Sarcocystis is a genus of parasites, the majority of species infecting mammals, and some infecting reptiles and birds.

The life-cycle of a typical member of this genus involves two host species, a definitive host and an intermediate host. Often the definitive host is a predator and the intermediate host is its prey. The parasite reproduces sexually in the gut of the definitive host, is passed with the feces and ingested by the intermediate host. There it eventually enters muscle tissue. When the intermediate host is eaten by the definitive host, the cycle is completed. The definitive host usually does not show any symptoms of infection, but the intermediate host does.

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

The name Sarcocystis is dervived from Greek: sarx = flesh and kystis = bladder.

"Sarcocystis" cyst in a sheep oesophagus. The cyst is approximately 4 mm across.
Sarcocystis cyst in a sheep oesophagus. The cyst is approximately 4 mm across.
Scientific classification
(unranked): SAR
Infrakingdom: Alveolata
Phylum: Apicomplexa
Class: Conoidasida
Order: Eucoccidiorida
Family: Sarcocystidae
Genus: Sarcocystis
Lankester, 1882
  • 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 calchasi
  • 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 fulicae
  • Sarcocystis fusiformis
  • Sarcocystis gallotiae
  • Sarcocystis garnhami
  • Sarcocystis gracilis
  • Sarcocystis grueneri
  • Sarcocystis halieti
  • 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 hjorti
  • Sarcocystis hofmanni
  • Sarcocystis hominis
  • Sarcocystis horvathi
  • Sarcocystis iberica
  • Sarcocystis idahoensis
  • Sarcocystis inghami
  • Sarcocystis jamaicensis
  • Sarcocystis jorrini
  • Sarcocystis kinosterni
  • Sarcocystis kirkpatricki
  • Sarcocystis kirmsei [1]
  • Sarcocystis klaseriensis
  • Sarcocystis kortei
  • Sarcocystis lacertae
  • Sarcocystis lamacanis
  • Sarcocystis leporum
  • Sarcocystis levinei
  • Sarcocystis lindemanni
  • Sarcocystis lindsayi
  • Sarcocystis linearis
  • Sarcocystis medusiformis
  • Sarcocystis melis
  • Sarcocystis mephitisi
  • Sarcocystis miescheriana
  • Sarcocystis mihoensis
  • Sarcocystis mitrani
  • Sarcocystis mongolica
  • Sarcocystis montanaensis
  • Sarcocystis morae
  • 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 silva
  • Sarcocystis singaporensis
  • Sarcocystis speeri
  • Sarcocystis stehlinii
  • Sarcocystis stenodactylicolubris
  • Sarcocystis strixi
  • Sarcocystis suicanis
  • Sarcocystis suihominis
  • Sarcocystis sulawesiensis
  • Sarcocystis sybillensis
  • Sarcocystis tarandi
  • Sarcocystis tarandivulpes
  • Sarcocystis tenella
  • Sarcocystis tilopodi
  • Sarcocystis turcicii
  • Sarcocystis turdi
  • Sarcocystis ursusi
  • Sarcocystis venatoria
  • Sarcocystis villivilliso
  • Sarcocystis wapiti
  • Sarcocystis zamani


The organism was first recognised in a mouse by Miescher in 1843.[2] His findings were not initially interpreted as involving a protist, and the literature referred to the structures he described as "Miescher's Tubules". Incidentally, Miescher's son — Johann Friedrich Miescher — discovered DNA. Similar structures were found in pig muscle in 1865 but these remained unnamed until 1899, when the name Sarcocystis miescheriana was proposed for them.

Initially, it was unclear whether these organisms were fungi or protozoa. This uncertainty was resolved in 1967 when electron microscopic studies showed that they were protozoa, related to Toxoplasma and Eimeria. The life cycle remained unknown until 1970, when bradyzoites from sarcocysts in bird muscles were inoculated into cultured mammalian cells and seen to undergo development into sexual stages and oocysts. Transmission studies with Sarcocystis of cattle (then considered a single species — Sarcocystis fusiformis) in dogs, cats and humans revealed three morphologically distinct species, which were named Sarcocystis bovicanis, Sarcocystis bovifelis and Sarcocystis bovihominis. This and post-1972 research on Sarcocystis was reviewed during the same decade.[3] The coverage of concepts in this review chapter is broader than reflected by its title and much of the important information therein does not appear in more recent publications.

