Abstract

Proliferative gastric lesions were recognized in the stomach of 6 yellowtail snappers (Ocyurus chrysurus), 1 lane snapper (Lutjanus synagris), 1 black grouper (Mycteroperca bonaci), 1 red grouper (Epinephalus morio), and 1 grouper of unknown species all housed in a large mixed species indoor marine environment. At necropsy, gross lesions were recognized in the 3 groupers and in the lane snapper and consisted of an irregular "cobblestone" appearance of the gastric mucosa. Foreign material was found in the stomach of the red grouper (stones) and lane snapper (plastic) at necropsy.

On histopathologic examination, gastric proliferative lesions included glandular epithelial hyperplasia (10/10 fish), adenoma (4/10), carcinoma in situ (6/10), and adenocarcinoma (6/10). Various combinations of these proliferative lesions were seen in all but 1 fish, a yellowtail snapper that had only evidence of mucosal hyperplasia. All 10 fish had perivascular to diffuse submucosal infiltrates of lymphocytes and plasma cells (mild to severe gastritis) and 6/10 fish had evidence of chronic granulomatous inflammation in the submucosa. Adenocarcinomas invaded into the gastric submucosa and were associated with a schirrous response. However metastasis was not a feature of this disease.

The presence of a "cluster" of similar neoplastic diseases in multiple fish from one environment suggests the possibility of a common cause. The cause of these unusual fish tumors is unclear. There have been reports of a propensity for polypoid gastric lesions in yellowtail snappers associated with irritation and trauma from stones and/or pelleted feed and perhaps aflatoxin exposure. Gastric adenomatous polyps have been previously identified in salmon subjected to aflatoxins. Trout treated with a variety of nitroso compounds developed malignant gastric tumors. Sections of liver from 2 of the affected yellowtail snappers in this report were negative for aflatoxin. The groupers and snappers in this report did not share a common food source.

We raise the possibility that chronic inflammation is the inciting cause of the hyperplastic and neoplastic lesions in these fish. We also suggest that a progression from preneoplastic change (hyperplasia) to adenoma to carcinoma in situ and eventually to invasive adenocarcinoma may also occur. The cause of chronic inflammation is unknown at this time but possibilities include chronic parasite migration/encystation, chronic ingestion of irritating foreign material, an irritant chemical present in the environment, or a combination of these factors.

Acknowledgements

We would like to thank Drs. Marilyn Wolfe and Jeff Wolf for their help in reviewing these cases and for reviewing this abstract. This project was performed in whole or in part by using services and funds provided by National Cancer Institute's Registry of Tumors in Lower Animals, operated under contract by Experimental Pathology Laboratories, Inc., N02-CB-27034.

References

1.  Bunton TE. 1996. Experimental chemical carcinogenesis in fish, Toxicol Pathol 24(5):603-618.

2.  Hendricks JD, DW Shelton, PM Loveland, CB Pereira, GS Bailey. 1995. Carcinogenicity of dietary dimethylnitrosomorpholine, N-methyl-N'-nitro-N-nitrosoguanidine and dibromoethane in rainbow trout, Toxicol Pathol 23(4):447-457.

3.  Kimura I, T Miyake, S Kubota, A Kamata, S Morikawa, Y Ito. 1976. Adenomatous polyps in the stomachs of hatchery-grown salmonids and other types of fishes, Prog Exp Tumor Res 20:181-194.