Abstract

A 12 year old, 160 kg, male California sea lion (Zalophus californianus) presented with a three week history of intermittent, partial anorexia and lethargy that progressed to extreme lethargy and complete anorexia and eventual death. The animal had previously exhibited infrequent bouts of deep coughing upon physical exertion. The second case was a 15 year old, 90 kg, female California sea lion that presented with a 2 week history of skin ulcers, and declining clinical condition. This animal was euthanized.

At necropsy, the male was thin and in good postmortem condition. The right, caudal lung lobe had an oval, approximately 4 cm diameter, fibrotic focus that centrally contained purulent exudate. The jejunum had a 1.5 x 3 cm rupture with rounded edges and the abdominal cavity was filled with abundant, dark brown to black, putrid fluid. Serosal surfaces of all abdominal organs were near-diffusely brown to black. Mesenteric lymph nodes were moderately enlarged, and there were no other significant gross findings. The female was in good nutritional and postmortem condition. There were numerous, 1-3 cm diameter, cutaneous ulcers throughout the body with central, caseous exudate. The lungs were dark purple-red, and contained numerous, miliary to 1 cm and occasionally up to 3 cm diameter, white, firm spherical to irregular nodules throughout. The spleen had a few, similar nodules, and there were no other significant gross findings.

Histologically in the male, the lungs had a spectrum of subacute to long-standing lesions: regions with extensive, interstitial to alveolar, granulomatous to pyogranulomatous infiltrate, and also areas with multifocal and coalescing abscesses to forming granulomas with extensive necrosis and with bands of granulation tissue and mature collagen intervening between abscesses and granulomas. The chronic lesions obliterated normal parenchyma, and pleura was also markedly fibrotic in these areas. Giant cells were common in all areas of inflammation. Blastomyces sp organisms were extremely numerous throughout, both extracellularly and within macrophages and giant cells. The organisms were 8-20 µm diameter, with a thick, double-contoured wall, and often exhibited broad-based budding. Extension of inflammation and organisms into larger airways, with occlusion in regions with chronic inflammation, was also present. Multiple veins and venules throughout sections had aggregates of inflammatory cells, fibrin and organisms often occluding the vessels. In the female, similar lesions were present though of subacute duration only.

Dissemination of the infection had occurred in both animals. The male had dissemination to the small intestine with transmural, chronic and active lesions in two locations. One of these sites was the grossly identified rupture site, and peritonitis with abdominal exudate was secondary to this rupture. Dissemination to the spleen and liver was also present in the male. In the female, dissemination had occurred to the skin and had caused the grossly identified ulcers. Additionally in the female, organisms and associated subacute inflammation were present in multiple lymph nodes and the spleen. Other clinically insignificant lesions identified included moderate hepatic hemosiderosis in both animals, nodular adrenal cortical and thyroid hyperplasia in the male, and aspermatogenesis in the male secondary to Lupron treatment. The male also had diffuse adrenal cortical hyperplasia likely secondary to the stress of chronic blastomycosis.

Death of the male was from the cumulative effects of disseminated blastomycosis and consequences of intestinal rupture caused by the transmural, Blastomyces sp-induced lesion, and clinical demise of the female also was due to disseminated blastomycosis. The causative agent likely was Blastomyces dermatitidis, though culture would have been required for specific identification; the lung culture in the female was overgrown by a contaminant, and material for culture was not available from the male. The infection in both animals was likely primary pulmonary with eventual dissemination considering the number of organisms present in the lungs and extent of lung lesions in both animals. Dissemination to the wall of the intestinal tract with rupture in the male is probably an unusual consequence of this infection, though this is speculative as there is scant information in the literature concerning blastomycosis in sea lions. The authors could find only one abstract in the literature describing lesions associated with blastomycosis in California sea lions.¹ No predisposing factor to the infection was found in either animal, thus Blastomyces sp was a presumptive primary pathogen.

Acknowledgments

The authors wish to thank Jane Chladny and the University of Illinois College of Veterinary Medicine Histopathology Laboratory for excellent technical assistance.

References

1.  Kennedy-Stoskopf S, R Russell. 1983. Blastomycosis in a California sea lion. 14th Annual Conference of the International Association of Aquatic Animal Medicine, p. 28.