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Biomedical subjects

E P Dolensek

Publications and source records attributed to E P Dolensek.

14 recordsLinked to original sources
PubMed1986

Congestive cardiomyopathy in neonatal artiodactyls.

From January 1982 through December 1985, 11 newborn artiodactyls died with clinical and/or pathologic evidence of cardiomyopathy. Clinical signs were inability to rise, depression, failure to nurse, hypothermia, and shivering. Macroscopically, the animals had mild to marked dilatation and thinning of the interventricular septum and left ventricular free wall. Histologic findings included thinning and waviness of myofibers and acute myodegeneration and myocytolysis.

Animals↗
PubMed1985

Cardiomyopathy and vitamin E deficiency in zoo animals and birds.

Cardiomyopathy associated with vitamin E deficiency was diagnosed in more than 100 ruminants and primates and in 106 embryos and newly hatched chicks and ducklings. Affected bird embryos failed to pip the eggshell and died inside. Newly hatched chicks and ducklings and neonatal ruminants were weak, had difficulty standing or rising, and died within a few days. Death usually occurred without premonitory signs of disease in juvenile and adult animals. On gross examination, the hearts of the neonatal ruminants had areas of mottled, pinkish-tan myocardium. The hearts of the embryos and newly hatched birds were edematous, pinkish, and pale. In the juvenile ruminants, irregular, whitish patches or pale areas were seen in the myocardium. Histologically, there was multifocal myocytolysis in the myocardium of the neonatal and juvenile ruminants and embryos and newly hatched birds. Focal disseminated or diffuse myocardial fibrosis and myocytolysis were observed in the hearts of the adult animals. Plasma alpha tocopherol values were low enough in all species to be considered deficient. These values increased significantly after the addition of alpha tocopherol and/or vitamin E to the diets of the animals. Cardiomyopathy has not been diagnosed in any of the same groups of animals since supplementation was initiated.

Animals↗
PubMed1984

Cardiomyopathy associated with vitamin E deficiency in seven gelada baboons.

Between November 1979 and July 1982, 7 captive gelada baboons (Theropithecus gelada) died; 5 of them died unexpectedly, 1 died after a 4-month history of heart failure, and 1 was anemic and dyspneic for 2 days before death. Of those that died unexpectedly, 1 was anemic and 4 were clinically normal. At necropsy, all baboons had white or pale patches of myocardium. Histologically, fibrosis and acute myocytolysis were observed in the myocardium. Three affected baboons were tested for plasma alpha-tocopherol content and were found deficient. Four unaffected baboons were given vitamin E for 24 months, and plasma alpha-tocopherol content returned to normal. Blood selenium content was determined in 1 affected baboon and was normal.

Anemia↗
PubMed1984

Listeriosis in seven bushy-tailed jirds.

Listeriosis was diagnosed in 7 bushy-tailed jirds (Sekeetamys calurus). Death in all cases was acute, and there were no clinical signs. Necropsy revealed necrotizing lesions in the liver, intestines, spleen, and hepatic and mesenteric lymph nodes. On histologic examination large numbers of gram-positive coccobacilli were seen in the lesions. Pneumonitis was seen in 6 jirds, and small numbers of bacteria were seen in the lungs in all cases except one. Diagnosis was based on bacterial culture of the liver in 2 jirds and on immunofluorescence of bacteria when tissue specimens from 2 other jirds were stained with fluorescein-labelled antiglobulins specific for Listeria monocytogenes.

Animals↗
PubMed1983

Myelopathy and vitamin E deficiency in six Mongolian wild horses.

Degenerative myelopathy was diagnosed in six Mongolian wild horses. Three of the horses had a history of ataxia dating from birth to 3 months of age. The clinical signs were uncoordinated movement of the hindlimbs and an abnormally wide-based gait and stance. The other 3 horses had mild ataxia. There were no gross lesions in the brain, vertebrae, or spinal cord. Histologic examination revealed degeneration of the neural processes in the ventral and lateral funiculi of all 6 horses. Myelin sheaths were dilated and vacuolated, and there were swollen, fragmented, or lysed axons. Neuronal degeneration, phagocytosis, and accumulation of periodic acid-Schiff-positive, xylol-insoluble lipopigment were observed in the affected neurons of the dorsal root ganglia. The plasma alpha-tocopherol values of 5 of the affected horses ranged from less than 0.03 to 0.08 (mean, 0.04 +/- 0.01) mg/dl. Seven clinically normal horses from the same herd had a range of less than 0.03 to 0.3 (mean, 0.11 +/- 0.02) mg/dl, which was low enough to be considered deficient.

Animal Population Groups↗
PubMed1982

Myopathy in the nyala.

Between January 1973 and June 1981, a total of 21 nyalas (Tragelaphus angasi) died with clinical and/or pathologic evidence of myopathy. The main clinical signs were stiffness, inability to rise, and failure to suckle in newborn fawns. Death usually occurred without premonitory signs of disease. Gross lesions were characterized by white or pale patches of skeletal or cardiac muscle. Histologically, acute degeneration or necrosis and mineralization were commonly observed in skeletal muscle. Acute necrosis of the myocardium with or without arteriolar fibrinoid necrosis was usually found in juvenile animals. Interstitial fibrosis of the myocardium with arteriosclerosis was commonly observed in adults. The plasma alpha tocopherol values of 3 affected nyalas ranged from 0.03 to 0.08 mg/dl (mean, 0.05 mg/dl). Unaffected nyalas from the same herd had a range of 0.09 to 0.24 mg/dl (mean, 0.13 mg/dl), which is low enough to be considered clinically deficient. The blood selenium values of the affected nyalas and other nyalas from the same herd ranged from 0.30 to 0.33 ppm (mean, 0.32 ppm), and were considered normal.

Animals↗
PubMed1975

Uniocular vascular occlusion in a paraplegic hybrid monkey. A clinicopathologic study.

One eye of a hybrid monkey showed ophthalmoscopic, fluorescein angiographic, and electroretinographic evidence of ophthalmic artery occlusive disease. Histopathologic examination of that eye revealed widespread atrophy of the choroid, retina and optic nerve. An associated paraplegia was presumed to be the result of vascular occlusive disease as well.

Animals↗