Iatrogenic Copper Toxicosis Induced by Administering Copper Oxide Boluses to Neonatal Calves

Hamar, Dwayne W.; Bedwell, Cathy L.; Johnson, Jerre L.; Schultheiss, Patricia C.; Raisbeck, Merle; Grotelueschen, Dale M.; Williams, Elizabeth; O’Toole, Donal; Paumer, Richard J.; Vickers, Matt G.; Graham, Timothy J.

doi:10.1177/104063879700900422

Cited by 17 publications

(17 citation statements)

References 15 publications

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“…7,13,14,24,26 Although chronic primary copper toxicosis generally occurs after multiple exposures to copper over a prolonged period of time ranging from weeks to even months, cases of copper intoxication in calves with hepatic and, in some instances, renal changes typical of chronic copper toxicosis have been reported several weeks after a single administration of timereleased boluses containing copper oxide wires as a neonate. 8,25 In addition, exposure to hepatotoxicants, including toxic plants, can also predispose animals to hepatic copper accumulation over time and cause what has been referred to as secondary chronic copper toxicosis. 12,15,21 In contrast to acute copper intoxication, which is initially characterized by gastroenteritis, the prehemolytic stage of chronic copper toxicosis often presents clinically as a hepatopathy 8,13,25,26 and, especially in the case of sheep, remains subclinical in the prehemolytic stage until large quantities of copper are suddenly released from hepatic stores.…”

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confidence: 99%

“…8,25 In addition, exposure to hepatotoxicants, including toxic plants, can also predispose animals to hepatic copper accumulation over time and cause what has been referred to as secondary chronic copper toxicosis. 12,15,21 In contrast to acute copper intoxication, which is initially characterized by gastroenteritis, the prehemolytic stage of chronic copper toxicosis often presents clinically as a hepatopathy 8,13,25,26 and, especially in the case of sheep, remains subclinical in the prehemolytic stage until large quantities of copper are suddenly released from hepatic stores. A stressful event, such as transportation, pregnancy, lactation, strenuous exercise and/or handling, or disease and malnutrition, can apparently trigger the breakdown of copper-containing lysosomes, resulting in severe hepatocellular disease and release of copper from the liver.…”

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Copper Toxicosis with Hemolysis and Hemoglobinuric Nephrosis in Three Adult Boer Goats

Bozynski¹,

Evans²,

Kim³

et al. 2009

J VET Diagn Invest

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Acute and, particularly, chronic copper exposures, along with defects in hepatic copper metabolism, altered excretion of copper, and/or nutritional imbalances between copper and other trace elements, can lead to hepatic accumulation of copper and primary copper toxicosis. There is interspecies variation in susceptibility to copper toxicosis, with sheep being the species most likely to develop this condition. Adult dairy goats and Boer crosses are generally considered resistant to chronic copper toxicosis, especially the hemolytic stage of this disease. The current report is rather unusual in that it describes instances of naturally occurring copper toxicosis with hemolysis and hemoglobinuric nephrosis in 3 adult Boer goats. In 2 of these goats, a possible source of excessive dietary copper was investigated but not definitively identified. In the third goat, the etiologic factors associated with the copper toxicosis were not determined. It appears that mature Boer goats are susceptible to the hemolytic stage of chronic copper toxicosis, which was not observed in a recent, large-scale copper intoxication involving lactating dairy goats. Copper analyses on both liver and kidney samples were necessary to confirm the diagnosis of copper toxicosis in all 3 goats. All feedstuffs associated with instances of copper toxicosis should be analyzed for iron, molybdenum, sulphur, and zinc as well as copper to determine what nutritional factors are contributing to the pathogenesis of this disease. Consideration also should be given to the ingestion of hepatotoxic plants and other toxic exposures, which could predispose an animal to secondary chronic copper toxicosis.

