Sarcocystosis is a disease that affects psittacines, primarily those of Australian, Asian and African origin. It is caused by a protozoan parasite (Sarcocystis falcatula) which is introduced into the aviary by opossums (Didelphis virginiana).
Index of Bird Diseases … Symptoms and Potential Causes … Bird Species and Diseases They are Most Susceptible to
Reprinted from: Schubot, R., et al. 1992. Psittacine Aviculture: Perspectives, Techniques, and Research. Willis Printing Group, Inc.; Loxahatchee, FL.
Sarcocystosis In Psittacine Birds
Susan L. Clubb
Sarcocystosis is a disease which affects psittacines, primarily those of Australian, Asian and African origin. It is caused by a protozoan parasite (Sarcocystis falcatula) which is introduced into the aviary by opossums (Didelphis virginiana). It is not infectious from one parrot to another; however, cases tend to occur in clusters because the infected opossum seeds the aviary grounds with infectious sporocyst. Diagnosis in the live bird is difficult primarily due to the hyperacute (rapidly fatal) nature of the disease. A treatment program has been developed for birds in which the disease is tentatively diagnosed. Prevention and control of the disease must be aimed at eliminating opossums from the aviaries and adjacent grounds. (1,4,5)
The Greek root sarco refers to flesh or muscle, with sarcocyst referring literally to a cyst in muscle. Sarcocystis is a genus of protozoan parasites that is associated with the presence of muscle cysts which are usually grossly evident, in straited muscle of an intermediate host species. The muscle cyst stage in the intermediate host is relatively benign. It is during the early developmental stages in other tissues of the intermediate host when infection can prove fatal.
Sarcocystis falcatula is the species associated with an acute fatal disease in psittacine birds. Disease occurs during the early stages of the infection as the parasite is undergoing schizogony (an asexual reproductive stage) in the lung.
The life cycle of Sarcocystis requires both definitive and intermediate hosts. The host in which sexual reproduction of the parasite takes place is called the definitive host, whereas the host in which asexual reproduction takes place is called the intermediate host.
The intermediate host is usually a herbivore or insectivore and becomes infected by ingesting foods contaminated by feces of the definitive host. The intermediate host range may be broad, as in this parasite involving several orders of birds. The degree to which the intermediate host is affected by the
Sarcocystis species typically have a limited definitive host range and cycle with little associated morbidity or mortality in mature individuals. The definitive host is typically a carnivore which becomes infected by eating an animal which has mature cysts in its muscles.
Muscle cysts have been noted in many species and are seldom associated with disease. Generalized early sarcocystosis in the intermediate host is not often recognized because in native species it is an insignificant temporary stage. However when excessive numbers of this stage develop, such as in exotic psittacine species, lesions develop which are often fatal. (1,5)
Sarcocystis falcatul cycles normally between the opossum as the definitive host and its prey cowbirds (Molothrus ater) and grackles (Quiscalus quiscula), as intermediate host species. When certain species of exotic birds accidentally ingest the sporocyst shed by infected opossums severe illness, often hyperacute and fatal, can occur.
Sarcocystosis has been observed in a variety of exotic species but is most prevalent among non-American (African, Asia and Australian) psittacine species. Cockatoos, cockatiels and African parrots are most commonly affected with the acute fatal illness. The disease has been diagnosed in virtually all species of cockatoos in U.S. aviculture. It has also been reported in eclectus parrots, great-billed parrots, ring-necked, moustache and Alexandrine parakeets, many species of lorys and lorikeets, king parrots and lovebirds.
