Sarcocystosis in a Major Mitchell’s Cockatoo (Cacatua leadbeateri)
Kelli L. Boyd and Kenneth S. Latimer
Department of Pathology, College of Veterinary Medicine, The University of Georgia, Athens, Georgia (USA) 30602-7388
Abstract. Sarcocystosis was diagnosed in a female Major Mitchell’s Cockatoo that died unexpectedly. Microscopically, merozoites were observed within pulmonary air capillaries. In addition, parasitic cysts containing metrocytes were observed within the myocardium. This case report describes the gross necropsy findings and histologic lesions associated with fatal sarcocystosis. The life cycle of the parasite is reviewed with attention to methods of disease prevention.
Key Words: Major Mitchell’s Cockatoo, Cacatua leadbeateri, Sarcocystosis, Sarcocystis falcatula, Opossum, Didelphis virginiana, Pulmonary disease, Cockroach
Introduction
Sarcocystis falcatula is a coccidian parasite of the Apicocomplexa family. The opossum (Didelphis virginiana) is the definitive host of the parasite in which gametogenesis and production of sporocysts occurs in the small intestine. Cockroaches may serve as intermediate transport hosts of the parasite and facilitate infection of birds, which serve as intermediate hosts. 1-5 In infected birds, asexual proliferation of the parasite results in the formation of meronts in pulmonary capillaries. Ultimately, the merozoites give rise to sarcocysts in striated muscle. The sarcocysts characteristically have a striated wall and contain numerous crescent-shaped merozoites. 4,5 This case report describes a fatal case of sarcocystosis in a Major Mitchell’s Cockatoo (Cacatua leadbeateri).
Case Report
A female Major Mitchell’s Cockatoo of unknown age was found dead in her cage at the Riverbanks Zoological Park in Columbia, South Carolina. The bird was housed in an outdoor aviary and appeared healthy the previous day.
The bird was examined by necropsy. Gross findings included dark red lungs and an enlarged spleen with multiple white foci. Representative portions of major organs and tissues were collected, preserved in 10% neutral-buffered formalin, and mailed to the Department of Pathology at The University of Georgia College of Veterinary Medicine for histopathologic examination. Upon receipt, the tissues were processed routinely, embedded in paraffin, sectioned at 3µm, stained with hematoxylin and eosin, and examined by light microscopy.
The major histologic findings were confined to the heart, lung, and liver. The lungs were congested and had parabronchial hemorrhage, edema, and fibrin deposition. An interstitial infiltrate of lymphocytes and plasma cells also was observed. Rare meronts and free merozoites were present within pulmonary endothelial cells and within capillary lumina (Fig. 1). Also present were multiple, elongate, variably-sized, parasitic cysts within the myocardium (Fig. 2). The cysts were sometimes bordered by a mildly striated wall and were filled with round to oval metrocytes. Crescent-shaped merozoites were sometimes observed in more mature sarcocysts. These morphological features were typical of Sarcocystis sp. The liver had multifocal infiltrates of lymphocytes and plasma cells within the parenchyma. The histological diagnoses were cardiac and pulmonary sarcocystosis with mild multifocal nonsuppurative hepatitis.
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| Fig. 1. Major Mitchell's Cockatoo, sarcocystosis, lung, H&E stain. A cluster of merozoites is present within the lumen of a dilated pulmonary capillary (center). |
Fig. 2. Major Mitchell's Cockatoo, sarcocystosis, myocardium, H&E stain. A sarcocyst is bordered by a striated wall and is filled with round to oval metrocytes (center). |
Additional portions of lung and myocardium were diced into 1 mm cubes, postfixed in osmium tetroxide, dehydrated in graded alcohols, and embedded in Spurr resin. Ultrathin tissue sections were placed on high-transmission nickel grids, stained with lead citrate and uranyl acetate, and examined by transmission electron microscopy. The myocardial cyst walls were approximately 700 nm thick with regularly spaced villous pleats (Fig. 3). Occasionally, microfilaments were observed within the pleats or folds. Internally, the cysts were compartmentalized, separating the developing metrocytes. Sections of pulmonary capillaries contained elongate meronts and free merozoites, often associated with degenerating endothelial cells (Fig. 4).
