Transmission and host response of Atlantic salmon to Moritella viscosa in winter ulcer disease

Moritella viscosa, responsible for winter ulcer disease, is one of the major health and welfare challenges in Atlantic salmon aquaculture. This study investigated whether pre-bath exposure to commensal skin bacteria influences Atlantic salmon susceptibility to M. viscosa, compared cohabitation and bath challenge models to evaluate infection routes, and examined host and tissue responses, including the bacterial binding capacity of skin mucins. Pre-exposure to Atlantic salmon skin commensals Pseudomonas, Psychrobacter and Aliivibrio, which was expected to stimulate the immune system, did not mitigate M. viscosa-induced damage. Both bath and cohabitant challenge models resulted in low mortalities (6.3% and 2.6%, respectively), although a subset of fish in each model developed severe skin ulcers. M. viscosa remained persistent across sample types. Ulcerated individuals in the cohabitation model formed a distinct subgroup showing reduced growth, elevated acute inflammation marker expression in skin and heart, decreased serum protein and albumin levels, diminished heterologous and M. viscosa-specific antibody titers, and reduced IL-22 and IFNγ concentrations. In non-ulcerated fish, the skin barrier was impaired and showed features associated with M. viscosa pathogenesis, as indicated by a numerical decrease in transepithelial resistance, disrupted tight junctions, compromised epidermal integrity, increased keratocyte gaps, and a shift from acidic to more neutral mucus. Additionally, skin mucus bound both the investigated commensal bacteria and the pathogens M. viscosa and Aeromonas salmonicida.