🔺Primary deficiency as a result of in inadequat opper in the diet. 

🔺Secondary copper deficiency is associated with antagonistic factors, particularly excess molybdenum and sulfur, which form thiomolybdates in the rumen.

🔺Thiomolybdates can bind copper in the rumen, or, if l insufficient copper is present, they are absorbed (especially tetrathiomolybdate) and bind to several enzymes and compounds that have diverse biological activities.  
🔺Dietary iron forms complexes with copper in the rumen, and so can exacerbate this process.

🔺Herd or flock problem, mainly in young growing ruminants (cattle, sheep, goats, and farmed deer) on pasture in spring and summer. 

🔺Primary deficiency occurs in sandy and heavily weathered soils; secondary in peat or muck soils high in molybdenum. Feed and water supplies may also contain molybdenum, sulfate, and iron salts, which interfere with copper absorption and metabolism. Some breeds of sheep, and possibly Simmental cattle, are more susceptible.

🔺Unthriftiness, altered hair color, chronic diarrhea in molybdenosis (secondary
deficiency), chronic lameness, neonatal ataxia in newborn lambs (swayback) 

🔺if ewes are copper deficient in midpregnancy, delayed ataxia in older lambs (enzootic ataxia), anemia in more prolonged deficiency, falling disease in adult cattle.

Low plasma and liver copper, low ceruloplasmin, anemia.

Demyelination in enzootic ataxia, anemia, emaciation, hemosiderosis, osteodystrophy, cardiomyopathy. 

Low liver and plasma copper, response to treatment.

🔺Copper deficiency must be differentiated from herd problems associated with the following:
🔹Unthriftiness as a result of intestinal parasitism
🔹Malnutrition as a result of energy– protein deficiency
🔹Lameness caused by osteodystrophy (calcium, phosphorus, and vitamin D imbalance)
🔹Anemia as a result of sucking lice
🔹Neonatal ataxia in lambs (congenital swayback and enzootic ataxia) from border disease; cerebellar hypoplasia
(daft lamb disease); hypothermia; meningitis
🔹Sudden death as a result of other causes

Oral slow-release bolus or capsule, parental copper glycinate, oral copper sulfate.

 Oral dosing with controlled release glass bolus or capsule with copper oxide needles; supplementation pasture by top-dressing with copper sulfate; parenteral administration of copper at strategic times; remove sulfates from water supply; genetic selection may be an option.