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| Fig. 3. Major Mitchell's Cockatoo, sarcocystosis, myocardium, electron micrograph. Parasitic cyst wall has characteristic pleats or folds; villi average 700 nm in length. |
Fig. 4. Major Mitchell's Cockatoo, sarcocystosis, lung, electron micrograph. Meront within a pulmonary capillary endothelial cell. |
Discussion
The opossum (Didelphis virginiana, Fig. 5) is the definitive host of Sarcocystis falcatula. While many orders of birds may serve as intermediate hosts, grackles (Cassidix mexicanus, Quiscalus quiscula) and cowbirds (Molothrus ater) are most commonly infected. The opossum, grackle, and cowbird have a host range that covers almost the entire continental United States. Sarcocystis falcatula undergoes sexual reproduction within the small intestine of the opossum. Infective sporocysts subsequently are shed in the feces. Ingestion of fecal-contaminated food, soil, or water results in intermediate infection of birds, especially grackles and cowbirds. The parasitic life cycle is completed when the opossum ingests infected birds or bird carcasses. 1
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| Fig. 5. Opossum (Didelphis virginiana) with young. |
In captive non-American psittaciformes such as the Major Mitchell's Cockatoo of this report, the course of infection is rapid and usually fatal. Pulmonary and hepatic disease are observed most commonly. Infective sporocysts are ingested from food or water bowls contaminated with opossum feces or by ingesting cockroaches that may serve as transport hosts for the parasite. Following ingestion, the infective sporozoites are released in the alimentary tract and subsequently localize in the pulmonary capillaries where two successive stages of merogeny occur. 4-6 This stage of parasite replication is often associated with acute death. Most birds do not show clinical signs of disease until a few hours before death. Clinical signs may include dyspnea, excretion of yellow-pigmented urates, and lethargy. Abnormally high lactate dehydrogenase and aspartate aminotransferase activities may be the only biochemical abnormalities. Birds that survive the initial illness will often die within a few days up to 2 weeks later, at which time parasitic cysts (sarcocysts) may be observed in myocardial and skeletal muscle. 2-6
In contrast, American psittacines are typically resistant to fatal parasite infection; however, nestlings may be affected and die. American species exposed to Sarcocystis falcatula appear to be more adapted to the parasite and usually exhibit no signs of illness. The parasite ultimately encysts in skeletal and cardiac muscle, forming typical sarcocysts. These sarcocysts are relatively common incidental histologic findings in American free ranging psittacines, as well as in grackles, cowbirds, and waterfowl. There generally is no reaction to the sarcocysts, but mild necrosis and granulomatous inflammation have been observed infrequently. 2
Typical postmortem findings include a bird in good body condition with clear fluid exuding from the mouth when the bird is lifted. The liver and spleen usually are enlarged. The lungs are often congested (dark red) and will exude serous fluid and blood when cut. 2
Microscopically, the lungs will typically be congested with some fibrin deposition, edema, and hemorrhage within parabronchi. Meronts may be observed within pulmonary capillary endothelium. In addition, free merozoites may be observed within the pulmonary capillary lumina or in the parabronchi in association with hemorrhage. Merozoites are elongate, crescent-shaped, and contain a single, prominent, basophilic nucleus. The number of merozoites observed in histologic sections may range from rare to numerous. In severe infestations, the merozoites may obstruct pulmonary capillaries. In addition to histopathology, Romanowsky-stained cytologic touch imprints of unfixed lung tissue may facilitate disease diagnosis by demonstrating individual merozoites. Sarcocysts occur in skeletal and cardiac muscle, are variably-sized, and may have a striated cyst wall. They may be filled with round to oval metrocytes (immature stage of the parasite) or thin, elongate, crescent-shaped merozoites (more mature stage of the parasite). Meronts also may be observed in monocyte-macrophages in the spleen, liver, pancreatic islets, and proventriculus. 2,3