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.[4] The life cycle of about 60 of these species is now known.

In outline gametogony and sporogony occur in the intestine of the definitive host while both schizogony which occurs in various tissues and the formation of sarcocysts (containing bradyzoites and metrocytes) occurs principally in the muscles of the intermediate host. In some cases a single species may act as both the definitive and intermediate host.

Oocysts are passed in the feces of an infected definitive host. The oocyst undergoes sporogony creating two sporocysts. Once this is complete the 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 (also known as "bradyzoic merozoites"[5]) that are infectious for the definitive host. The 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.


Although sarcocysts were first reported in the muscles of birds by Kuhn in 1865 not until 1977 was the first life cycle involving a bird (Gallus gallus) and a carnivore (Canis familiaris) described by Munday et al.[6] In 1986 the first life cycle involving birds as both the definitive (Northern goshawk — Accipiter gentilis) and intermediate (Atlantic canary — Serinus canaria) hosts was described by Cern and Kvasnovsk.[7]


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. Within this clade Toxoplasma and Neospora appear to be sister clades. Isospora also appear to belong to this clade and this clade is a sister to Sarcocystis. Frenkelia appears to be very closely related to Sarcocystis.

Several molecular studies have suggested that Frenkelia is actually a species of Sarcocystis. This genus was distinguished from Sarcocystis on the basis of its tendency to encyst within the brain rather than within muscle. This distinction may not be taxonomically valid.

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.[8] Frenkelia also groups with this clade.


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: 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 (approximately 46 cases reported by 1990). These figures represent a gross underestimate of the human burden of disease.

The extremes of age reported to date are a 26-day-old infant and a 75-year-old man. Infections have been reported from Africa, Europe (Germany, Spain and Poland), the United States (California), Central and South America, China, India, Tibet, Malaysia and Southeast Asia.

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 mortem 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).[9]

An outbreak affecting 93 persons was reported in 2012 in Malaysia.[10] Sarcocystis nesbitti was confirmed to the cause in several cases.


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.[11] This species was named by Rivolta after Lindemannl in 1898.

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 are currently considered to be capable of causing human infection: S. bovihominis (S. hominis) and S. suihominis. Other species including Sarcocystis nesbitti have occasionally been reported infecting humans.

Route of infection

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.

It has been suggested that contaminated water may be able to cause infection but this presently remains a theoretical possibility.


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.

Clinical features

In volunteer studies with infected beef symptoms appeared 3–6 hours after eating. These included anorexia, nausea, abdominal pain, distension, diarrhea, vomiting, dyspnoea and tachycardia. All symptoms were transient and lasted about 36 hours. In a second series symptoms — abdominal pain, distension, watery diarrhea and eosinophilia — appeared at 1 week and resolved after 3 weeks.

Clinical cases have been associated with acute fever, myalgias, bronchospasm, pruritic rashes, lymphadenopathy, subcutaneous nodules associated with eosinophilia, elevated erythrocyte sedimentation rate and elevated creatinine kinase levels. Symptoms may last as long as five years. Segmental necrotizing enteritis has been reported on one occasion.


Definitive diagnosis by biopsy of an infected muscle. Sarcocysts are identifiable with hematoxylin and eosin. The PAS stain may be helpful but variable uptake of stain is common. Along with the sarcocysts inflammatory cells may be found. Other findings include myositis, myonecrosis, perivascular and interstitial inflammation, vasculitis and eosinophilic myositis.


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.

Amprolium and salinomycin was effective in preventing severe illness and death in experimentally infected calves and lambs. These agents have not been tried in humans to date.


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: Non human

Sarcocystis in pig muscle
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.[12]

Sheep may be infected by four recognized 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.[13] S. arieticanis and S. tenella both produce extra intestinal disease. Anemia, anorexia, ataxia, and abortions are the chief clinical signs. Myositis with flaccid 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.In modern times are used to dismantle fallen Sarcocystis protozoa as they are administered in counterfeit ampoules or so-called nano needle packs.

