Managing lead exposure and toxicity in cow-calf herds to minimize the potential for food residues.

Lead poisoning is commonly diagnosed in cattle. In this study, 3 groups of cattle from different herds accidentally exposed to discarded lead batteries on pasture were intensively studied to determine the extent and severity of exposure. The losses from acute death due to lead toxicity were substantial in all the 3 study groups at 12%, 17%, and 4%. Blood samples were taken from all cattle around the time of the first diagnosis and then later in 2 of the 3 herds to monitor the change in lead concentrations over time. Asymptomatic lead toxicosis was observed in these herds. In these 3 groups, between 4% and 12% of asymptomatic cattle had blood lead concentrations consistent with acute lead poisoning (> 0.35 ppm), and between 7% and 40% of these asymptomatic animals were in the high-normal range (0.1-0.35 ppm). Because of the consistently high number of asymptomatic cattle with elevated lead levels, all cattle potentially exposed to a lead source should be tested before sale or slaughter to minimize the entry of lead into the food chain. The blood lead concentrations, which were monitored for months after the initial diagnosis, decreased slowly after the cattle were removed from the lead source. The prolonged retention of lead may be due to continued release and absorption of lead from metal particles in the reticulum or rumen. The mean reduction in the lead level was 0.046 ppm (95% CI, 0.017-0.075 ppm) every 30 days for these 2 herds. Using a single-component exponential model, the half-life of lead in the animals retested from Herds 1 and 2 was highly variable. The median half-life was 63 days (interquartile range, 34-107 days). One out of 8 pregnant heifers with high blood levels had a stillborn calf. There were no abortions or calf mortalities in this group. Blood samples were'collected from the calves around the time of birth. The concentrations of lead in the blood of the calves exposed in utero were low (0.010-0.095 ppm).     

Long-term follow-up of blood lead levels and haematological and biochemical parameters in heifers that survived an accidental lead poisoning episode

Four of 10 heifers that survived an episode of lead poisoning caused by an old broken battery in the pasture were periodically monitored from days 14 to 205 after the episode, with the aim of (i) determining the time-course of lead clearance from blood; and (ii) assessing whether the exposed cattle showed changes in haematological parameters or serum markers of hepatic and renal function (e.g. serum creatinine level) that might be useful as indicators of subclinical toxicity. On the first sampling day, lead levels in blood varied between 0.478 and 0.758 mg/l. The half-life of lead in blood was rather variable, ranging from 68 to 266 days. Despite the high blood lead levels, no significant changes were detected in haematological parameters or hepatic/renal markers, all of which remained within normal ranges. In conclusion, these cattle that survived an episode of lead poisoning may constitute a risk for human consumers, but do not appear to have suffered severe health consequences themselves.     

Treatment of lead poisoning in wild geese.

Twenty-seven wild geese (Anser albifrons) suffering from lead poisoning caused by ingestion of lead shot were treated with disodium calcium ethylenediaminetetraacetate. The concentration of lead in blood ranged from 0.4 to 23.0 micrograms/ml, with a mean concentration of 5.6 micrograms/ml. In 22 of the birds, 1 to 48 lead pellets (mean, 10.5 pellets/bird) were seen on radiographs of their gizzards. Eleven of 27 birds recovered 3 to 8 weeks after the initiation of treatment. In the birds that recovered, the lead pellets were rapidly eroded as the birds recovered their appetites in response to treatment, and disappeared radiographically between treatment days 17 and 52. The birds that did not survive died within 4 weeks, despite decreased concentrations of lead in blood. Of these 16 birds, 15 had radiographic evidence of impaction of the proventriculus at the first examination and no evidence of resolution of the impaction at the time of death. In contrast, only 2 of the 11 geese that recovered had impaction of the proventriculus at the time of admission. Thus, the condition of the proventriculus seems to be the first consideration to evaluate in the prognosis of lead poisoning in geese.     

Background lead levels in dairy cattle: updated values for 1986

Lead poisoning continues to be a problem in cattle. The toxicologic significance of blood lead levels requires the differentiation of background blood lead from toxic levels. A ten-fold variation of background blood lead levels reported in previous studies has prompted us to conduct our own survey. Our results indicate significantly lower background blood lead levels in New York State cattle analyzed in 1986 than in those levels previously reported elsewhere.     

