Abstract
Sarcocystosis is caused by the apicomplexan protozoan parasite, Sarcocystis spp., including Sarcocystis neurona.1,2 Opossums (Didelphis virginiana) are the S. neurona definitive host, with various species acting as intermediate hosts.1-4 Other species can become infected and be aberrant hosts, notably horses that can develop equine protozoal myeloencephalitis.2,3 The parasite undergoes sexual reproduction within the opossum’s intestinal epithelium and with fecal shed of infective sporocysts.2 Intermediate and aberrant hosts ingest the sporocysts that migrate through the body and encyst in a variety of tissues, typically muscle or brain;2,5 however, the heart, liver, diaphragm, and esophagus can be affected2,6. Sarcocystosis has been well documented in free-ranging marine mammals,4,7 particularly pinnipeds,1,2,8 but rarely documented in managed care3,5,8,9. Free-ranging California sea lions (Zalophus californianus) commonly present to stranding facilities with polymyositis and rhabdomyolysis causing severe muscle weakness and atrophy.1,2,6 Harbor seals (Phoca vitulina) differ as they present with neurological signs caused by meningoencephalitis, particularly affecting the cerebellum.3,8 Similarly, sea otters (Enhydra lutris) present with neurological signs.2,4
During the summer of 2023, the New York Aquarium diagnosed sarcocystosis in two pinniped species in an outdoor exhibit. A nine-year-old female California sea lion presented with lethargy, partial anorexia, and chest scooting with tucked fore flippers. After minimal response to supportive care for five days, she was immobilized for diagnostic evaluation. Clinical findings included severe myoglobinuria with marked increases in creatine kinase (13,618 U/L), alanine aminotransferase (755 U/L), aspartate aminotransferase (435 U/L), and phosphorus (7.6 mg/dL). Sarcocystis neurona protozoal serology was strongly positive at 1:20,480.10 Six weeks later, a 16-year-old female harbor seal presented with acute lethargy, partial anorexia, and progressive ataxia and tremors leading to inability to ambulate and swim normally, with significant head tremors. Diagnostic evaluation revealed clinically unremarkable CBC and biochemistries, but S. neurona serology was strongly positive at 1:5,120. Within seven days of presentation, both animals began anti-protozoal therapy1,2 (ponazuril 10 mg/kg PO q 24 h, clindamycin 10 mg/kg PO q 12 h, and tapering dexamethasone starting at 0.15 mg/kg PO q 24 h). Within seven days of treatment, clinical signs and appetite in both animals improved. Corticosteroids were discontinued after six weeks in both animals. Clindamycin and ponazuril were discontinued in the sea lion after eight and 14 weeks, respectively, following resolution of clinical signs. At the time of abstract submission, the harbor seal continues with ponazuril and clindamycin after 12 weeks with intermittent, mild head tremors.
Epidemiological investigation included evaluation of pest management, seawater sources, weather changes, and exhibit infrastructure. Infective sporocysts are highly resistant to environmental degradation and can persist in soil long after excretion.2 Despite opossums not being observed or trapped around the exhibit, it is presumed infections occurred by ingestion of exhibit water contaminated with dirt from extensive rainwater run-off from exhibit landscaping caused by exhibit infrastructure deterioration. Even after 30 years, with no previous sarcocystosis cases reported in this exhibit, climate change must be considered as a potential contributing factor. Sarcocystis neurona may be more common in pinnipeds under managed care than previously believed and should be considered for any cases of lethargy, weakness, or neurological signs.
Acknowledgments
The authors wish to thank W. Hana, H. Walters, J. Rant, and the animal care team for their dedicated care of these animals. The authors would also like to thank P. Toledo, V. Jemec, and T. Howell for their veterinary technical support during these cases.
*Presenting author
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