No abstract

Sarcocystis falcatula is an apicomplexan parasite with a broad range of avian intermediate hosts. The pathology and pathogenesis of infection with this parasite has been studied experimentally in the budgerigar (Melopsittacus undulatus). The present study quantitatively examines the pathology of this parasite in canaries (Serinus canarius) and pigeons (Columba livia) and compares it with that found in budgerigars. The general progression of merogony and cyst formation is similar qualitatively to that seen in budgerigars, but it differs quantitatively. The principal site of precystic merogony is in pulmonary endothelial cells. The magnitude of pulmonary meront burdens (at similar inoculated dosages) varies in different intermediate host species. Merogony is less persistent than in budgerigars. Among the various species of birds, the magnitude of precystic merogony correlates differently with the magnitude of skeletal muscle cyst burdens. The distribution of cyst burdens among various muscles also differs. The composition of inflammatory cells differs among various avian species' response to S. falcatula. Pathologic changes quantitatively parallel tissue meront burdens (except possibly in the liver of canaries), resulting in an interstitial pneumonitis, hepatitis, and mild inflammatory lesions of other organs.

This report describes acute interstitial pneumonitis due to an apicomplexan parasite with schizogony in endothelial cells of pulmonary vessels accompanied by early and metrocyte stages of sarcocysts in the heart of a thick-billed parrot (Rhynchopsitta pachyrhyncha). The pattern of this disease is similar to that of the acute phase (approximately 10-15 days postinoculation) of experimental infections of budgerigars, Melopsittacus undulatus, with high doses of sporocysts of Sarcocystis falcatula.

Forty-four budgerigars (Melopsittacus undulatus) were administered sporocysts of Sarcocystis falcatula orally and were examined at necropsy intervals from less than 12 hr to 168 days. Tissue were examined by touch preparations (of organ cut surfaces), light microscopy, and electron microscopy. Meront and cyst burdens were determined in various organs and correlated with duration of infection, inoculum, and the meront or cyst burdens of other organs. Host inflammatory tissue reactions were quantitated and correlated with meront and cyst burdens. Quantitation of meronts was more accurate in tissue sections than in touch preparations, but quantitation of merozoites was better in touch preparations. More than 97% of meronts were found in capillary, venular, and venous endothelial cells. Cysts were found only in cardiac and skeletal myocytes. Merogony began in the lamina propria of the small intestine less than 12 hr postinoculation (PI). Meronts were in liver and lung by the second day PI and in other organs by 3-7 days PI. Mean meront burdens were highest in lung (33 meronts/mm2), lower in liver and kidney (1-3 meronts/mm2), and infrequent in other organs (less than 0.9 meronts/mm2). Cysts were first seen in cardiac myocytes 7 days PI. They developed through the metrocyte stage and then degenerated, rarely reaching maturity. Cysts were first noted in skeletal muscle at 8 days PI. In leg, upper esophagus, and tongue, cysts matured between 44 and 77 days PI. In pectoral muscles, the majority of cysts degenerated during the late metrocyte and early intermediate stages (28-42 days PI). In addition to a previously reported and often fatal acute interstitial pneumonitis, S. falcatula-infected budgerigars also sustained a chronic active hepatitis, interstitial myocarditis, myositis, nephritis, splenitis, and encephalitis. These lesions weakly correlated with meront burdens in most sites during early infection (up to 50 days PI).

The normal microscopic and submicroscopic structure of the lower respiratory tract of the budgerigar (Melopsittacus undulatus) is described and compared with other birds and mammals. Granular (type II) pneumocytes are confined to linings of air sacs, parabronchi, and their atria; however, their secretions (surfactant) cover the surfaces of the infundibula and respiratory space. Infundibula extend from the atria and give rise to the air capillaries, which branch and anastomose freely with those of adjacent infundibula and other parabronchi (interparabronchial septa are not found). Infundibula and the respiratory labyrinth are lined by a continuous epithelium of squamous pneumocytes, whose perikarya are concentrated in the infundibula and whose peripheral cytoplasm is markedly attenuated. The squamous pneumocytes of the respiratory labyrinth share a basal lamina with the blood capillaries that they envelop.