American or neotropical (Mexico, and South and Central America) psittacine species appear to be resistant to the disease as adults however, young birds are sporadically affected. For example, in one facility one to two percent of conure chicks (Aratinga sp.) Removed from the nest for hand feeding at five to seven days of age succumbed to sarcocystosis. This indicates that chicks of neotropical species are more susceptible than adults, and that the disease can be transmitted to the young birds which are being fed by adults that do not themselves succumb to the disease. Rarely were all chicks in a clutch affected. For instance, in a clutch of military macaws pulled from the nest, one chick died acutely at 18 days of age, the second died at 21 days and the third was never ill. (4)
Death in adult neotropical psittacine birds is uncommon. Acute fatal disease was documented in a yellow-faced Amazon (Amazona xanthops), a thick-billed parrot (Rhynchopsitta pachyrhyncha) and a Pacific parrotlet (Forpus coelestis). Both the thick-billed parrot and Pacific parrotlet are species which occur in arid, high altitude habitats not within the natural ranage of the opossum. (4)
Todd reported muscle cysts of Sarcocytis in a half-mooned conure (Aratinga canicularis). He cited reports of muscle cysts in green-rumped parrotlets (Forpus passerinus), gold-capped conures (Aratinga auricapilla), blue and gold macaws (Ara ararauna) and orange-chinned parakeets (Brotogeris jugularis). This would indicate that these species are more resistant. Fewer asexual reproductive stages develop in the lung and the complete development to the muscle cysts could take place. (12)
Exotic columbiforms (pigeons) such as blue crowned pigeons (Goura sp.) And pheasant pigeons are also susceptible and succumb to acute fatal disease associated with schizogony in the lung.
Clinical Signs And Course Of The Disease
Pulmonary sarcocystosis is a hyper acute disease and birds are often found dead or near death without showing previous signs of illness. Birds may die unexpectedly after being observed as normal just a few hours before. Clear fluid usually exudes from the mouth when the dead bird is lifted. Birds are typically in good condition with no weight loss or other indications of chronic disease. Smith et al. found that budgerigars usually died within two to four weeks of experimental infection. (11)
Males appear to be affected more often than females. This may be associated with the male working the nest box and incidentally ingesting sporocyst. Often cage mates die within days of each other; however, many birds survive after the death of their mates.
In birds found ill prior to death, clinical signs include severe dyspnea (labored breathing), excretion of yellow pigmented urates and lethargy. Birds often show elevated serum enzymatic activities, including LDH (lactate dehydrogenase), and AST (aspartate aminotranferase). Other serum chemistry values are typically within normal ranges. (4) Birds which survive the initial pulmonary sarcocystosis often die within a few days to two weeks following the initial illness, and may show early muscle cysts.
Antemortem diagnosis is difficult to confirm because the disease is hyperacute and there are no specific diagnostic tests available. Affected birds do not shed sporocyst. Changes in CBC and serum chemistries are non-specific. Differential diagnosis could include any systemic infection producing an acute onset of pneumonia and/ or hepatitis. Clinical history, species susceptibility and the potential for exposure are keys to making a presumptive diagnosis.
The antemortem clinical diagnosis can only be confirmed by lung biopsy; however biopsy could not be recommended as a routine procedure due to the high risk. Lung biopsies have been accomplished in birds utilizing gaseous anesthesia. (A) The bird is placed in lateral recumbency. An incision is made in the upper intercostal area cranial to the 6th rib. Intercostal muscle is bluntly dissected to expose the caudal aspect of the lung. A section of lung tissue is removed using cutting biopsy forceps.
(b) For best results, the biopsy should contain some tissue from within the lung parenchyma rather than just a small piece of the surface of the lung which may not be diagnostic. Application of pressure to the biopsy site or cautery may be helpful to reduce hemorrhage. Closure involves immobilization of the ribs and suture of the skin. The biopsy specimen can be submitted for histopathology or a lung smear can be prepared for rapid diagnosis.
Surgical risks include hemorrhage and hemoaspiration. Birds which are clinically ill with this disease are poor surgical risks due to their compromised respiratory capability. Therefore this diagnosis procedure should not be considered lightly but is rather of more academic importance. The exception being that presentation is very similar to acute pulmonary mycosis and the treatment protocol for the two diseases are very different. In case of a presumptive diagnosis, initiation of therapy instead of lung biopsy may be prudent.
