In recent lab‐based experiments, some post‐smolt Atlantic salmon (Salmo salar) held at 3°C for 5 weeks exhibited a range of clinical signs. They became lethargic and swam at the water's surface, developed ulcers to the head and jaw (clinical signs similar to tenacibaculosis in Norwegian salmon aquaculture) and had fin erosion, and this was associated with significant mortalities. In addition, when fish with ‘early’ and ‘advanced’ stages of these different clinical signs were further examined, their livers were found to be large, pale and friable. Fish with this aetiology also had elevated aspartate aminotransferase levels (indicative of liver damage), elevated plasma [Na+], [Cl−] and osmolality (indicating osmoregulatory impairment), low glucose levels (likely limiting metabolic responses to maintain homeostasis) and high circulating cortisol levels (∼100 ng/mL). This suite of physiological disturbances is very similar to that observed in a condition referred to as ‘Winter Syndrome’ or ‘Winter Disease’ (WS/WD) in cultured gilthead sea bream (Sparus aurata) and other fish species. Thus, it appears that WS/WD described here for the first time in Atlantic salmon, alone or in combination with opportunistic infections, results in lipid deposition in the liver, compromising liver function and osmoregulatory capacity, and metabolic collapse that ultimately results in significant losses.