Copper toxicosis in a dairy goat herd

CASE DESCRIPTION: A closed herd of 400 mixed-breed dairy goats was examined because of a decrease in milk production and increase in mortality rate. Nine animals had died within a 1-month period. CLINICAL FINDINGS: Clinical signs were evident only in lactating goats and included anorexia and recumbency. In the most severely affected goats, signs progressed to neurologic abnormalities and death. Serum aspartate aminotransferase activity, gamma-glutamyltransferase activity, and total bilirubin concentration were high in clinically affected does, but no evidence of hemolysis was found. A diagnosis of copper toxicosis was made on the basis of high liver and kidney copper concentrations and histologic evidence of hepatic necrosis. Goats were found to have been fed a mineral mix containing 3,050 ppm copper for 9 months prior to the onset of copper toxicosis. Overall, there was no consistent relationship between serum hepatic enzyme activities, serum copper concentration, and liver copper concentration. TREATMENT AND OUTCOME: Clinically affected goats were treated with penicillamine, ammonium molybdate, sodium thiosulfate, and vitamin E. Penicillamine increased urine copper excretion in treated does versus untreated control animals. An increased incidence of infectious disease was identified in the herd 9 months later. Liver vitamin E concentration was low in 10 of the 12 goats that underwent necropsy. CLINICAL RELEVANCE: Findings suggested that penicillamine may be an effective treatment for goats with copper toxicosis. Production losses months after the diagnosis was made suggested that the intoxication had a prolonged animal welfare and economic impacts.     

Copper toxicity in a New Zealand dairy herd

Chronic copper toxicity was diagnosed in a Jersey herd in the Waikato region of New Zealand following an investigation into the deaths of six cattle from a herd of 250 dry cows. Clinical signs and post-mortem examination results were consistent with a hepatopathy, and high concentrations of copper in liver and blood samples of clinically affected animals confirmed copper toxicity. Liver copper concentrations and serum gamma-glutamyl transferase activities were both raised in a group of healthy animals sampled at random from the affected herd, indicating an ongoing risk to the remaining cattle; these animals all had serum copper concentrations within normal limits. Serum samples and liver biopsies were also collected and assayed for copper from animals within two other dairy herds on the same farm; combined results from all three herds showed poor correlation between serum and liver copper concentrations.To reduce liver copper concentrations the affected herd was drenched with 0.5 g ammonium molybdate and 1 g sodium sulphate per cow for five days, and the herd was given no supplementary feed or mineral supplements. Liver biopsies were repeated 44 days after the initial biopsies (approximately 1 month after the end of the drenching program); these showed a significant 37.3% decrease in liver copper concentrations (P <0.02). Also there were no further deaths after the start of the drenching program. Since there was no control group it is impossible to quantify the effect of the drenching program in this case, and dietary changes were also made that would have depleted liver copper stores.Historical analysis of the diet was difficult due to poor record keeping, but multiple sources of copper contributed to a long term copper over supplementation of the herd; the biggest source of copper was a mineral supplement. The farmer perceived this herd to have problems with copper deficiency prior to the diagnosis of copper toxicity, so this case demonstrates the importance of monitoring herd copper status regularly. Also the poor correlation between liver and serum copper concentrations in the three herds sampled demonstrates the importance of using liver copper concentration to assess herd copper status.     

Phosphorus supplements and fluorosis in cattle—a northern Australian experience

SUMMARY Chronic fluoride toxicosis caused lameness, dental lesions and illthrift in an extensive beef cattle herd in northern Australia. Up to 15% of the herd was lame and the disease forced the culling of large numbers of cows. The source of fluoride was fertiliser-grade monoammonium and diammonlum phosphate fed as part of a mineral supplement. Large quantities of mineral supplement were provided to the cattle because lameness was attributed to phosphorus deficiency, which is endemic in the area. Most lameness developed in the late dry season in the post-lactation phase. Severe lameness was caused by fractured pedal bones.     

Clostridium botulinum type B toxicosis in a herd of cattle and a group of mules

Clostridium botulinum type B toxicosis was diagnosed as the cause of generalized weakness and death in a group of cows and mules fed from the same batch of rye silage. One severely affected cow was treated and recovered, as did other less severely affected cows. All affected mules died. The remaining cattle in the herd were then vaccinated before continued feeding of the silage.     

