Abiotic Stressors and Infectious Disease in Aquaculture: Emerging Evidence for Environmental Contaminants as Hidden Disease Drivers

Infectious disease in aquaculture is shaped by interactions among pathogens, hosts and the surrounding environment. Temperature, salinity and other physicochemical conditions are established modifiers of several aquatic diseases, whereas environmental contaminants have been studied predominantly for their direct toxic effects. Whether contaminant exposure also alters subsequent infection has received much less integrated attention. We critically evaluate evidence linking environmental contaminants with viral, bacterial and parasitic infections in aquatic animals, while using established physicochemical stressors as a reference framework. Direct challenge studies show that pesticides, persistent organic contaminants, microplastics, mycotoxins and other pollutants can alter pathogen replication, infection severity or infection‐associated mortality in specific host–pathogen systems. Several studies report altered infection outcomes after sublethal exposure despite limited or absent mortality, growth impairment or overt cytotoxicity before pathogen challenge. Pathogen challenge can therefore reveal functional effects of contaminant exposure that may be missed by conventional apical toxicity endpoints. However, the relationship is not uniform. Null, non‐monotonic and occasionally protective effects have also been reported, and most direct evidence remains confined to laboratory studies in fish and shrimp. Evidence for transmission, commercial production systems, molluscs and parasitic diseases is comparatively scarce. Environmental contaminants should therefore be regarded as context‐dependent modifiers of infectious‐disease risk rather than universal causes of disease outbreaks. Where contaminant‐associated susceptibility is demonstrated, disease control may need to address both the relevant contaminant exposure and the pathogen. This evidence supports exploring dual‐function interventions that restore or mitigate contaminant‐induced host dysfunction while directly inhibiting the pathogen.