Page 468 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Iron Chapter | 28 435

VetBooks.ir of iron-containing vitamins or molluscicide applied to rid the very low liver iron stores in newborn pigs, the low
expression of duodenal iron transporters in the first few
gardens of snails and slugs. Baby pigs are iron deficient
days postpartum (Lipinski et al., 2010), and the need to
at birth and require iron supplementation, which can
result in peracute or acute toxicity. Limited cases of iron supplement the small amounts of iron that they receive in
poisoning have occurred in horses and cattle through the sow’s milk. Because of their low iron stores at birth, iron-
use of iron supplements. In general, toxicity occurs in the deficiency anemia can occur in nonsupplemented baby
GI mucosa (oral exposure), liver, myocardium, and other pigs within 2 4 weeks after birth. This is manifested
tissues when the iron-binding capacity of the body is clinically in the pigs as dyspnea, anorexia, increased
overwhelmed, and free iron causes oxidative damage. infections, and poor growth, with some deaths. It is pre-
Genetic iron storage diseases are uncommon, but have vented by oral or parenteral injection of iron-containing
been reported in mynah birds, blackbirds (and other mem- compounds (Underwood, 1977; Osweiler et al., 1985).
bers of the Turdidae family), toucans, Saler cattle, When comparing routes of administration of the same
Egyptian fruit bats, and rarely in horses. iron compound, the potential for toxicity is the greatest
after intravenous injection followed by intramuscular
Acute Toxicity in Dogs, Cattle, Pigs injection with oral administration being the least toxic. In
acute iron toxicosis of pigs, two syndromes are recog-
and Adult Horses
nized. The first is a peracute syndrome which is charac-
Acute iron toxicity has been reported in dogs (Greentree terized by sudden death minutes to a few hours after iron
and Hall, 1983), cattle (Ruhr et al., 1983), pigs (Velasquez injection. In some ways, this resembles an anaphylactic
and Aranzazu, 2004), horses (Arnbjerg, 1981), and reaction in its rapidity of onset, vascular collapse and
humans. In dogs, toxicosis primarily occurs through the death, but the exact mechanism is not known. This pera-
accidental ingestion of large amounts of iron-containing cute syndrome has also been reported in horses following
vitamins or other iron supplements. In addition, acute tox- administration of iron compounds (Lannek and Persson,
icity can occur in dogs as the result of ingestion of mollus- 1972; Bergsjoe, 1974). The second syndrome described in
cicide containing iron phosphate and/or iron EDTA (Buhl pigs is a subacute to acute syndrome characterized by GI
et al., 2013; Haldane and Davis, 2009) In cattle, horses, necrosis, severe depression, coma and death, which can
and pigs, it has occurred through accidental administration occur in the four stages described above. Pigs born to
of excess amounts of iron supplements by oral or paren- sows deficient in vitamin E and selenium are reported to
teral routes. Diagnosis is based on history, appropriate be more susceptible to iron toxicosis (Osweiler et al.,
clinical signs, and radiography in small animals as 1985; Velasquez and Aranzazu, 2004).
iron-containing pills are radiodense. In general, if the
animals remain asymptomatic for greater than 8 h follow-
Neonatal Horses
ing a single exposure, it is reported that they are unlikely
to develop iron toxicity. In all species, ingestion of a toxic Although reports of iron toxicosis in horses and ponies
dose (roughly greater than 20 mg/kg in dogs) initially are rare, several cases in the 1980s are of note. Newborn
results in necrosis of the GI mucosal cells. This is followed foals, 2 5 days old, were given an oral nutritional supple-
by fluid loss, direct cardiotoxicity, and widespread organ ment containing ferrous fumarate. They became ill,
damage through the mechanisms described above. Fluid icteric, weak, and died of liver failure within 1 5 days
loss and decreased cardiac output can lead to circulatory following administration. The histologic lesions in the
shock. Iron toxicity has been described as occurring in four livers of these foals were remarkable in that they had the
stages. Stage I occurs 0 6 h postingestion and is character- appearance of longer-term chronic lesions even though
ized by vomiting, diarrhea, abdominal pain, and depres- they were as little as 24 h old. These hepatic lesions con-
sion. Stage II occurs from 6 to 24 h postingestion and is sisted of prominent bile ductule proliferation, hepatic cell
characterized by apparent recovery. Stage III begins at necrosis, and periportal fibrosis (Divers et al., 1983;
12 96 h with commencement of additional vomiting, Acland et al., 1984). Through experimental administra-
diarrhea, abdominal pain, GI hemorrhage, weakness, shock, tion, it was determined that ferrous fumarate, adminis-
and possibly death. Stage IV, if it occurs, begins 2 6 tered orally to foals within the first few days after birth,
weeks after ingestion and is characterized by GI fibrosis caused the liver failure seen in the earlier clinical cases
and obstruction (Greentree and Hall, 1983). (Mullaney and Brown, 1988). The increased sensitivity of
the neonatal foals is thought to be from increased absorp-
tion in the GI tract and lower systemic iron-binding
Neonatal Pigs
capacity (Poppenga, 2002). The iron overload in these
Paradoxically, iron toxicity in piglets resulting from oral foals, resulting from oral administration of ferrous fuma-
supplementation or parenteral injection occurs because of rate, caused hepatic necrosis with bile ductule