Acute microcystin exposure induces reversible histopathological changes in Chinook Salmon (Oncorhynchus tshawytscha) and Atlantic Salmon (Salmo salar)

• Published in: Journal of fish diseases Vol. 45; no. 5; pp. 729 - 742
• Main Authors: Shartau, Ryan B., Snyman, Heindrich N., Turcotte, Lenora, McCarron, Pearse, Bradshaw, Julia C., Johnson, Stewart C.
• Format: Journal Article
• Language: English
• Published: England Blackwell Publishing Ltd 01-05-2022
• Subjects: Algae; Animals; Atlantic Salmon (Salmo salar); Chemical analysis; Chinook Salmon (Oncorhynchus tshawytscha); Cyanobacteria; Exposure; Fish Diseases - chemically induced; Fish Diseases - pathology; Freshwater fishes; Hepatotoxicity; hepatotoxin; Histopathology; Lesions; Liver; Liver diseases; Marine fishes; microcystin; Microcystins; microcystis aeruginosa; net‐pen liver disease; Oncorhynchus tshawytscha; Salmo salar; Salmon; Salmonids; Seawater; Toxins; Water analysis; Chinook Salmon (Oncorhynchus tshawytscha); hepatotoxin; Atlantic Salmon (Salmo salar); cyanobacteria; net-pen liver disease; microcystis aeruginosa; microcystin
• ISSN: 0140-7775; 1365-2761
• DOI: 10.1111/jfd.13599

Atlantic Salmon (Salmo salar) and Chinook Salmon (Oncorhynchus tshawytscha) develop a severe liver disease called net‐pen liver disease (NPLD), which is characterized by hepatic lesions that include megalocytosis and loss of gross liver structure. Based on studies where salmonids have been exposed to microcystin (MC) via intraperitoneal injection, NPLD is believed to be caused by MC exposure, a hepatotoxin produced by cyanobacteria. Despite the link between MC and NPLD, it remains uncertain if environmentally relevant MC exposure is responsible for NPLD. To determine if we could produce histopathology consistent with NPLD, we compared the response of Atlantic and Chinook Salmon sub‐lethal MC exposure. Salmon were orally gavaged with saline or MC containing algal paste and sampled over 2 weeks post‐exposure. Liver lesions appeared by 6 h but were resolved 2‐weeks post‐exposure; histopathological changes observed in other tissues were not as widespread, nor was their severity as great as those in the liver. There was no evidence for NPLD due to the absence of hepatic megalocytosis. These results indicate that the development of NPLD is not due to acute MC exposure but may be associated with higher MC concentration occurring in food, long‐term exposure through drinking of contaminated seawater and/or interactions with other marine toxins.