Sarcocystis: Wikis


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Sarcocystis cyst in a sheep oesophagus. The cyst is approximately 4mm across.
Scientific classification
Kingdom: Protista
Phylum: Apicomplexa
Class: Conoidasida
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Sarcocystis

Sarcocystis accipitris
Sarcocystis alces
Sarcocystis alceslatrans
Sarcocystis ameivamastigodryasi
Sarcocystis americana
Sarcocystis arieticanis
Sarcocystis asinus
Sarcocystis atheridis
Sarcocystis aucheniae
Sarcocystis bertrami
Sarcocystis bigemina
Sarcocystis booliati
Sarcocystis bovicanis
Sarcocystis bovifelis
Sarcocystis bovihominis
Sarcocystis buffalonis
Sarcocystis cameli
Sarcocystis camelopardalis
Sarcocystis campestris
Sarcocystis chamaleonis
Sarcocystis cernae
Sarcocystis cervi
Sarcocystis cervicanis
Sarcocystis canis
Sarcocystis capracanis
Sarcocystis cornixi
Sarcocystis crotali
Sarcocystis cruzi
Sarcocystis cuniculi
Sarcocystis cymruensis
Sarcocystis danzani
Sarcocystis dasypi
Sarcocystis debonei
Sarcocystis diminuta
Sarcocystis dirumpens
Sarcocystis dispersa
Sarcocystis dubeyella
Sarcocystis dubeyi
Sarcocystis equicanis
Sarcocystis falcatula
Sarcocystis fayeri
Sarcocystis felis
Sarcocystis fusiformis
Sarcocystis gallotiae
Sarcocystis garnhami
Sarcocystis gracilis
Sarcocystis grueneri
Sarcocystis hoarensis
Sarcocystis fusiformis
Sarcocystis gallotiae
Sarcocystis gerbilliechis
Sarcocystis gigantea
Sarcocystis giraffae
Sarcocystis gongyli
Sarcocystis gracilis
Sarcocystis greineri
Sarcocystis grueneri
Sarcocystis hardangeri
Sarcocystis hemioni
Sarcocystis hemionilatrantis
Sarcocystis hericanis
Sarcocystis hircicanis
Sarcocystis hirsuta
Sarcocystis hofmanni
Sarcocystis hominis
Sarcocystis horvathi
Sarcocystis idahoensis
Sarcocystis inghami
Sarcocystis jorrini
Sarcocystis kinosterni
Sarcocystis kirkpatricki
Sarcocystis kirmsei
Sarcocystis klaseriensis
Sarcocystis kortei
Sarcocystis lacertae
Sarcocystis lamacanis
Sarcocystis leporum
Sarcocystis levinei
Sarcocystis lindemanni
Sarcocystis lindsayi
Sarcocystis medusiformis
Sarcocystis melis
Sarcocystis mephitisi
Sarcocystis miescheriana
Sarcocystis mihoensis
Sarcocystis mitrani
Sarcocystis mongolica
Sarcocystis montanaensis
Sarcocystis mucosa
Sarcocystis moulei
Sarcocystis murinotechis
Sarcocystis muris
Sarcocystis muriviperae
Sarcocystis neotomafelis
Sarcocystis nesbitti
Sarcocystis neurona
Sarcocystis odoi
Sarcocystis odocoileocanis
Sarcocystis ovicanis
Sarcocystis ovifelis
Sarcocystis oviformis
Sarcocystis ovalis
Sarcocystis phacochoeri
Sarcocystis phoeniconaii
Sarcocystis podarcicolubris
Sarcocystis poephagi
Sarcocystis poephagicanis
Sarcocystis porcifelis
Sarcocystis porcihominis
Sarcocystis rangi
Sarcocystis rangiferi
Sarcocystis rauschorum
Sarcocystis rileyi
Sarcocystis rodentifelis
Sarcocystis roudabushi
Sarcocystis scandinavica
Sarcocystis sebeki
Sarcocystis sibirica
Sarcocystis sigmodontis
Sarcocystis singaporensis
Sarcocystis speeri
Sarcocystis stehlinii
Sarcocystis stenodactylicolubris
Sarcocystis suicanis
Sarcocystis suihominis
Sarcocystis sulawesiensis
Sarcocystis sybillensis
Sarcocystis tarandi
Sarcocystis tarandivulpes
Sarcocystis tenella
Sarcocystis tilopodi
Sarcocystis turcicii
Sarcocystis turdi
Sarcocystis ursusi
Sarcocystis villivilliso
Sarcocystis wapiti
Sarcocystis zamani

Sarcocystis is a genus of protozoa. Species in this genus infect reptiles, birds and mammals. The name is dervived from Greek: sarx = flesh and kystis = bladder.

