Poisoning (termed saturnism or plumbism) occurs by:
licking of lead-based paint, the most frequent cause of plumbism, particularly
in young calves with pica;
ingestion of fodder contaminated by industrial pollutants;
ingestion of foodstuffs stored in containers with a lead base (notably
ingestion of water which has been standing in lead pipes (these
are usually protected by a coating of insoluble lead carbonate, however subsequent
repairs to the pipes may remove or destroy this protective layer, resulting in
a surge of lead from the pipe once flushed and refilled with water);
ingestion of vegetables which have been grown in soils saturated with lead
(e.g. pastures established on waste soil around the site of old lead mines);
ingestion of waste oil containing lead, or fragments of discarded batteries
or old wallpaper (decorated with lead-based paints);
for ducks, geese and swans (or other wild birds), ingestion of lead weights
or lead shot used in fishing and hunting; once lodged in the alimentary tract,
the lead progressively dissolves;
urban and atmospheric pollution from car exhaust gases.
(Note: the use of tetraethyl lead as an anti-knock agent in petrol contributes
to atmospheric lead. However, the increased use of lead-free petrol should reduce
the amount of lead from this source.) Pets and domestic animals may play a role as
biological indicators of lead pollution. The contamination of land by lead also occurs
in the immediate vicinity of motorways, busy roads and junctions.
Cumulative thiol-depriving poison, capable of blocking particular enzyme processes,
notably those involved in haemopoiesis.
Toxic oral doses in mg/kg (lead acetate):
LD (single exposure):
LD (multiple exposures):
6-10 mg/kg per day
Toxicity varies according to the different lead salts. Repeated doses of sufficient
quantity may induce a syndrome of acute lead poisoning.
Clinical features Acute intoxication in ruminants
neurological effects predominate but vary in their presentation; in order of
decreasing frequency: blindness, shaking, irritability, depression or convulsions,
ataxia, abnormal or erratic behaviour (walking round in circles, pacing, grinding
of the teeth);
gastrointestinal effects are common but occur less frequently than those described
above; in order of decreasing frequency: salivation, anorexia, diarrhoea,
abdominal pain, colic;
abortions, opisthotonos, lacrimation, nasal discharge and paralysis of the pharynx
may also be observed; general deterioration and coma; death may occur within
several hours to several days.
gastrointestinal symptoms present initially and predominate: anorexia, vomiting,
diarrhoea with colic, and abdominal pain;
followed by neurological signs: convulsions, hyperexcitability, opisthotonos,
blindness, lassitude and apathy, leading to paralysis;
death may occur and is relatively slow in its onset (several days).
birds (swans, waterfowl)
anorexia, weight loss, ruffled dull feathers;
conjunctivitis, ataxia, immobility with intermittent periods of collapse
and falling to the ground, convulsions, abnormal stance or postures (e.g.
head on the ground);
may lead to a rapid death, generally occurring within a few hours of exposure.
(Relatively uncommon in animals, or more correctly, more difficult to identify and
to diagnose accurately.) The clinical features are non-specific, of variable intensity
and are often transient:
anorexia, flatulence, abdominal pain and cramps, diarrhoea or constipation, reduction
in milk output, loss of weight;
the onset of clinical signs is very slow: several months.
Not well characterized, but from observations made in veterinary practice:
fatty degeneration of the liver and kidneys;
petechiae on the myocardium, epicardium and kidneys (the subcortical region);
relatively severe gastroenteritis;
EDTA, calcium disodium edetate, 25-50 mg/kg dissolved in normal saline or glucose
given intravenously, the dose repeated if necessary two to three times at 24-hour
dimercaprol (BAL) by deep im injection, 2-3 mg/kg every 16 hours for 24 hours;
8 hourly in the next 24 hours, then twice daily until a complete recovery is
Symptomatic and supportive care
hepatic protective agents; regimen to support hepatic failure;
tranquillizers or sedatives if necessary;
fluids and electrolytes; regimen to support renal failure.
samples of liver and kidney (post-mortem);
urine taken at 6 hours and 24 hours after treatment with EDTA (to confirm that
lead is being chelated and excreted);