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.[14] Infection by S. tilopodi of muscle tissue in the Guanaco has been reported.[15]

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

H&E micrograph showing Sarcocystis in a 3-year-old sheep cardiac muscle tissue (40X)

Infection with Sarcocystis is common. Rates in pigs vary: 18% in Iowa,[16] 27% in the Philippines,[17] 43% in Spain,[18] 57% in Uruguay,[19] and 68% in India [20] The infection rate in sheep is commonly above 90%.[18][21][22][23] Camels have a similarly high incidence of infection.[21][23] Rates above 80% are known in cattle and goats.[21][22] The incidence in water buffaloes, yak and hainag exceeds 80%[21][23] while the incidence in horses, donkeys and chickens is lower.[22][23]


The diagnosis is usually made post mortem 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 mortem 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. Heated safranin + methylene blue has been used for staining as well.[24] PCR amplification of the rRNA may also be used.

Cell walls

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.

Differential diagnosis

There are several other genera of heteroxenous and cyst-forming coccidia[25] including Besnoitia, Cystoisospora, Frenkelia, Hammondia, Neospora and Toxoplasma.[26] Related but monoxenous spore forming genera include Isospora. Differentiating these genera from Sarcocystis in diagnostic material may be difficult without immunochemical stains.


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.


S. neurona is the subject of an ongoing (as of September 2011) genome project.


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. 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.

See also


  1. ^ Garnham, P. C. C.; Duggan, A. J.; Sinden, R. E. (1979). "A new species of Sarcocystis in the brain of two exotic birds". Annales de Parasitologie Humaine et Comparée. 54 (4): 393–400. doi:10.1051/parasite/1979544393. open access
  2. ^ Miescher, F. (1843). "Ueber eigenthiimliche Schlauche in den Muskeln einer Hausmaus. Ber. u.d". Verhandl. Naturf. Ges. Basel. 5: 198–202.
  3. ^ Markus, MB (1978). "Sarcocystis and sarcocystosis in domestic animals and man". Advances in Veterinary Science and Comparative Medicine. 22: 159–193. PMID 104559.
  4. ^ Markus, MB; Killick-Kendrick, R; Garnham, PCC (1974). "The coccidial nature and life cycle of Sarcocystis". Journal of Tropical Medicine and Hygiene. 77 (11): 248–259. PMID 4219030.
  5. ^ Markus, MB (1987). "Terms for coccidian merozoites". Annals of Tropical Medicine and Parasitology. 81 (4): 463. doi:10.1080/00034983.1987.11812147. PMID 3446034.
  6. ^ Munday BL, Humphrey JD, Kila V (1977). "Pathology produced by, prevalence, of, and probable life-cycle of a species of Sarcocystis in the domestic fowl". Avian Dis. 21 (4): 697–703. doi:10.2307/1589428. JSTOR 1589428. PMID 415727.
  7. ^ Cerná Ž, Kvašňovská Z (1986). "Life cycle involving bird-bird relation in sarcocystis coccidia with the description of Sarcocystis accipitris sp.n" (PDF). Folia Parasitologica. 33 (4): 305–9.
  8. ^ Elsheikha HM, Lacher DW, Mansfield LS (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): 345–57. doi:10.1007/s00436-005-1396-5. PMID 16133298.
  9. ^ Wong KT, Pathmanathan R (1992). "High prevalence of human skeletal muscle sarcocystosis in south-east Asia". Trans. R. Soc. Trop. Med. Hyg. 86 (6): 631–2. doi:10.1016/0035-9203(92)90161-5. PMID 1287922.
  10. ^ Abubakar S, Teoh BT, Sam SS, Chang LY, Johari J, Hooi PS, Lakhbeer-Singh HK, Italiano CM, Omar SF, Wong KT, Ramli N, Tan CT (2013). "Outbreak of human infection with Sarcocystis nesbitti, Malaysia, 2012". Emerging Infect. Dis. 19 (12): 1989–91. doi:10.3201/eid1912.120530. PMC 3840867. PMID 24274071.
  11. ^ Baraban M. Le and Saint-Remy M. G.(1894) Sur un cas de tubes psorospermiques observés chez l'homme. Compt. Rend. Soc. Biol. 46: 231-203
  12. ^ Markus, MB; Van Der Lugt, JJ; Dubey, JP (2004). Sarcocystosis. Chapter 20 in: Infectious Diseases of Livestock (eds JAW Coetzer & RC Tustin), Volume 1 (2nd ed.). Oxford University Press. pp. 360–375. ISBN 978-0195782028.
  13. ^ Dubey JP, Lindsay DS, Speer CA, Fayer R, Livingston CW (1988). "Sarcocystis arieticanis and other Sarcocystis species in sheep in the United States". J. Parasitol. 74 (6): 1033–8. doi:10.2307/3282228. JSTOR 3282228. PMID 3142990.
  14. ^ La Perle KM, Silveria F, Anderson DE, Blomme EA (1999). "Dalmeny disease in an alpaca (Lama pacos): sarcocystosis, eosinophilic myositis and abortion". J. Comp. Pathol. 121 (3): 287–93. doi:10.1053/jcpa.1999.0321. PMID 10486166.
  15. ^ C. Michael Hogan. 2008. Guanaco: Lama guanicoe,, ed. N. Strömberg Archived 2011-03-04 at the Wayback Machine
  16. ^ Dubey JP, Powell EC (1994). "Prevalence of Sarcocystis in sows from Iowa". Vet. Parasitol. 52 (1–2): 151–5. doi:10.1016/0304-4017(94)90045-0. PMID 8030181.
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External links