Due to the difficulty of making an antemortem diagnosis, treatment of confirmed cases has not been documented. However, several birds which survived the death of cage mates and in which a presumptive diagnosis was made survived following treatment. Although the disease was not confirmed, clinical signs (dyspnea, biliverdinuria, elevation of serum enzyme activities) were consistent with clinical signs seen in other cases that were subsequently confirmed on necropsy, and the birds had the potential for exposure.
Therapy included a combination of drugs with antiprotozoal activity in combination with supportive care. Pyrimethamine, a drug used for treating toxoplasmosis and other systemic protozoal infections, was used in conjunction with trimethoprim-sulfadiazone in an attempt to control the organism. Pyrimethamine was administered by gavage twice daily, 0.5 mg/kg for two to four days, then reduced to 0.25 mg/kg for 30 days. © Trimethoprim-sulfadiazone was administered by injection at the rate of 5 mg/kg BID for seven days. (d) Supportive care included administration of oxygen and feeding by gavage. Furosemide was used in an attempt to relieve pulmonary edema and was administered parenterally at the rate of 1.6 mg/kg BID. (e)
Post Mortem Findings
Generalized sarcocystosis in psittacines is a systemic disease affecting multiple organ systems, but the primary site of pathology is the lungs. The lungs are congested and deep red to grey in color with serous (clear) fluid exuding from the surface. Liver and spleen are markedly enlarged, especially the spleen. Bacterial cultures of liver, spleen, lung and heart blood usually yield no bacterial or fungal growth. There is typically no muscle wasting or other signs of long standing disease.
Microscopic lung lesions consist of diffuse interstitial edema extending into the alveoli, with mononuclear cell infiltration and reticulo-endothelial cell hyperplasia. Protozoal schizonts and merozoites are present in the capillary endothelium. Individual merozoites measure about 2 x 7 um and occur in clusters of a few to up to 40 merozoites, often obstructing capillaries. Schizonts and merozoites are also found in reticuloendothelial cells of the spleen and other organs, including liver, proventriculus and pancreatic islets.
Microscopic lesions may be confused with those of Toxoplasma gondii and Isospora serini. Definitive identification of schizonts in tissue is not possible by light microscopy; however, characteristic morphological features are recognizable by electron microscopy (Photo 20-1). Tissue phases of blood parasites such as Haemosporidia and Haemogregarines can be ruled out by their absence on peripheral blood smears.
Rapid in-house diagnosis can be made by preparing a squash preparation of lung tissue from an affected bird. A small piece of lung tissue is blotted to remove edema fluid then squashed between two microscope slides. The squash preparation can be stained with stains appropriate for blood smears. Extracellular merozoites can be seen by light microscopy under oil-immersion (Photo 20-2).
Life Cycle And Pathogenesis
The life cycle of S. Falcatula is complex, involving several reproductive stages in the definitive and intermediate hosts. For simplicity the life cycle is illustrated in Figure 20-1.
Infective sporocysts are shed in the feces of an opossum. Sporocysts are ingested by the intermediate host (bird) directly from the soil or via a transport carrier such as a cockroach. (9) The sporocyst contains sporozoites which are released on the day of ingestion in the intestine of the bird. Sporozoites invade the host’s gut wall, migrate via the blood vessels to the walls of venules where they undergo schizogony. The nucleus of the schizont divides (schizogony) to form merozoites.
Smith, et al. experimentally inoculated budgerigars with sporocysts collected from infected opossums in order to study the early pulmonary pathology of S. Falcatula infection. Early schizogony and merogony of S. Falcatula occurs first in endothelial cells lining pulmonary capillaries, then in venules and veins. The development of enlarging schizonts in these endothelial cells results in hypertrophy of the cells. This hypertrophy narrows or occludes the lumen of capillaries and venules producing obstruction of blood outflow in affected areas of the lung, and endophlebitis. Schizonts rupture, releasing merozoites which are found free in capillaries or in edema fluid filling respiratory spaces. Merozoites then penetrate other endothelial cells producing more schizonts or migrate to muscle cells and form cysts. Leukocytes, platelets and fibrin attach to denuded cell membranes at the site of rupture of the schizont. This results in endophlebitis and formation of fibrin-platelet thrombi (blood clots) which contribute to venous obstruction.
