Lead poisoning in livestock
Lead poisoning in livestock
Lead poisoning in
animals and people is a major concern worldwide.
Poisoning in animal
populations may serve as a sentinel to assess the extent of environmental contamination
and human health problems related to lead.
In veterinary medicine,
lead poisoning is most common in dogs and cattle. Lead is the most common cause
of cattle poisoning. Lead poisoning in other species is limited by reduced
accessibility, more selective eating habits, or lower susceptibility.
Animals die or perform
poorly after accidentally ingesting lead. Gradual poisoning may also occur in
areas with heavy industrial pollution.
Causes
Old lead acid batteries are the
most common cause of lead poisoning in livestock. Battery cases become brittle
over time and are easily broken by inquisitive cattle. The lead and lead salts
that they contain are easily accessed and readily eaten by stock. One broken
tractor battery was reported to have fatally poisoned 28 cattle over several
weeks, though a small number of sick animals recovered. Another 200 cattle in
the same paddock were unaffected. Skimmings and ‘slag’ taken from molten lead during
attempts to recover the metal from old batteries are also highly toxic to stock
(as well as exposing the operators to health risks).
Other causes of lead
poisoning in stock include: licking and eating lead based paint from old paint tins,
buildings or other painted materials; eating ashes left after burning old
painted materials; eating linoleum; and drinking sump oil. Silage contaminated
by lead shot, automotive grease and oil filters, caulking, putty and even
access to leadlight windows have caused fatal lead poisoning in stock. Lead
fragments from collars used in pipeline joins (e.g.on large water pipe lines)
can pose a poisoning hazard and has been identified as a likely cause of fatal
lead poisoning.
In cattle, many cases
are associated with seeding and harvesting activities when used oil and battery
disposal from machinery is handled improperly. With the elimination of
tetraethyl lead from gasoline in many countries, the number of lead poisoning
cases attributed to oil consumption has declined in recent years. Other sources
of lead include paint, linoleum, grease, lead weights, lead shot, and
contaminated foliage growing near smelters or along roadsides. To prevent
future occurrences of lead poisoning, it is crucial to identify the source.
Lead poisoning is also encountered in urban environments and during the
renovation of old houses that have been painted with lead-based paint, leading
to exposure of small animals and children. The consumption, through grooming,
of dust containing lead has been reported in cats. Improper disposal of
lead-poisoned animal carcasses may result in toxicoses in nontarget scavenger
animals. Scavenging by endangered species such as the condor raises unique
concerns.
Even a small amount of lead can
kill cattle. Cattle will readily drink crankcase oil, lick grease from
machinery and chew on lead plumbing and batteries. Other frequent causes of
poisoning include flaking high lead paint, ash from fires in which lead
materials were burnt, lead shot from shooting. The lead in these materials
settles in the stomachs of cattle, where stomach acids gradually change the
lead into poisonous salts. Cattle are
at most risk of lead poisoning because they are very inquisitive and commonly
‘taste test’ new finds – including old batteries, flaking lead paint, sump oil,
ashes and just about any other potential lead source they come across. Lead and
other heavy materials tend to lodge in the reticulum (fore-stomach) of ruminant
animals. This provides a reservoir from which lead can continue to be absorbed
into the bodies of cattle, sheep and goats. Lead in old paint pigments is
finely ground and quite soluble. Lead previously exposed to acid conditions in
batteries and silage is also more easily absorbed from an animal’s gut than
clean metallic lead and thus presents a higher poisoning risk. Lead poisoning
is most common among calves because they are curious feeders, and both milk and
milk substitutes increase the amount of lead absorbed by calves. Sucking
animals can also receive lead in their milk.
Lead poisoning risks
can increase during drought. Hungry stock may develop a depraved appetite (pica),
particularly if also suffering trace element or mineral deficiencies. Hungry
stock are also more inclined to breaking into ‘no-go’ areas, such as around
farm sheds or the farm rubbish tip where there is some residual feed, or stock
may be held in house paddocks to make feeding easier. Less pasture cover makes
it more likely that stock will find hazards such as old batteries.
Lead is quite a
different story as various sources of lead are present and in daily use on most
farms. Lead is a persistent chemical in the environment and in stock. It should
be taken into account during any on-farm risk assessment for persistent chemicals.
Remember that people, particularly children, can be at risk from lead poisoning
as well as farm livestock and other domestic animals.
Pathogenesis
Absorbed
lead enters the blood and soft tissues and eventually redistributes to the
bone. The degree of absorption and retention is influenced by dietary factors
such as calcium or iron levels. In ruminants, particulate lead lodged in the
reticulum slowly dissolves and releases significant quantities of lead. Lead
has a profound effect on sulfhydryl-containing enzymes, the thiol content of
erythrocytes, antioxidant defenses, and tissues rich in mitochondria, which is
reflected in the clinical syndrome. In addition to the cerebellar hemorrhage
and edema associated with capillary damage, lead is also irritating,
immunosuppressive, gametotoxic, teratogenic, nephrotoxic, and toxic to the
hematopoietic system.
