Lead poisoning follows ingestion of lead-containing materials
such as material from discarded car batteries; lead-based paints
are now rare.
Lead poisoning follows ingestion of lead-
containing materials such as material from discarded car
Lead poisoning is characterised by acute brain disease.
Irrespective of the rate of uptake of lead, the clinical
signs of intoxication are sudden in onset and characterised by
behavioural changes. Affected cattle become isolated and depressed
but are over- reactive to touch and sound.
They are blind but show no clinical lesions
in the eyes and may press the head into corners and against
Cattle with lead poisoning become isolated and
As the disease progresses, cattle become frenzied, bellow,
stagger and crash into obstacles. There may
be signs of abdominal pain including kicking at the abdomen and
frequent teeth grinding. Death may occur suddenly or within
Cattle with lead poisoning may show head pressing
In the advanced stages of lead poisoning, cattle
become frenzied, bellow, stagger and crash into
Your veterinary surgeon will also consider:
- Hypomagnesaemic tetany (staggers)
The diagnosis of lead poisoning
is based upon clinical signs and the presence of a lead
source. Confirmation depends upon increased kidney and liver lead
Cattle with severe neurological signs
of several days' duration may have extensive brain
pathology that is unlikely to respond to treatment. Slow
intravenous injections of a 5% solution of sodium calcium edentate
and oral solutions of magnesium sulphate are the treatments of
choice but are rarely successful once severe neurological signs are
present. Your veterinary surgeon will decide whether treatment or
euthanasia for welfare reasons is the better course of action, and
which drugs to administer.
Prevention is a matter of good management by not allowing
cattle access to sources of lead.
Regulatory authorities, such as the Food Standards Agency, may
recommend withdrawal periods before milk and/or meat from exposed
cattle may enter the food chain.
Toxicity may result from inadvertent dietary supplementation or
incorporation of a feedstuff with a high copper content, possibly
as the result of contamination. Acute
toxicity is rare. Copper
toxicity in cattle is much less common than in sheep. Ingestion of
high copper content in the ration over several
weeks/months will result in a
high liver copper content. Sudden release causes an
acute intravascular haemolytic crisis.
Toxicity may result from inadvertent dietary
supplementation or incorporation of a feedstuff with a
high copper content, possibly as
the result of contamination.
Acute copper toxicity causes severe gastro-enteritis with
colic signs, diarrhoea and rapid
dehydration. The affected cattle are very depressed, do not eat,
and death usually ensues within three days.
In cases of chronic copper toxicity the appearance of clinical
signs is associated with the destruction of red blood cells which
may be precipitated by stress. Affected cattle are weak, very dull
and depressed and separate from others in the group. They have a
poor appetite and often foetid diarrhoea. There
is jaundice (yellowing) of mucous membranes. Death is
preceded by recumbency.
Your veterinary surgeon will also consider
- Post-parturient haemoglobinuria
- Kale poisoning.
The diagnosis is based upon history, a source of excess copper,
and clinical findings of jaundice in chronic toxicity.
The diagnosis is supported by laboratory findings of
increased serum copper and liver enzyme concentrations.
The suspected copper source must be removed immediately. There
is no ammonium tetrathiomolybdate preparation licensed for use in
food-producing animals and its use in suspected cases
of chronic copper toxicity is poorly defined from a
Copper supplementation must be carefully considered after first
establishing a deficiency situation.
Historically, fluorosis resulted from
industrial pollution of grazing land where chronic disease
results after ingestion over many months/years but is rare in the
Growing cattle develop mottling of the enamel and premature loss
of teeth. Adult cattle show insidious onset lameness
affecting the hindlegs caused by periarticular exostoses of the
long bones. Fracture of the pedal bone may occur but there
are other more common causes of such sudden inset lameness. There
is no specific treatment.
Brassica plants and fertilisers are potential sources of
Brassica plants are potential sources of
Fertilisers are also potential sources of nitrates.
Note storage of fertilisers adjacent to cattle feed
- there is the possibility of feed
Acute poisoning with cyanosis, weak
rapid pulse, and dyspneoa, is seen within hours of
ingestion progressing rapidly to weakness, recumbency and
Causes of sudden death your veterinary surgeon will consider
- Lightning strike
Diagnosis is based upon classical clinical signs and exposure to
Intravenous injection of 4 mg/kg methylene blue as a
2 per cent solution.
Overdosage and accidental exposure to
organophosphates lead to toxicity.
Failure to correctly dispose of concentrated
dip (not an OP in this case) can lead to
Profuse salivation, colic and diarrhoea are followed by
muscle tremors, stiffness progressing
to paralysis. At this stage cattle show marked depression
with increasing severity of colic,
sweating and breathing difficulties followed rapidly by death.
Based upon clinical signs and history of exposure to/treatment
Atropine sulphate (0.1 mg/kg injected slowly intravenously
followed by 0.4 mg/kg injected subcutaneously) is repeated as
Correct storage and disposal of empty containers containing
Urea is used as a source of non-protein nitrogen (NPN) in feed
supplements especially in beef cattle. Nitrogen from urea is
released in the rumen as ammonia in the rumen. Accidental
urea intoxication occurs sporadically and can cause severe losses.
One incident resulted in the death
of 17 of 29 suckler cows within six hours
after the contamination of their drinking water with urea
Poisoning episodes typically occur after sudden access to urea,
which may simply involve only a break of several days' supply then
free access. Urea is highly soluble and will wash out of the
diet/feed blocks following heavy rain then cattle may drink the
puddles with a high urea content.
Signs of urea poisoning can appear within several hours and
include muscle twitching, teeth grinding, frothy salivation, bloat,
colic, frequent urination, forced rapid breathing, staggering,
bellowing, and terminal seizure activity. Often, animals are found
dead near the source of the urea supplement.
Your veterinary surgeon will also consider:
- Clostridial disease such as Blackleg
Diagnosis is based upon a history of access to urea, and the
50 litres of cold water then several litres of 6 per cent
vinegar have been recommended.
- Ensure thorough mixing of the ration.
- Gradual introduction to urea feeding with an uninterrupted