PULMONARY ARTERIAL DISEASE ASSOCIATED WITH RIGHT-SIDED CARDIAC HYPERTROPHY AND CONGESTIVE HEART FAILURE IN ZOO MAMMALS HOUSED AT 2,100 M ABOVE SEA LEVEL.

Subacute and chronic mountain sickness of humans and the related brisket disease of cattle are characterized by right-sided congestive heart failure in individuals living at high altitudes as a result of sustained hypoxic pulmonary hypertension. Adaptations to high altitude and disease resistance vary among species, breeds, and individuals. The authors conducted a retrospective survey of right-sided cardiac hypertrophy associated with pulmonary arterial hypertrophy or arteriosclerosis in zoo mammals housed at Africam Safari (Puebla, México), which is located at 2,100 m above sea level. Seventeen animals with detailed pathology records matched the study criterion. Included were 10 maras (Dolichotis patagonum), 2 cotton-top tamarins (Saguinus oedipus oedipus), 2 capybaras (Hydrochaeris hydrochaeris), and 1 case each of Bennet's wallaby (Macropus rufogriseus), nilgai antelope (Boselaphus tragocamelus), and scimitar-horned oryx (Oryx dammah). All had right-sided cardiac hypertrophy and a variety of arterial lesions restricted to the pulmonary circulation and causing arterial thickening with narrowing of the arterial lumen. Arterial lesions most often consisted of medial hypertrophy or hyperplasia of small and medium-sized pulmonary arteries. All maras also had single or multiple elevated plaques in the pulmonary arterial trunk consisting of fibrosis, accompanied by chondroid metaplasia in some cases. Both antelopes were juvenile and died with right-sided congestive heart failure associated with severe pulmonary arterial lesions. To the authors' knowledge, this is the first description of cardiac and pulmonary arterial disease in zoo mammals housed at high altitudes.

Spongiosis Hepatis in a Wild Aquarium-Maintained Red Irish Lord.

An aquarium-maintained female Red Irish Lord Hemilepidotus hemilepidotus presented with severe coelomic distension. The fish was anesthetized for ultrasonographic examination, which highlighted multiple cyst-like lesions in the liver and a distended ovary that was filled with follicles and an inspissated egg mass. Multiple exploratory celiotomies were performed for egg mass removal, liver biopsy, ovariosalpingectomy, and body wall rupture repair. Fourteen weeks after original presentation, and subsequent to 2 weeks of anorexia, the fish died. At necropsy, the liver was severely enlarged and distorted by multiple, coalescing, cyst-like spaces with no grossly normal liver parenchyma. The spleen also contained a raised cyst-like structure. Microscopically, the liver had well-demarcated foci of hepatocyte loss with retained meshworks of interconnected, perisinusoidal stellate cells. The fluid-filled spaces surrounded by stellate cells were not lined by epithelium or endothelium. The spleen had similar fluid-filled spaces formed of stellate cells. The cyst-like lesions in the liver were consistent with spongiosis hepatis; however, the concurrent development of a morphologically comparable lesion in the spleen is not typical of spongiosis hepatis cases. This case may represent the first report of spontaneously occurring spongiosis hepatis in a fish maintained in a public aquarium, as well as the first report in a fish of spongiosis hepatis-like lesions in an organ other than the liver.