Cerebrospinal Nematodiasis Due to Baylisascaris sp. in Golden-Headed Lion Tamarins (Leontopithecus chrysomelas): Implications for Management
American Association of Zoo Veterinarians Conference 1997
Allan P. Pessier1, DVM; Cynthia Stringfield2, DVM; Jimmy Tragle3,4, DVM; H.J. Holshuh5, DVM; Donald K. Nichols1, DVM; Richard J. Montali1, DVM
1Department of Pathology, National Zoological Park, Washington, DC, USA; 2The Los Angeles Zoo, Los Angeles, CA, USA; 3The Salisbury Zoological Park, Salisbury, MD, USA; 4Whaleyville Animal Hospital, Whaleyville, MD, USA; 5Los Angeles County Veterinary Public Health, Long Beach, CA, USA


Visceral larval migrans (VLM) caused by nematode parasites in the genus Baylisascaris has been described in a wide variety of mammalian and avian species.5 Experimental infection of nonhuman primates with B. procyonis, the raccoon ascarid, has been well described,6 and increasingly natural infections of captive primates are being reported.2,3 Previously, the only report of Baylisascaris sp. infection in callitrichids was of B. columnaris, the skunk ascarid, in several species of marmoset (Callithrix sp.).1,4 In this report, we describe cases of VLM due to Baylisascaris sp. in golden-headed lion tamarins (Leontopithecus chrysomelas) from two zoos. Observations regarding exhibit design and tamarin behavior possibly predisposing to infection in this species are also discussed.

Two histologically confirmed cases occurred at the Salisbury Zoo in Salisbury, MD. These tamarins were housed in a screen-topped, outdoor exhibit with abundant overhanging foliage, which was shared with a two-toed sloth and several iguanas. In March of 1996, an 8-year-old, male golden-headed lion tamarin was examined for a recent onset of ataxia and a mild head tilt. Over the next 5 months, partial improvement was observed with intermittent courses of antibiotics and prednisone given orally. In August of 1996, the monkey’s condition worsened, and it could no longer feed itself; euthanasia was performed. At about the time this animal was euthanatized, its cagemate, a 7-year-old female began showing similar neurologic signs. Treatment with antibiotics and prednisone resulted in only slight improvement. Euthanasia was performed in September 1996. Histologic examination of both monkeys revealed focally extensive areas of granulomatous and eosinophilic encephalitis, which was most severe in the cerebellum and occipital lobes of the cerebrum. In both animals, foci of inflammation contained cross sections of nematode larvae ranging from 30–67 µm in diameter, with a single pair of prominent lateral alae and paired triangular excretory columns that were smaller than the central intestine. These findings were considered to be consistent with Baylisascaris sp. Lesions consistent with parasite migration tracts were also observed in the spinal cord of the male and the optic nerve and retina of one eye in the female tamarin. Review of clinical and necropsy records revealed two other tamarins over the preceding 3 years with similar neurologic signs, one of which had a granulomatous and eosinophilic encephalitis consistent with larval migrans; no larvae, however, were demonstrated histologically. Raccoons had been a persistent problem within the park despite an aggressive trapping program, and several raccoon latrines were observed adjacent to the tamarin exhibit. Fecal flotation of raccoon feces obtained from one of these latrines contained large numbers of ascarid ova. The two-toed sloth has remained asymptomatic.

Additional cases involved a family group of three golden-headed lion tamarins from the Los Angeles Zoo housed in an outdoor exhibit with a chain-link top and overgrowing foliage that allowed debris to fall into the exhibit. This exhibit also contained white-fronted marmosets separated from the tamarins by a wall. Between September 1992 and September 1993, all three tamarins in this group began to display neurologic signs characterized by a head tilt, intention tremors, weakness, and ataxia. Hematologic and serum biochemical analyses, as well as routine radiography were all within normal limits. Animals were treated with varying regimens that included prednisone and antibiotics, and they had a variable clinical course characterized by periods of improvement and resolution followed by return of clinical signs. In October of 1994, magnetic resonance imaging was performed on two animals, including the most severely affected monkey, with negative results. All three tamarins had negative serologic tests for toxoplasmosis and lymphocytic choriomeningitis virus. The most severely affected animal had negative results for blood lead. In July 1994, all three tamarins were treated weekly for 4 weeks with oral ivermectin (0.03 ml of 1% ivermectin solution/monkey) because of suspected VLM. In August 1994, the tamarins were removed from the exhibit because of suspected repeated ascarid infection associated with soil contamination. In November of 1994, a 2.5-year-old male from this group was euthanatized because of persistent, severe clinical signs. A complete necropsy was performed, and histologic examination of the brain demonstrated a granulomatous meningoencephalitis that was most severe in the cerebellum, basal ganglia and occipital lobes. Cross sections of a larval nematode parasite consistent with Baylisascaris sp. were demonstrated in inflammatory foci. The remaining two tamarins eventually recovered sufficient neurologic function to breed and raise offspring. Skunks and raccoons had been persistent pests within the zoo. Fecal flotation of skunk feces obtained within the park have been positive for ascarid eggs. The white-fronted marmosets within the enclosure have remained asymptomatic.

