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Overview of Sarcocystosis

By Gastón A. Moré, MV, DVM, Laboratorio de Inmunoparasitología, Universidad Nacional de La Plata, Argentina

In sarcocystosis, the endothelium and muscles and other soft tissues are invaded by Apicomplexan protozoans of the genus Sarcocystis. As the name implies, Sarcocystis spp (from Greek sarkos: muscle and kystis: cysts) form cysts in muscles of various intermediate hosts—people, horses, cattle, sheep, goats, pigs, birds, rodents, camelids, wildlife, and reptiles. The cysts vary in size from a few micrometers to centimeters, depending on the host and species. Most Sarcocystis spp infections are distributed worldwide.

Etiology, Transmission, and Pathogenesis:

Sarcocystis spp normally develop in two-host cycles consisting of an intermediate host (prey) and the final host (predator). Species-specific prey-predator life cycles have been demonstrated for cattle-dog (S cruzi), cattle-cat (S hirsuta), cattle-human (S hominis), sheep-dog (S capracanis, S hircicanis), sheep-cat (S gigantea, S medusiformis), goat-dog (S capracanis, S hircicanis), goat-cat (S moulei), pig-dog (S meischeriana), pig-human (S suihominis), pig-cat (S porcifelis), horse-dog (S fayeri), llama-dog (S aucheniae), pigeon-hawk (S calchasi), and others. S sinensis has been detected affecting muscles of buffalo and cattle, but its final host remains unknown. Some wildlife may serve as intermediate hosts (such as raccoons, rodents, birds, etc) or final hosts (coyotes, opossums, snakes, etc) for some species of Sarcocystis.

About 1–2 wk after ingesting muscle tissue that contains Sarcocystis cysts (sarcocysts), the final host begins to shed infective sporocysts in the feces; shedding continues for several months. After ingestion of sporocysts by a suitable intermediate host, sporozoites are liberated and initiate development of schizonts in vascular endothelia of mesenteric arterioles and mesenteric lymph nodes. Merozoites are liberated from the mature schizonts and produce a second generation of endothelial schizonts in capillaries from several organs. Merozoites from this second generation subsequently invade the muscle fibers and develop into the typical sarcocysts. Initially, sarcocysts contain only a few metrocytes—round, noninfective parasites that give rise to the banana-shaped infective bradyzoites found in mature cysts beginning 2–3 mo after infection. Sarcocysts of some species are easily visible with the unaided eye (S aucheniae, S hirsuta, S gigantea). The presence of such sarcocysts as well as those of zoonotic species can cause condemnation of the carcass during meat inspection. Sarcocysts of other species remain microscopic, even though tremendous numbers of cysts may be present in the muscles. The identification of different species could be achieved by molecular studies and cyst wall morphology (mainly ultrastructure).

S cruzi produce microscopic cysts, principally in myocardium, and can affect 100% of some cattle populations. S hirsuta has been primarily responsible for cattle condemnation for visible sarcocysts. S meischeriana is the most important species affecting pigs and may affect meat quality. Macroscopic cysts of S aucheniae are an important cause of condemnation of llama meat. Sarcocysts are easily recovered from esophagus, diaphragm, and heart muscle.

In general, Sarcocystis spp infections are considered of low pathogenicity except induced infection with S cruzi sporocysts from canine feces, which may cause acute disease in calves; eosinophilic myositis in cattle; and abortions, stillbirths, and deaths in pregnant cows. Two cases of necrotic encephalitis in heifers have been reported. Similar pathogenicity has been demonstrated for S tenella in lambs and ewes and for S miescheriana in pigs. An outbreak of myositis affecting 20 ewes with flaccid paralysis was a result of heavy Sarcocystis infection. Immune status of the host and the dose of sporocysts may be the most important factors for the development of clinical disease. Pathologic changes in myocardium and skeletal muscles were more pronounced in cows with lymphatic leukemia. “Immunization” using small doses of sporocysts appears to prevent development or reduce severity of clinical disease in sheep when challenged with large doses later (premunitive immunity). In dogs, a longer prepatent period and shortened patent period resulted after repeated infection. Pigs can also have persistent acquired immunity after immunization infections.

