Acorns are the fruits (achenes) of different species of oak. Common in England
and Northern Europe are:
Quercus ilex (holm oak, evergreen oak);
Quercus pedunculata (pedunculate oak);
Quercus robur (common oak, English oak);
Quercus petraea syn sessihflora (sessile oak, durmast oak).
Animals most affected
Cattle, (sheep, horses).
Ingestion of extremely large quantities of acorns in autumn, especially during periods
of food shortage or drought. Poisoning is extremely frequent and, in certain regions,
particularly serious, affecting mainly young animals.
Contains pyrogallic acids, up to 8%, although the amounts vary according to the age
of the acorn. Unripe, green acorns contain the highest levels of pyrogallic acids,
and certain species of oak (e.g. the pedunculate oak) are more toxic than others.
In addition, the age of the tree is significant, with youngest trees having the greatest
levels of pyrogallic acids and tannins.
Ingestion over a period of 1-4 weeks is necessary before toxic signs become apparent.
(Pigs are resistant to pyrogallic and tannic acids.)
Present first (within 7-10 days), and are severe and persistent:
anorexia, lack of rumination, abdominal pain;
severe constipation, followed by dark foetid diarrhoea, often haemorrhagic, (flatulence,
colic and salivation appear less frequently).
Equally intense and persistent, but presenting later:
cessation of lactation, inappetence, loss of weight and body fat, hypothermia
(Not persistent, or regular in their presentation)
haematuria or haemoglobinuria (rare).
(Infrequent and appearing towards the endstage of poisoning):
tremor, grinding of the teeth, ataxia, sluggishness, weakness in the hindquarters.
epistaxis, subcutaneous haemorrhages.
ventral oedema, jaw oedema and oedema of limbs (presentation rare and delayed);
abortion, patchy sweating (occasional).
A fatal outcome is common (up to 80% of animals with renal signs).
If blood urea levels reach 1-3 g/l, the prognosis is guarded;
if uraemia is >3 g/l, a fatal outcome should be anticipated.
general congestion of the carcase with an attendant odour of stale urine;
haemorrhagic gastroenteritis with necrosis of the muscular-serous layers;
occasional degeneration of the liver, with hypertrophy of the gallbladder;
congestion and degeneration of the kidneys, which appear large and pale, with
or without petechial haemorrhages;
frequently peri-renal oedema;
abdominal fat appears yellow in colour, is soft and has an odour of urine;
degeneration of muscles with suffusions of blood.
No antidote. Symptomatic and supportive care only:
gastrointestinal demulcents, liquid paraffin, mild oleaginous or mucilagenous
laxatives (infusion of linseed);
hepatic protective agents;
iv infusions of serum with added glucose and bicarbonates.
To avoid or prevent poisoning:
prune back oaks surrounding grazing areas;
prevent access to acorns;
isolate animals with sigus of a toxic syndrome indicative of acorn ingestion.