Location: Animal Parasitic Diseases LaboratoryTitle: Atypical fatal sarcocystosis associated with Sarcocystis neurona in a white-nosed coati (Nasua narica molaris) Author
|Trupkiewicz, John - Philadelphia Zoo|
|Verma, Shiv - Non ARS Employee|
|Adedoyin, Gloria - National Instiute Of Allergy And Infectious Diseases (NIAID, NIH)|
|Georoff, Tim - Philadelphia Zoo|
|Grigg, Michael - National Instiute Of Allergy And Infectious Diseases (NIAID, NIH)|
Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/7/2017
Publication Date: 10/17/2017
Citation: Dubey, J.P., Trupkiewicz, J.G., Verma, S.K., Mowery, J.D., Adedoyin, G., Georoff, T., Grigg, M. 2017. Atypical fatal sarcocystosis associated with Sarcocystis neurona in a white-nosed coati (Nasua narica molaris). Veterinary Parasitology. 247:80-84. https://doi.org/10.1016/j.vetpar.2017.10.003.
DOI: https://doi.org/10.1016/j.vetpar.2017.10.003 Interpretive Summary: Toxoplasma and Sarcocystis are related single celled parasites of livestock and humans. While Toxoplasma has long been recognized to cause neurologic disease in many warm blooded hosts, including humans, parasites in the related genus Sarcocystis also cause serious disease in livestock and even in humans. Sarcocystis neurona causes a fatal neurological disease in horses called Equine Protozoal Myeloencephalitis (EPM) in Americas. Facial nerve paralysis, muscular atrophy, and limb abnormalities are the most common clinical signs of EPM. In the present study, the authors report on clinical and parasitological findings of acute sarcocystosis in a White-nosed coati at the Philadelphia zoo. Atypical for S. neurona, parasites were disseminated throughout virtually all tissues and, most especially, in abdominal tissues. Molecular characterization revealed the infection to stem from a new strain of the parasite. Whether this severe parasitism was related to the host or the parasite needs further investigation. These results will be of interest to veterinarians, parasitologists, and zoo keepers.
Technical Abstract: The protozoan parasite Sarcocystis neurona is an important cause of disease in horses (equine protozoal myeloencephalitis, EPM) and in marine mammals. Isolated reports of clinical EPM-like disease have also been documented in a zebra, raccoon, domestic cat, domestic dog, ferret, skunk, mink, lynx, Red panda and fisher. The predominant cause is encephalomyelitis associated with schizonts in neural tissues. Here, we report disseminated sarcocystosis of many tissues but not the brain of a captive White-nosed coati (Nasua narica molaris). Schizonts were located in many cell types, and differed morphologically from S. neurona schizonts in horses. The 14 year old, neutered male coati was euthanized due to progressive weakness, lethargy, and inappetence. Examination of Giemsa-stained impression smears of the lung taken at necropsy revealed schizogonic stages of S. neurona-like organisms, including free and intracellular merozoites, immature and mature schizonts in fibroblasts, neutrophils, and mononuclear cells. Histologically, protozoa-associated lesions (in decreasing order of intensity) were seen in lungs, adrenal and thyroid glands, stomach, skeletal muscle, gallbladder, small intestine, liver, urinary bladder, spleen, pancreas, salivary glands, kidneys, and eye. Few sarcocysts were seen in skeletal muscle and in the myocardium. Immunohistochemcally, the protozoa reacted positively to S. neurona but not to Toxoplasma gondii antibodies. PCR amplification of the DNA derived from the lung tissue of the coati yielded amplicons for all coccidian markers tested. PCR-DNA sequencing at the 18S, 28S and ITS-1 was consistent with S. neurona as the coccidian agent infecting the coati. PCR-DNA sequencing performed using primer pairs against antigenic surface proteins (SnSAG3, SnSAG4, SnSAG1-5-6) and microsatellite markers (SN7, SN9) revealed that the S. neurona strain infecting the coati was new. Although it was similar to the widely distributed Type VI strain, it possessed a novel allele at SnSAG5, and a different MS combination of repeats at SN7 and SN9, than what is expected for the widely distributed Type VI strain. Whether this severe parasitism was related to the host or the parasite needs further investigation.