Page 469 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

436 SECTION | V Metals and Micronutrients

VetBooks.ir proliferation and fibrosis. It is speculated that what was pills (surgically if necessary), and increase excretion.
Because the body has limited ability to excrete excess
histologically interpreted as proliferation of bile ductules
iron (other than through bleeding), urinary excretion can
was, in fact, proliferation of hepatic stem cells (oval cells)
in response to the severe hepatic damage (personal obser- be enhanced through the use of a chelating agent. A spe-
vation). Experimentally, adult ponies have been adminis- cific chelator of iron, deferoxamine, has been used in the
tered iron as ferrous sulfate at 50 mg/kg/day orally for up treatment of iron toxicity. Deferoxamine has a strong
to 8 weeks. Through the study and for 20 weeks after the affinity for iron and a low affinity for calcium and com-
end of dosing, no adverse clinical signs or hepatic damage petes effectively for iron in ferritin and hemosiderin but
were reported (Pearson and Andreasen, 2001). not in transferrin, hemoglobin or heme-containing
enzymes. It is poorly absorbed orally and so is given par-
enterally by slow intravenous drip. Since it is excreted
Iron Storage Disease
primarily by the kidneys, it should be given carefully to
Iron storage disease, resulting in hemosiderosis and hemo- patients with renal insufficiency (Osweiler et al., 1985;
chromatosis, has been reported in several different species Goyer and Clarkson, 2001; Poppenga, 2002).
of animals. Hemochromatosis is the pathologic accumula-
tion of iron in tissues, while hemosiderosis is the non-
pathologic accumulation of iron. In birds, iron storage CONCLUDING REMARKS AND FUTURE
disease has been reported in mynah birds, toucans, birds DIRECTIONS
of paradise, quetzals, and birds of the Turdidae family
(blackbirds, song thrushes, fieldfares, and redwings, Iron is essential for normal physiological functioning.
Pavone et al., 2014). The clinical signs are dyspnea, Iron-deficiency anemia is common in humans and also
hepatic damage/insufficiency, and death in mynah birds. occurs in piglets, veal calves and parasitized animals.
Sudden death has been reported in toucans. It has been Therefore, iron supplements are readily available and
shown that the cause in mynah birds is due to mainte- widely used. In addition, some species have a propensity
nance of iron uptake from the GI tract, despite excess for genetic iron storage diseases. Fortunately, both acute
hepatic iron accumulation (Mete et al., 2003). The treat- and chronic iron toxicoses are rare in animals. When toxi-
ment in birds can consist of a low iron diet with phlebot- cosis does occur, cellular damage is caused by the pres-
omy or the use of iron chelators (Rodenbusch et al., ence of free iron in excess of the body’s capacity to bind
2004). A genetic, inheritable defect resulting in hemo- and sequester it. The free iron then initiates the generation
chromatosis, clinical wasting, and skeletal defects can of ROS in excess of cellular oxidant defenses resulting in
occur in Salers cattle beginning at 9 22 months of age lipid peroxidation of membranes, protein and DNA cross-
(O’Toole et al., 2001; Norrdin et al., 2004). Egyptian fruit linking, and cell death.
bats (Rousettus aegyptiacus) are also known to have
genetic iron storage disease. In these bats, it was found
that if the sum of transferrin saturation and serum iron REFERENCES
was greater than 51, the individual bat had a high proba-
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