There are about 130 recognised species in this genus. Revision of the taxonomy of this genus is ongoing, and it is possible that all the currently recognised species may in fact be a single species or much smaller number of species that can infect multiple hosts.

While the majority of the species in this genus infect mammals, about a dozen are known to infect snakes.



The organism was first recognised in a mouse by Miescher in 1843.[1] His findings were not recognised as a protist initially and the literature referred to the structures he described as "Miescher's Tubules". Incidentally Miescher's son — Johann Friedrich Miescher — discovered DNA.

Life cycle

The heteroxenous (more than one obligatory host in its life cycle) life cycle of these apicomplexan parasites remained obscure until 1972 when the prey-predator relationship of its' definitive and intermediate hosts was recognised.

Oocysts are passed in the feces of an infected definitive host. The oocyst undergoes sporogony creating two sporocysts. Once this is complete oocyst itself undergoes lysis releasing the sporocysts into the environment. Sporocysts typically contain 4 sporozoites and measure 15-19 by 8-10 micrometres.

An intermediate host such as a cow or pig then ingests a sporocyst. Sporozoites are then released in the body and migrate to vessels where they undergo the first two generation of asexual reproduction. These rounds result in the development of meronts. This stage lasts about 15 to 16 days after ingestion of sporocysts. Merozoites emerge from the second generation meronts and enter the mononucleate cells where they develop by endodyogeny. Subsequent generations of merozoites develop downstream in the direction of blood flow to arterioles, capillaries, venules, and veins throughout the body subsequently developing into the final asexual generation in muscles.

Merozoites entering muscle cells round up to form metrocytes and initiate sarcocyst formation. Sarcocysts begin as unicellular bodies containing a single metrocyte and through asexual multiplication numerous metrocytes accumulate and the sarcocyst increases in size. As the sarcocyst matures, the small, rounded, noninfectious metrocytes give rise to crescent-shaped bodies called bradyzoites that are infections for the definitive host. Time required for maturation varies with the species and may take 2 months or more.

In species in which symptoms develop these typically occur 20–40 days after ingestion of sporocysts and during the subsequent migration of sporozoites through the body vessels. Acute lesions (oedema, hemorrhages and necrosis) develop in the affected tissues. The parasite has a predilection for skeletal muscle (myositis), cardiac muscle (petechial hemorrhages of cardiac muscle and serosae), and lymph nodes (oedema, necrosis and hemorrhage). These lesions are associated with maturation of second generation of meronts within the endothelial and subendothelials cells. Occasionally mononuclear infiltration or hyperemia has been observed in the lamina propria of the small intestine. After the acute phase cysts may be found in various muscular tissues, generally without pathology.

Once the intermediate host is eaten by the definitive host such as a dog or human, the parasite undergoes sexual reproduction within the gut to create macrogamonts and microgamonts. Most definitive hosts do not show any clinical sign or symptoms. Fusion of a macrogamont and a microgamont creates a zygote which develops into an oocyst. The oocyst is passed through the faeces completing the life cycle.

A second life cycle has more recently been described whereby carnivores and omnivores pass the infectious stages in their faeces. Ingestion of this material may lead to successful infection of the ingesting animal.


The taxonomy of this genus and its relationship to other protozoal genera is currently under investigation.

Related genera include: Besnoitia, Caryospora, Cystoisospora, Frenkelia, Isospora, Hammondia, Hyaloklossia, Lankesterella, Neospora and Toxoplasma.

Sarcocystis is the largest genus within the family Sarcocystidae and consists of species which infecting a range of animals including mammals, birds and reptiles. Frenkelia, another genus within this family, consists of parasites that use rodents as intermediate hosts and birds of prey as definitive hosts.

It appears that Besnoitia, Hammondia, Neospora and Toxoplasma form a single clade. Isospora also appear to belong to this clade and that this clade is a sister to Sarcocystis.

Within the genus a number of clades have been identified. These include one that contains S. dispersa, S. lacertae, S. mucosa, S. muris, S. neurona and S. rodentifelis.[2]


These protozoa are mostly found in mammals. They do not appear to infect mammals of the superorder Afrotheria and infect only two species of the Xenarthra. Because of this pattern the genus may have evolved in the Northern hemisphere from a preexisting protozoan species that infected mammals.

Alternatively because a number of Australian marsupials are also infected by this genus, marsupials may have been the original hosts of this genus and the parasites were spread to the Northern hemisphere by birds.

A third possibility is that the genus originally infected birds and was spread world wide by these hosts.