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Copper Toxicosis with Hemolysis and Hemoglobinuric Nephrosis in Three Adult Boer Goats

Bozynski¹,

Evans²,

Kim³

et al. 2009

J VET Diagn Invest

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“…18 In cases of chronic Cu poisoning, clinical manifestations are only observed during the hemolytic crisis, or a few days before, so it is very difficult to establish an early diagnosis of this disease based only on clinical signs. 6,11 Consequently, several researchers have tried to establish parameters of clinical diagnosis based on laboratory analyses. 9,11,13 Serum Cu and other traditional biochemical variables have limited diagnostic value in terms of Cu accumulation, 9,13 and the best results were observed in sheep in association with alterations of hepatic enzymes.…”

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“…11 Although the frequency of this intoxication is lower in other species of ruminants, Cu intoxication in cattle has recently evolved as an emerging disease, with descriptions of cases of acute and chronic intoxication in several countries, including Brazil. [2][3][4]6,12,16 Recent research 1 has shown that there is an increase in the number of cases in cattle and has described 14 outbreaks within 6 months. However, in buffalo, there is only 1 description of this intoxication, during which young animals that received reconstituted Cu-enriched powdered milk for a few months demonstrated signs indicative of chronic Cu poisoning and died suddenly.…”

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Predictive Values of Aspartate Aminotransferase and Gamma-Glutamyl Transferase for the Hepatic Accumulation of Copper in Cattle and Buffalo

et al. 2008

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Abstract. Ten cattle and 10 buffalo were divided into 2 groups (control [n 5 8] and experimental [n 5 12]) that received daily administration of copper. Three hepatic biopsies and blood samples were performed on days 0, 45, and 105. The concentration of hepatic copper was determined by spectrophotometric atomic absorption, and the activities of aspartate aminotransferase (AST) and gamma-glutamyl transferase (GGT) were analyzed. Regression analyses were done to verify the possible existing relationship between enzymatic activity and concentration of hepatic copper. Sensitivity, specificity, accuracy, and positive and negative predictive values were determined. The serum activities of AST and GGT had coefficients of determination that were excellent predictive indicators of hepatic copper accumulation in cattle, while only GGT serum activity was predictive of hepatic copper accumulation in buffalo. Elevated serum GGT activity may be indicative of increased concentrations of hepatic copper even in cattle and buffalo that appear to be clinically healthy. Thus, prophylactic measures can be implemented to prevent the onset of a hemolytic crisis that is characteristic of copper intoxication.

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“…Cu poisoning (Gummow 1996, Hamar et al 1997, Auza et al 1999, Mendel et al 2007). This value is used in cases of chronic Cu poisoning (CCP).…”

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Renal cortex copper concentration in acute copper poisoning in calves

et al. 2012

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The aim of this study was to estimate the diagnostic value of renal cortex copper (Cu) concentration in clinical cases of acute copper poisoning (ACP). A total of 97 calves that died due to subcutaneous copper administration were compiled in eleven farms. At least, one necropsy was conducted on each farm and samples for complementary analysis were taken. The degree of autolysis in each necropsy was evaluated. The cases appeared on extensive grazing calf breeding and intensive feedlot farms, in calves of 60 to 200 kg body weight. Mortality varied from 0.86 to 6.96 %, on the farms studied. The first succumbed calf was found on the farms between 6 and 72 hours after the susbcutaneous Cu administration. As discrepancies regarding the reference value arose, the local value (19.9 parts per million) was used, confirming the diagnosis of acute copper poisoning in 93% of the analyzed kidney samples. These results confirm the value of analysis of the cortical kidney Cu concentration for the diagnosis of acute copper poisoning.

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Iatrogenic Copper Toxicosis Induced by Administering Copper Oxide Boluses to Neonatal Calves

Cited by 17 publications

References 15 publications

Copper Toxicosis with Hemolysis and Hemoglobinuric Nephrosis in Three Adult Boer Goats

Copper Toxicosis with Hemolysis and Hemoglobinuric Nephrosis in Three Adult Boer Goats

Predictive Values of Aspartate Aminotransferase and Gamma-Glutamyl Transferase for the Hepatic Accumulation of Copper in Cattle and Buffalo

Renal cortex copper concentration in acute copper poisoning in calves

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