Pulmonary edema (collection of fluid) in the interstitium results as blood flow is obstructed by enlarging schizonts and blood pools around affected capillaries and venules, edema causes displacement of the myelinoid surfactant layer lining the pulmonary alveoli. This layer is a fatty surface in which gaseous exchange occurs. Retraction and degeneration of pneumocytes making up the alveoli follows. Interstitial edema formation results in what is recognized as congestion of the lungs on gross examination. Edema fluid first appears in the interstitium, and subsequently fills airspaces. Fluid wells up in alveoli spilling into bronchi. Death due to asphyxiation occurs in heavily infected birds in which significant portions of the lung are affected. Schizogony also occurs in endothelia of liver, kidney, brain, heart and skeletal muscle. (10-13)
The hyperacute form of the disease is related to the rapid proliferation of the parasite in a susceptible host. Smith found schizonts in the lungs as early as two days post inoculation. Schizonts increase in size and divide to form merozoites. Mature schizonts rupture releasing merozoites which form more schizonts. The number of schizonts increases progressively from the second day postinoculation with the highest number occurring between eight to ten days postinoculation. It is at this time that the hyper acute form of the disease is most likely to occur. Smith estimated a schizont would contain 72 to 333 merozoites. Data on number of schizonts/mm2 suggest a biphasic pattern (two peaks in population) of parasite burdens, the first at eight to ten days and the second at four weeks postinoculation. Two peaks of inflammation lag slightly behind the peak parasite burdens.
It is apparent that the disease can also have a chronic aspect which would also be virtually impossible to confirm without lung biopsy. Smith found that interstitial edema was evident at four days postinoculation and reached a peak at eight to nine days post infection. Edema then waned, but was still prominent in heavily infected birds at four to six weeks postinoculation. Schizonts still occurred in the lungs of sacrificed budgerigars five to five and a half months postinoculation.
In birds infected for four weeks, transudate often contained bacteria or fungi. The edema, loss of surfactant layer and degeneration of pneumocytes resulted in atelectasis. Some alveoli become over distended resulting in emphysema.
At eleven weeks to five and a half months postinoculation edema was supplanted by collagen deposition, severely restricting respiratory exchange because of pulmonary fibrosis. Healing involved migration of pneumocytes into affected areas but as a result of collagen deposition (scar tissue formation) in tissues, affected birds had foci of emphysema and atelectasis. (11)
In order for the immediate host (grackles or cowbirds) to transmit the infection to the definitive host (opossums), it must survive schizogony in the lung or other tissues so merozoites can migrate to skeletal muscle and form typical muscle cysts. These tissue cysts also form in psittacine species if they survive initial lung schizogony. The cyst form more frequently in neotropical psittacines. Spindle-shaped muscle cysts in infected birds contain metrocytes which become infectious bradyzoites several weeks after infection (7).
Sexual development of Sarcocystis occurs in the gut of the opossum. Upon ingestion, bradyzoites are released from the muscle cysts by proteolytic enzymes in the opossum’s small intestine. Bradyzoites penetrate the intestinal mucosa where fertilization takes place producing oocysts. In most coccidia unsporulated oocysts are shed in the feces. However, Sarcocystis sporulates (divides) to form two sporocysts, each containing 4 sporozoites in the intestinal mucosa of the opossum (lamina propria). Tiny sporocysts (11-12 um by 7-8 um) and an occasional oocyst shed in the feces. Sporocysts are infectious at the time they emerge from the intestinal lining and are shed in small numbers over an extended period of weeks of months.
