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

            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.

Differential diagnosis

            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.

            In dogs, rabies, distemper, and hepatitis may appear similar to lead poisoning.

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.