Summary
The clinical signs of EPM depend on the location(s) of parasite-associated lesions in the CNS, and include inco-ordination, stumbling, frequent interference, difficulty backing up, ataxia, head tilting, loss of reflexes, loss of sensation, muscle atrophy and sometimes sudden collapse. Neurological deficits can be unilateral - the more frequent, or bilateral. In some horses the clinical signs develop very rapidly, in others slowly.
Taxonomy
Class: Conoidasida
Subclass: Coccidiasina
Order: Eucoccidiarida
Suborder: Eimeriorina
The taxonomy of species within the genus Sarcocystis is somewhat uncertain, but a number of distinct species have been identified in domestic and free-ranging animals and birds, and in people. Sarcocystis neurona is the cause of equine protozoal myeloencephalitis (EPM), a disease of horses in the Americas. The species was first described only in 1991, its definitive host (the opossum) identified in 1995, and an intermediate host (the domestic cat) identified in 2000.
When a Sarcocystis was first associated with EPM there was some uncertainty as to whether the species was S. falcatula, which cycles between opossums and various birds. It is now generally accepted that S. neurona and S. falcatula are both valid species, and that S. falcatula is not associated with EPM.
Note: Our understanding of the taxonomy of helminth, arthropod, and particularly protozoan parasites is constantly evolving. The taxonomy described in wcvmlearnaboutparasites is based on that in the seventh edition of Foundations of Parasitology by Larry S Roberts and John Janovy Jr., McGraw Hill Higher Education, Boston, 2005.
Morphology
The sporocysts of S. neurona in the faeces of opossum definitive hosts are sub-spherical, measure approximately 10 to 12 µm by 6 to 8 µm, and each contains four sporozoites.
Host range and geographic distribution
Sarcocystis neurona in horses is restricted to the Americas and its geographic distribution matches that of the definitive hosts. In the United States opossums are found in approximately the eastern half of the country and along the west coast. In Canada they are present in areas of southern Ontario and southern British Columbia. Only six cases of EPM have been reported in Canada, four in Ontario and two in Saskatchewan, where opossums do not occur. All these cases were reported before S. neurona was identified as the cause of the disease and diagnosis was based on the presence of typical clinical signs and organisms and/or pathology. The origins and travel histories of the horses are unknown.
Life cycle - indirect
Infection of intermediate hosts is by ingestion of the sporocysts. In these hosts the sporozoites are released and invade the intestinal mucosa, then blood vessels, where they enter the endothelial cells and undergo one or more cycles of asexual reproduction (merogony or schizogony), each resulting in the production of meronts containing merozoites. Finally the merozoites enter muscle cells and form sarcocysts containing large numbers of bradyzoites. Ingestion of the sarcocysts by opossums completes the life cycle. Until recently it was believed that development of S. neurona in horses did not proceed beyond the meront stage and that meronts occurred only in the central nervous system (brain and spinal cord). Recently, however, sarcocysts have been reported in the skeletal muscle of a young horse, indicating that they can be true intermediate hosts.
Several mammals and birds can become infected with non-intestinal S. neurona, including cats, dogs, raccoons, skunks, armadillos, sea otters, ferrets, and cowbirds. Of these hosts species some develop sarcocysts in muscle tissues and can likely be a source of infection for opossums, and thus serve as true intermediate hosts, while others simply become infected without complete parasite development to sarcocysts, and can be considered as "dead-end" or "aberrant" hosts. Neurological signs associated with S. neurona have been reported in most intermediate hosts species, although in horses, and likely in the other intermediate host species, clinical disease is much less common than is infection. Initially horses were thought to be aberrant hosts for S. neurona, but sarcocysts have recently been described in muscle tissues of a naturally infected horse. Given the broadly based diet of opossums, it is probable that additional species of intermediate host will be identified.
Epidemiology
Pathology and clinical signs
The key lesions associated with the parasite are in the central nervous system - meronts and free merozoites within neuron cytoplasm. Parasite development can occur in any part of the CNS but the spinal cord is more frequently affected than the brain. Typical pathology includes necrosis, haemorrhage, and inflammatory infiltrations surrounding neurons containing meronts and/or merozoites. The parasites can also be found unassociated with lesions.
The clinical signs of EPM depend on the location(s) in the CNS affected and include inco-ordination, stumbling, frequent interference, difficulty backing up, ataxia, head tilting, loss of reflexes, loss of sensation, muscle atrophy and sometimes sudden collapse. Neurological deficits can be unilateral - the more frequent, or bilateral. In some horses the clinical signs develop very rapidly, in others slowly. .
Diagnosis
At post-mortem the diagnosis of EPM can be based on the presence of typical lesions and organisms, although the latter may be few and difficult to find, especially in H and E stained sections. Immunohistochemistry is very useful in identifying Sarcocystis, and antibodies specific for S. neurona are available. PCR can also be used on parasite DNA recovered from tissues.
Treatment and control
Public health significance
References
Dubey, JP et al., (2001) A review of Sarcocystis neurona and equine protozoal myeloencephalitis. Veterinary Parasitology 95: 89-131.