People may also serve as intermediate hosts and suffer myositis and vasculitis, but this tissue phase is rare, and the source of such human infection has never been determined. Human intestinal illness as final host, with clinical signs of nausea, abdominal pain, loss of appetite, vomiting, and diarrhea that lasted as long as 48 hr, has followed ingestion of sarcocysts of S suihominis in uncooked pork and S hominis in uncooked beef. Differentiation between cysts of S sinensis and S hominis in beef is extremely important to avoid unjustified rejections.

Clinical Findings:

Sarcocystis spp infections are quite prevalent in farm animals; however, there have been few outbreaks of clinical disease. Most animals are asymptomatic, and the parasite is discovered only at slaughter. In cattle severely affected by S cruzi, the signs include fever, anorexia, cachexia, decreased milk yield, diarrhea, muscle spasms, anemia, loss of tail hair, hyperexcitability, weakness, prostration, and death. Cows infected in the last trimester of pregnancy may abort. After recovery from acute illness, calves failed to grow well and eventually died in a cachectic state. Anemia, hepatitis, and myocarditis were the primary lesions in acute ovine sarcocystosis after experimental challenge with S tenella sporocysts. Cases of encephalomyelitis in sheep were associated with a Sarcocystis sp infection. After recovery from acute illness, some sheep may lose their wool. S tenella may also induce abortion in sheep. At necropsy, acutely affected animals have hemorrhage of the serous membranes of the viscera and myocardium. Sarcocystis spp infections are probably most important in growing ruminants and swine, in which they can result in subclinical anemia and reduced weight gain.

Equine protozoal myeloencephalitis (EPM, see Equine Protozoal Myeloencephalitis) is caused principally by S neurona in American horses. Only asexual stages of this parasite have been found in horses, and they may be located in neurons and leukocytes of the brain and spinal cord. Opossums (Didelphis virginiana and D albiventris) are its definitive hosts. Clinical signs in horses include gait abnormalities such as ataxia, knuckling, and crossing over. Muscle atrophy of the hindlimb, which is usually unilateral, is frequent. The lesions are typically focal, and brain-stem involvement is common. Depression, weakness, head tilt, and dysphagia are other possible signs. EPM can mimic many neurologic diseases. Horses may also develop a myopathy. Multifocal myositis has been reported and is possibly due to another Sarcocystis species with horses as the intermediate host, S fayeri. PCR is an important diagnostic method. S calchasi can produce pigeon protozoal encephalitis with severe brain lesions and muscle cysts at the same time.


Livestock become infected by sporocysts from the feces of carnivores. Because most adult cattle, sheep, and many pigs harbor cysts in their muscles, dogs and other carnivores should not be allowed to eat raw meat, offal, or dead animals. Supplies of grain and feed should be kept covered; dogs and cats should not be allowed in buildings used to store feed or house animals. Amprolium (100 mg/kg/day for 30 days), fed prophylactically, reduced illness in cattle inoculated with S cruzi. Prophylactic administration of amprolium or salinomycin also protected experimentally infected sheep. Therapeutic treatment of the chronic stage (tissue cysts) has been ineffective. Vaccines are not available. Experimental work demonstrated that infected pork and beef could be made safe for consumption by cooking at 70°C (158°F) for 15 min or by freezing at –4°C (24.8°F) for 2 days or –20°C (-4°F) for 1 day.

Pyrimethamine and sulfadiazine (1 mg/kg/day and 20 mg/kg/day, respectively, for 120 days or longer) is the traditional therapy to treat horses with EPM. Diclazuril and toltrazuril (5 mg/kg) are potentially useful prophylactic agents against S neurona.

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