Sarcocystis spp

From Bird
Representative life cycle of Sarcocystis spp.
The Virginia opossum (Didelphis virginiana) is the definitive host of Sarcocystis falcatula.
Cockroaches may serve as transport hosts in the distribution of Sarcocystis falcatula sporocysts.

Sarcocystis spp are a group of protozoan parasites of birds.

All coccidia are classified in the phylum Apicomplexa and in the suborder Eimeriorina. The genus Sarcocystis falcatula is a cyst forming coccidian that infects many species of animals, including psittacine birds. Initially, S. falcatula was thought to be synonymous with S. neurona, the causative agent of equine protozoal myeloencephalitis (EPM), but this has been disproven[1].

New World psittacines have adapted to the parasite and may remain asymptomatic following infection, while Old World psittacine birds experience severe disease or death when infected with this coccidian. Sarcocystosis is of concern in psittacine birds, especially when housed outdoors or when their food is not stored correctly. Sarcocystis falcatula is known to cause a fatal pulmonary disease in psittacine birds, especially Old World (non-American) psittacines including cockatoos, cockatiels, Eclectus parrots, and African parrots. New world (American) psittacines such as conures, Amazon parrots, and macaws seem to be resistant to infection possibly due to co-habitating with the definitive host, the Virginia opossum (Didelphis virginiana). Difficulty in controlling sarcocystosis also is compounded by the fact that S. falcatula can be transmitted by cockroaches. If birds eat these paratenic (transport) hosts or if birds eats food that is contaminated by cockroach feces, they may develop sarcocystosis[2].

Life Cycle

Sarcocystis spp are protozoan parasites that have an obligatory two-host life cycle. Sexual reproduction occurs in the gastrointestinal tract of the definitive host, forming infective sporocysts that are excreted in the feces. Asexual reproduction occurs in the intermediate host, eventually forming cysts in the skeletal muscle (sarcocysts) that are filled with bradyzoites.

The definitive host for S. falcatula is the Virginia opossum (Didelphis virginiana); while the intermediate host appears to be several different orders of birds[3]. Raccoons and skunks, also have been identified as intermediate host as well[4].

The intermediate host (bird) becomes infected by ingesting infective sporocysts that are shed in the opossum's feces or that are transported by cockroaches. Furthermore, birds can develop sarcocytstosis if they eat a cockroach that has ingested feces containing S. falcatula sporocysts or if they eat food contaminated by cockroach feces. The sarcocysts usually are found in the skeletal muscle of the intermediate host, but also can be found in cardiac muscle, brain, and gastrointestinal tract. The definitive host (opossum) becomes infected after eating a bird carcass that contains sarcocysts[5].

Initially, the intermediate hosts were identified as cowbirds (Molothrus ater) and grackles (Cassidix mexicanus, Quiscalus quiscula), which are commonly found across America. Further research studies and clinical case reports have demonstrated that other orders of birds may be infected with S. falcatula, including Psittaciformes (budgerigars) and Columbiformes (pigeons)[6]. However, many of these species of birds develop acute, fatal, pulmonary illness. Passeriformes (canaries, zebra finches, cowbirds, and grackles) and Galliformes (chickens and guinea fowl) usually survive pulmonary schizogony and then develop sarcocysts in striated muscle. It is speculated that the birds that survive pulmonary schizogony with sarcocyst formation are more resistant to fatal pulmonary disease because of environmental coevoultion with the opossum.

Clinical signs

Old World psittacine birds with S. falcatula infection often appear healthy just hours before being found dead in the cage. Clear fluid may exude from the mouth as they are lifted. Because the course of disease is rapid, dead birds lack weight loss or more chronic signs of disease. If the birds are found ill but alive, clinical signs may include severe dyspnea, lethargy, and yellow-pigmented urates.


Historically, definitive antemortem diagnosis of sarcocystosis has been accomplished via skeletal muscle biopsy in New World psittacines, although a lung biopsy would be a better choice in an Old World bird psittacine bird[7]. Serologic testing has been performed experimentally using fluoresence microscopy; however, a variable seropositive status was observed in infected cowbirds (Molothrus atar). Serum electrophoresis in the same study indicated early inflammation, but electrophoretogram changes were not pathognomonic for sarcocystosis[8].

Suspicion of S. falcatula infection usually is based on the medical history (outdoor aviary, exposure to cockroaches and opossums) and clinical signs, if present. Clinical chemistry studies may reveal increased activity of lactate dehydrogenase and aspartate aminotransferase; all other serum chemistry and complete blood count values are usually within the reference interval.

There is no specific and easy antemortem test to diagnose S. falcatula infection. The only antemortem diagnostic technique that can be done is a lung biopsy; however, this procedure entails a high amount of risk in a patient with compromised pulmonary function. In summary, a presumptive diagnosis of S. falcatula infection is based upon a high index of suspicion of sarcocystosis, acute unexplained death of an otherwise healthy bird, clinical signs of dyspnea, exposure to opossums or cockroaches, and species of bird (Old World psittacine)[9].

Post mortem findings in psittacine brids that die acutely of S. falcatula infection primarily involve the lungs, but also affect other organ systems. The lungs generally appear congested, deep red, and exude a clear, serous fluid when cut. All of these findings suggest pulmonary edema and hemorrhage. Hepatomegaly and splenomegaly typically are present.