Copper poisoning in a dairy herd fed a mineral supplement

Copper poisoning in a dairy herd resulted in the death of 9 of 63 (14%) adult Holstein cows. Clinical signs were acute anorexia, weakness, mental dullness, poor pupillary light reflexes, and scant nasal discharge. These were followed by recumbency, chocolate-colored blood, jaundice, and death. Four animals exhibited signs of hyperesthesia and/or rumen stasis prior to death. At necropsy there was generalized icterus of body tissues, with the liver appearing orange and the kidneys dark blue. Histologically, there was accumulation of hemosiderin in Kupffer cells, and severe to moderate hepatocellular necrosis in all cases. Ammonium molybdate added to the ration, combined with the cessation of mineral supplementation, arrested the outbreak.

These cases illustrate significant mortality, due to copper poisoning, in adult cattle fed a low-dose mineral dietary supplement for over two years. Dietary copper intake of the herd (on a dry matter basis) was 37.5 mg/kg for lactating cows and 22.6 mg/kg for dry cows.

     

Acute, fatal illness in cattle exposed to boron fertilizer

Twenty-six cows died after accidental exposure to boron fertilizer. Cows developed diarrhea, weakness, ataxia, signs of depression, and died, usually within a few hours. Seizure-like behavior was noticed in 2 cows, and 2 were suspected of aborting. High boron concentrations in tissues from affected cows confirmed ingestion of an appreciable amount of boron fertilizer. In an attempt to confirm the diagnosis of boron poisoning, boron fertilizer was administered to goats. A kid goat given 3.6 g of fertilizer/kg of body weight developed clinical signs similar to those seen in the cattle. Boron compounds such as sodium borate and boric acid have been considered generally nontoxic, and reports of livestock toxicosis are uncommon. This case report suggests that these compounds may be palatable under certain circumstances leading to ingestion of toxic quantities.     

Polioencephalomalacia in cattle consuming water with elevated sodium sulfate levels: A herd investigation

Polioencephalomalacia (PEM), hereafter used to refer to the specific lesion of cerebrocortical necrosis, developed in 11 of 110 mature cattle on pasture in central Saskatchewan. The primary water source contained a markedly elevated level of sodium sulfate (7200 ppm). The significant clinical findings of the herd investigation included depression, ataxia, cortical blindness, dysphagia, and death. Diagnosis of PEM was confirmed by histopathological evidence of cerebrocortical and subcortical necrosis with microvascular fibrinoid necrosis predominantly in the thalamic region of three affected cattle. The histopathology of sulfate-associated PEM observed in this herd appears to be unique and its features are presented and discussed. Mean levels for serum transketolase, copper, red blood cell transketolase activity, and thiamine (vitamin B₁) in all exposed young (n = 100) and mature (n = 99) animals did not reveal evidence of deficiencies. Although the blood thiamine status of the seven surviving, affected animals was not evaluated before treatment with exogenous thiamine, 199 members of the herd had blood thiamine levels within the reference range at the time of the outbreak. The outbreak resolved after cattle were moved to a water source containing acceptable levels of sodium sulfate.     

Serum selenium concentrations and glutathione peroxidase activities in cattle grazing forages of various selenium concentrations

In cows from 15 dairy herds (n = 210), serum selenium (Se) concentrations ranged from 0.021 to 0.789 microgram/ml, whereas 0.05 to 0.40 microgram/ml is the reported range for adequate serum Se concentrations in cattle. Serum Se concentrations of dairy cattle appeared to follow a geographic distribution pattern. On the basis of herd mean serum Se concentrations, adequate serum Se concentrations were found in cattle from only 1 of 5 herds grazing forage in the geographic area classified as Se deficient for cattle. Adequate mean serum Se concentrations were found in cattle from 4 of 5 herds located in geographic areas described as having variable forage Se concentrations (Se-marginal areas). Of the 10 herds from these 2 areas, there were only 2 herds in which 95% of the cattle had serum Se concentrations in the Se-adequate range (0.05 to 0.40 microgram/ml). In 2 selected neighboring farms in the Se-deficient area, cattle in 1 herd had adequate serum Se concentrations and cattle in the other herd had less than adequate serum Se concentrations (less than 0.05 microgram/ml). Therefore, more cattle are at risk of developing Se-deficiency disease than is commonly believed and forage of neighboring farms may have different Se concentrations. Serum Se concentrations (up to 0.789 microgram/ml) correlated with glutathione peroxidase enzyme activity; this serum Se concentration (0.789 microgram/ml) is approximately 6.2 times higher than previously reported in dairy cattle. Therefore, RBC glutathione peroxidase activity may be useful in determining the diagnosis of chronic Se toxicosis.     

