Lead poisoning in a cat

Lead poisoning was suspected in a 3-year old Persian cat with depression, anorexia and sporadic vomiting. Laboratory tests disclosed an increased urinary delta aminolevulinic acid (δ-ALA) concentration but normoblastaemia or basophilic stippling of erythrocytes. Treatment for lead poisoning with calcium ethylenediamine tetraacetate for 5 days brought clinical improvement and reduction of urinary δ-ALA concentration but signs of toxicosis recurred in the next week. Repeated chelation therapy brought prompt improvement. A dog and another cat in the household had increased urinary δ-ALA concentrations, indicating metabolic effects of lead exposure, but were clinically well and were not treated. The source of lead was believed to be old paint.     

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.     

Chronic plumbism in rabbits: a comparison of three diagnostic tests.

Three groups of rabbits (A, B, and C; 6 rabbits/group) were fed a lead supplement of 25, 50, and 100 mg of Pb/kg of live weight/day for 87 days to compare the efficacies of 3 diagnostic tests--whole blood lead concentration, urinary delta-aminolevulinic acid (UALA), and fluorescent erythrocyte test (FET)--and to determine the clinicopathologic changes of experimentally induced lead poisoning in rabbits. All rabbits given lead had whole-blood lead concentrations greater then the maximum value (0.030 mg/dl) for control rabbits (group D), indicating that this measurement is a reliable indicator of lead ingestion. All group A rabbits (fed 25 mg of Pb/kg) and 66% negative UALA test results, with values less than the maximum value (0.12 mg/dl) for group D (control) rabbits. Only group C rabbits (fed 100 mg of Pb/kg) had consistently positive UALA FINDINGS. The test was therefore considered unreliable for detecting daily lead intakes less than 100 mg/kg of live weight of rabbits. All rabbits given lead had erythrocytes which fluoresced red when exposed to light rays with wavelenghts from 320 to 400 nm; fluorescence was not observed in erythrocytes of control rabbits. The FET appears to be a convenient and reliable diagnostic test for lead ingestion. In groups B and C, clinical signs of lead poisoning were mild, nonpersistent anemia characterized by the presence of poikilocytes, hupochromic erythrocytes, target cells, erythroblasts, erythrocytes with punctate basophilic stippling, reduced mean corpuscular hemoglobin concentrations, and relative lymphocytosis, neutropenia, and eosinopenia. One rabbit from the group fed the largest dose displayed partial anorexia.     

A biochemical profile for predicting the chronic exposure of sheep to Microscystis aeruginosa, an hepatotoxic species of blue-green alga

Sheep which grazed on the shoreline of a freshwater lake which had a toxic bloom of Microcystis aeruginosa were studied for evidence of chronic poisoning, and a serum biochemical profile was developed to indicate sub-lethal, chronic poisoning in the sheep which had been exposed to microcystins. The profile included measurements of glutamate dehydrogenase (GLDH), γ-glutamyl transferase (γGT), bile acids, bilirubin and albumin. Of 18 sheep which were exposed to M aeruginosa for more than three months, 100 per cent had high serum concentrations of bile acids, 94 per cent had high activities of gldh and γgt, 83 per cent had high bilirubin and 72 per cent had low albumin concentrations compared with the median values of unexposed animals. Other sheep which were exposed for shorter periods, showed evidence of hepatic injury after one week of exposure. The majority of the sheep showed no preference for an alternative, uncontaminated source of water.     

Feline Precursor. porphyria, characterized by persistent delta. Aminolevulinic aciduria

A female domestic shorthaired cat had frequent seizures and vague gastrointestinal signs. Lead poisoning was suspected because of increased urinary delta aminolevulinic acid concentration. However, abnormalities continued despite repeated chelation therapy and blood lead concentration was normal. Delta aminolevulinic aciduria persisted, but concentrations of porphobilinogen in urine and of porphyrins in blood, urine and faeces were normal. An inherited porphyric disorder was suspected, involving deficiency of aminolevulinic acid dehydrase, an enzyme active in haem biosynthesis. Accumulation of aminolevulinic acid in vivo could explain the observed signs.     