Besnoitia bennetti

Besnoitia bennetti is a parasite that can cause besnoitiosis infections in donkeys. The range of this organism ranges from Africa to the United States. B. bennettii shares similar characteristics with Toxoplasma, Neospora, and Sarcocystis genera. Lab work onB. bennetti is conducted at biosafety level 1.


The Caulleryellidae are a family of parasites in the phylum Apicomplexa. Species in this family mostly infect dipteran larvae.


Eimeriorina is a suborder of phylum Apicomplexa.All species in this clade are homoxenous or facultatively homoxenous. Merogony, gamogony and oocyst formation all occur within the same host. The hosts may be vertebrates or invertebrates.

Erroneous identifications of species is a major problem in coccidian systematics and it is likely that some of the genera and species will be revised.

Equine protozoal myeloencephalitis

Equine protozoal myeloencephalitis (EPM), is a disease caused by the apicomplexan parasite Sarcocystis neurona that affects the central nervous system of horses.


The Eucoccidiorida are an order of microscopic, spore-forming, single-celled parasites belonging to the apicomplexan class Conoidasida. Protozoans of this order include parasites of humans, and both domesticated and wild animals including birds. Among these parasites are the Toxoplasma gondii that cause toxoplasmosis and Isospora belli, which results in isosporiasis.


Frenkelia is a genus of parasites in the phylum Apicomplexa. The species in this genus infect the gasterointestinal tracts of birds of prey (definitive hosts) and the tissues of small rodents (intermediate hosts).


Karyolysidae is a family of parasitic alveolates of the phylum Apicomplexa.


Polarella is a genus of dinoflagellates.

It includes the species Polarella glacialis.


Ponazuril (INN), sold by Merial, Inc., now part of Boehringer Ingelheim, under the trade name Marquis® (15% w/w ponazuril), is a drug currently approved for the treatment of equine protozoal myeloencephalitis (EPM) in horses, caused by Sarcocystis neurona. More recently, veterinarians have been preparing a formulary version of the medication for use in small animals such as cats, dogs, and rabbits against coccidia, an intestinal parasite. Coccidia treatment is far shorter than treatment for EPM.

Pyrenophora tritici-repentis

Pyrenophora tritici-repentis (telomorph) and Drechslera tritici-repentis (anamorph) is a necrotrophic plant pathogen of fungal origin, phylum Ascomycota. The pathogen causes a disease originally named yellow spot but now commonly called tan spot, yellow leaf spot, yellow leaf blotch or helminthosporiosis. At least eight races of the pathogen are known to occur based on their virulence on a wheat differential set.The tan (yellow) spot fungus was first described by Nisikado in 1923 in Japan . and was later identified in Europe, Australia and the USA, in the mid 1900s. The disease is one of the most important fungal disease on wheat and the fungal pathogen is found to infect in all parts of the world wherever wheat and other susceptible host crops are found. P. tritici-repentis overwinters on stubble, and due to recent heavily no-till/residue retention cultural practices, increased incidence and yield loss of up to 49% has been witnessed if ideal conditions occur. It forms characteristic, dark, oval-shaped spots of necrotic tissue surrounded by a yellow ring. It is responsible for losses that account for up to 30% of the crop, due to its effects reducing photosynthesis. Pathogenesis and toxicity in P. tritici-repentis is controlled by a single gene, transformations of this gene cause the pathogen to become benign when interacting with wheat. This has major implications for those in agriculture seeking to combat the effects of this fungus.

