Abstract
West Nile virus (WNV), a mosquito-born, single-stranded RNA virus in the Flaviviridae family, has widespread distribution and was one of the first arboviruses to be described in humans.1,2 Infection can be asymptomatic or produce a range of signs and outcomes, including death.1 Since the introduction of WNV into North America in 1999, natural infection has been documented in >100 wild mammal species across the Americas.3-5 Disease due to WNV infection has been reported in marine mammals, including a killer whale (Orcinus orca), harbor seals (Phoca vitulina), and a northern sea otter (Enhydra lutris kenyoni).1,6-9
In fall 2023, a two-year-old male, rehabilitated southern sea otter (Enhydra lutris nereis) under managed care presented with decreased food consumption and activity. Due to a recent Sarcocystis neurona infection in two pinnipeds housed near the otter, anti-protozoal therapy was initiated but discontinued after negative serology results were received. Clinical pathology abnormalities included moderate leukopenia (2,700 leukocytes) with relative mature neutrophilia (69%), absolute neutropenia (1,863), relative (17%) and absolute (459) lymphopenia, relative (14%) monocytosis, and mildly elevated creatine kinase (524 U/L). Clinical signs abated temporarily with initial treatments but returned to include an intermittent unilateral paresis followed by bilateral forelimb and cervical spinal weakness, increased vocalizations, and anorexia. Diagnostic imaging and physical exam findings were unremarkable. Subsequent signs included facial tremors, focal facial seizures, muscle fasciculations, and tonic seizures that progressed to convulsive seizures lasting up to five minutes. Despite aggressive treatment with anticonvulsant medications (midazolam, levetiracetum), a non-convulsive status epilepticus event occurred with minimal response to treatment. Eight days after initial presentation, the animal was placed under general anesthesia with ventilation and medical support in an attempt to control the seizures. The animal was stable for more than 16 hours but arrested during recovery. WNV serology results received the day after death were strongly positive for WNV at 1:10,240.
Notable gross postmortem findings included generalized lymphadenomegaly and meningeal congestion. The brain and spinal cord were grossly unremarkable. Significant histopathologic findings included moderate to severe diffuse meningoencephalitis and myelitis with lymphoplasmacytic perivascular cuffs, neuronal necrosis, and satellitosis. WNV PCR was positive in brain samples, and in situ hybridization for WNV localized viral RNA in areas of inflammation and within necrotic neurons and glia. All additional ancillary diagnostics from brain samples were negative. This included PCR for eastern equine encephalitis virus, canine distemper virus, avian influenza virus, SARS CoV2, and apicomplexan protozoa; aerobic and anaerobic bacterial culture; and Sarcocystis culture. Toxicologic screening (GC/MS; liver) was also negative.
The southern sea otter is endangered. West Nile virus infection has generally been considered a disease of little clinical significance in sea otters, with only one case referenced in the literature in a northern sea otter.9 This and our case suggest it should be a differential in animals with neurologic signs. They also highlight the need for a better understanding of its effects in otters, its significance from a conservation perspective, and the efficacy and safety of WNV vaccination, especially in endangered species.
Acknowledgements
The authors wish to thank the Animal Care and Animal Health teams of New York Aquarium for their dedicated care of this animal; Dr. Cara Field and Crystal Luna for their assistance with the case; Drs. Devinn Marie Sinnott, Karen Shapiro, and Lauren Camp from the University of California–Davis and staff at the Cornell Animal Health Diagnostic Center for ancillary diagnostics testing; and Dr. Melissa Miller, California Fish and Wildlife, for consultation.
*Presenting author
+Student presenter
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