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Marine survival of anadromous salmon species is highly variable, and causes of this variability are often unknown. In the 1990s, cultured pink salmon Oncorhynchus gorbuscha alevins from 2 different regions in Alaska, USA, had years with increased postemergent mortality that could not be attributed to viruses, bacteria, or parasites. In both regions, lifetime marine survival of the most severely affected fish groups was as low as 1.1% in 1 region and 0.13% in the other region. To determine causes of morbidity, alevins from both regions were sampled for detailed histopathology (n = 144 and 36). Microscopic lesions associated with increased postemergent mortality included ruptured yolk sacs or 'coagulated yolk' (up to 38% of abnormal fish affected) and invasive fungi in the stomach or swimbladder (up to 39% of abnormal fish affected). The diagnosis of a ruptured yolk sac was based on the presence of yolk protein in the peritoneal cavity. Putative yolk proteins sometimes also distended peritoneal macrophages, systemic vessels, hepatocyte cytoplasm, splenic macrophages, and renal ducts. The most severe case of visceral fungi had hyphae invading from the stomach into the swimbladder and kidney. In the hatchery with the greatest postemergent mortality, 38% of the abnormal fish sampled had no significant microscopic lesions. We hypothesize that ruptured yolk sacs and visceral fungi occurred in fish that were predisposed to develop these lesions because of poor body condition. High prevalence of these lesions might be a useful marker for predicting poor marine survival.

Ruptured yolk sacs and visceral fungi in emergent pink salmon alevins: histopathology and relation to marine survival