Sarcocystis neurona is a protozoan parasite, and is closely related to Toxoplasma gondii (Dubey, 2022a). It is an important cause of a serious neurological syndrome in horses called Equine Protozoal Myeloencephalitis (EPM). It has emerged as a common cause of mortality in marine mammals, especially sea otters (Enhydra lutris) (Thomas et al., 2007, Dubey et al., 2015). EPM-like illness has also been recorded in several other mammals including domestic dogs and cats. The genus Sarcocystis has more than 200 species, and most of the species are host-specific, cycling between intermediate hosts (usually herbivores) and definitive hosts (usually a carnivore). The sexual cycle occurs only in the intestine of the definitive host, which excretes environmentally-resistant oocysts/sporocysts in a fully infective stage. Unlike most species of Sarcocystis, S. neurona has an unusual life cycle. The North American opossum (Didelphis virginiana) and the South American opossum (Didelphis albiventris) are its known definitive hosts. Hosts supporting sarcocyst maturation (skunk, raccoon, sea otter and armadillo) qualify as established intermediate hosts. Several other intermediate hosts are suspected. In some hosts (such as the horse), only schizonts have been identified; hence these appear to represent aberrant hosts which fail to contribute to further transmission. Among intermediate hosts, the raccoon (Procyon lotor) likely contributes most to transmission (Dubey et al., 2015). The parasite’s asexual development, leading to formation of infectious sarcocysts, was documented in laboratory-raised raccoons after oral inoculation of S. neurona sporocysts (Stanek et al., 2002).

The finding of S. neurona in raccoon as an intermediate host is important because clinical signs resemble those of rabies infection. Although most infections in raccoons are considered asymptomatic, there are four histopathological reports of isolated cases of raccoons (Dubey et al., 1990, Dubey and Hamir, 2000; Hamir and Dubey, 2000; Stoffregen et al., 1991; Thulin et al., 1992; Supplementary Table S1). In two of these, concurrent Morbilli Virus Infection (MVI; also called Canine Distemper Virus [CDV]) aggravated clinical disease. However, histological evidence of MVI was not detected in two raccoons with myocarditis (Hamir and Dubey, 2001). No MVI information was available from the fifth case. In four of these five cases, diagnosis was confirmed by immunohistochemical (IHC) staining with S. neurona-specific antibodies (Dubey et al., 2015).

The objective of the present report is the documentation of an outbreak of S. neurona-associated disease in raccoons, and the first molecular confirmation of the parasite from brain and muscle of naturally infected raccoons. The opportunity was taken to supplement information on the genome of S. neurona sequenced and annotated by Blazejewski et al. (2015).