Copper deficiency and toxicity in ruminants (Proceedings)
Copper deficiency occurs when the diet contains an abnormally low amount of copper (primary copper deficiency) or when copper absorption or metabolism is adversely affected (secondary copper deficiency). If inadequate amounts of copper are available to tissues in the form of essential metalloenzymes, the signs of copper deficiency (hypocuprosis) may occur. Clinical signs in ruminants include diarrhea, decreased weight gain, unthrifty appearance, anemia, changes in coat color (achromotrichia) or wool quality, anemia, spontaneous fractures, lameness (epiphysitis) and demyelinization (enzootic ataxia of sheep and goats, or swayback). One of these syndromes usually predominates in a given herd.
The minimum recommended dietary copper concentration (dry matter basis) is 4 to 10 ppm (mg/kg) for cattle, 5 ppm for sheep, and 7 ppm for merino sheep. Young animals and fetuses are more susceptible to copper deficiency than mature animals, and cattle are more susceptible than sheep. Secondary copper deficiency is associated with high dietary levels of molybdenum, sulfates, zinc, iron, or other compounds. Secondary copper deficiency often presents with clinical signs of diarrhea and weight loss or unthriftiness. It has been called teart, peat scours, renguerra, pine, and salt lick disease.4 Salt sickness in Florida appears to be the result of combined copper and cobalt deficiencies. The cause of copper deficiency in clinical cases is often multifactorial and can be difficult to quantify. In addition, unknown factors cause clinical expression of copper deficiency in ruminants to be manifested as a variety of syndromes.
Clinical syndromes and differential diagnosisProfuse watery diarrhea with poor weight gains and/or weight loss is a common syndrome seen in ruminants with copper deficiency. When it occurs on boggy pastures that contain high concentrations of molybdenum, it has been referred to as teart. Decreased weight gains or weight loss as a herd problem can have many other causes, including parasitism, trace mineral deficiencies (selenium, cobalt), protein calorie malnutrition, and Johne's disease. A syndrome characterized by epiphyseal enlargement, stiffness, and unthriftiness is seen in young ruminants and is the result of copper deficiency and is sometimes called pine. Copper deficiency can cause spontaneous fractures in ruminants. Enzootic neonatal ataxia (swayback) of lambs and kids is characterized by progressive incoordination and recumbency that begins with the hind limbs and progresses to the front limbs. It has also been reported in deer and pigs. Inadequate keratinization of wool and achromotrichia is the result of imperfect oxidation of free thiol groups during hair growth and keratinization. Subsequently, the wool fibers do not crimp normally, and they appear to be "stringy" or "kinky". A copper containing enzyme, tyrosinase (polyphenyloxidase), is needed to convert ltyrosine to melanin. With copper deficiency, this conversion is slow and hair is lighter in color than normal (achromotrichia). Loss of wool crimp and pigmentation changes in sheep or cattle, respectively, occur late in the course of copper deficiency. In addition to the above clinical syndromes that may occur alone or jointly, copper deficiency may be associated with anemia6 (altered iron metabolism) or infertility. Infertility is probably multifactorial and may not respond to an increase in copper intake alone. Copper deficiency also seems to result in decreased immune function in ruminants.