Myocardial fibrosis has increasingly been documented as an important cause of mortality in zoo primates. The changes have been associated with hypertensive heart disease, atherosclerosis, obesity, and hypovitaminosis E.1-7 Viral infections have been discussed, but the pathogenesis is more probably a noninfectious disease. Histologically the lesions are similar to chronic ischemic heart disease in elderly humans, except that in the great apes, atherosclerotic lesions may be absent, and deaths occur in middle-aged animals.5
A 16-year-old male Sumatran orangutan (Pongo pygmaeus), born in an English zoo, lived in a Swedish zoo for 12 years together with a clinically healthy female without producing any offspring. During a 22-month period, recurrent diffuse respiratory symptoms were treated with a variety of antibiotics, bromhexine, and prednisolone. The male was continuously lethargic and at times uncoordinated, and only prednisolone appeared to alleviate some of the symptoms.
The ape was found dead and necropsy was performed the same day. The orangutan weighed 192 kg and was obese. The major gross finding was severe effusion, with hydropericardium (>0.8 L), hydrothorax in the left pleural cavity (>0.7 L) and hemothorax (>3.0 L) on the right side. The lungs were congested, compressed and edematous. Approximately 1 L of clear watery fluid was found in the air sacs. The liver was severely enlarged with a reticulated appearance. A large amount of deeply infiltrating subcutaneous edema was present in the torso, and the eyelids were swollen and edematous. The heart appeared normal in shape; the myocardium and the valves were grossly unremarkable.
Histologic examination showed a severe diffuse fibrosis of the myocardium without any inflammatory cells present. The myocytes were multifocally hypertrophied and alternatively atrophic, with fibrous connective tissue in between muscle cells. Signs of atherosclerosis was not seen. Chronic pulmonary congestion with severe perivascular and interstitial fibrosis as well as chronic liver congestion was noted. Moderate focal lymphocyte airsacculitis was seen. Vitamin E and selenium levels in muscle and liver tissue were found to be within normal range.
The diagnosis was myocardial fibrosis. As no inflammatory reaction was seen in the heart, a viral infection was considered as less likely to have caused the long-term symptoms and extensive changes in the heart. The respiratory symptoms could have been due to both repeated infections and to heart disease, but the chronic changes in lungs and liver tissues point to a heart problem. A hypertensive heart disease together with obesity had probably over time produced the extensive fluid effusions and finally ended with a ruptured pulmonary vessel leading to a fatal hemorrhage to the pleural cavity. As this condition has been increasingly documented in captive great apes, further investigations are needed in the possible pathogenesis. Considering the comparative histology of the human condition of chronic ischemic heart disease, an overview of diets and management of the captive primates may be called for.
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