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.

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.

Salmonella enterica serovar Infantis (S. Infantis) poses a growing issue in the poultry sector, with phage-based products emerging as a safe and effective control measure. This study investigated the emergence of reduced-phage-susceptibility variants (RPSV) of S. Infantis in PhagoVet-treated broilers, given that RPSV could undermine phage treatment efficacy. The bacteriophages in the PhagoVet product were characterized using transmission electron microscopy (TEM), genome sequencing, and infection profiling. Furthermore, two broiler trials were conducted: a challenge group (T1) and a challenge-and-treated group (T2). The S. Infantis infective dose was set at 10⁴ and 10⁶ colony-forming units (CFUs) per animal, with PhagoVet administration at 10⁶ and 10⁸ plaque-forming units (PFUs) per animal, in Trials 1 and 2, respectively. The results revealed that the four PhagoVet bacteriophages belonged to different genera. PhagoVet evidenced broad-spectrum efficacy against 271 strains representing 18 Salmonella serovars. In Trial 1, PhagoVet reduced bacterial counts in feces to nearly undetectable levels by day 42, with no RPSV detected. However, in Trial 2, three and five RPSVs were detected in feces and ceca, respectively. Consequently, PhagoVet demonstrated efficacy against S. Infantis in broilers, and the potential impact of RPSV is deemed unlikely to compromise its efficacy.

Corticosterone (CORT) is the primary avian stress hormone and regulates key physiological processes, but chronically elevated levels can be detrimental. This study simulated chronic stress by exogenously increasing CORT to assess effects on gait score, bone morphometry, immune indicators, and fluctuating asymmetry (FA) in broiler chickens. A total of 60 one-day-old male Ross 308 broiler chickens were allocated to six treatment groups (T0–T5; n = 10 per group). T0 received a placebo and served as the control group, while T1–T5 were gavaged daily with increasing corticosterone doses (1–5 mg/kg body weight). Treatments were administered from day 1 to day 42. CORT did not affect gait score on day 11 (p = 0.232) or day 42 (p = 0.112), but gait score was significantly correlated with body weight (day 11: p < 0.001; day 42: p = 0.004). Elevated CORT reduced bursa diameter (p < 0.001) and increased bursa follicle scores (p < 0.001), while heterophil-to-lymphocyte ratios remained unaffected (p = 0.349). Carcass and bone dimensions decreased consistently with higher doses (p < 0.001), and body weight correlated positively with all bone traits (p < 0.001). Length-to-width ratios increased with CORT dose (p < 0.001). Composite carcass FA showed dose-related variation in carcass asymmetry, with highest in T4, intermediate in T2, T3, and T5, and lowest in T0–T1 (p = 0.026). Trait-specific FA effects were detected for metatarsus length (p = 0.005) and wattle (p = 0.018), while bone FA remained unaffected (p = 0.272). Overall, exogenously increasing CORT impaired growth, suppressed immune function, and increased fluctuating asymmetry, indicating reduced developmental stability.