Abstract
Over a 2-year period, a pair of adult giant anteaters (Myrmecophaga tridactyla) died of cardiac insufficiency associated with severe dilated biventricular cardiomyopathy. The female died with clinical signs of prolonged, progressive exercise intolerance and dyspnea. The male was diagnosed with progressive and chronic dilated cardiomyopathy by ultrasonography. Although the female never began treatment, the male was given oral cardioactive drugs, but was unresponsive. At necropsy, the heart of each animal appeared globoid with thin, flaccid ventricular walls. Histopathology supported the gross findings of cardiomyopathy with associated chronic passive hepatic and pulmonary congestion. The clinical pattern is parallel to that shown by taurine-deficient domestic felines.
Introduction
Dilated cardiomyopathy is an occasional finding in domestic dogs1,3,6 and cats4,5 and less frequently in foxes, raccoons, opossums, ferrets, and skunks.7 Secondary myocardial disease of this pattern is observed in domestic cats due to insufficient dietary taurine.8 Biventricular dilatation and associated cardiac insufficiency are the hallmarks of a taurine-deficient cardiomyopathy in domestic cats.8-10 They also develop sequelae of retinal degeneration, reproductive and developmental anomalies, increased platelet aggregation, and decreased white blood cell immune function.4 In felines, taurine and carnitine supplementation can ameliorate the clinical signs, and, in many cases, improve cardiac condition and size to near normal parameters.4,8,11 To date, dilated cardiomyopathy due to a diet restricted in taurine has only been described in felines, but has been suggested in dogs and foxes.3,7
Case Report
Two giant anteaters (Myrmecophaga tridactyla) were exhibit-mates and developed similar clinical signs suggestive of chronic cardiac insufficiency and congestive heart failure over a period of 2 years. The female presented first with clinical signs of slowly progressive dyspnea and decreased physical activity, which went largely unnoticed. The animal eventually died from this problem without any treatment attempted. Following the female’s death, the male was examined in April of 2000. The animal was immobilized with tiletamine/zolazepam (Telazol, Fort Dodge Animal Health, Fort Dodge, IA, USA, 240 mg IM) and isoflurane (AErrane, Baxter Healthcare Corp., Deerfield, IL, USA, 1% by face mask). Radiographs revealed an apparently enlarged heart, but electrocardiography was unrevealing. No other abnormalities were noted.
The male developed similar clinical signs in February of 2001, evidencing a marked decrease in physical activity and partial anorexia. The animal was immobilized with tiletamine/zolazepam (Telazol, Fort Dodge Animal Health, Fort Dodge, IA, USA, 160 mg IM) and isoflurane (AErrane, Baxter Healthcare Corp., Deerfield, IL, USA, 2% by face mask). A tentative diagnosis of anemia was made based on findings at that time (Hct 7%; ISIS mean 35.5%). These results later proved to be lab error on re-examination. The animal was re-immobilized in March with tiletamine/zolazepam (Telazol, Fort Dodge Animal Health, Fort Dodge, IA, USA, 200 mg IM) and isoflurane (AErrane, Baxter Healthcare Corp., Deerfield, IL, USA, 2% by face mask). Physical exam revealed a hematocrit within expected limits (Hct 32%; ISIS mean ±35.5%), progressive weight loss, pulmonary edema, and ascites. The hemogram and serum chemistries were within expected limits for the species, except for a rise in hepatocellular enzymes, most likely associated with hepatic congestion.
Eventually, the animal could not walk without inducing dyspnea and open-mouthed breathing. Peripheral edema progressed to anasarca. By late May, the animal was induced with sevoflurane (Ultane, Abbott Laboratories, Abbott Park, IL, USA, 4% by face mask) for in-depth examination. A severely enlarged heart with a characteristic globoid appearance was documented by radiography. Transthoracic echocardiography imaged extremely thin myocardial free walls and virtually no ventricular excursion during systole. Tricuspid regurgitation (pressure estimated at 42 mm Hg) and mitral regurgitation, with an apparently normal aortic valve, led to diagnosis of dilated cardiomyopathy with a reduced ejection fraction (approx. 5–10%). The images indicated a very poor forward flow of blood from the ventricles when compared to the domestic cat. Normal values for the anteater have not been established, but work is underway to do so. Electrocardiograms were consistent with the changes noted on echocardiography. Abdominal ultrasonography revealed moderate ascites and bilateral hydronephrosis. Punction of the abdomen yielded approximately 600 ml. of an acellular transudate, as confirmed by in-house cytology.
The animal was treated with furosemide (Lasix furosemide, Taylor Pharmaceuticals, Decatur, IL, USA, 100 mg PO BID for 10 days) for 1 week prior to restraint, and digoxin (Digoxin, Carr Drugs, New Orleans, LA, USA, 2 mg PO BID for 2 days) immediately following the exam. It died 2 days after examination.
A globoid heart with thin left and right ventricular walls was apparent at necropsy of both animals. Histopathology supported the gross finding of bilateral dilated cardiomyopathy with associated passive congestion of lungs and liver in both animals. Mineralization of the aorta and stomach was also found in the male. Vitamin A and E serum concentrations were within normal limits for carnivores (vitamin A 90 ng/ml, National Research Council mean 100; vitamin E 0.32 µg/ml, National Research Council mean 0.35 µg/ml), while the blood taurine level (plasma 18 nmol/ml, whole blood 75 nmol/ml) was significantly lower than the values from another female anteater (plasma 33 nmol/ml, whole blood 280 nmol/ml) held at a different institution (San Francisco Zoo) showing no clinical signs of heart disease.
Discussion
Due to reports of hyperostosis associated with hypervitaminosis D in tamanduas fed commercial feline diets,2 changes in the diet of captive anteaters were made. In the diet for these giant anteaters, recommendations made by the zoo’s consulting nutritionist changed the commercial cat food-based diet to a paste made of moistened lamb and rice dog food (Nature’s Recipe Lamb Meal, Rice, and Barley Canine Formula, Nature’s Recipe Pet Foods, Corona, CA, USA) and Leafeater (Marion Leafeater, Marion Zoological, Plymouth, MN, USA), with yogurt, and vitamin supplements (The Missing Link Omega 3, Designing Health Inc., Valencia, CA, USA and K-Sol Vitamin K, Vetamix Inc., Shenandoah, IA, USA). The new diet was readily accepted by the animals. Daily treats of banana and avocado, plus rotten logs and insects were added for enrichment.
The dog food-based diet was analyzed for taurine on two separate occasions (June 01, 2001 and July 24, 2001) using the “as fed” diet. Analysis was provided by the Amino Acid Analysis Laboratory (Department of Molecular Biosciences, School of Veterinary Medicine, UC Davis, CA, USA). The resulting levels of taurine were 0.18 g and 0.11 g taurine/kg of dry matter. These levels indicate that taurine concentrations are severely deficient when compared to the levels required by the domestic cat, which are of 1 g/kg DM for dry expanded food, according to the National Research Council (1986; Nutrient Requirements of Cats, Revised Edition, National Academy Press, Washington, DC, USA. Pp. 13–15). The clinical signs, pathogenic course, and postmortem results of these cases are strongly suggestive of a nutritional deficiency. The pattern is similar to secondary cardiomyopathy of domestic felines with taurine deficiency.
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