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Copper Deficiency / Molybdenum Excess in Cattle, Goats and Sheep

Description
Copper Deficiency / Molybdenum Excess


Clinical signs.
Signs include profuse watery diarrhea, poor weight gain/weight loss, poor haircoats, depigmentation, pale mucous membranes, and microcytic hypochromic anemia (iron deficiency). Loss of wool crimp and depigmentation can develop in affected sheep. Epiphyseal enlargement and stiff gait occurs in many young ruminants. Copper deficiency in kids and lambs causes "enzootic neonatal ataxia" (swayback); it is characterized by pelvic limb ataxia that progresses to the forelimbs. Spontaneous fractures are also reported in association with copper deficiency.

Pathogenesis.
Copper is an essential cofactor in many mammalian enzymes (iron utilization, prevention of cellular oxidative damage, collagen synthesis, pigment formation, etc.). Dietary copper deficiency as well as impairment of alimentary absorption of copper produces the disease. There is an important dietary relationship between dietary copper, sulfate and molybdenum. If dietary sulfur or molybdenum are fed in excessive amounts, copper absorption in the GI tract is drastically reduced. Excessive dietary calcium also interferes with copper absorption.

Diagnosis.
Liver copper levels are the most reliable test for the copper status of the animal, but antemortem sampling (liver biopsy) involves some risk to a living animal. Blood testing is less useful, as these levels are the last to fall in a deficient state. However, they are often employed since testing is noninvasive. Feed analysis (copper, sulfur, molybdenum).

Treatment and prevention.
Treatment: SQ copper glycinate, or dietary copper supplementation in a salt-mineral mix. Copper oxide wire boluses are a useful way to supply longterm (4.5 mos) therapy. The boluses lodge in the rumen and slowly release copper.
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