Janis A. Raines, DVM
A 1.5-year-old male three-toed sloth (Bradypus variegatus) presented moribund and unresponsive in its enclosure. Venipuncture of the femoral rete was performed for a complete blood count and blood chemistry panel. Blood glucose was performed in house on a glucometer (Encore, Bayer Corporation, Elkhart, IN, USA) and was 30 mg/dl. Glucose supplementation (30 ml 25% dextrose SQ) was initiated and within 30 minutes, the animal began to behave normally again and began to feed. This unusual behavior and periodic hypoglycemia repeated itself every 24 hours for three days and resolved after supportive therapy. Bloodwork at each occasion was unremarkable, save an increased alkaline phosphatase that is attributed to the animal’s young age, a severe hypoglycemia, and monocytosis of unknown origin.8 In addition, the red blood cells were noted as having a pallor to them. Iron-deficiency anemia was a differential, even though no anemia was found in this sloth, as this clinical presentation was similar to another sloth that had been anemic.
For the next four days, behavior, mentation, and feeding response of this animal was apparently normal. Blood glucose concentration during this time were normal. However, this animal was receiving oral electrolyte supplementation (Biolyte, Pharmacia & Upjohn Co., Kalamazoo, MI, USA; 60 ml PO SID), gastrointestinal motility enhancers, (Metoclopramide: oral-Morton, Grove Pharmaceutical, Inc., Morton Grove, IL; 0.1 mg/kg PO once; Injectable-A-H Robins, Richmond, VA, USA; 0.05 mg/kg, IM SID for 3 days), and gastric protectants (Cimetidine, Abbott Labs, N. Chicago, IL, USA; 10 mg/kg IM once). One week after initial presentation, the sloth was again found moribund and unresponsive with a glucometer reading of 15 mg/dl, but no resolution of clinical signs occurred following the same regimen that was previously successful. The animal refused to feed and was tube-fed a slurry (blended mixture of Chorisia spp., Ficus elastica, and an electrolyte solution) that has been successfully used in other anorectic sloths. These “moribund” animals can be enterally supported as often just the stimulation from the placement of the tube in the esophagus and subsequent gastric distension is sufficient to bring these animals out of an unresponsive state. Due to severe hemodepression, intravenous catheter placement was not possible. Intraosseous catheter placement was attempted but unsuccessful due to inability to access marrow cavity. The marrow cavity was reduced in this animal due to a suspected abnormal growth pattern from an improper diet as a hand-reared neonate.7 Although the animal appeared to be resting quietly in a sling and overnight reports were unremarkable, the sloth was found dead the following morning.
One of the challenges of keeping Bradypus spp. successfully in captivity is providing proper husbandry and environment.1,3,6 For a phylogenetically primitive animal, they are very sensitive to changes in temperature and diet.4 Loss of gut flora is deadly and excessive stress can lead to anorexia which is followed closely by death due to complete ileus.4 The challenge to this case, besides the unusual normal behavior of the animal involved, is determining the extent of illness once the animal starts showing clinical signs. It is difficult to assess cardiac disease in Bradypus spp. This is attributed to their dorsoventrally flattened thorax and the extremely close placement of the ribs.2,5,9
Gross necropsy revealed appropriately digested foodstuff within the gastrointestinal tract and no other grossly significant lesions within the rest of abdominal viscera. The pericardial sac was thickened and the interior of the sac grainy in appearance. The epicardium was thickened, grainy, and heavily inflamed. The interior of the cardiac chambers was grossly normal, no gross dilation, nor any abnormalities of the valve leaflets were noted. Histopathologic evaluation indicated multifocal areas of hemorrhage, neutrophils, and macrophages in the epicardium. The epicardium was covered by large colonies of bacterial cocci admixed with fibrin, and degenerate and necrotic neutrophils. Strands of fibrin admixed with bacterial cocci adhered to the epicardium and produced multifocal vasculitis. Microscopic lesions in other organ systems were consistent with bacterial emboli: pneumonitis, multifocal acute tubular nephrosis, and segmental membranoproliferative glomerulonephropathy. In this case, bacterial cultures taken at necropsy were nondiagnostic because of contamination. The histopathology suggested Streptococcus as the primary differential for infecting organism. It is probable that the epicarditis was the nidus from which a systemic septicemia began, affecting other organs, and producing the clinical hypoglycemia.
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