Ultrastructurally, the sarcocyst wall is 700 nm thick with densely packed, regularly spaced folds or villous protrusions (675nm long x 100 nm wide) that occasionally appear as vesicles on transverse section. Extensions from the inner wall divide the cysts into compartments. Merozoites within the pulmonary capillaries have ultrastructural features typical of other coccidia. 3
In captive non-American psittaciformes such as the Major Mitchell's Cockatoo of this report, the course of infection is rapid and usually fatal. Pulmonary and hepatic disease are observed most commonly. Infective sporocysts are ingested from food or water bowls contaminated with opossum feces or by ingesting cockroaches that may serve as transport hosts for the parasite. Following ingestion, the infective sporozoites are released in the alimentary tract and subsequently localize in the pulmonary capillaries where two successive stages of merogeny occur. 4-6 This stage of parasite replication is often associated with acute death. Most birds do not show clinical signs of disease until a few hours before death. Clinical signs may include dyspnea, excretion of yellow-pigmented urates, and lethargy. Abnormally high lactate dehydrogenase and aspartate aminotransferase activities may be the only biochemical abnormalities. Birds that survive the initial illness will often die within a few days up to 2 weeks later, at which time parasitic cysts (sarcocysts) may be observed in myocardial and skeletal muscle. 2-6
In contrast, American psittacines are typically resistant to fatal parasite infection; however, nestlings may be affected and die. American species exposed to Sarcocystis falcatula appear to be more adapted to the parasite and usually exhibit no signs of illness. The parasite ultimately encysts in skeletal and cardiac muscle, forming typical sarcocysts. These sarcocysts are relatively common incidental histologic findings in American free ranging psittacines, as well as in grackles, cowbirds, and waterfowl. There generally is no reaction to the sarcocysts, but mild necrosis and granulomatous inflammation have been observed infrequently. 2
Typical postmortem findings include a bird in good body condition with clear fluid exuding from the mouth when the bird is lifted. The liver and spleen usually are enlarged. The lungs are often congested (dark red) and will exude serous fluid and blood when cut. 2
Microscopically, the lungs will typically be congested with some fibrin deposition, edema, and hemorrhage within parabronchi. Meronts may be observed within pulmonary capillary endothelium. In addition, free merozoites may be observed within the pulmonary capillary lumina or in the parabronchi in association with hemorrhage. Merozoites are elongate, crescent-shaped, and contain a single, prominent, basophilic nucleus. The number of merozoites observed in histologic sections may range from rare to numerous. In severe infestations, the merozoites may obstruct pulmonary capillaries. In addition to histopathology, Romanowsky-stained cytologic touch imprints of unfixed lung tissue may facilitate disease diagnosis by demonstrating individual merozoites. Sarcocysts occur in skeletal and cardiac muscle, are variably-sized, and may have a striated cyst wall. They may be filled with round to oval metrocytes (immature stage of the parasite) or thin, elongate, crescent-shaped merozoites (more mature stage of the parasite). Meronts also may be observed in monocyte-macrophages in the spleen, liver, pancreatic islets, and proventriculus. 2,3
Ultrastructurally, the sarcocyst wall is 700 nm thick with densely packed, regularly spaced folds or villous protrusions (675nm long x 100 nm wide) that occasionally appear as vesicles on transverse section. Extensions from the inner wall divide the cysts into compartments. Merozoites within the pulmonary capillaries have ultrastructural features typical of other coccidia. 3
