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 3–7 days after consumption of large quantities of young oak leaves in the spring or green acorns in the fall. Fallen trees associated with a recent storm are often reported with outbreaks. Mortality as high as 70% may be 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 pyrogallol, gallotannins, polyhydroxyphenolic compounds, or their metabolites produced by microbial activity in the rumen, causes GI and renal dysfunction.Signs include anorexia, depression, emaciation, brisket edema, 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, which is evident 4–6 days after exposure, may be characterized by increased BUN and creatinine, proteinuria, glucosuria, hyperbilirubinuria, 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. Evidence of hepatotoxicity characterized by elevated liver enzymes may also be present.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, aminoglycoside antibiotic poisoning, oxalate poisoning, and ochratoxicosis. |