Lead causes anemia when
it combines with red blood cells and bone marrow. It damages the small blood
vessels, causing bleeding, and deprives the nerves, the brain and other organs
of oxygen. Lead severely damages the kidney and liver. It also causes
sterility, fetal death and abortion.
Clinical Findings
Clinical Findings
Acute lead poisoning is more common in young animals. The prominent
clinical signs are associated with the GI and nervous systems. In cattle, signs
that appear within 24–48 hr of exposure include ataxia, blindness, salivation,
spastic twitching of eyelids, jaw champing, bruxism, muscle tremors, and
convulsions.
Subacute lead poisoning, usually seen
in sheep or older cattle, is characterized by anorexia, rumen stasis, colic,
dullness, and transient constipation, frequently followed by diarrhea,
blindness, head pressing, bruxism, hyperesthesia, and incoordination.
Chronic lead poisoning, occasionally
seen in cattle, may produce a syndrome that has many features in common with
acute or subacute lead poisoning. Impairment of the swallowing reflexes
frequently contributes to the development of aspiration pneumonia.
Embryotoxicity and poor semen quality may contribute to infertility.
GI
abnormalities, including anorexia, colic, emesis, and diarrhea or constipation
are predominant manifestations in dogs. Anxiety, hysterical barking, jaw
champing, salivation, blindness, ataxia, muscle spasms, opisthotonos, and
convulsions may develop. CNS depression rather than CNS excitation may be
evident in some dogs. In horses, lead poisoning usually produces a chronic
syndrome characterized by weight loss, depression, weakness, colic, diarrhea,
laryngeal or pharyngeal paralysis (roaring), and dysphagia that frequently
results in aspiration pneumonia.
In
birds, anorexia, ataxia, loss of condition, wing and leg weakness, and anemia
are the most notable signs.
Symptoms
Although clinical signs
of poisoning normally precede death, most animals are simply found down or dead
on the pasture. Symptoms include:
Depression; Loss of
appetite; Occassionally diarrhea; Apparent blindness; Odd behaviour including
grinding teeth, bobbing head, twitching eyes/ ears; Frothing at mouth; Muscle
tremors; Staggers; Excitable; Convulsions.
Often the first sign of
lead poisoning is finding dead stock – often near a fence or some other obstacle.
Where affected animals are observed they show signs of central nervous system damage.
They generally cease grazing and appear very dull and unresponsive. They are
often blind and may walk aimlessly, including into fences and other obstacles,
before becoming comatose and dying. In some cases these symptoms are
accompanied by muscle twitches that may be more obvious around the face, ears
and eyelids but can involve any area of the body. Paralysis of the tongue, circling
and ‘star-gazing’ are also reported in some cases. Immediate veterinary advice
should be sought for any livestock showing nervous signs. Lead poisoning can
cause symptoms similar to those of other diseases affecting the nervous system including
some plant poisonings, PE (polioencephalomalacia) and metabolic diseases like
low blood magnesium (hypomagnesaemia or grass tetany). An accurate early
diagnosis is vital to help prevent continuing losses and to determine the
appropriate treatment for sick animals.
Lesions
Animals
that die from acute lead poisoning may have few observable gross lesions. Oil
or flakes of paint or battery may be evident in the GI tract. The caustic
action of lead salts causes gastroenteritis. In the nervous system, edema,
congestion of the cerebral cortex, and flattening of the cortical gyri are
present. Histologically, endothelial swelling, laminar cortical necrosis, and
edema of the white matter may be evident. Tubular necrosis and degeneration and
intranuclear acid-fast inclusion bodies may be seen in the kidneys.
Osteoporosis has been described in lambs. Placentitis and accumulation of lead
in the fetus may result in abortion.
Diagnosis
Diagnosis of lead
poisoning is based on a history of access to lead and the clinical signs. Post-mortem
examination will usually reveal lead particles in the reticulum of affected
ruminants. Lead poisoning can be confirmed by testing tissue samples (liver or
kidney) taken at post-mortem or by testing blood from live animals. Animals
that have had an abnormal lead intake will show elevated blood lead levels for
some weeks before they slowly fall to near normal levels. Lead levels in the
liver and kidney of survivors can remain elevated for many months. Animal
tissues containing elevated lead levels are not acceptable for human
consumption. Lead concentrations in various tissues may be
useful to evaluate excessive accumulation and to reflect the level or duration
of exposure, severity, and prognosis and the success of treatment.
Concentrations of lead in the blood at 0.35 ppm, liver at 10 ppm, or kidney
cortex at 10 ppm are consistent with a diagnosis of lead poisoning in most
species. Many countries have deemed blood lead concentrations >0.05–0.10 ppm
to be a notifiable disease in food-producing animals
Haematologic
abnormalities, which may be indicative but not confirmatory of lead poisoning,
include anemia, anisocytosis, poikilocytosis, polychromasia, basophilic
stippling, metarubricytosis, and hypochromia. Blood or urinary δ-aminolevulinic
acid and free erythrocyte protoporphyrin levels are sensitive indicators of
lead exposure but may not be reliable indicators of clinical disease.
Radiologic examination may be useful to determine the magnitude of lead
exposure.
