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Quercus Poisoning : Introduction
(Oak bud poisoning, Acorn poisoning)
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Most animals are susceptible to Quercus poisoning, although cattle and sheep are affected most often. Most species of oak ( Quercus spp ) found in Europe and North America are considered toxic. Clinical signs occur several days after consumption of large quantities of young oak leaves in the spring or green acorns in the fall. High mortality is often observed. Malformed calves and abortions have been reported in dams consuming acorns during the second trimester of pregnancy. The toxic principle, which appears to be gallotannins, polyhydroxyphenolic compounds, or their metabolites, causes GI and renal dysfunction. Signs include anorexia, depression, emaciation, dehydration, rumen stasis, tenesmus, smell of ammonia on the breath, serous ocular or nasal discharge, polydipsia, polyuria, hematuria, icterus, and constipation followed by mucoid to hemorrhagic diarrhea. Renal insufficiency may be evidenced by increased BUN and creatinine, proteinuria, hyperphosphatemia, hypocalcemia, and urine with a low specific gravity. Pale swollen kidneys, perirenal edema, subcutaneous edema, ascites, and hydrothorax are common necropsy findings. Edema and subserosal petechial or ecchymotic hemorrhage of intestinal mucosa and ulceration of the esophagus and rumen may be seen. Diagnosis is based on clinical findings, necropsy, history, and histopathologic examination of the kidney (ie, nephrosis). Other common diseases that resemble oak poisoning include pigweed ( Amaranthus spp ) poisoning and aminoglycoside antibiotic poisoning.
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Quercus spp (oak)

Quercus spp (oak)
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Quercus spp (oak), leaves

Quercus spp (oak), leaves
Consumption of a pelleted ration supplement (1 kg/head/day) containing 10-15% calcium hydroxide plus access to more palatable feeds may be used as a preventive measure if exposure to acorns or oak leaves cannot be avoided. Calcium hydroxide, ruminatorics, and purgatives (such as mineral oil [1 L/500 kg], sodium sulfate [1 kg/400 kg], or magnesium sulfate [450 g/400 kg]) may be effective antidotes if administered early in the course of disease. Fluid therapy to correct dehydration and acidosis and transplantation of ruminal microflora may be beneficial. Clinical recovery usually occurs within 60 days but is rare if renal dysfunction is severe.

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