Bovine anaplasmosis: susceptibility of seronegative cows from an infected herd to experimental infection with Anaplasma marginale

Adult cows from an Anaplasma marginale-infected herd that were negative to the A marginale rapid card agglutination (RCA) and complement fixation (CF) tests for 1 to 4 years developed acute anaplasmosis after inoculation with 0.5 ml of blood from an A marginale carrier cow. The test cattle were as susceptible as the control cattle of similar ages. Also, 2 cows that had seroconverted from RCA/CF-positive to RCA/CF-negative status naturally were fully susceptible to anaplasmosis when they were experimentally infected. Results of the study indicated that indigenous seronegative cattle in anaplasmosis-enzootic regions probably do not have acquired or natural immunity to A marginale infection.     

Arsenic toxicosis and suspected chromium toxicosis in a herd of cattle

Arsenic toxicosis and suspected chromium toxicosis were diagnosed in a herd of cattle that ingested ashes from lumber treated with copper, chromium, and arsenic. Findings included peracute death, depression, ataxia, weakness, recumbency, and watery diarrhea. Chemical analyses of liver, kidney, abomasal contents, rumen contents, and ashes revealed high concentrations of arsenic and chromium. Histologically, specimens of abomasum and duodenum had diffuse mucosal degeneration and engorged capillaries. Epithelial cells of the proximal convoluted tubules and distal collecting tubules of the kidney were swollen and had mild granular cytoplasmic degeneration. Burning lumber treated with copper, chromium, and arsenic does not remove the heavy metals from them, and ingestion of the ashes from the wood constitutes a hazard to livestock health.     

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.     

Cardiomyopathy of ruminants induced by the litter of poultry fed on rations containing the ionophore antibiotic, maduramicin. I. Epidemiology, clinical signs and clinical pathology.

The epidemiological, clinical and clinical pathological findings in 20 cattle and 4 sheep from 15 outbreaks of poultry litter toxicity in South Africa over the past 6 years are documented. In 6 outbreaks, the litter emanated from batteries where maduramicin had been incorporated into rations of broilers. According to circumstantial evidence the litter involved in the 9 other outbreaks was also derived from broilers which had been fed on rations containing an ionophore. The litter was fed ad libitum to the affected stock or constituted 30-80% by volume of their rations. The principal sign manifested was sudden mortality of up to 70% of the herd or flock, usually within 20-40 days of commencement of feeding of poultry litter. A few cattle developed signs of congestive heart failure, and stiffness was commonly seen in sheep. In a dosing trial with poultry litter involving 1 steer and 6 sheep, the steer and a sheep died suddenly and a second sheep was destroyed in extremis. Tachycardia and/or cardiac arrythmia were recorded in 5 sheep, and the activity of aspartate transaminase (AST) and/or lactate dehydrogenase (LD) in the sera of 4 was elevated. Since the cardiac lesions in field cases were similar to those of ionophore poisoning and broiler rations containing maduramicin was a common factor in several outbreaks, toxic litter from some of these outbreaks were tested for the presence of this compound. Analysis by high performance liquid chromatography of litter from 2 specimens of outbreaks revealed that they contained 2.5 ppm and 6.1 ppm maduramicin.(ABSTRACT TRUNCATED AT 250 WORDS)     

CHRONIC COPPER POISONING IN DAIRY COWS

SUMMARY Chronic copper poisoning in a dairy herd fed supplementary copper is recorded. Most cows received 11 g of copper sulphate per day but high milk producers received 22,0 g and within 6 months, 3 of them became ill and died. The signs shown by the 3 cows were anorexia, decreased milk production, frequent recumbency and jaundice. Within 4 days of showing signs, the cows died. The autopsy findings were dehydration, anaemia, jaundice, liver damage and intestinal haemorrhage. Liver copper values varied from 1,250 to 2,410 ppm DM.     

