Page 766 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Avian Toxicology Chapter | 53 725

VetBooks.ir 15 30 min. Frequent vocalization, incoordination, tre- lead concentration does not always correlate with the
mors and seizures are the common clinical signs reported
severity of clinical signs.
Emaciation, atrophy of breast muscles, hydropericar-
in birds (Bischoff et al., 2001). There are no specific post-
mortem lesions associated with 4-AP poisoning. dium, pale musculature or viscera consistent with anemia,
Diagnosis is usually confirmed by the detection of 4- renal or visceral gout, air sacculitis, and fat atrophy have
AP in the grain/bait, gastrointestinal contents, or liver. been reported in various avian species. Bile stasis leading
to an engorged gallbladder, dark-green viscous bile, bile-
stained gastric and intestinal mucosa, and a greenish
METALS appearance to the liver have been reported in raptors
(Locke and Thomas, 1996). Histologically, myelin degen-
Lead
eration of peripheral nerves, renal necrosis with or with-
Occurrences of lead exposure and intoxication in birds out intranuclear inclusion bodies, hemosiderosis in liver,
continue to be detected worldwide along with increasing lung, and kidneys, and patchy necrosis of gizzard mus-
awareness and regulation. Though wild raptors, water- cles may be observed (Dvm et al., 2016; Locke and
fowl, and upland game birds are groups that have been Thomas, 1996).
subjected to lead intoxication, there are few reports of Measurement of whole blood lead concentration in
lead exposure in backyard chickens (Bautista et al., 2014; live birds or in the liver and kidney of dead birds is
Trampel et al., 2003). Various species-specific and employed for diagnosis and is widely available. A whole
habitat-linked factors of lead exposure are unique to birds. blood lead concentration of 0.20 ppm (20 μg/dL) or
Often, birds consume lead shot or other lead objects mis- greater is considered to be consistent with lead exposure.
taken as seed or grit. The curious nature of pet birds leads Because lead associates with red blood cells, serum and
them to ingest shiny objects easily. Temporal and spatial plasma are not appropriate for testing. Generally, 4 ppm
patterns of lead intoxication in California condors coin- wet weight or greater lead concentration in the avian liver
ciding with anthropogenic activities such as big game and kidney is likely to be significant.
hunting have been recorded (Cade, 2007). Various chelation therapies are employed for the
Inorganic lead salts and organic forms are more bio- treatment of lead intoxication. Several chelators can
available than elemental lead; however, the acidic envi- effectively bind lead, including CaNa 2 EDTA, succimer,
ronment in the proventriculus and ventriculus increases D-penicillamine, and British anti-Lewisite (BAL).
the solubility of elemental lead. Lead is actively trans- CaNa 2 EDTA and succimer are currently the chelators of
ported across the GI tract through the same transport choice, although no veterinary-approved forms are
mechanism used for calcium absorption. Irrespective of available. Symptomatic and supportive care including
its form, ingested lead is mostly excreted in the feces seizure control, fluid and electrolyte therapy for birds
without being absorbed. Red blood cells contain a major- experiencing diarrhea, and vitamin supplementation may
ity of the absorbed lead, with smaller amounts being further aid in patient stabilization and therapy.
bound to albumin or existing as free lead in plasma. Bone
is a long-term storage depot for lead and bone remodeling
Zinc
can result in release of stored lead. In chickens, a signifi-
cant amount of lead can result in eggs especially shells Galvanized cage wires and accessories, pennies minted
21
since divalent lead (Pb ) can alternate for calcium after 1982, and contaminated soil, water, and feed are
21
(Ca ) during shell formation. some of the documented sources of zinc associated with
Clinical signs consistent with lead intoxication are avian toxicosis (Puschner and Poppenga, 2009). Zinc is
related to nervous, GI, hematopoietic, and renal systems. absorbed in the proventriculus and small intestine.
Signs of intoxication can also be nonspecific and limited Postabsorption, zinc is distributed to pancreas, liver, kid-
to regurgitation, anorexia, weakness, and weight loss neys, intestinal mucosa, and brain where it binds to
(Puschner and Poppenga, 2009). Lethargy, wing droop, metallothionein.
leg paresis, changes in phonation, head tilt, ataxia, blind- The toxic effects of zinc are observed on the GI tract,
ness, circling, head tremors, and seizures are liver, kidneys, pancreas, red blood cells, and brain. High
notable signs related to nervous system dysfunction. GI intracellular zinc concentrations lead to increased cellular
signs include regurgitation and decreased motility of the reactive oxygen species production, reduced cellular ATP
upper GI tract (esophagus, proventriculus, and ventricu- concentrations, and loss of mitochondrial membrane
lus) resulting in impaction and greenish diarrhea that potential (Dineley et al., 2003).
stains feathers around the vent. Anemia as a result of Clinically affected birds may exhibit neurological signs
increased erythrocyte fragility and decreased erythrocyte such as intermittent head bobbing and ataxia. Other signs
replacement is observed in affected birds. Whole blood are lethargy, anorexia, polyuria, polydipsia, hematuria,