S. gracilis

S. gracilis may refer to:

Sageretia gracilis, a shrub species with slightly shiny dark green leaves and yellow-green flowers

Sarcocystis gracilis, a parasitic protozoan species in the genus Sarcocystis infecting dogs

Saurida gracilis, the gracile lizardfish, a fish species found in the Indo- pacific region

Scaphispatha gracilis, a plant species endemic to South America

Sellosaurus gracilis, a prosauropod dinosaur species of Triassic Europe

Senoculus gracilis, a spider species in the genus Senoculus found from Guyana to Argentina

Sepiadarium gracilis, a cuttlefish species native to the Indo-Pacific

Sillago gracilis, the trumpeter whiting, a fish species

Sloanea gracilis, a plant species endemic to Suriname

Smilodectes gracilis, an adapiformes primate species from the early Eocene

Smilodon gracilis, the slender smilodon, an extinct carnivorous mammal species

Spartina gracilis, the alkali cordgrass, a plant species

Sphodromantis gracilis, a praying mantis species found in the Transvaal

Spilogale gracilis, the Western spotted skunk

Spratelloides gracilis, the slender sprat, a sprat fish species

Stemonoporus gracilis, a plant species endemic to Sri Lanka

Streptocephalus gracilis, a crustacean species endemic to South Africa

Syrnolopsis gracilis, a gastropod species

Sabin–Feldman dye test

A Sabin–Feldman dye test is a serologic test to diagnose for toxoplasmosis. The test is based on the presence of certain antibodies that prevent methylene blue dye from entering the cytoplasm of Toxoplasma organisms. Patient serum is treated with Toxoplasma trophozoites and complements as activator, and then incubated. After incubation, methylene blue is added. If anti-Toxo antibodies are present in the serum, because these antibodies are activated by complements and lyse the parasite membrane, Toxoplasma trophozoites are not stained (positive result); if there are no antibodies, trophozoites with intact membrane are stained and appear blue under microscope (negative result).

The dilution of the test serum at which 50% of the tachyzoites are thin, distorted and colorless is reported as antibody titer of the test serum.

The test is highly sensitive and specific with no false positives reported so far.

Drawbacks of this test:

1. Difficulty in maintaining the live tachyzoites.

2. It detects immunoglobulin G(IgG) antibodies, hence cannot differentiate between recent or past infection.

3.False positive for Sarcocystis,Trypanosoma lewisi,Trichomonas vaginalis


The Sarcocystidae are a family of Apicomplexa associated with a variety of diseases in humans and other animals.

Sarcocystis accipitris

Sarcocystis accipitris is a species of parasites of the genus Sarcocystis.

Sarcocystis calchasi

Sarcocystis calchasi is an apicomplexan parasite. It has been identified to be the cause of Pigeon protozoal encephalitis (PPE) in the intermediate hosts, domestic pigeons (Columba livia). PPE is a central-nervous disease of domestic pigeons. Initially there have been reports of this parasite in Germany, with an outbreak in 2008 and in 2011 in the United States. Sarcocystis calchasi is transmitted by the definitive host Accipter hawks.

Sarcocystis host–parasite relations

Sarcocystis is a genus of parasitic Apicomplexan alveolates. Species in this genus infect reptiles, birds and mammals. The name is derived from Greek: sarkos = 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.

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

Further material on this genus can be found on the Sarcocystis page.

Sarcocystis nesbitti

Sarcocystis nesbitti is a species of Apicomplexa.

Sarcocystis neurona

Sarcocystis neurona is primarily a neural parasite of horses and its management is of concern in veterinarian medicine. The protozoan Sarcocystis neurona is a protozoan of single celled character and belongs to the family, Sarcocystidae, a group called coccidia. The protozoan, S. neurona, is a member of the genus Sarcocystis, and is most commonly associated with equine protozoal myeloencephalitis (EPM). The protozoan, S. neurona, can be easily cultivated and genetically manipulated, hence its common use as a model to study numerous aspects of cell biology.


Tokophrya is a genus of suctorians. An example is Tokophrya lemnarum.


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