Experimental lead intoxication in dogs: a comparison of blood lead and urinary delta-aminolevulinic acid following intoxication and chelation therapy.

Intravenous lead administration to dogs produced an acute syndrome of lead intoxication charcterized by depression, vomiting, anorexia and weight loss. The effect of chelation therapy with calcium disodium ethylene diamine tetraacetate, penicillamine or both was determined by serially monitoring changes in blood lead and urine delta-aminolevulinic acid. Following therapy, blood lead values were significantly lower in chelated dogs than non-treated lead exposed dogs on days 7 and 10. Urine delta-aminolevulinic acid at day 7 was significantly higher in untreated lead exposed dogs than in other groups. There was no significant difference in blood lead or urine delta-aminolevulinic acid between lead intoxicated dogs which underwent the indicated chelation therapy protocols. There was, however, a trend for higher urinary delta-aminolevulinic acid excretion in those intoxicated dogs undergoing calcium disodium ethylene diamine tetraacetate therapy as opposed to those undergoing penicilamine therapy. There was no significant correlation between blood lead and urinary delta-aminolevulinic acid previous to lead exposure. However, after lead exposure significant correlation was present at days 4, 7, 10 and 14. Certain lead exposed dogs following chelation therapy were noted to have normal blood lead levels but elevated urinary delta-aminolevulinic acid suggesting that blood lead does not always correlate with metabolic effects of lead in the body. Urinary delta-aminolevulinic acid was therefore recommended as an additional laboratory parameter which improved assessment of lead exposure in dogs, particularly in determining adequacy of chelation therapy.     

Copper poisoning in a flock of sheep. Copper excretion patterns after treatment with molybdenum and sulfur or penicillamine

During an outbreak of chronic copper poisoning, fecal and urinary copper excretion were measured following treatment with molybdenum and sulfur supplementation of the feed (0.1 g ammonium molybdate plus 1 g sodium sulfate/sheep/day) or oral penicillamine (50 mg/kg bodyweight/day) using rams in metabolism cages. Serum glutamic-oxaloacetic transaminase activities and liver levels of molybdenum and copper in sheep that died were also monitored. Within four days of starting molybdenum and sulfur supplementation a highly significant increase in fecal copper excretion was evident and the increase persisted throughout the monitoring period (five weeks — general treatment of the flock continued for another three weeks). There was no effect of the molybdenum and sulfur supplementation on urinary excretion of copper. The molybdenum and sulfur supplementation was very effective, resulting in a rapid marked decrease in mortality. Oral penicillamine treatment induced cupruresis but did not affect fecal copper excretion. The results indicated that, while the cost of penicillamine may be a limiting factor for general treatment of a flock, it may be the drug of choice for the therapy of valuable breeding animals because cupruresis may be accurately and individually controlled. Serum glutamicoxaloacetic transaminase activities were a valuable aid in diagnosing chronic copper toxicosis as well as for monitoring recovery. High initial liver copper levels were gradually reduced following molybdenum and sulfur treatment. However, at the end of the study the liver copper levels of dead sheep varied within wide limits and there were still some sheep with high liver copper levels.     

Acute and long-term effects of exposure to sodium monofluoroacetate (1080) in sheep

Acute and long-term effects of a single, relatively high oral dose (0.25 and 0.30 mg/kg) of sodium monofluoroacetate (1080) on the survival and productivity of sheep were evaluated to establish a better understanding of 1080 poisoning and identify more specific changes diagnostic of toxicosis. In survivors, clinical signs of acute 1080 toxicosis such as salivation and lethargy were generally very mild. Fasted animals were more prone to 1080 toxicity. In animals that died, more severe signs, including tachypnoea, dyspnoea, and tremors occurred for 15-20 min prior to death. 1080 concentrations were highest in the blood > heart > skeletal muscle > liver. 1080 could not be detected in any of these organs of the animals that survived. Serum citrate concentrations were elevated for 4 days after dosing. No clinical or biochemical abnormalities were found in any animal after 4 days. Histopathological lesions were most marked in the heart and lung with inflammation, necrosis, and scattered foci of fibrous tissue in the myocardium, pulmonary oedema and inflammation of the lung. No adverse long-term effects on general health or reproductive performance were observed in any sheep that survived the first 4 days following exposure to 1080. The most reliable diagnostic indicators of 1080 exposure in sheep were measurement of its residues in blood, skeletal muscle and ruminal contents, increased serum citrate concentration, elevated heart rate, and characteristic electrocardiograph changes (up to 4 days after exposure). Death from 1080 is most likely to occur within 96 h, and animals that survived this period appeared normal.     