These are the first reports of Baylisascaris sp. larval migrans in golden-headed lion tamarins. Cases from the Salisbury Zoo were most likely due to Baylisascaris procyonis, based on recurring problems in controlling wild raccoon populations and on the discovery of infected raccoon latrines adjacent to the exhibit. At the Los Angeles Zoo, cases could have been due to either B. procyonis or B. columnaris because of recurring problems with skunks as well as raccoons. Clinical signs common to both groups of tamarins included a head tilt and ataxia. As is evident from these clinical histories, long clinical courses extending over many months may be observed in affected tamarins. While Baylisascaris sp. infection was not confirmed in the two surviving tamarins from the Los Angeles zoo, VLM is the most likely explanation for the clinical signs observed in these animals. Based on this observation, it appears that some golden-headed lion tamarins may be able to survive infection with Baylisascaris sp.

In both zoos, tamarins were housed in outdoor exhibits that provided overhead access by wildlife. Open outdoor exhibits, such as these with dense overhanging foliage, may create situations that are attractive to raccoons and subsequently predispose an exhibit to contamination with Baylisascaris sp. eggs. In particular, raccoons are known to create latrines in wooded areas at the bases of trees, tree forks, and raised horizontal surfaces.5 These cases emphasize the need to aggressively control raccoon and skunk populations in zoological parks and to design exhibits that have a minimal chance of becoming contaminated by feces containing eggs of Baylisascaris sp.

Of particular interest is that in both zoos, tamarins were housed adjacent to or with other primate species that did not demonstrate clinical signs of infection with Baylisascaris sp. Keepers from both zoos reported subjectively that the tamarins would spend greater amounts of time on the ground foraging compared to the other primate species. Such a difference in behavior indicates that the tamarins might have contact with a greater number of ascarid eggs with an increased likelihood of VLM. Alternatively, golden-headed lion tamarins may be naturally more susceptible to disease caused by Baylisascaris sp. migration.


Dr. Pessier was supported by a Friends of the National Zoo Fellowship (97-3545A). The authors acknowledge helpful discussions with Dr. Kevin R. Kazacos.

Literature Cited

1.  Armstrong D.L., Montali R.J., Doster A.R., and Kazacos K.R. 1989. Cerebrospinal nematodiasis in macaws due to Baylisascaris procyonis. J. Zoo Wildl. Med. 20(3): 354–359.

2.  Ball R.L., Wilson S., Dryden M., and Veatch J. 1995. Cerebrospinal nematodiasis in a white-handed gibbon (Hylobates lar) due to Baylisascaris procyonis. Proc. Am. Assoc. Zoo Vet. 354–355.

3.  Garlick D.S., Marcus L.C., Pokras M., and Schelling S.H. 1996. Baylisascaris larva migrans in a spider monkey (Ateles sp.) J. Med. Primatol. 25: 133–136.

4.  Huntress S.L. and Spraker T. 1985. Baylisascaris infection in the marmoset. Proc. Am. Assoc. Zoo Vet. 78.

5.  Kazacos K.R., Boyce W.M. 1989. Baylisascaris larva migrans. J. Am. Vet. Med. Assoc. 195(7): 894–903.

6.  Kazacos K.R., Wirtz W.L., Burger P.P., and Christmas C.S. 1981. Raccoon ascarid larvae as a cause of fatal central nervous system disease in subhuman primates. J. Am. Vet. Med. Assoc. 179(11): 1089–1094.


Speaker Information
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Allan P. Pessier, DVM
Department of Pathology
National Zoological Park
Washington, DC, USA

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