Opossums start to shed sporocysts five days after eating an infectious meal. Shedding has been reported for at least 15 weeks after infection. Prolonged shedding occurs because sporocyst are trapped beneath epithelial cells within the interstitial layer of intestinal villi by intestinal contraction. Sporocysts are distributed throughout the small intestine with a predominance in the upper middle section.
Sarcocystosis occurs sporadically during the year, however heaviest losses are experienced from late fall to spring in south Florida. Losses can be isolated or clustered. Affected birds have been housed in a variety of cages and aviaries, including suspended cages, large flight cages, and even screened porches. While psittacines may not have direct access to opossum feces, transmission can be accomplished by mechanical carriers.
In order to prove this route of transmission, an opossum was trapped on one facility where the disease had occurred. It was found to be shedding sporocysts of Sarcocystis falcatula. This opossum was housed in a room with birds which included some cockatoos. Several cockatoos died of sarcocystis even though they had no direct contact with the feces of the opossum. Transmission by cockroaches was suspected. Feces from the opossum were fed to cockroaches which were subsequently blenderized and fed to cockatoos by gavage. These experimentally inoculated birds died of pulmonary sarcocystosis at 10 to 14 days post-inoculation.
Cockroaches are known to be coprophagic (eat feces). It was proven that cockatoos will eat cockroaches by adding them to feed (with their legs pulled off to prevent escape). Cockroaches were placed in feed bowls along with feed. Feeding was recorded on videotape where cockatoos were seen consuming the insects. It is also possible that cockroaches could contaminate feed with their feces. (9)
Box, et al. investigated the life cycle and host range of Sarcocystis falcatula. In laboratory experiments which included cats, rats and a dog , only opossums were found to be suitable definitive hosts for S. falcatula. The intermediate host spectrum of S. falcatula was investigated by feeding sporocysts to birds of four orders, including Psittaciformes (budgerigars), Passeriformes (canaries and zebra finches), Galliformes (chickens and guinea fowl) and Columbiformes (pigeons). Budgerigars and pigeons experienced acute fatal illness, but canaries, zebra finches, chickens and guinea fowl survived the lung schizogony stage and developed muscle cysts.
Due to the vast distribution of both the definitive and intermediate host species, the natural life cycle of S. falcatula can occur over most of the U.S., placing psittacines in outdoor facilities at potential risk.
The range of the opossum extends over most of the continental U.S. with the exception of the Rocky Mountains, the desert southwest and the extreme northern areas.(3), The brown-headed cowbird ranges over the entire continental U.S., and the common grackle ranges over the continental U.S. east of the Rocky Mountains. Both are in the order Passeriformes (Perching Birds).(8)
Psittacine diets spilled from cages attract both cockroaches and opossums which feed around cage areas at night. Opossums easily hide during the day in rubbish piles, heavy vegetation or under outbuildings, making their presence on a farm difficult to detect. Opossums are strictly nocturnal and arboreal often covering several miles in an evening. They can easily climb fences and move around through the trees and over the roofs of aviaries. Feces deposited on the roof of an aviary can serve as a source of infection. Since sporocysts of S. falcatula are shed over a prolonged period of time, a single infected opossum visiting a farm regularly could seed the farm with infectious sporocysts which parrots might ingest resulting in sporadic cases.
The higher incidence of disease from late fall to spring may be related to a massive influx of migratory grackles and cowbirds at that time, and their subsequent breeding season. Many cowbird or grackle chicks fall from the nest and are easy prey for opossums. Adults birds consume large quantities of insects in order to raise their chicks, some of which may have fed on the feces of opossums. Opossums are known to prey on birds and may feed on chicks around rookeries. A diet high in infected birds would increase the contamination of areas with Sarcocystis sporocysts. In Sarcocystis muris, both primary infection and reinfection of the definitive hosts leads to shedding. (9)
The relative resistance of adult neotropical psittacines to acute fatal sarcocystosis is possibly related to natural selection of these species in an environment where opossums infected with S. falcatula are prevalent. Non-American species, evolved in an environment free of opossums, have not been naturally selected for resistance and show a variable outcome of infection.
