decrease in the thickness of the tunica muscularis and an increase in T-lymphocyte infiltration in the gut mucosa. Also more and larger goblet cells were observed in the animals with high macroscopic dysbacteriosis scores. Although the exact aetiology still remains to be identified, dysbacteriosis in broiler chickens thus coincides with an inflammatory reaction in the gut mucosa.

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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.

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.

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.