Page 460 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
P. 460

Copper Chapter | 26  427




  VetBooks.ir  membranes. There may be hemoglobinuria, and death is  to liver biopsy to assess liver copper concentrations. The
                                                                addition of elemental zinc to the diet (100 200 mg/day
             common among severely affected animals. Postmortem
                                                                as the acetate) should be considered to reduce copper
             findings include icterus, swollen liver, enlarged spleen,
             and the kidneys appear dark, often referred to as gunmetal  absorption.
             blue or black kidneys. Antemortem testing of serum cop-
             per often shows an elevation above normal, but this
                                                                CONCLUDING REMARKS AND FUTURE
             decreases over time with a rapid decrease following fluid  DIRECTIONS
             therapy. Postmortem diagnostic testing for copper should
             be performed on both liver and kidney. Mobilization of  In trace amounts, copper is an essential element, but in
             copper from the liver may reduce copper concentrations  excess it is a toxicant. In general, sheep and certain breeds
             to normal levels but the mobilized copper is then accumu-  of dogs are more susceptible to copper poisoning. Copper
             lated in the kidney. The ratio should be tested for both  produces toxicity by multiple mechanisms. Poisoned ani-
             copper and molybdenum. The close environment of the  mals are usually treated with ammonium molybdate and
             sheep should be inspected for extraneous sources of  sodium thiosulfate. In addition, supportive care including
             copper.                                            fluid therapy and blood transfusion are beneficial.
                Young dogs with genetic susceptibility to chronic cop-
             per toxicosis may develop an acute syndrome of weak-  REFERENCES
             ness, vomiting, and anorexia. Older dogs may present
             with a more chronic syndrome of weight loss and    Bremner, I., 1998. Manifestations of copper excess. Am. J. Clin. Nutr.
             anorexia, which may progress to ascites and neurological  67 (Suppl), 1069S 1073S.
             signs related to a developing hepatic encephalopathy. If  Dirksen, K., Spee, B., Penning, L.C., et al., 2017. Gene expression pat-
             untreated, the animal may succumb to liver dysfunction,  terns in the progression of canine copper-associated chronic hepati-
             and postmortem findings may include a cirrhotic liver.  tis. PLoS One. 12 (5), 1 19.
                                                                Du, Z., Hemken, R.W., Harmon, R.J., 1996. Copper metabolism of
             Antemortem diagnostics would include an evaluation of
                                                                  Holstein and Jersey cows and heifers fed diets high in cupric sulfate
             liver enzymes. In suspect cases, a liver biopsy should be
                                                                  or copper proteinate. J. Dairy Sci. 79, 1873 1880.
             used to confirm elevated copper content (Taboada and
                                                                Engle, T.E., 2014. Copper and lipid metabolism in beef cattle: a review.
             Thompson, 1997).                                     J. Anim. Sci. 89, 591 596.
                                                                Fieten, H., Gill, Y., Martin, A.J., et al., 2016. The Menkes and Wilson
             TREATMENT                                            disease genes counteract in copper toxicosis in Labrador retrievers:
                                                                  a new canine model for copper-metabolism disorders. Dis. Model
             Treatment of animals acutely poisoned with copper    Mech. 9, 25 38.
             mainly consists of supportive treatment directed at the  Forman, O.P., Boursnell, M.E.G., Dunmore, B.J., et al., 2005.
             shock, dehydration, and damage to the GI tract.      Characterization of the COMMD1 (MURR1) mutation causing cop-
                Treatment of sheep with severe clinical signs follow-  per toxicosis in Bedlington terriers. Anim. Genet. 36, 497 501.
             ing hemolytic crisis is often unrewarding. Supportive care  Gaetke, L.M., Chow-Johnson, H.S., Chow, C.K., 2014. Copper: toxico-
                                                                  logical relevance and mechanisms. Arch. Toxicol. 88, 1929 1938.
             should include fluid therapy and the consideration of a
                                                                Galey, F.D., Maas, J., Tronstad, R.J., et al., 1991. Copper toxicosis in
             blood transfusion. Ammonium or sodium molybdate
                                                                  two herds of beef calves following injection with copper disodium
             (50 500 mg) and sodium thiosulfate (0.3 1 g) should be
                                                                  edetate. J. Vet. Diagn. Invest. 3, 260 263.
             used daily as a drench for up to 3 weeks not only in  Gummow, B., 1996. Experimentally induced chronic copper toxicity in
             affected animals but also in other animals that have  cattle. Onderstepoort J. Vet. Res. 63, 277 288.
             received the same diet. Ammonium tetrathiomolybdate  Keswani, T., Mitra, S., Bhattacharyya, A., 2013. Copper-induced immu-
             has been suggested as a treatment but is difficult to  notoxicity involves cell cycle arrest and cell death in the liver.
             obtain. It can be administered IV or SQ at 1.7 3.4 mg/kg  Environ. Toxicol. 30, 411 421.
             on alternate days for three treatments. Molybdenum in the  National Research Council (NRC), 2005. Copper. Mineral Tolerance of
             diet can be increased to 5 ppm and zinc can be supple-  Animals. second revised ed. The National Academies Press,
             mented at 100 ppm to reduce copper absorption.       Washington, DC, pp. 134 153.
                                                                Speeti, M., Eriksson, J., Saari, S., et al., 1998. Lesions of subclinical
                Dogs affected with chronic copper toxicosis should be
                                                                  Doberman hepatitis. Vet. Pathol. 35, 361 369.
             fed a low copper diet, e.g., avoiding organ meats that are
                                                                Taboada, J., Thompson, L.J., 1997. Copper hepatopathy. In: Tilley, L.P.,
             usually higher in copper. The use of oral chelating agents
                                                                  Smith, F.W.K., MacMurray, A.C. (Eds.), The 5 Minute Veterinary
             is suggested to enhance urinary excretion of copper. The
                                                                  Consult: Canine and Feline. Williams and Wilkins, Baltimore, MD,
             use of D-penicillamine at 10 15 mg/kg PO twice daily or  pp. 478 479.
             the use of trientine hydrochloride at 10 15 mg/kg PO  Wu, X., Leegwater, P.A., Fieten, H., 2016. Canine models for copper
             twice daily have been suggested. Liver enzymes should  homeostasis disorders. Int. J. Mol. Sci. 17, 196 209.
             be monitored every 6 months and consideration be given
   455   456   457   458   459   460   461   462   463   464   465