Lead concentrations in the blood and eggs of backyard laying hens

AIMS: To investigate the prevalence of lead exposure in hens and eggs from backyard poultry in a sample of Auckland households, the relationship between concentrations of lead in the blood of the hens and in the shells and yolks of eggs from the same household, and to examine associations with measures of hen health, environment and husbandry factors.

METHODS: Thirty households participated in the study from August to November 2016, each providing one adult hen for sampling, an egg from the household if available, and completing a questionnaire on hen husbandry. Concentrations of lead in blood were determined using a portable lead analyser. Eggs were analysed for concentrations of lead in the yolk and shell using inductively coupled plasma mass spectrometry after biological digestion with a mixture of nitric and hydrochloric acid.

RESULTS: Twenty three of 30 hens (77%) showed evidence of lead exposure, with median concentrations of lead in blood of 0.77 (min?<0.16, max 8.02) μmol/L. All eggs showed evidence of lead exposure, with concentrations of lead in the yolk ranging from 0.003–1.07?mg/kg, and concentrations of lead in the eggshell ranging from <0.1–0.82?mg/kg. A positive correlation existed between concentrations of lead in the blood of a hen and concentrations of lead in egg yolk from the same hen (R²=0.97), and both the yolk (R²=0.58) and shell (R²=0.30) of an egg from her flock. No association was found between concentrations of lead in blood and hen health indices measured in this study. Concentrations of lead in blood were higher in hens from properties with homes built before 1941 than between 1941–1960 (p=0.03), and in hens from properties with weatherboard homes than brick homes (p=0.049).

CONCLUSIONS AND CLINICAL RELEVANCE: There was a high prevalence of lead exposure in this sample of Auckland backyard chickens, with the majority of hens being sub-clinically affected. Associations were found between concentrations of lead in the blood of the hens, and properties with homes built before 1941 and clad in weatherboard. Concentrations of lead in over half the egg yolks sampled were at levels sufficient to warrant human health concern. The assessment of concentrations of lead in backyard poultry and eggs intended for human consumption is recommended to protect human and bird health.     

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.     

An outbreak of lead poisoning in dogs

SUMMARY An outbreak of lead toxicosis in working dogs on a sheep farm is described. The affected dogs exhibited neurological signs which appeared to be initiated by straineous physical activity. Radiological examination and estimation of urinary delta aminolevolonic acid (U-ALA) was not found to be useful for clinical diagnosis but blood lead estimation was helpful in detecting and confirming dogs that were exposed to lead. Gross pathological lesions were absent in a lead poisoned dog. However, histopathological lesions were seen in brain and bone. Acid-fast lead inclusion were not detected in liver and kidney epithelial cells but were present in osteoclasts.     