Assessment of the potential toxicity of a poison for rabbits, pindone (2-pivalyl 1, 3 indandione), to domestic animals

The toxicity of pindone, a rabbit poison, to horses, cattle, goats, chickens, dogs and cats was investigated, using extension of prothrombin time (PT) as an index of poisoning. The daily dose of pindone, administered for 5 days, ranged from 0.3 mg/kg for dogs to 2.5 mg/kg for chickens. This range of dose rates was considered to be indicative of the worst possible case that could arise following a campaign of baiting for rabbits. Although significant elevations in PT (more than double baseline values) were noted in all species other than horses, clinical signs of anticoagulant poisoning were not observed in any of the species tested. From the observed PT, cattle and cats appeared to be the most susceptible, and horses the least susceptible, to pindone toxicity. The half-lives of the elevated PT were calculated as 3.1 days for cattle, 2.8 days for goats and chickens, 1.9 days for horses and dogs and less than one day for cats. It is proposed that these half-lives can be used as a guide for determining the duration of treatment of pindone-affected animals.     

Bovine lead poisoning in Alberta: A management disease

Lead poisoning was the most common toxicosis diagnosed in cattle by Alberta Animal Health Laboratories between 1964 and 1985 (n = 738 cases, = 33.5 cases per year). Seasonal variation in incidence was evident, and occurrence was frequently associated with change in housing or pasture. Discarded batteries or used crankcase oil were implicated in more than 80% of cases for which the source of lead was determined.

Pulmonary congestion, marked congestion and hemorrhage of thymus and heart, and presence of oil or lead particles in the ingesta were the most common postmortem findings. Eighty-six percent of cases were confirmed by elevated lead levels in tissues.

Lead poisoning represents a significant, unnecessary loss to producers. Increased producer awareness and improved waste management on farms could significantly reduce the incidence of lead poisoning in cattle.

     

Lead poisoning in cattle and its implications for food safety

The lead poisoning incidents in cattle investigated by the Veterinary Laboratories Agency between 1990 and 2003 are reviewed. Lead poisoning was most commonly encountered in young calves, but cattle of all ages were affected. The lead was derived mainly from lead paint, lead accumulator batteries and lead in soil from old mine workings. Paint was responsible for the majority of cases of poisoning in young calves; yearling animals were most at risk from discarded batteries, and adult cows were most commonly poisoned by geochemical sources of lead. There was a marked seasonal incidence, with most cases occurring after turnout in the spring and early summer.     

Terbufos poisoning in a dairy herd

This report describes the accidental poisoning of over 200 head of Holstein cattle by the organophosphate, terbufos. The ingestion of an acutely toxic dose (approximately 7.5 mg/kg) of terbufos by 84 heifers resulted in severe respiratory distress as the primary clinical sign and death within 12 hours. There was no response to treatment with atropine sulfate. One hundred and twenty milking cows received a portion of the contaminated feed diluted approximately ten times. These cattle had typical signs of organophosphate poisoning and responded to atropine sulfate. Severely affected cows received pralidoxime chloride and activated carbon 48 h after terbufos ingestion but did not respond to the drugs. Diagnosis of organophosphate poisoning was confirmed by tissue and feed analysis for terbufos and measurement of whole blood cholinesterase activity.     

Icterus and amaurosis caused by lead poisoning in a cynomolgus monkey (Macaca fascicularis)

The diagnosis and treatment of a case of lead poisoning in a cynomolgus monkey (Macaca fascicularis) are described. The clinical signs were jaundice and amaurosis. Clinicopathological findings suggested cholestasis. A tentative diagnosis of lead poisoning was made when basophilic stippling of erythrocytes was observed in a peripheral blood smear. The diagnosis was confirmed by finding a lead concentration of 2280 micrograms/litre in a venous blood sample. Cage bars painted with red lead appeared to be the source of the poison. The lead was chelated by the intramuscular administration of 2,3 dimercapto-1-propanol (BAL) and calcium disodium edetate for seven days, followed by oral D-penicillamine for five weeks. The encephalopathy was treated with dexamethasone sodium phosphate. Recovery from the blindness was noted after 10 days and marked improvement of the general well being of the animal was observed after one month.     

Lead poisoning in cattle

Lead poisoning is a frequent cause of poisoning in domestic animals. Signs of encephalopathy and gastroenteritis are commonly observed in cattle following lead poisoning. This article discusses the etiology, epidemiology, pathogenesis, clinical signs, diagnosis, postmortem findings, and treatment of lead poisoning in cattle.     