A final possibility because of the existence of life cycles where both the intermediate and final hosts are reptiles, the genus may have originated in reptiles and spread from there to other genera.

The resolution of this question awaits the outcome of further molecular studies.

Clinical notes: Human

Infection with this parasite is known as sarcosporidiosis. Because of initial confusion over the taxonomy of this parasite it was originally referred to as Isospora hominis. The older literature may refer to this organism.

Human infection is considered rare with less than one hundred published cases of invasive disease. These figure represent a gross understimate of the human burden of disease. Stool examinations in Thai laborers showed that sarcocystis infection had a prevalence of ~23%. Virtually all cases appeared to be asymptomatic which probably explains the lack of recognition. A study of 100 human tongues obtained at post mortum in Malaya revealed an infection rate of 21%. There was no sex difference and the age range was 16 to 57 years (mean 37.7 years).[3]

The first report of human infection was by Lindemannl in 1868. Although several additional reports were subsequently published, these early descriptions were not considered definitive. The first generally agreed definitive description of this disease was published in 1894 by Baraban and Saint-Remy [4]. This species was named by Rivolta after Lindemannl in 1898.

The pathology is of two types: a rare invasive form with vasculitis and myositis and an intestinal form that presents with nausea, abdominal pain, and diarrhea. While normally mild and lasting under 48 hours, the intestinal form may occasionally be severe or even life threatening. The invasive form may involve a wide variety of tissues including lymph nodes, muscles and the larynx.

The invasive forms were considered to belong to a single species - S. lindemanni - and the intestinal form due to S. hominis (from undercooked beef) or S. suihominis (from undercooked pork). The description of S. lindemanni has since been considered to be unsatisfactory and has been declared a nomem nudum (a name without a recognised species). Two species currently considered to be capable of causing human infection: S. bovihominis (S. hominis) and S. suihominis.

Infection occurs when undercooked meat is ingested. The incubation period is 9–39 days. Human outbreaks have occurred in Europe. Rats are a known carrier.

Because infection is rarely symptomatic, treatment is rarely required. There have been no published trials so treatment remains empirical. Agents that have been used include albendazole, metronidazole and cotrimoxazole for myositis. Corticosteroids have also been used for symptomatic relief.

Infection can be prevented by cooking the meat before eating. Alternatively freezing the meat at -5C for several days before ingestion will kill the sporocysts.

Clinical notes: Other

Sarcocysts within pig skeletal muscle. Note the readily visible striated border.

Four recognised species infect cattle: S. bovifelis, S. bovihominis (S. hominis) S. cruzi (S. bovicanis) and S. hirsuta. S. cruzi is the only species known to be pathogenic in cattle. A number of clinical syndromes have been reported in connection with this parasite: eosinophilic myositis; abortions, stillbirths and deaths in pregnant cows; two cases of necrotic encephalitis in heifers have also been reported. Typical clinical signs of acute bovine sarcocystosis are: anorexia, pyrexia (42C or more), anemia, cachexia, enlarged palpable lymph nodes, excessive salivation and loss of hair at the tip of the tail.

Sheep may be infected by four recognised species of Sarcocystis: S. arieticanis and S. tenella (S. ovicanis) are pathogenic; S. gigantea (S. ovifelis) and S. medusiformis are non-pathogenic. Infection with these parasites is common in the US with over 80% of sheep examined showing evidence of infection[5]. S. arieticanis and S. tenella both produce extra intestinal disease. Anemia, anorexia, ataxia, and abortions are the chief clinical signs. Myositis with flacid paralysis has been reported as a consequence of infection. Ovine protozoan myeloencephalitis is a recognised syndrome that may occur in outbreaks. The usual pathological findings in such cases are multifocal spinal cord white matter oedema and necrosis, glial nodules and mild to moderate nonsuppurative encephalomyelitis. The diagnosis may be established finding protozoan bodies (12.7-23.0 micrometres) that stain immunocytochemically for Sarcocystis epitopes.

Four recognised species infect pigs: S. medusiformis, S. meischeriana (S. suicanis), S. porcifelis and S. suihominis. S. porcifelis is pathogenic for pigs causing diarrhea, myositis and lameness.

Five species infect horses: S. asinus, S. bertrami, S. equicanis, S. fayeri and S. neurona (S. falcatula). All utilize canids as definitive hosts: transplacental infection has also been reported. S. neurona causes equine protozoal myeloencephalitis. Exposure to this parasite appears to be common in the United States with serological surveys indicating that 50-60% percent of all horses in the Midwest United States have been exposed to it. Clinical signs include gait abnormalities including ataxia, knuckling and crossing over. Muscle atrophy, usually unilateral, may occur. The lesions are typically focal. Brain-stem involvement is common. Depression, weakness, head tilt and dysphagia also occur.