Distribution and environmental risk factors for paratuberculosis in dairy cattle herds in Michigan.

OBJECTIVE: To determine prevalence of paratuberculosis among dairy cattle herds and to identify associated soil-related risk factors. SAMPLE POPULATION: Serum and soil samples for 121 Michigan dairy herds. PROCEDURE: Blood samples were collected from cows at each farm and tested for Mycobacterium paratuberculosis, using an antibody ELISA. Soil samples were collected from pastures and exercise lots; pH and available iron content were determined. A questionnaire was administered to collect data regarding farm management practices and productivity. RESULTS: 55% of the herds tested had > or = 2 M paratuberculosis-positive cattle. Adjusting sample prevalence for distribution of herd size strata yielded a statewide herd prevalence of 54%. Of 3,886 cattle tested, 267 had positive results. Prevalence of test-positive cattle was 6.9%. For every part per million (ppm) increase in soil iron content, there was a 1.4% increase in the risk of a herd being test-positive. An increase in soil pH of 0.1 was associated with a 5% decrease and an increase in soil iron content of 10 ppm was associated with a 4% increase in the number of test-positive cattle. Application of lime to pasture areas was associated with a herd being only 10% as likely to be paratuberculosis positive and with a 72% reduction in number of test-positive cattle. CONCLUSIONS AND CLINICAL RELEVANCE: Prevalence of paratuberculosis-positive dairy herds in Michigan (54%) was greater than expected, but prevalence of paratuberculosis-positive cattle (6.9%) was within anticipated values. These prevalences were associated positively with acidic soil and increased soil iron content. Application of lime to pasture areas was associated with reduced risk of paratuberculosis.     

An outbreak of dictyocaulosis in lactating cows on a dairy farm

CASE DESCRIPTION: The owner of a herd of 74 Holstein-Friesian cattle reported decreased milk production, weight loss, and coughing among lactating cows. Owner-initiated antimicrobial treatment was unsuccessful; 1 lactating cow died, and 50% of the lactating cows had clinical signs of respiratory distress, such as tachypnea and coughing. CLINICAL FINDINGS: On the basis of history, physical examination findings, and fecal examination results, affected animals were determined to have Dictyocaulus viviparus (lungworm) infestation. The disease history suggested that the herd contained cows with subclinical patent lungworm infestations; after introduction of susceptible heifers, the pastures had become heavily infested with D viviparus and clinical problems subsequently developed in both newly introduced and resident cows. TREATMENT AND OUTCOME: Affected and unaffected heifers and adult cows were treated with a pour-on formulation of eprinomectin (0.5 mg/kg [0.23 mg/lb]). One animal died, but 2 weeks after treatment, clinical signs among affected cattle were markedly improved. Ten weeks after treatment, milk production improved from 23 kg/cow/d (51 lb/cow/d) to 28 kg/cow/d (62 lb/cow/d). CLINICAL RELEVANCE: The outbreak provides additional evidence that dictyocaulosis is becoming more common among adult dairy cattle, rather than almost exclusively affecting young stock. This may be attributable to anthelmintic use and management practices on dairy farms. Combined with anecdotal reports of an increase in the incidence of dictyocaulosis among adult cattle in North America, D viviparus infestation should be included as a differential diagnosis for decreased milk production, weight loss, and coughing among adult dairy cattle.     

Effect of adding superphosphate to the drinking water on the fertility of dairy cows.

Mean serum inorganic phosphorus concentrations of cows in an infertile dairy herd of 170 cows in the Hunter Valley increased from less than 4.5 mg/100 ml to greater than 5.8 mg/100 ml after defluorinated superphosphate was added to their drinking water at the rate of 2.5 kg/450 1 once weekly from September, 1976. The first service pregnancy rate increased from 36.5% to 63.2%, the mean calving to conception interval decreased from 109 days to 85 days and the number of cows culled each year for infertility fell from 15 to 5. The pasture fed to the milking cows contained on average greater than 17% crude protein, greater than or equal to 0.39% phosphorus, greater than or equal to 9 ppm copper and 38--46 ppm manganese according to the dominant species. The Ca/P ratio ranged from 2 to 5.5:1. Of these, only the Ca/P ratio and the manganese concentrations appeared to be abnormal.     

