An Update on Toxoplasma gondii and Sarcocystis neurona Infections in California Sea Otters
IAAAM Archive
Melissa A. Miller1; David Jessup1; Erin Dodd1; Mike Harris1; Jack Ames1; Patricia Conrad2; Ian Gardner2; Christine Kreuder2; Linda Lowenstine2; Jonna Mazet2; Karen Worcester3; David Paradies4; Michael Grigg5
1California Department of Fish and Game, MWVCRC, Santa Cruz, CA, USA; 2School of Veterinary Medicine, University of California, Davis, CA, USA; 3Central Coast Regional Water Quality Control Board, San Luis Obispo, CA, USA; 4Bay Foundation of Morro Bay, Morro Bay, CA, USA; 5Stanford Medical School, Palo Alto, CA


Two species of protozoan parasites, Toxoplasma gondii and Sarcocystis neurona, are associated with fatal meningoencephalitis in southern sea otters (Enhydra lutris neries), a federally-listed threatened species.1,2,6 The environmentally-resistant oocysts or sporocysts of these parasites are shed in the feces of infected terrestrial animals, specifically cats (T. gondii) and opossums (S. neurona). To date, no other "egg"-shedding hosts have been identified, and otters rarely, if ever, consume recognized intermediate hosts, such as mice and birds. Since 1998, we have completed systematic necropsies of all freshly dead otters submitted to our facilities, along with serological testing, parasite isolation in cell culture and brain immunohistochemistry for T. gondii and S. neurona. Because of the apparent terrestrial origin of both parasites, we expected to find that natural infections of sea otters were uncommon. However, we detected active T. gondii brain infections in 36 percent of freshly dead California sea otters examined between 1997 and 2001. In addition, 4 percent of otters were positive for S. neurona.

We developed indirect fluorescent antibody tests, (IFATs) to screen live and dead sea otters for evidence of protozoal exposure. The T. gondii IFAT was validated for otters using serum from necropsied sea otters with confirmed T. gondii infections, and was then used to screen sera from live, free-ranging sea otters from California, Washington and Alaska.4 Thirty-six percent of freeranging California sea otters were seropositive for T. gondii, compared to 38 percent of Washington otters and 0 percent of Alaskan otters.

To investigate the apparent emergence of T. gondii infections in California sea otters, we examined spatial, environmental, and demographic data from 223 live and dead sea otters for associations with T. gondii seropositivity, with the ultimate goal of identifying risk factors for T. gondii infection.5 Risk factors associated with T. gondii seropositivity included male gender and older age class. Spatial analysis revealed two "high-risk" sites for T. gondii exposure along the central California coast. Most important, otters sampled near areas of heavy freshwater outflow were almost three times more likely to be seropositive to T. gondii than otters sampled near areas of low flow. More recently, molecular characterization of 35 T. gondii isolates obtained from California sea otters revealed a striking bias toward an atypical parasite genotype in sea otter brain tissue.

Between 1998 and 2002 we detected over 10 cases of meningoencephalitis due to brain infection by Sarcocystis neurona, and the parasite was successfully isolated in cell culture from eight California sea otters. In contrast to T. gondii, no incidental S. neurona infections were detected in necropsied otters; in all cases, the S. neurona-associated brain inflammation was moderate to severe, and was associated with varying degrees of tissue necrosis. Simultaneous T. gondii and S. neurona brain infections were suspected or confirmed for three sea otters and one Pacific harbor seal (Phoca vitulina richardsi).3

The association between anthropogenic environmental disturbance, pathogen pollution and the emergence of infectious diseases in wildlife has been postulated, but not always well supported by the epidemiology. These studies provide specific evidence of contamination of the coastal marine ecosystem with the zoonotic pathogen, Toxoplasma gondii and the related parasite Sarcocystis neurona, and reveals extensive infection of the threatened California sea otter population. It also supplies statistical evidence implicating land-based surface runoff as a source of T. gondii infection for sea otters. Sea otters and humans compete for some of the same benthic invertebrate prey. Thus, if otters are ultimately found to be exposed to T. gondii and other pathogens through consumption of filter-feeding prey, this study has potent implications for human health.


This research was supported through funding from the National Sea Grant Program (NA06RG0142 R/CZ-169), PKD Trust, Morris Animal Foundation, the San Francisco Foundation, UC Davis Wildlife Health Center, the Lindbergh Foundation, Friends of the Sea Otter, the Marine Mammal Center (TMMC) and the California Department of Fish and Game (CDFG). The authors wish to acknowledge the excellent assistance of staff and volunteers from CDFG, TMMC, the Monterey Bay Aquarium, and USGS-BRD for sea otter carcass recovery.


1.  Cole RA, DS Lindsay, CL Roderick, JP Dubey NJ Thomas, LA Baeten. 2000. Biological and molecular characterizations of Toxoplasma gondii obtained from southern sea otters (Enhydra lutris nereis). J. Parasitol. 86:526-530.

2.  Miller MA, PR Crosbie, K Sverlow, K Hanni, BC Barr, N Kock, MJ Murray, LJ Lowenstine, PA Conrad. 2001. Isolation and characterization of Sarcocystis from brain tissue of a free-living southern sea otter (Enhydra lutris nereis) with fatal meningoencephalitis. Parasitol Res. 87: 252-257.

3.  Miller MA, KW Sverlow, PR Crosbie, BC Barr, LJ Lowenstine, FM Gulland, A Packham, PA Conrad. 2001. Isolation and characterization of parasitic protozoa from a Pacific harbor seal (Phoca vitulina richardsi) with meningoencephalitis. J. Parasitol. 87:816-822.

4.  Miller MA, IA Gardner, A Packham, JK Mazet, KD Hanni, D Jessup, J Estes, R Jameson, E Dodd, BC Barr, LJ Lowenstine, FM Gulland, PA Conrad. 2002. Evaluation of an indirect fluorescent antibody test (IFAT) for demonstration of antibodies to Toxoplasma gondii in the sea otter (Enhydra lutris). J. Parasitol. 88: 594-599.

5.  Miller MA, IA Gardner, C Kreuder, DM Paradies, KR Worcester, DA Jessup, E Dodd, MD Harris, JA Ames, AE Packham, PA Conrad. 2002. Coastal freshwater runoff is a risk factor for Toxoplasma gondii infection of southern sea otters (Enhydra lutris nereis). Int. J. Parasitol. 32: 997-1006.

6.  Thomas NJ, RA Cole. 1996. The risk of disease and threats to the wild population. Endangered Species Update Special Issue: Conservation and management of the southern sea otter. 13: 23-27.

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Melissa A. Miller

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