S. fayeri may cause myositis in horses.

Fatal infection of an alpaca (Lama pacos) with an unnamed species has been reported. Findings included disseminated eosinophilic myositis, abortion and haemoabdomen. The myositis was associated with hameorrhage, necrosis and degeration.[6] Infection by S. tilopodi of muscle tissue in the Guanaco has been reported.[7]

S. hemionilatrantis infects mule deer. Death from experimental inoculation have been reported.

These parasites can also infect birds producing three different clinical forms: an acute pulmonary disease, muscular disease and neurological disease. Symptoms include lethargy, shortness of breath, tail bobbing, yellow tinted droppings and sudden death.

The presence of the cysts in the muscle of wild birds is known as "rice breast".

Incidence in animals

Infection with Sarcocystis is common. Rates in pigs vary: 18% in Iowa,[8], 27% in the Philippines [9], 43% in Spain [10], 57% in Uruguay [11], and 68% in India [12] The infection rate in sheep is commonly above 90%.[10][13][14][15] Camels have a similarly high incidence of infection.[13][15] Rates above 80% are known in cattle and goats.[13][14] The incidence in water buffaloes, yak and hainag exceeds 80%[13][15] while the incidence in horses, donkeys and chickens is lower.[14][15]


There are several other genera of heteroxenous and cyst-forming coccidia including Besnoitia, Cystoisospora, Frenkelia, Hammondia, Neospora and Toxoplasma. Related but monoxenous spore forming genera include Isospora. Differentiating these genera from Sarcocystis in diagnostic material may be difficult without immunochemical stains.

The diagnosis is usually made post mortum by examination of the skeletal muscle. In some species the cysts may be visible to the naked eye (ducks, mice, rabbits and sheep) but in most microscopic examination is required. Ante mortum diagnosis may be made with the use of dermal sensitivity testing or complement fixation tests. Muscle biopsy is also diagnostic but this is much less commonly used.

Oocysts with two sporocysts or individual sporocysts in human feces are diagnostic of intestinal infection. These first appear 14 to 18 days after ingesting beef (S. hominis), and 11 to 13 days after ingesting pork (S. suihominis). Flotation based on high-density solutions incorporating sodium chloride, cesium chloride, zinc sulfate, sucrose, Percoll, Ficoll-Hypaque or other such density gradient media is preferred to formalin-ethyl acetate or other sedimentation methods. Sporocysts of S. hominis average 9.3 by 14.7 micrometres and those of S. suihominis average 10.5 by 13.5 micrometres. Because of the overlap in size, size alone is not reliable as a diagnostic criterion of the species. Confirmatory staining with the periodic acid-Schiff (PAS) can be performed as the walls stain positively. PCR amplification of the rRNA may also be used.

The walls of the sarcocyst may be helpful in species diagnosis with 24 wall types identified in 62 species. S. hominis and S. suihominis both have walls of type 10. The wall of S. hominis is up to 6 micrometres thick and appears radially striated from villar protrusions up to 7 micrometres long. Its bradyzoites are 7 to 9 micrometres long. The wall of S. suihominis is 4 to 9 micrometres thick, with villar protrusions up to 13 micrometres long. Its bradyzoites are 15 micrometres long.


Current treatments are not entirely satisfactory. Amprolium (100 mg/kg, sid for 30 days), fed prophylactically, reduced illness in cattle inoculated with S. cruzi. Prophylactic administration of amprolium or salinomycin also protected experimentally infected sheep.

In horses treatment has been confined to dihydrofolate reductase inhibitors such as the sulfonamides and pyrimethamine. Sulfadiazine (20 mg/kg orally) once or twice a day is a commonly used. Infected horses should also be placed on pyrimethamine at the dose of 1.0 mg/kg given once a day orally for 120 days or longer. Diclazuril and Toltrazuril and other coccidiostats are being evaluated to treat EPM.


No vaccines are currently known. Experimentally inoculated pigs appear to develop a persistent immunity so a vaccine may be possible.

Host-parasite relations

The parasite's life cycle typically involves a predator and a prey animal. A single species may infect multiple prey or predator animals. In at least 56 species definitive and intermediate hosts are known. Many species are named after their recognised hosts.

A listing of the known host-parasite relations can be found on the page Sarcocystis: Host-parasite relations.


Hoareosporidium is now considered a synonym of Sarcocystis.

