S. Kennedy-Stoskopf; M. K. Stoskopf; J. D. Strandberg; M. Eckhaus
Division of Comparative Medicine, Johns Hopkins School of Medicine,
Baltimore, MD
A California sea lion (Zalophus californianus) exhibiting recurrent
ulcerative skin lesions was biopsied for viral isolation by explantation. Fibroblastic outgrowth
of explanted skin developed large areas of multinucleated syncytia. Electron microscopy
demonstrated virus particles characteristic of spumaviruses in the family Retroviridae. Similar
skin lesions developed on a harbor seal (Phoca vitulina) about one month after
introduction into the sea lion exhibit. Scattered areas of multinucleated syncytia developed in
the explanted skin fibroblasts from this animal, though virus was not recovered. No syncytia
developed in fibroblasts from a harbor seal which had no history of skin lesions and no contact
with the sea lion exhibit. Skin lesions reoccurred in the otherwise asymptomatic sea lion 4
months after the initial biopsy. The animal was rebiopsied and died suddenly 4 days later after
24 hours of anorexia and pyrexia. At post mortem, death was attributed to a Pasteurella
multocida pericarditis and septicemia. Lung, kidney, spleen, and lymph nodes were explanted in
an effort to determine the extent of the spumavirus infection. Cellular outgrowths of the lung
occasionally developed syncytia but more frequently were lysed. Elimination of the cell culture
by EM showed virus particles characteristic of a herpesvirus. Spumaviruses are not known to
cause clinical disease. They do cause a persistent infection of the reticulo-endothelial system
possibly altering the host's immune response. Herpesviruses cause a wide variety of clinical
diseases and latent infections. Neither spumaviruses nor herpesviruses have been previously
described in pinnipeds. The role of these viruses in pathogenesis of disease in pinnipeds
remains speculative, but either might predispose an animal to a fatal secondary infection.