Equine protozoal myeloencephalitis

Equine protozoal myeloencephalitis

J P DUBEY

Introduction

Equine protozoal myeloencephalitis (EPM) is a neurological disease of horses in the Americas caused by Sarcocystis neurona. The clinical syndrome was recognized in the USA by Rooney86 in the 1960s and protozoa were first demonstrated in lesions in 1974.2, 12, 26 Initially, the protozoa were considered to be Toxoplasma gondii.12, 37, 93 A protozoan was first cultured in vitro from the spinal cord of an affected horse in 1991 and was named Sarcocystis neurona by Dubey et al.27 The development of a serological test in 199356 based on antigen prepared from in vitro cultured S. neurona merozoites led to the discovery that S. neurona infection is common in horses in the Americas.3, 4, 34, 45, 100 The history of EPM and its biology have recently been reviewed.37

Aetiology and life cycle

Sarcocystis neurona is a coccidian belonging to the family Sarcocystidae. Opossums of the genus Didelphis (D. virginiana and D. albiventris) are the definitive hosts and the horse is an aberrant intermediate host (Figure 24.1).21, 25, 35, 36, 49, 52 Sea otters and several other mammals are also aberrant intermediate hosts.37

The natural intermediate hosts of S. neurona are unknown. The sarcocyst stage of S. neurona and an experimental intermediate host were recently identified.41 Laboratoryraised cats fed sporocysts from a naturally infected opossum developed sarcocysts in their skeletal muscles. The sarcocysts were microscopic (about 700 μm long) with a 1 to 2 μm thick cyst wall. The bradyzoites were slender and tiny (about 5 μm long). Laboratory-raised opossums fed infected cat muscles shed sporocysts. The sporocysts were 10 × 8 μm in size.

A sexual cycle occurs in the lamina propria of the intestines of opossums. After gametogony, oocysts sporulate in the lamina propria of the small intestine and are excreted in the faeces. Sporocysts contain four sporozoites and a residual body.

Horses become infected by ingesting food and water contaminated with sporocysts. The only stages of S. neurona found in the horse are schizonts and merozoites which are confined to the brain and spinal cord27 (Figure 24.2). The time period and the route of dissemination of the parasite in the horse are unknown. In an experimental aberrant host, the immunodeficient gamma interferon knockout (KO) mouse, sporozoites excyst in the small intestine and can be found in peripheral blood within one day of feeding sporocysts.22, 23 Sarcocystis neurona first multiplies in visceral tissues and eventually resides in the central nervous system (CNS).22

Sarcocystis neurona schizonts are found in neurons, various glial cells and resident macrophages in the brain,26, 53, 94 and divide by endopolygeny.94 In endopolygeny, the parasite nucleus becomes multilobed and eventually each nuclear lobe is incorporated into two budding merozoites (Figure 24.3 and Figure 24.4). Schizonts in tissue sections are approximately 5–35 × 5–20 μm in size and contain up to 40 merozoites, often arranged in a rosette sometimes around a residual body37 (Figure 24.4). Merozoites are approximately 5 × 1 μm in size. Ultrastructurally, S. neurona schizonts are located in the host cell cytoplasm without a parasitophorous vacuole (Figure 24.4). Merozoites contain conoid, micronemes, a nucleus, a prominent lipid body posterior to the nucleus, but no rhoptries37, 94 (Figure 24.4).

Epidemiology

Equine protozoal myeloencephalitis has been reported only in horses born and raised in the Americas, including Canada, the USA, Panama and Brazil.1, 5–8, 18, 26, 38, 39, 46, 48, 51, 55, 57, 61, 63, 72–74, 81, 89 Although fatal EPM has been diagnosed in other parts of the world, including South Africa, 85 it occurs only in horses imported from the Americas. The distribution of EPM follows the geographic range of the opossum (D. virginiana) in North America and its relative D. albiventris in Central and South America.36

Figure 24.1  Life cycle of Sarcocystis neurona

Figure 24.2  Sarcocystis neurona in sections of the spinal cord of a horse. Haematoxylin and eosin stain

  1. Perivascular infiltration and necrosis. Two infected neurons (arrows) but parasites are barely visible at this magnification
  2. Neuron containing several schizonts (arrows)
  3. Four schizonts (arrows) in various stages of development
  4. Intracellular and extracellular individual merozoites (arrow heads)

Serological surveys indicate that about 30 to 50 per cent of horses in the USA, Brazil, and Argentina have been exposed to S. neurona. 3, 4, 34, 45, 99 Although antibodies to S. neurona have been found in horses, donkeys, and mules,88 bona fide clinical disease has not been reported in animals other than horses, with the exception of a Grant’s zebra (Equus burchelli bohmi)in a zoo.40, 80 The prevalence of S. neurona antibody increases with age and is not related to breed, sex, and category (race/draught) of the horse.88 Although horses of any breed or age may suffer from EPM, clinical disease occurs most frequently in three- to five-year-old Thoroughbreds and Standardbreds. There are no documented cases of congenital S. neurona infection.

Sarcocystis neurona-like organisms have been found in the CNS of raccoons (Procyon lotor)29, 31, 44, 96, 98 (Figure 24.5 and Figure 24.6), mink (Mustela vison),32 skunks (Mephitis mephitis),30 a domestic cat,33 Pacific harbour seals (Phoca vitulina richardsi),65 Southern sea otters...

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