with Phil Rennie
Do you have any Oak trees on your property? If so it’s good to be aware that most animals are susceptible to Quercus poisoning, although cattle and sheep are affected most often.
Most species of oak (Quercus spp) found in New Zealand and elsewhere in the world are considered toxic.
Clinical signs occur three to seven 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.
Feed restriction before exposure plays a crucial role enhancing susceptibility. Mortality as high as 70 per cent may be seen.
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 hydrolysis in the rumen, binds and precipitates proteins, which results in GI and renal dysfunction.
Signs and symptoms
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 four to six days after exposure, may be characterised by increased BUN and creatinine, proteinuria, glucosuria, hyperbilirubinuria, hyperphosphatemia, hypocalcemia, and urine with a low specific gravity.
Pale swollen kidneys characterised by coagulative necrosis of the proximal convoluted tubular cells, 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 characterised by increased liver enzymes may also be present.
Diagnosis is based on clinical findings, necropsy, history, and histopathologic examination of the kidney (i.e., nephrosis).
Other common diseases that resemble oak poisoning include pigweed (Amaranthus spp) poisoning, aminoglycoside antibiotic poisoning, oxalate poisoning, and ochratoxicosis.
Antidotes and precautions
Consumption of a pelleted ration supplement (1 kg/head/day) containing 10-15 per cent 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, activated charcoal, 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.
Polyethylene glycol (1 g/kg/day) administered in the feed or water will bind tannins and reduce tissue damage.
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.
Improved range management to limit grazing in immature oak stands will prevent development of the syndrome.
While typical at this time of year with oak leaf fall, other diseases may also result in animals to become sick suddenly. If you suspect that your animals may be suffering from one of these toxicities, please contact your local vet clinic for advice.