Iron Deficiency Anemia
Johanna L. Watson • Gary P. Carlson • Monica Aleman
Iron is present in most forages and grains. In neonates, the major source of iron is colostrum (≈0.79 mg/L in mare's milk).1
■ BOX 37.2
Causes of Depression Anemia
Nutritional Deficiency
Iron deficiency Copper deficiency Cobalt deficiency
Vitamin B12 deficiency
Folic acid deficiency
Anemia of Inflammatory Disease
Chronic infection
Chronic inflammation
Fractures and severe trauma
Neoplasia
Anemia Secondary to Organ Dysfunction
Chronic liver disease
Chronic renal disease
Chronic gastrointestinal disease Parasitism (trichostrongylosis)
Bone Marrow Damage/Dysplasia
Myeloid and megakaryocytic bone marrow hypoplasia in Standardbred horses
Bracken fern poisoning
Congenital dyserythropoiesis and keratosis in polled Hereford calves
Trichloroethylene-extracted soybean meal toxicity Myelophthisic disorders (myeloproliferative disease, lymphoma) Aplastic anemia
Soil, dam's feces, and milk are other important sources of iron.1 Iron deficiency is most commonly associated with chronic blood loss due to internal or external parasitism, bleeding GI lesions, or hemostatic defects.
Dietary iron deficiency is seldom the sole cause of anemia, even in neonates on an all-milk diet, unless they are raised on cement or in barns or hutches with no access to the soil. A modest anemia is anticipated in veal calves. The anemia seen in some young calves during the first few days to weeks of life is apparently the result of congenital iron deficiency.2 Altered immune function, high incidence of infection, and reduced growth performance are reported in veal calves on low-iron diets.3 Alterations in GI pH may alter absorption of iron by the small intestine. States of inflammation and infection cause iron sequestration, not deficiency, by the reticuloendothelial system and lactoferrin. Iron deficiency has been well documented in calves and piglets housed exclusively indoors or in hatches with no access to soil.4 Absolute iron deficiency anemia is not commonly reported in horses.5-8Circulating erythrocytes account for about two-thirds of the total iron reserves found in the body. The remaining iron stores are distributed in the liver, spleen, and bone marrow. With chronic blood loss anemia, iron depletion is first indicated by decreased marrow iron, which can be appreciated with special staining of the bone marrow with Prussian blue stain for iron. As blood loss continues and iron deficiency progresses, serum iron is decreased, whereas iron-binding capacity may actually increase. Late in this process, iron-deficient erythropoiesis results in the typical microcytic, hypochromic erythrocytes generally thought to be characteristic of iron deficiency anemia (decreased PCV, hemoglobin concentration, mean corpuscular volume, and mean corpuscular hemoglobin concentration). Other laboratory findings include echinocytosis, keratocytosis, schistocytosis, acanthocytosis, ovalocytosis, hypoferritinemia, and hypoferremia.5-8 The observed RBC morphologic abnormalities are thought to be due to oxidative damage. Normal serum iron and iron-binding capacity for most domestic animals is 100 and 300 ug/dL, respectively.
Treatment
Treatment of iron deficiency anemia is contingent on evaluation of the cause and correction or resolution of the process responsible for chronic blood loss. Iron is usually supplied as an oral supplement or feed additive, and many commercial preparations are available. Injectable iron dextran intended for use in baby pigs should be avoided in horses and cattle, because it can induce anaphylaxis, especially if administered repeatedly.9 An injectable iron preparation intended for use in horses was reported to result in acute iron overload, massive hepatic necrosis, and severe death losses in a group of young cattle.10 Iron overload has resulted in acute death losses in neonatal foals fed an iron-containing microbial supplement and in hemochromatosis and extensive liver damage in adult horses.11
Copper Deficiency
Johanna L.
Watson • Gary P. CarlsonCopper deficiency can occur as a primary problem in milk-fed animals or in pastured animals in copper-deficient areas. More commonly, copper deficiency occurs secondarily in association with other trace mineral imbalances such as dietary molybdenum excess and is influenced by the sulfur and zinc content of the diet. Copper is an essential cofactor for a wide variety of enzymatic reactions, and copper deficiency produces a constellation of clinical signs related to impairment of these reactions.12 Clinical signs of copper deficiency are most prominent in young, growing animals and may include reduced growth rate, rough and depigmented hair, diarrhea, osteoporosis with spontaneous fractures, and anemia. In lambs, copper deficiency can produce a demyelinating syndrome known as swayback or enzootic ataxia. Copper deficiency has also been associated with hemolytic anemia in postparturient dairy cattle in New Zealand.10 Copper plays an important role in iron transport from the gut to the marrow and in the incorporation of iron into the heme moiety. The anemia produced by copper deficiency is generally moderate and slowly progressive. It closely resembles iron deficiency in that it is usually a microcytic, hypochromic anemia. Bone marrow evaluation often reveals intracellular accumulations of iron known as sideroblasts. This finding indicates that the principal problem is a function of altered incorporation of iron into the erythrocyte hemoglobin rather than an actual deficiency of iron. Copper deficiency can be documented by measuring serum copper as ceruloplasmin, erythrocyte superoxide dismutase, or the copper content of hair, liver, or kidney. Serum iron tends to be low in animals with copper deficiency. Copper can be supplied as a dietary supplement or as an injectable copper glycinate preparation.