Immune Dysfunction as a Driver of Antimicrobial Demand and Resistance Selection in Poultry: A Mechanistic Review

Antimicrobial resistance (AMR) in poultry is driven immediately by antimicrobial exposure, but recurrent flock-level treatment often reflects earlier biological failures. This mechanistic review examines immune dysfunction, mucosal-barrier injury and physiological stress as upstream determinants of antimicrobial demand. Viral immune-organ injury, toxin-related effects, coccidial epithelial damage, early-life vulnerability and heat stress may impair vaccine responsiveness, colonization resistance, tissue integrity or medication delivery, thereby increasing susceptibility to bacterial colonization, disease, shedding or recurrence. Flock-level antimicrobial treatment then creates selection pressure in pathogens and the wider microbiome. Evidence is strongest for infectious bursal disease virus (IBDV), for which controlled studies demonstrate enhanced Campylobacter colonization and shedding following IBDV-associated immune dysfunction. Evidence for chicken anemia virus, Marek’s disease virus, mycotoxins, coccidiosis, heat stress and poor chick quality is more indirect and context-dependent. The review distinguishes direct evidence from mechanistic inference and presents a trigger-based diagnostic and surveillance framework linking immune and barrier indicators with antimicrobial use and AMR outcomes. Preventing avoidable bacterial disease may reduce selection opportunity while preserving diagnosis-led treatment for birds that need it.