Abstract
Prairie voles (Microtus ochrogaster) from 1 of the 3 laboratory animal facilities experienced increased unexpected deaths with no clinical signs. There was a total of 30 deaths in the affected facility and 16 deaths in the other 2 unaffected facilities in the same period. Significant gross findings included cardiomegaly (6/30, 20%) and pleural effusion (4/30, 13%). Heart weights (P = .0049) and widths (P = .0047) were significantly higher in M. ochrogaster from the affected facility than the other 2. Histology revealed cardiomyocytes with intracytoplasmic basophilic granular material in most M. ochrogaster from the affected facility (25/30, 83%). Of the affected animals, other changes included myocardial fibrosis (18/25, 72%), myocarditis (9/25, 36%), and atrial thrombosis (6/25, 24%). M. ochrogaster from the 2 other facilities, that died naturally or were euthanized for unrelated causes, did not reveal similar cardiac changes. Histochemical stains and immunohistochemical assays characterized the intracytoplasmic material as von Kossa negative and periodic acid-Schiff with diastase positive, that immunolabeled for myogenin and sarcomeric actin. Transmission electron microscopy showed the granular material as autolysosomes, with microtubular or filamentous dense aggregates, that were product of mitochondria and myofibrillar degradation. Affected and unaffected colonies are housed similarly, with identical husbandry except for water; reverse osmosis water was used in the affected facility and tap water in the unaffected. Water testing revealed significant differences in mineral content between reverse osmosis and tap water, with marked depletion in calcium, chloride, magnesium, potassium, sodium, zinc, sulfate, and orthophosphate. We speculate that the autolysosomal dysfunction is a result of mineral imbalance.
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