The original type species was Sarcocystis miescheriana. Its description has since been considered less than satisfactory and S. muris has been proposed as the type species.

S. turdi may not be a valid species.

Isospora bigemina has been reclassified as Sarcocystis bigemina.

Isospora hominis has been reclassified as Sarcocystis hominis.



S. bertrami is a synonym of S. equicanis.

S. bovihominis is a synonym of S. hominis.

S. cruzi is a synonym of S. bovicanis.

S. gigantea is a synonym of S. ovifelis.

S. hirsuta is a synonym of S. bovifelis.

S. idahoensis and S. roudabushi may be the same species.

S. miescheriana is a synonym of S. suicanis

S. neurona is a junior synonym of S. falcatula. S. neuroma is the more commonly used name for this species.

S. poephagi may be the same species as S. hirsuta.

S. poephagicanis may be the same species as S. cruzi.

S. tenella is a synonym of S. ovicanis.


  1. ^ Miescher, F. (1843) Ueber eigenthiimliche Schlauche in den Muskeln einer Hausmaus. Ber. u.d. Verhandl. Naturf. Ges. Basel 5: 198-202
  2. ^ Elsheikha H.M., Lacher D.W., Mansfield L.S. (2005) Phylogenetic relationships of Sarcocystis neurona of horses and opossums to other cyst-forming coccidia deduced from SSU rRNA gene sequences. Parasitol. Res. 97(5):345-357
  3. ^ Wong K.T., Pathmanathan R. (1992) High prevalence of human skeletal muscle sarcocystosis in south-east Asia. Trans. R. Soc. Trop. Med. Hyg. 86(6):631-632.
  4. ^ Baraban M. Le and Saint-Remy M. G.(1894) Sur un cas de tubes psorospermiques observes chez 1' homme. Compt. Rend. Soc. de Biol. 46: 231-203
  5. ^ Dubey J.P., Lindsay D.S., Speer C.A., Fayer R., Livingston C.W. Jr. (1988) Sarcocystis arieticanis and other Sarcocystis species in sheep in the United States. J. Parasitol. 74(6):1033-1038
  6. ^ La Perle K.M., Silveria F., Anderson D.E., Blomme E.A. (1999) Dalmeny disease in an alpaca (Lama pacos): sarcocystosis, eosinophilic myositis and abortion. J. Comp. Pathol. 121(3):287-293
  7. ^ C. Michael Hogan. 2008. Guanaco: Lama guanicoe,, ed. N. Strömberg
  8. ^ Dubey J.P., Powell E.C. (1994) Prevalence of Sarcocystis in sows from Iowa. Vet. Parasitol. 52(1-2):151-155
  9. ^ Claveria F.G., De La Peña C., Cruz-Flores M.J., Saleque A., Bhatia B.B. Freyre A., Chifflet L., Mendez J. (2001) Sarcocystis miescheriana infection in domestic pigs (Sus scrofa) in the Philippines. J. Parasitol. 87(4):938-939.
  10. ^ a b Pereira A., Bermejo M. (1988) Prevalence of Sarcocystis cysts in pigs and sheep in Spain. Vet. Parasitol. 27(3-4):353-355
  11. ^ Freyre A, Chifflet L., Mendez J. Sarcosporidian infection in pigs in Uruguay. Vet. Parasitol. 41(1-2):167-171
  12. ^ Saleque A., Bhatia B.B. (1991)Prevalence of Sarcocystis in domestic pigs in India. Vet. Parasitol. 40(1-2):151-153
  13. ^ a b c d Latif B.M., Al-Delemi J.K., Mohammed B.S., Al-Bayati S.M., Al-Amiry A.M. (1999)Prevalence of Sarcocystis spp. in meat-producing animals in Iraq. Vet. Parasitol. 84(1-2):85-90
  14. ^ a b c Woldemeskel M., Gebreab F. (1996) Prevalence of sarcocysts in livestock of northwest Ethiopia. Zentralbl Veterinarmed B. 43(1):55-58.
  15. ^ a b c d Fukuyo M., Battsetseg G., Byambaa B. (2002) Prevalence of Sarcocystis infection in meat-producing animals in Mongolia. Southeast Asian J. Trop. Med. Public Health. 33(3):490-495.

External links

See also

Dr. Michael Kent. Oregon State University. "Sarcocystis". May 5, 2006.

Simple English

The Sarcocystis is a genus of protozoa, a kind of disease. Species in this genus can infect reptiles, birds, and mammals, and sometimes pigs as well. The name came from the Greek language, sarx, which meant flesh, and kystis, which meant bladder. The organism was first found in a mouse by Miescher in 1843.


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