Sheep scab control using trans-cinnamic acid

A series of in vitro and in vivo assays were conducted to examine the effects of trans-cinnamic acid ethyl ester on Psoroptes mange mites. In vitro, 24h after exposure to the test material at concentrations of 10, 1 or 0.1% (v/v), 100, 74 and 20% of mites had died, respectively, compared to 8% following exposure to the control (0.05% SDS only). The different life-cycle stages were affected similarly by the test compound. The concentration required to produce 95% mortality 24h after exposure to the test compound was 6.29% (95% confidence interval 4.98-8.88). Tarsal contact of the mites with the test compound was also sufficient to achieve high levels of mortality; 100% death was observed when the mites were placed in contact with either sheep skin circles treated to give 0.01 ml/cm(2) or polyester cloth circles treated with 0.03 ml/cm(2). However, the residual activity of both skin and cloth treated with 0.03 ml/cm(2) was completely lost after 7 days. In vivo, trans-cinnamic acid ethyl ester suspended in 2% (w/v) lecithin was applied as a spray formulation to eight sheep with active artificial infestations of sheep scab. Seven of the 8 treated sheep were cured and remained completely clear of scab mites for 56 days. However, 33 days after treatment 2 adult female mites were observed on one of the eight treated sheep and the mite population on this sheep subsequently recovered. In contrast, in a control group of two infested sheep, treated with a 2% (w/v) lecithin only, mite populations increased as expected in a typical scab infestation, but eventually self-cured in one animal. The data suggest that, with appropriate development of suitable application technology, trans-cinnamic acid ethyl ester could have a role as a potential therapeutic treatment for active sheep scab, however the short residual period of activity is likely to limit its use in commercial sheep flocks.     

Copper poisoning in the Kruger National Park: field investigation in wild ruminants

Chronic copper poisoning was investigated in ruminants within the Phalaborwa area of the Kruger National Park (KNP). Exposure of ruminants to environmental copper pollution resulting form copper smelting operations of a mine in the area was examined by comparing impala faecal copper concentrations in dung heaps and tissue (liver, lung and kidney) copper concentrations of organs collected from impala and buffalo culled within three risk zones (high, moderate and low) of the study area in relation to the distance from the smelter over a period of 4 years. An additional area within the KNP not exposed to the environmental copper pollution from the mine served as control. Tissue copper accumulation was also determined in tracer impala placed in the highest risk zone. The results of this study confirmed the occurrence of chronic copper poisoning in impala and indicated an inverse relationship in extent of impala faecal copper elimination and in tissue copper accumulation in impala and buffalo with distance from the copper smelter. Impala liver copper concentrations were shown to be a reliable indicator of copper accumulation for these ruminants. The presence lung copper concentrations, indicating the exposure to airborne copper were the highest in impala culled in the zone closest to the smelter. Liver copper concentrations above the diagnostic limit of 150 ppm for chronic copper poisoning in domestic sheep were consistently found in impala within the highest risk zone. Clinical pathological measurements suggested that AST activity could possibly be used as an indicator for chronic copper poisoning in impala. It is concluded that, in addition to the environmental and geo-botanical evidence previously reported, the copper smelter of a nearby copper mine is the most likely source of copper pollution responsible for chronic copper poisoning in impala and the occurrence of high copper concentrations in buffalo in the Phalaborwa area of the KNP.     

Performance of sheep grazing in pastures of Brachiaria decumbens,Brachiaria brizantha,Panicum maximum,and Andropogon gayanus with different protodioscin concentrations

Brachiaria spp. are the most important grasses for ruminants in central-western Brazil. However, the use of these pastures is limited by their toxicity due to steroidal saponins. This experiment was conducted for 60 days to demonstrate the resistance of sheep raised on Brachiaria spp. pastures to steroidal saponin poisoning. The experiment was composed by 48 animals randomly divided into four groups (n?=?12). Among them, 32 4- to 5-month-old castrated male crossbred Santa Inês sheep, originating from flocks that had been grazing on Brachiaria spp. for more than three consecutive years, and 16 were non-adapted (naïve) sheep from flocks that never had prior contact with pastures of Brachiaria spp. were randomly divided into four groups. Each of the four experimental groups was composed by eight adapted and four non-adapted animals. The four experimental groups were introduced into paddocks, each of which contained a single grass: either Brachiaria decumbens, Brachiaria brizantha, Panicum maximum, or Andropogon gayanus. The addition of the naïve sheep to the groups was designed to detect pastures’ toxicity to naïve sheep and to adjust the stocking rate to optimize the use of forage. The weight gains of sheep grazing on B. decumbens, B. brizantha, and P. maximum were similar; however, the A. gayanus group showed lower weight gains compared with the other groups (P?<?0.05). The mean serum activities of γ-glutamyltransferase in the sheep grazing on B. decumbens were higher than those in the sheep from the other groups. No significant differences among the groups were found in aspartate aminotransferase, creatinine, albumin, or total protein serum concentrations. No clinical signs were observed in the adapted sheep in any of the pastures. Of the four non-adapted sheep introduced into the B. decumbens pasture, two showed clinical signs of steroidal saponin poisoning, and one died. No clinical signs were observed in the non-adapted sheep in the other pastures. The saponin (protodioscin) concentrations in the pastures varied from 3.3 to 12.2 g/kg DM in B. decumbens, from 2.8 to 9.1 g/kg DM in B. brizantha, and from 1 to 1.5 g/kg DM in A. gayanus. No saponins were found in P. maximum. It is concluded that sheep from flocks reared in pastures of B. decumbens and B. brizantha were resistant to steroidal saponin poisoning and showed similar weight gains to those of sheep grazing in other tropical pastures.     

