Abstract

The etiology of goldfish ulcer disease, which causes ulcerations of the skin and musculature in this species, was investigated in this study. Diseased goldfish from several sources were examined for the presence of parasites, viruses and bacteria. Most fish were infected with external parasites, but the parasites observed were varied. No viral cytopathic effects were detected on two cell lines (FHM and CAR) inoculated with lesion and organ homogenates. A nonmotile gram-negative rod closely resembling Aeromonas salmonicida achromogenes was isolated from diseased fish from all sources and was most prevalent in early-stage lesions. Aeromonas hydrophila and other bacteria were frequently isolated from late-stage lesions. Bacteria were generally absent from the kidneys of all fish excepting those with extremely deep, late-stage lesions.

Attempts were made to reproduce goldfish ulcer disease in clinically normal fish by exposing them to kidney and lesion ultrafiltrates, A. hydrophila and the A. salmonicida-like bacterium. Fish were injected intraperitoneally, intramuscularly and subcutaneously with the material, and infection was also attempted by scraping off a small patch of scales and dropping the material onto the denuded area (scrape patch technique). Lesion formation was consistently induced by exposing the fish to the A. salmonicida-like bacterium by the scrape patch technique, while fish injected with the bacterium died without forming lesions. Exposure to the ultrafiltrates or A. hydrophila by injection or the scrape patch technique did not result in consistent lesion formation or death. Later experiments showed that a waterborne challenge with the A. salmonicida-like organism without prior scale removal was sufficient to induce lesion formation.

Histopathological aspects of the disease were also studied.

Notes

Economic losses from ulcer disease include deaths and non-saleability due to lesions. The disease is most prevalent in the spring and fall when the water temperature is 50-75°F.

Diagnosis is made by doing wet mounts of skin, gills and internal organs as well as histopathology of lesions. The lesions are at first difficult to detect grossly. They start as a small fuzzy patch on the surface of the skin. Histopathologically one sees epidermal hyperplasia. There is an inflammatory response with necrosis and clumps of bacteria visible.

Aeromonas is sensitive to chloramphenicol, erythromycin, tetracycline and the sulfa drugs. The lesions may also heal with heat treatment. A vaccine is presently being formulated.