This topic brings me back during our voluntary practical work in Institute Veterinar Malaysia (IVM). Upon going to visit sheep and goat farm this Thursday, I'd better refresh the most common nutrition problem in sheep.
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Kidney damage cause by copper toxicity
Copper requirement in sheep
Sheep are unique among food and farm animals in the way they utilize copper. Copper is a required mineral for all farm animals and also is potentially toxic to all of the food-producing animals. Sheep are the most susceptible of all food-producing animals to copper toxicosis. Copper status of sheep is influenced by breed, age of animal, health status of animal, levels of other minerals consumed, and even levels of some feed additives in the diet.
Copper is essential for life. It is required for normal iron metabolism, synthesis of elastin and collagen, melanin production and integrity of the central nervous system. It is essential in keratin (wool) production. More recently, it has been shown that copper is one of the key trace minerals required for an effective immune response. Signs of deficiency include anemia, brittle or fragile bones, loss of hair or wool pigmentation and poor wool growth. In sheep, stringy wool and "swayback" are commonly reported.
Generally, sheep require about 5 ppm (parts per million or mg/kg) of Cu in their total diet. Toxicity can occur at levels above 25 ppm. However, dietary molybdenum (Mo) levels also affect copper requirements, as Mo forms an insoluble complex with Cu to prevent copper absorption. If molybdenum levels are low ( less than 1 ppm), sheep are more susceptible to Cu toxicity. If Mo intakes exceed 10 ppm, Cu deficiency may occur on diets that would normally be adequate. Sulfur (S) further complicates the Cu:Mo relationship by binding with the Mo.
Molybdenum and sulfur act as antagonists to copper. The presence of these compounds bind with copper and prevent gut absorption and increase excretion of absorbed copper in the liver and body tissues. Molybdenum is often added to sheep diets to try to help prevent copper toxicity.
Copper toxicity in sheep
Copper toxicity in sheep usually results from the accumulation of excess Cu in the liver over a period of a few weeks to more than a year with no clinical signs, followed by a sudden release of liver Cu stores to cause toxicity (rapid breakdown of red blood cells).
Copper toxicity can be of two types: chronic or acute. The acute form of copper toxicity occurs quickly, shortly after ingestion of high amounts of copper. The chronic form occurs when sheep are fed diets over a period of time that are marginally higher in copper content relative to level of copper antagonists in the diet. This could be over a period of weeks or months, depending on actual copper intake by the sheep. What happens is that sheep bind absorbed copper very tightly in the liver. Copper buildup in the liver occurs because sheep do not excrete copper from the body as efficiently as other animal species.
When the liver becomes saturated with copper, tissue damage occurs in the liver and large amounts of copper are released into the bloodstream. This causes the death of red blood cells and subsequent tissue damage. Often, the first very noticeable sign of copper toxicity is dead sheep. This many times may follow some stressful event for the sheep.
Affected sheep are lethargic and anemic. They may grind their teeth incessantly and experience extreme thirst. Membranes are very pale and may appear yellow, as jaundice sets in. Urine is a bloody color. Death usually occurs 1 to 2 days after the onset of clinical symptoms. At post-mortem, tissues are pale to dark yellow and the kidneys are a very dark color.
*From Merck's Veterinary Manual
Hemolysis and hemoglobinuria may develop after 3 days if the animal survives the GI disturbances. The sudden onset of clinical signs in chronic copper poisoning is associated with the hemolytic crisis. Affected animals exhibit depression, weakness, recumbency, rumen stasis, anorexia, thirst, dyspnea, pale mucous membranes, hemoglobinuria, and jaundice. Several days or weeks before the hemolytic crisis, liver enzymes, including ALT and AST, are usually increased. During the hemolytic crisis, methemoglobinemia, hemoglobinemia, and decreases in PCV and blood glutathione are usually seen.
Acute copper poisoning produces severe gastroenteritis with erosions and ulcerations in the abomasum of ruminants. Icterus develops in animals that survive >24 hr. Tissues discolored by icterus and methemoglobin are characteristic of chronic poisoning. Swollen, gunmetal-colored kidneys, port-wine-colored urine, and an enlarged spleen with dark brown-black parenchyma are manifestations of the hemolytic crisis. The liver is enlarged and friable. Histologically, there is centrilobular hepatic and renal tubular necrosis.
Bloody color of urine of affected sheep
In contrast, cattle require about 10 ppm of Cu in their diet and can tolerate Cu levels ten times higher than sheep. Non-ruminants, such as pigs and chickens, tolerate even higher levels of Cu. Growing pigs are often fed 100 to 250 ppm to improve performance. The toxic level of Cu in the diet of chickens ranges from 250 to 800 ppm.
Thus, due to species differences, it is necessary to purchase grain rations or mineral premixes which have been specifically formulated for sheep. It is recommended that sheep NOT be fed poultry litter or other waste products which contain high levels of copper. In addition, there have been instances where high levels of Cu have been traced to the fertilization of pasture with pig manure.
If and when copper toxicity is suspected, the diagnosis needs to be confirmed by a veterinarian or diagnostic laboratory. Sources of copper need to be promptly identified. It is important to know the Cu and Mo status of all feeds and forages being fed. Grains are lower in copper than forages. Most forages will contain copper at levels equal to or above the NRC requirement for ruminants; however, as plants mature, the bio-availability of the copper decreases. Errors in feed mixing should also be considered as a possible source of excess copper. Water should not be overlooked as a source.
Treatment
Although prevention is much preferred, there are times when treatment is warranted to prevent further losses. The most common treatment is to give a drench daily containing 50 to 100 mg of ammonium molybdate and 0.5 to 1.0g of sodium sulfate.
Though more data is needed, observations suggest that goats are more tolerant of copper than sheep.
Sources: The Merck Veterinary manual, copper toxicity in sheep, Susan Schoenian Small ruminant info sheet University Of Maryland, copper toxicity in sheep, Mike Neary, Purdue University.
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