In captive non-American psittaciformes such as the Major Mitchell's Cockatoo of this report, the course of infection is rapid and usually fatal. Pulmonary and hepatic disease are observed most commonly. Infective sporocysts are ingested from food or water bowls contaminated with opossum feces or by ingesting cockroaches that may serve as transport hosts for the parasite. Following ingestion, the infective sporozoites are released in the alimentary tract and subsequently localize in the pulmonary capillaries where two successive stages of merogeny occur. 4-6 This stage of parasite replication is often associated with acute death. Most birds do not show clinical signs of disease until a few hours before death. Clinical signs may include dyspnea, excretion of yellow-pigmented urates, and lethargy. Abnormally high lactate dehydrogenase and aspartate aminotransferase activities may be the only biochemical abnormalities. Birds that survive the initial illness will often die within a few days up to 2 weeks later, at which time parasitic cysts (sarcocysts) may be observed in myocardial and skeletal muscle. 2-6
In contrast, American psittacines are typically resistant to fatal parasite infection; however, nestlings may be affected and die. American species exposed to Sarcocystis falcatula appear to be more adapted to the parasite and usually exhibit no signs of illness. The parasite ultimately encysts in skeletal and cardiac muscle, forming typical sarcocysts. These sarcocysts are relatively common incidental histologic findings in American free ranging psittacines, as well as in grackles, cowbirds, and waterfowl. There generally is no reaction to the sarcocysts, but mild necrosis and granulomatous inflammation have been observed infrequently. 2
Typical postmortem findings include a bird in good body condition with clear fluid exuding from the mouth when the bird is lifted. The liver and spleen usually are enlarged. The lungs are often congested (dark red) and will exude serous fluid and blood when cut. 2
Microscopically, the lungs will typically be congested with some fibrin deposition, edema, and hemorrhage within parabronchi. Meronts may be observed within pulmonary capillary endothelium. In addition, free merozoites may be observed within the pulmonary capillary lumina or in the parabronchi in association with hemorrhage. Merozoites are elongate, crescent-shaped, and contain a single, prominent, basophilic nucleus. The number of merozoites observed in histologic sections may range from rare to numerous. In severe infestations, the merozoites may obstruct pulmonary capillaries. In addition to histopathology, Romanowsky-stained cytologic touch imprints of unfixed lung tissue may facilitate disease diagnosis by demonstrating individual merozoites. Sarcocysts occur in skeletal and cardiac muscle, are variably-sized, and may have a striated cyst wall. They may be filled with round to oval metrocytes (immature stage of the parasite) or thin, elongate, crescent-shaped merozoites (more mature stage of the parasite). Meronts also may be observed in monocyte-macrophages in the spleen, liver, pancreatic islets, and proventriculus. 2,3
Ultrastructurally, the sarcocyst wall is 700 nm thick with densely packed, regularly spaced folds or villous protrusions (675nm long x 100 nm wide) that occasionally appear as vesicles on transverse section. Extensions from the inner wall divide the cysts into compartments. Merozoites within the pulmonary capillaries have ultrastructural features typical of other coccidia. 3
References
1. Fenger CK, Granstrom DE, Langemier JL, Stamper S, Donahue JM, Patterson JS, Gajadhar AA, Marteniuk JV, Xiaomin Z, Dubey JP: Identification of opossums (Didelphis virginiana) as the putative definitive host of Sarcocystis neurona. J Parasitol 81:916-919, 1995.
2. Clubb SL, Frenkel JK: Sarcocystis falcatula of opossums: Transmission by cockroaches with fatal pulmonary disease in psittacine birds. J Parasitol 78:116-124, 1992.
3. Latimer KS, Perry RW, Mo IP, Nietfeld JC, Steffens WL, Harrison GJ, Ritchie BW: Myocardial sarcocystosis in a Grand Eclectus parrot (Eclectus roratus) and a Moluccan cockatoo (Cacatua moluccensis). Av Dis 34:501-505, 1990.
4. Smith JH, Neill PJG, Dillard EA, Box ED: Pathology of experimental Sarcocystis falcatula infections of canaries (Serinus canarius) and pigeons (Columba livia). J Parasitol 76:59-68, 1990.
5. Smith JH, Meier JL, Neill PJG, Box ED: Pathogenesis of Sarcocystis falcatula in the budgerigar. I. Early pulmonary schizogony. Lab Invest 56:60-71, 1987.
6. Smith JH, Meier JL, Neill PJG, Box ED: Pathogenesis of Sarcocystis falcatula in the budgerigar. II. Pulmonary pathology. Lab Invest 56:72-84, 1987. This Page Last Updated May 15, 1998 |