Foremilk and bovine mastitis

Abstract

Lambs grazing cobalt-deficient pastures and injected with hydroxocobalamine gained significantly more weight and excreted significantly less methylmalonic acid in the urine than untreated controls. Lambs with liver vitamin B₁₂ levels in the range 0.1–0.2?g/g excreted less than 25 ?g of methylmalonic acid per ml of urine, whereas lambs with liver vitamin B₁₂ concentrations of less than 0.1 ?g/g excreted greater amounts. Lambs in both groups had serum vitamin B₁₂ concentrations less than 500 pg/ml.

No consistent diurnal variation in urinary methylmalonic acid concentrations was found for four lambs studied.

There was a decrease in the methylmalonic acid levels of urine after storage for more than 24 hours which could be prevented by acidification of the urine.

A mean urinary methylmalonic acid concentration greater than 30 ?g/ml for 10 animals randomly selected from a flock would indicate a cobalt deficiency in the flock as a whole.     

Superphosphate poisoning of sheep: a study of natural outbreaks

Superphosphate poisoning is typically a disease of pregnant and lactating ewes under nutritional stress. Poisoning has been observed only in the late winter and spring. Most episodes occurred when hungry sheep were forced to graze short pastures top-dressed within one week prior to the onset of clinical signs. Fine weather which is favourable for the application of fertiliser also favours the occurrence of poisoning. Clinical signs include anorexia, thirst, diarrhoea, weakness and incoordination. Death usually occurs within 48 hours of the onset of clinical signs. In some outbreaks the presenting signs are those of hypocalcaemia but response to calcium therapy is transient. Poisoning results in a toxic tubular nephritis and uraemia. No satisfactory treatment can be suggested but poisoning can be prevented by avoiding exposure of sheep to top-dressed pastures.     

Experimental lead toxicosis in swine

Thirty pigs, weighing 17 to 24 kg, were exposed to lead or sodium acetate orally or intraperitoneally (IP) 6 days each week for 13 weeks. These pigs were extremely tolerant of lead. Only mild clinical signs of lead toxicosis were observed in orally lead-exposed pigs despite blood lead concentrations of up to 290 micrograms/dl. Four IP lead-exposed pigs died, but eight other IP lead-exposed pigs survived the exposure period despite blood lead concentrations up to 14,300 micrograms/dl. Lead exposure caused marked decreases in blood delta-aminolevulinic acid dehydratase activities of all pigs and moderate decreases of blood hemoglobin concentrations, hematocrit percentages, mean corpuscular volumes, mean corpuscular hemoglobin concentrations, and mean corpuscular hemoglobins in IP lead-exposed, but not in orally lead-exposed pigs. Basophilic stippling was observed in erythrocytes of lead-exposed pigs, but not in those of control pigs.     