Lead poisoning may be
confused with other diseases that cause nervous or GI abnormalities. In cattle,
such diseases may include polioencephalomalacia, nervous coccidiosis, tetanus,
hypovitaminosis A, hypomagnesemic tetany, nervous acetonemia, organochlorine insecticide
poisoning, arsenic or mercury poisoning, brain abscess or neoplasia, rabies,
listeriosis, and Haemophilus infections.
Treatment
Treatment for acute lead poisoning is seldom effective. The disease has
usually progressed too far to be treated once clinical signs are seen.
Treatment only stops or lessens the clinical signs of lead poisoning and must
be begun early if an animal is to be saved. The treatment of stock affected by
lead poisoning is often unsuccessful. Animals in the early stages of poisoning
are more likely to respond than those that are seriously affected. However, the
outlook is poor for any animal that has ingested a large amount of lead from
sources such as old batteries, lead paint or other forms of lead that are more readily
absorbed from the gut.
Cattle that eat lead
will likely die. If you suspect lead poisoning in cattle, remove cattle from
the affected area immediately. A veterinarian can help confirm the poisoning.
The cause should be identified and the risk removed.
More intensive
treatment options are available, including injections to increase the rate with
which lead is eliminated from the body. However, these options are unlikely to
be cost-effective for commercial livestock. Injections of thiamine hydrochloride
(vitamin B1) can reduce the effects of lead on the central nervous system.
Drenching with small amounts of magnesium sulfate (Epsom salts) may also help
to reduce absorption of lead from particles held in the reticulum of cattle,
sheep and other ruminants. These relatively low-cost treatments may improve the
survival rate of clinically affected animals. If tissue damage is extensive,
particularly to the nervous system, treatment may not be successful.
In livestock, calcium disodium edetate (Ca-EDTA) is
given IV or SC (110 mg/kg/day) divided bid for 3 days; this treatment should be
repeated 2 days later. In dogs, a similar dose divided qid is administered SC
in 5% dextrose for 2–5 days. After a 1-wk rest period, an additional 5-day
treatment may be required if clinical signs persist. No approved veterinary
product containing Ca-EDTA is currently commercially available.
Thiamine (2–4 mg/kg/day, SC) alleviates
clinical manifestations and reduces tissue deposition of lead. Combined Ca-EDTA
and thiamine treatment appears to produce the most beneficial response.
d-Penicillamine can be administered PO
to dogs (110 mg/kg/day) for 2 wk. However, undesirable adverse effects such
as emesis and anorexia have been associated with this treatment. d-Penicillamine
is not recommended for livestock.
Succimer (meso 2,3-dimercaptosuccinic acid, DMSA) is a chelating
agent that has proved to be effective in dogs (10 mg/kg, PO, tid for
10 days) and is also useful in birds. Fewer adverse effects have been
associated with DMSA than with Ca-EDTA.
Cathartics
such as magnesium sulfate (400 mg/kg, PO) or a rumenotomy may be useful to
remove lead from the GI tract. In cattle, surgery to remove particulate lead
material from the reticulum after the ingestion of batteries is rarely
successful. Barbiturates or tranquilizers may be indicated to control
convulsions. Chelation therapy, in combination with antioxidant treatment, may
limit oxidative damage associated with acute lead poisoning. Antioxidants such
as n-acetylcysteine (50 mg/kg/day, PO) have been used in combination with DMSA.
Mobilization
of lead at parturition, excretion of lead into milk, and lengthy withdrawal
times in food-producing animals raise considerable controversy regarding the
rationale for treatment from both public health and animal management
perspectives. The half-life of lead in the blood of cattle ingesting
particulate lead is usually >9 wk. Withdrawal times, which may be >1 yr,
should be estimated by periodic monitoring of blood lead concentrations. In a
herd of cattle with confirmed cases of lead poisoning, all potentially exposed
cattle should be evaluated. A small but significant portion of the asymptomatic
cattle may have concentrations of lead in tissues that exceed recognized food
safety standards.
Prevention
There are several steps you can take to protect your cattle and the
human food chain from lead contamination. You should:
- check your fields and barns for vehicle batteries, building materials, flaking lead paint, putty, lead flashing;
- remove or fence off fly-tipped material;
- prevent access to burnt out cars and old machinery that might contain lead;
- prevent cattle access to bonfire ash.
On farms with high lead soils, you should:
- keep your cows' soil consumption as low as possible;
- avoid waterlogged land and poached land for grazing;
- avoid overgrazing and maintain adequate sward height;
- fence off bare areas of soil;
- calibrate cutters when making silage to minimize soil uptake;
- flatten any molehills prior to cutting grass for silage;
- provide salt licks and mineral supplements;
- use main water or tested borehole water rather than natural run-off water from high lead soils.
Prevention is the best cure. Stock
are expert at finding old batteries, lead-based paint, sump oil and similar
poisoning risks in the farm rubbish tip or around the machinery shed. Batteries
powering electric fences and other farm equipment also need to be secured from
stock. Where possible, remove any old batteries from your property by taking
them to an approved recycling facility. Make sure that any broken battery cases
and spilled contents are also removed.
Cattle with lead
poisoning are not fit for human consumption.
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