Because of its sporadic nature, control of the disease in psittacines by prophylactic drug therapy is impractical. Control efforts must be aimed at the disseminators of infection. Opossums should be excluded from psittacine breeding areas by use of livestock electric fences. Electric wires can be affixed to insulators on the exterior of existing fencing or may be free standing. In southern coastal areas of the United States, control of cockroaches in heavily planted outdoor areas is difficult, if not impossible. Chickens may be utilized to eat cockroaches and reduce the chance of transmission. Chickens readily feed on cockroaches and are resistant to S. falcatula infection. The use of flightless chicken breeds, such as silky chickens, will help avoid roosting of chickens on the top of cages and soiling cages, food and water bowls, which may result in contamination with other infectious agents. It is also possible that some sporocysts of Sarcocystis could pass through the intestines of both cockroaches and chickens.
Outdoor aviculture of non-American psittacines in southern coastal areas of the U.S. can be limited by sarcocystosis. For success with these species, exclusion of opossums must be considered in aviary design and management procedures.
1. Box, J.Meier and J.H. Smith, 1984., Description of Sarcocystis falcatula, stiles, J. Protozoal. 31:521-524. 1983.
2. Box, E.D. and J.H. Smith, The intermediate Host Spectrum in Sarcocystis Species in Birds. J. Parasitol. 64:668-673. 1982
3. Burt, W.H. and R.P. Grossenheider., A field Guide to the Mammals, Houghton Mifflin Company, Boston, MA. 1964.
4. Clubb, S.L., J.K. Frenkel, C.H. Gardiner and D.L. Graham, An Acute Fatal Illness in Old World Psittacine Birds Associated with Sarcocystis falcatula of Opossums, Proc Annual Conference of Association of Avian Veterinarians., pp 139-150, 1986.
5. Dubey, J.P., C.A. Speer, R. Fayer., Sarcocystosis of Animals and Man. CRC Press, Boca Raton, Fl. 1989.
6. Frenkel, J.K., Tissue-dwelling Intercellular Parasites; Infection and Immune response in the Mammalian Host to Toxoplasma, Sarcocystis and Trichinella. American. Zoological. 29:455-467. 1989
7. Neill, P.J.G., J.H. Smith and E.D. Box. Pathogenesis of Sarcocystis falcatula (Apicomplexa: Sarcocystidae) in the Budgerigar (Melopsittacus undulatus). IV. Ultrastructure of Developing, Mature and Degenerating Sarcocysts. J. Protozool. 36:430-437. 1989
8. Robbins, C.S., B. Bruun, and H.S. Zim. Birds of North America, Golden Press, New York, N.Y. 1966.
9. Smith, D.D. and J.K. Frenkel. Cockroaches as Vectors of Sarcocystis muris and Other Coccidia in the Laboratory. J. Parasitol. 64(2):315-319. 1978
10. Smith, J.H., J.L. Meier, P.J.G. Neill anad E.D. Box. Pathogenesis of Sarcocystis falcatula in the Budgerigar. I. Early Pulmonary Schizogony. Lab Invest. 56 (1): 60-71. 1987.
11. Smith, J.H., J.L. Meier, P.J.G. Neill and E.D. Box. Pathogens of Sarcocystis falcatula in the Budgerigar. II. Pulmonary pathology. Lab Invest. 56 (1) : 72-84. 1987.
12. Todd, K.S., A.M. Gallina and W.B. Nelson. Sarcocystis Species in Psittacine Birds. J. Zoo Animal Med. 6:21 – 24. 1975.
13. Smith, J.H., P.J.G. Neill and E.D. Box, Pathogenesis of Sarcocystis falcatula (Apicomplexa: Sarcocystidae) in the Budgerigar (Melopsittacus undulatus) III. Pathologic and Quamtitative Parasitologic Analysis of Extrapulmonary Disease, journal of Parasitologic Analysis of Extrapulmonary Disease, Journal of Parasitology, Vol. 75 (2): pp. 270-287, 1989.
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