The effect of shade, shearing and wool type in the protection of Merino sheep from Hypericum perforatum (St John's wort) poisoning

OBJECTIVE: To investigate the roles of shade, fleece length and wool type in the protection of sheep from Hypericum perforatum poisoning. ANIMALS: Adult Merino ewes of superfine, fine and medium wool type. DESIGN: Seventy sheep were divided into seven equal groups. During late spring and summer a series of successive, replicate experiments was conducted, each using one group and lasting 5 days. The sheep carried 14 to 24 weeks wool growth. In each experiment the treatments tested were Hypericum +, sunlight + (n = 7); Hypericum +, sun - (n = 1); Hypericum -, sun + (n = 1); Hypericum -, sun - (n = 1). Next, 24 sheep in two equal groups were used in experiments of similar design to the above. Each group consisted of nine recently (1 to 3 weeks previously) shorn and three wool covered (25 to 26 weeks growth) sheep. The treatments tested were Hypericum +, sunlight +, fleece - (n = 9); Hypericum +, sun -, fleece + (n = 1); Hypericum -, sun +, fleece + (n = 1); Hypericum -, sun -, fleece + (n = 1). PROCEDURES: Finely milled Hypericum was administered by gavage to provide 3 mg hypericin / kg body weight. Sheep were sheltered from direct sunlight or were exposed for 5 h per day for 4 successive post-treatment days. Rectal temperatures were measured immediately before and at the end of each sunlight exposure session. Rectal temperature above 40 degrees C was considered indicative of hypericin poisoning. RESULTS: After Hypericum treatment hypericin poisoning was displayed by 26.5% of woolled sheep that were exposed to sunlight, but by none of those that were fully shaded. In similarly treated but recently shorn sheep 94% displayed hypericin poisoning when exposed to sunlight. In the wool covered group the percentages of poisoned animals based on wool type were: superfine 14%, fine 28.5%, medium 33.3%. In the recently shorn group the percentage for all three approached 100%. CONCLUSIONS: A majority of Merinos with at least 14 weeks wool growth will not be poisoned by a single oral dose of 3 mg hypericin /kg, but because hypericin persists in the blood circulation for several days this safe dose will be lowered by continuous daily ingestion. Sheep with access to substantial areas of shade could safely ingest much greater amounts of hypericin. Wool removal greatly increases the risk of poisoning. Superfine Merinos with a wool cover should be able to ingest more hypericin than comparable, medium wool types, without any increased risk of poisoning. The ability of ruminant livestock to safely ingest Hypericum is probably determined more by the amount of skin protection they have against incident sunlight than by differences in hypericin metabolism and excretion capacity.     

Protective effects of antioxidants on bitterweed (Hymenoxys odorata DC) toxicity in sheep

Antidotal effects of the 2 antioxidants butylated hydroxyanisole (BHA) and ethoxyquin (EQ) were evaluated in bitterweed (Hymenoxys odorata DC) toxicosis in sheep. Bitteerweed contains a toxic sesquiterpene lactone, hymenoxon, the toxicity of which is reduced by cysteine. Both BHA and EQ are known to induce hepatic glutathione production in rodents. Treatment of sheep with EQ (2.5 g/sheep/day for 9 days before poisoning) gave significant protection from toxic doses of bitterweed, but the protective effect of BHA was insignificant. Of 6 sheep given EQ in the feed, 5 survived 7 doses of bitterweed (4 g/kg/day or higher for 7 days), whereas 5 of 7 controls and 4 of 7 sheep given feed with added BHA died. The added EQ in the feed decreased the serum alkaline phosphatase activity and total protein, albumin, and calcium concentrations. Seemingly, EQ is the first protective agent with field application potential for bitterweed toxicity.     

Superphosphate poisoning of sheep: a study of natural outbreaks

Superphosphate poisoning is typically a disease of pregnant and lactating ewes under nutritional stress. Poisoning has been observed only in the late winter and spring. Most episodes occurred when hungry sheep were forced to graze short pastures topdressed within one week prior to the onset of clinical signs. Fine weather which is favourable for the application of fertiliser also favours the occurrence of poisoning.

Clinical signs include anorexia, thirst, diarrhoea, weakness and incoordination. Death usually occurs within 48 hours of the onset of clinical signs. In some outbreaks the presenting signs are those of hypocal- caemia but response to calcium therapy is transient.

Poisoning results iu a toxic tubular nephritis and uraemia.

No satisfactory treatment can be suggested but poisoning can be prevented by avoiding exposure of sheep to topdressed pastures.