Serum copper concentrations in beef cows and heifers

OBJECTIVE: To characterize serum copper status of cows and heifers in beef cow-calf herds throughout the United States and to evaluate use of copper supplements in those herds. DESIGN: Cross-sectional survey. ANIMALS: 2,007 cows and heifers from 256 herds in 18 states. PROCEDURES: Producers participating in a health and management survey conducted as part of the National Animal Health Monitoring System voluntarily allowed serum samples to be obtained from cows and heifers for determination of copper concentration. Results were categorized as deficient, marginally deficient, or adequate. The proportion of cattle and herds (on the basis of mean value of the tested cattle) in each category was determined. Copper concentrations were compared between herds that reportedly used copper supplements and those that did not. RESULTS: Overall, 34 of 2,007 (1.7%) cows and heifers were deficient in copper, and 781 (38.9%) were marginally deficient. In each region, at least a third of the cattle were deficient or marginally deficient. For herds, 92 of 256 (35.9%) were marginally deficient, and 22 (0.8%) were deficient. Approximately half of the producers reported use of copper supplements, but a sizeable proportion of those producers' cattle and herds were classified as marginally deficient or deficient. CONCLUSIONS AND CLINICAL RELEVANCE: Copper deficiency is not restricted to a single geographic region of the United States. Copper deficiency can persist despite reported use of supplements by producers. Veterinarians dealing with beef cow-calf herds that have problems consistent with copper deficiency should not rule out copper deficiency solely on the basis of geographic region or reported use of copper supplements for the herd.     

Chronic copper toxicity in a dairy herd

The addition of excessive copper to a commercially prepared dairy ration caused chronic copper toxicity in a dairy herd. A formulation error by a feed company resulted in copper levels of 800 to 1,000 mg/kg in the “as fed concentrate,” amounting to about 400-500 mg copper/kg of the whole ration. Five animals died with typical signs of acute copper toxicity, including intravascular hemolysis and methemoglobinemia. A further 39 cows died on the farm from a combination of debilitation and secondary infectious causes, and 215 were sent to slaughter because of debilitation and poor milk production. The mortality of calves born to dams that had been fed the toxic concentrate was approximately 50%.

We postulate that dairy cows, particularly pregnant cows, may be more susceptible to copper toxicity than other cattle, and suggest reexamination of the presently allowable maximum levels of copper supplementation of diets for dairy cattle.

     

Suckling calves with symptoms of swayback

Within a 1-year period, three calves from the same herd developed ataxia of the hind limbs and urinary incontinence at about 6 months of age. Signs progressed and the calves were slaughtered 1-8 months after the onset of signs. The calves belonged to a suckling beef herd of 35 cattle. Blood samples from 11 cattle of different ages were collected and glutathione peroxidase and copper levels were measured. Glutathione peroxidase levels were below the normal range in all cattle and copper levels were below the normal range in 7 of ll cattle. Pathological examination of an affected calf revealed a Wallerian type of degeneration of myelinated nerve fibres in the lateral and ventral spinal cord tracts. In addition, the hepatic copper content was very low. Copper deficiency is a well-known cause of swayback in young sheep and goats. To our knowledge, this is the first report of a possible association between a swayback-like syndrome and copper deficiency in calves.     

Dicoumarol toxicity in cattle associated with ingestion of silage containing sweet vernal grass (Anthoxanthum odoratum)

A diagnosis of dicoumarol toxicity in a herd of Friesian cattle was made following investigation of the deaths of three mature cows and eleven yearling heifers. Affected stock had been fed wrapped, bailed silage containing approximately 90% sweet vernal grass ( Anthoxanthum odoratum ). Sweet vernal grass contains coumarin, which can be converted to dicoumarol, a vitamin K antagonist, through the action of moulds. Most deaths were preceded by lethargy, severe anaemia and subcutaneous and internal haemorrhage. Dicoumarol toxicosis was suspected based on clinical signs, necropsy findings and prolonged prothrombin and activated partial thromboplastin times. Dicoumarol analysis of blood from affected animals and silage confirmed the diagnosis.