Lead poisoning in calves due to old white lead paint

A case of poisoning by chronic ingestion of lead in calves with a peracute clinical course is described. The source of lead was a prime coat of white lead on old white painted doors. These doors originated from an institution for aged people and had been used as pen walls for fattening calves. About 12 weeks later five animals died within hours after onset of CNS-symptoms. The post mortem examination of three animals revealed one with multifocal laminar edema and mild vasculitis in the cerebrocortex, one with acid fast intranuclear inclusion bodies in the renal tubular epithelial cells and one without lesions. Liver, kidney and abomasal contents of two animals were analysed for lead content. The concentration was diagnostic for lead poisoning in one case only.     

Toxic effects seen in a herd of beef cattle following exposure to ash residues contaminated by lead and mercury

Lead poisoning was diagnosed in three cattle along with increased mercury levels in the liver and kidney tissues of two of these animals. The clinical signs were different in each case and included salivation, anorexia, delayed menace response, delayed withdrawal reflex, head pressing, localized muscle fasciculation, reduced tongue tone, ataxia, rumen atony and seizures. Blood lead concentration was increased in all three cases to 0.76, 0.37 and 0.454ppm. Post mortem changes characteristic of lead poisoning were only recognized in one case and included cerebro-cortical oedema, cortical neuronal necrosis and endothelial proliferation, especially at the tips of the cerebral gyri. The animals were poisoned by ingestion of lead-contaminated ash residues from a bonfire. The abnormal levels of mercury in the liver and kidney tissues of two animals may also be at least partly attributable to the intake of the metal in the ash residues. The levels of mercury in the three samples from the ash residue were relatively low (1.31, 0.7 and 2.1ppm).     

Lead concentrations in blood and milk from periparturient dairy heifers seven months after an episode of acute lead toxicosis

In September 1988, 100 of 300 yearling dairy heifers developed blindness, tachypnea, foaming at the mouth, chewing, and facial fasciculations. Twenty-five animals died. Lead toxicosis was diagnosed based on the clinical signs and the presence of excessive concentrations of lead in whole blood, liver, kidney, and rumen contents of affected animals. The source of the lead was sudan grass silage that had been contaminated by soil that contained up to 77,000 mg/kg of lead. Lead concentrations were determined approximately 7 months after the acute episode of lead toxicosis. Whole blood and milk samples were obtained from heifers and a group of control cows 2 weeks prior to (blood only), at the time of, and 2 and 4 weeks after freshening. No lead was found in any of the milk samples (detection limit = 0.055 mg/liter). Animals that had been severely affected by lead toxicosis experienced a transient increase in whole blood lead concentrations at freshening that was not high enough to be considered toxic. No similar increases in blood lead were observed for control cows or heifers that had experienced milder toxicosis. These findings suggest that at parturition lead is mobilized into the blood of cattle previously exposed to excessive lead.     

Clinical findings in dogs and cats with lead poisoning

Over an 11-year period, 68 cases of lead poisoning were diagnosed in dogs and three in cats, accounting for 58.6% and 21.4% of the accidental poisonings in dogs and cats, respectively, presented at the Small Animal Clinic, University of Queensland. Of the dogs, 94% showed alimentary tract involvement and 67.6% central nervous system signs. Blood lead concentrations above 0.3 ppm were considered to indicate toxicity when associated with alimentary tract or central nervous system abnormalities. The percutaneous absorption of lead in dogs is proposed as a factor for intoxication.     

Demographic data and treatment of small companion animals with lead poisoning: 347 cases (1977-1986)

Three hundred forty-seven cases of lead poisoning in small animals, diagnosed after 1976, were reviewed. The types of treatments used and their outcomes were analyzed. Changes in blood lead concentrations following various treatments, as well as the sources of lead exposure, were also reviewed. The geographic origins of the cases were traced, and demographic factors were studied to determine possible correlates that might explain the regional distribution of cases.     

Blood lead and urinary delta aminolevolonic acid (U-ALA) in the diagnosis of lead toxicosis of dogs

A comparative evaluation of the usefulness of blood lead and urinary delta aminolevolonic acid estimations in the diagnosis of canine lead poisoning was made in 2 dogs which were given increasing quantities of lead by mouth for extended periods. In both lead administered dogs the blood lead levels remained elevated throughout the experimental period of 18 weeks. This contrasted with the results of U-ALA determinations in which elevated levels were detected only infrequently and at erratic intervals lacking relationship to lead exposure.     

