Abstract

A previously beach-stranded, juvenile, male, bottlenose dolphin (Tursiops truncatus) with a 2-year history of antibiotic treatment for vertebral osteomyelitis died after an acute onset of vomiting, profuse diarrhea, anorexia, and lethargy with marked leukopenia of 24 hours duration. Histopathological examination of the intestine revealed superficial necrotizing enteritis with a uniform population of gram-positive cocci within the lumen. Staphylococcus aureus isolated from the intestine tested positive for the gene for staphylococcal enterotoxin A (SEA) by polymerase chain reaction (PCR). The osteomyelitis of the coccygeal vertebral body proved to be locally extensive and contained sequestra, granulomata, fistulae and osteophytes. While no etiologic agent was identified in specially stained tissue sections, a Brucella species was isolated on culture of swabs made from this lesion. Diffuse lymphocellular depletion was detected in the spleen and other reticuloendothelial organs. A marked lymphohistiocytic portal hepatitis was observed along with hepatic arteriolar sclerosis and reduplication, portal fibrosis, biliary hyperplasia, and paucity of portal vein ramifications. Consistent with the isolation of a pyrogenic toxin superantigen (PTSAg)-producing staphylococcal isolate, some of the systemic symptoms in this animal resembled those in human toxic shock syndrome. The simultaneous isolation of S. aureus and Brucella species raises the possibility that synergistic activity of PTSAgs and endotoxin could have contributed to the rapidly lethal course of disease. Furthermore, this is the first detection of a staphylococcal isolate with this gene in association with necrotizing enteritis in a chronic rehabilitation setting and serves as a signal case to demonstrate that such organisms can be selected for and cause lesions, as is the case in humans treated chronically with antibiotics.