Case 180126 -3

Adult male river otter (Lontra canadensis)

The otter was found near the Petaluma River and was taken in by a wildlife rescue because he was emaciated and lethargic. The otter was hospitalized at the rescue for three days and had an excellent appetite. The otter’s marked lethargy, cage licking, and occasional frantic behavior were suggestive of neurologic abnormalities. The otter was found dead on the morning of the fourth day.

Postmortem decomposition was mild and the otter was emaciated. The left ventricle of the heart was moderately dilated with a thinned ventricular free wall and slight pallor in the myocardium. The cardiac apex was rounded. The stomach, as well as small and large intestines, contained a small to moderate amount of viscous, dark brown to black ingesta.

This section of brain is affected by multifocal regions of inflammation with associated rarefaction as well as prominent perivascular cuffing and meningeal inflammation. Large areas of the meninges and nearby perivascular spaces are infiltrated by moderate numbers of lymphocytes, fewer plasma cells, and macrophages. The associated cortex, and occasionally white matter, are rarified and are infiltrated by aggregates of histiocytes, lymphocytes, plasma cells, neutrophils, and glial cells. Within inflammatory aggregates are moderate numbers of shizonts that are approximately 15 to 30 um in diameter, ovoid with a thin to indistinguishable wall, and contain abundant ovoid 1 x 3 um to 2 x 4 um, basophilic zoites. Schizonts are both scattered throughout the neuropil and are occasionally within neurons, astrocytes, and histiocytes. Free zoites are similarly distributed. The nearby neuropil is rarefied or necrotic, and neurons within these areas are shrunken and angled with hypereosinophilic cytoplasm and pyknotic nuclei (acute necrosis).

Immunohistochemistry stains for Toxoplasma, Neospora, and Sarcocystis were all performed on the brain to identify the protozoa. Sarcocystis IHC was strongly immunoreactive with the protozoa and some of the associated inflammatory cells while Toxoplasma and Neospora IHC were both nonreactive. Distemper IHC on the brain and kidney were both nonreactive.

Cerebrum: severe, multifocal to coalescing, chronic, histiocytic, neutrophilic, lymphoplasmacytic meningoencephalitis with large numbers of protozoal schizonts, and associated necrosis and gliosis

The primary cause of clinical signs in this case is attributed to the severe, chronic, meningoencephalitis cause by Sarcocystis sp. Infectious S. neurona sporocysts are shed only in the feces of Virginia opossums (Didelphis virginiana), which are now widespread throughout California. To our knowledge, there are no reports of Sarcocystis induced meningoencephalitis in river otters. However, Sarcocystis has been reported to cause severe often fatal systemic disease, with meningoencephalitis being a common component, in a wide range of animals including horses, harbor seals and sea otters. One of the most common causes of mortality in west coast sea otters is protozoal meningoencephalitis. Thirty nine of 344 (11.3%) California and Washington state sea otters examined from 1985 to 2004 had histopathological evidence of significant protozoal meningoencephalitis. Both Toxoplasma gondii and Sarcocystis neurona are the most commonly identified protozoa. Sarcocystis is considered the more pathogenic of the two as T. gondii is commonly present in a quiescent form within the brain while S. neurona is commonly in an active form. Additionally, of the sea otters that died of meningoencephalitis, the ones that exhibited neurologic signs prior to death always had the active form of S. neurona within their brain lesions. In the current case, the immunohistochemistry is only able to characterize the protozoal organisms as Sarcocystis sp., but cannot further speciate as further molecular diagnostics would be necessary. There was no evidence of a Distemper infection or any other signs of immunosuppression that would predispose this animal to develop a Sarcocystis infection.

Interestingly, this river otter had a dilated cardiomyopathy, which is one of the changes that has been reported in sea otters with Sarcocystis associated meningoencephalitis. Additionally, there has been an association made between domoic acid exposure and dilated cardiomyopathy in sea otters. The hippocampal, dentate gyrus, and thalamic lesions commonly associated with domoic acid toxicity were not apparent in this case, so it’s possible that the Sarcocystic/meningoencephalitis could be significantly associated with the cardiac dilation.

References

1. Kreuder, Christine, et al. "Evaluation of cardiac lesions and risk factors associated with myocarditis and dilated cardiomyopathy in southern sea otters (Enhydra lutris nereis)." American journal of veterinary research 66.2 (2005): 289-299.

2. Miller, Melissa A., et al. "A protozoal-associated epizootic impacting marine wildlife: Mass-mortality of southern sea otters (Enhydra lutris nereis) due to Sarcocystis neurona infection." Veterinary parasitology 172.3 (2010): 183-194.

3. Thomas, N. J., et al. "Protozoal meningoencephalitis in sea otters (Enhydra lutris): a histopathological and immunohistochemical study of naturally occurring cases." Journal of comparative pathology 137.2 (2007): 102-121.