Determination of delta aminolevulinic acid in the urine of cows in acute mass lead poisoning

The concentration of delta aminolevulinic acid (ALA) in the urine of dead heifers (n = 3), diseased cows (n = 13) and clinically healthy cows (n = 29) was determined in the course of acute mass intoxication with lead. At the same time, the content of lead was determined in kidney, liver, in rumen contents of dead heifers and in the beet pulp fed to the animals. The ALA concentrations were converted to values per uniform specific weight of urine and per gram of creatinine secreted with urine. As found, the determination of ALA concentration per gram of creatinine is diagnostically insignificant in the case of lead poisoning. The average ALA values in the urine of the dead and clinically diseased cows (221.0, 119.9 and 72.3 mumol per litre) markedly differed from the average values of ALA concentrations in the urine of the clinically healthy animals (41.2, 32.8 and 25.6 mumol per litre). Owing to the wide variability of the determined ALA concentration in urine it appeared useful in cases of suspicion of lead poisoning of cattle to determine ALA concentration in the urine of the group of clinically diseased animals and in the group of clinically healthy animals in order to compare ALA secretion with urine in the two groups. A 2.9-fold average increase of ALA in the urine of clinically diseased animals, compared with the ALA values in the urine of clinically healthy animals, already testifies to lead intoxication.     

EXPERIMENTAL POISONING OF HORSES AND CATTLE WITH SWAINSONA CANESCENS VAR HORNIANA

Horses and cattle fed swainsona ( Swainsona canescens var horniana ) over a period of 8 to 10 weeks lost condition and became incoordinated and hypersensitive. Histotogical examination of tissues from affected animals revealed the characteristic changes of widespread cellular vacuolation and axonal spheroids in the CNS.
Cattle withdrawn from the toxic plant after being fed for varying periods up to 8 weeks returned to normal.
Serum α-mannosidase activity declined significantly in cattle during the test period, whereas in horses the activity rose. Serum alkaline phosphatase levels increased significantly in cattle but not in horses.
The similarity of the clinical signs of disease in horses was noted to those seen in Indigofera linnaei poisoning (Birdsville disease). Differential diagnosis can be made by botanical observations and by an increased frequency of vacuolated lymphocytes in the blood in swainsona poisoning.     

Cestrum parqui (green cestrum) poisoning in cattle

SUMMARY Naturally occurring cases of poisoning of cattle by Cestrum parqui were characterised by ataxia, depression, recumbency, convulsions and death. Three cattle were dosed experimentally by intrarumenal administration of fresh plant material. One calf died 48 h after receiving 30 g (wet weight) of plant /kg body weight. Doses of 11 and 17 g/kg caused only mild intoxication, with dullness and anorexia lasting 2 days. In natural and experimental cases the main lesion was hepatic periacinar necrosis. Elevated levels of plasma aspartate transaminase and prolonged prothrombin times were demonstrated in experimental cases. Haemorrhage beneath the serosa and into the intestinal lumen occurred in field cases, but not in the experimental. It is concluded that C. parqui poisoning in cattle is a primary hepatotoxicity.     

Acute lead poisoning in cows due to feeding of lead contaminated ash residue

In a dairy herd of 21 cows which were on pasture during the day at the end of May 2002, four eight years old cows were suddenly inappetent and showed severe diarrhoea consisting of black discolorate feces. A few days after the onset of the disease, three affected cows exhibited neurological disorders. These cows were admitted to the IInd Medical Clinic of the University for Veterinary Medicine in Vienna. Following clinical signs were observed: circulatory weakness, anorexia, atony of the rumen, diarrhoea and in accordance with acute lead poisoning typical signs of the central nervous system. One cow died and the other two animals were euthanized. Results of blood testing were anaemia, basophil spotting of erythrocytes, increase of liver enzymes and CK, hypocalcaemia, decrease of potassium and phosphate. The cerebrospinal fluid of two cows showed increased CK-, LDH- and AST-values. The lead contents of whole blood samples were between 0.486 and 0.928 mg/kg, of liver samples 13.3 to 114.4 mg/kg, of kidney samples 172.2 to 448 mg/kg and of rumen content 59 mg/kg fresh matter. At necropsy, enteritis, liver fluke disease and severe interstitial and alveolar pulmonary emphysema were found. Pathohistologically typical ischaemic necrosis of neurons predominantly at the tips of the gyri, disseminated petechial hemorrhages and moderate diffuse neovascularisation, but no acid-fast intranucleolar inclusion bodies in the renal tubules were observed. As causative agent of the acute lead poisoning a residue on combustion, taken up by the cows on the pasture, was confirmed. The ash residue was formed by combustion of three tires which contained 450 g heavy weights of 96.5% lead for wheel balance. The lead content of the ash residue was between 2.9 and 28 g/kg dry matter.