Microscopically, the lungs have a diffuse interstitial pneumonia and meronts of S. falcatula may be observed in air capillaries. Hemorrhage and fibrin deposition also may be observed in parabronchi[10]. During early merogony, pulmonary capillary obstruction occurs due to the multiplying meronts. As pulmonary vascular outflow is impeded, pulmonary edema and hemorrhage occur producing a respiratory crisis[11].

Definitive diagnosis of S. falcatula infection can be accomplished by cytology, histology, or electron microscopy. Crescent-shaped meronts may be observed on lung imprints stained with Romanowsky (Wright, Leismann, Giemsa, or Diff-Quik) stains. Histologically, meronts may be observed within pulmonary air capillaries and small blood vessels of other tissues and organs, including the brain. Skeletal and cardiac muscle may have developing sarcocysts containing metrocytes (more oval organisms) or sporozoites (elongated organisms) contained within a striated cyst wall.

Ultrastructurally, different developmental stages of the protozoan can be seen in lung, skeletal muscle, cardiac muscle, and neural cells. These stages of development include merozoites, metrocytes, schizonts, bradyzoites, and entire sarcocysts. S. falcatula has a characteristic striated cyst wall with long slanted microvilli that project from the outer surface, an undulating cyst wall and unique bradyzoite ultrastructure. These features are distinctive from other protozoa, including Toxoplasma gondii, Neospora caninum, and even other Sarcocystis spp.


Antemortem treatment for S. falcatula is difficult because of the relatively short clinical course of disease. If S. falcatula infection is suspected or has been confirmed in a group of birds, anti-protozoal treatment is recommended with pyrimethamine (Daraprim) and trimethoprim sulfadiazine (Tribrissin). The suggested treatment protocol includes administration of pyrimethamine at 0.5 mg /kg body weight twice daily administered by gavage for 2 –4 days. The dosage of pyrimethamine is then reduced to 0.25 mg/kg for the next 30 days. Trimethoprim sulfadiazine is administered by intramuscular injection at a dosage of 5 mg/ kg body weight /day for seven days.

Trimethoprim sulfadiazinemay cause muscle necrosis, especially in cockatoos. Therefore, continued oral treatment with the drug (30 mg /kg body weight per os every 12 hr for 30 days) would be a suitable alternative. Supportive care also is important and may include tube feeding by crop gavage, oxygen administration if dyspnea is present, and furosemide (1.6 mg/kg twice daily) to relieve pulmonary edema. This treatment protocol has been most effective in birds that are suspected to be infected with S. falcatula (e.g., the cagemate died of sarcocystosis) but are not showing clinical signs of disease.

Prevention is the key to controlling S. falcatula infections, especially when birds are housed outdoors. The opossum must be excluded from bird enclosures and food storage areas. This can be done by elevating birdcages off the ground, using an electric wire fence around the facility, and using dogs for biological control of opossums. All bird food should be stored in closed containers that exclude both opossums and cockroaches. Cockroaches can be controlled by screening and keeping flightless (silky) chickens at the facility. Flightless chickens will feed on the cockroaches that could be carrying S. falcatula, but the chickens themselves are not susceptible to a fatal infection. Using flightless chickens is important because they will not be able to fly on top of the birdcages, minimizing any risk of sporocyst distribution from their feces.


  1. Dame JB, MacKay RJ, Yowell CA, et al (1995) Sarcocystis falcatula from passerine and psittacine birds: Synonmy with Sarcocystis neurona, agent of equine protozoal meningitis. J Parasitol 81:916-919
  2. Clubb SL, Frenkel JK (1992) Sarcocystis falcatula of opossums: Transmission by cockroaches with fatal pulmonary disease in psittacine birds. J Parasitol 78:116-124
  3. Porter RA, Ginn PE, Dame JB, et al (2001) Evaluation of the shedding of Sarcocystis falcatula sporocysts in experimentally infected Virginia opossums (Didelphis virginiana). Vet Parasitol '95:313-319
  4. Smith JH, Meier JL, Neill PJG, et al (1987) Pathogenesis of Sarcocystis falcatula in the budgerigar. I. Early pulmonary schizogony. Lab Invest 56:60-71
  5. Bolon B, Greiner EC, Calderwood Mays, MB (1989) Microscopic features of Sarcocystis falcatula in skeletal muscle from a Patagonian Conure. Vet Pathol 26:282-284
  6. Suedmeyer WK, Bermudez AJ, Barr BC, et al (2001) Acute pulmonary Sarcocystis falcatula-like infection in three Victoria crowned pigeons (Goura victoria) housed indoors. J Zoo Wildl Med 32:252-256
  7. Page CD, Schmidt RE, English JH, et al (1992) Antemortem diagnosis and treatment of sarcocystosis in two species of psittacines. J Zoo Wildl Med 23:77-85
  8. Cray C, Greiner E, Zielezienski K (1996) Serologic diagnosis of sarcocystosis. Proc Assoc Avian Vet Annual Conf pp:205-208
  9.; Reprinted from: Schubot, R., et al. 1992. Psittacine Aviculture: Perspectives, Techniques, and Research. Willis Printing Group, Inc., Loxahatchee, FL. With permission from Scott Schubot, Owner/Director of Avicultural Breeding and Research Center
  10. Latimer KS, Perry RW, Mo IP, et al (1990) Myocardial sarcocystosis in a Grand Eclectus parrot (Eclectus roratus) and a Moluccan cockatoo (Cacatua moluccensis). Avian Dis 34:501-505, 1990
  11. Smith JH, Meier JL, Neill PJG, et al (1987) Pathogenesis of Sarcocystis falcatula in the budgerigar. II. Pulmonary pathology. Lab Invest 56:72-84