Page 474 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Lead Chapter | 29 441

VetBooks.ir small lead objects around the house. Both cats and dogs white matter. Astrocytic proliferation was also observed.
Blood capillaries were congested with enlarged and
have been exposed to lead by the renovations of older
increased endothelial cells. Meningeal blood vessels were
homes containing leaded paints. The main route seems to
be the ingestion of fine dust by the grooming habits of prominently congested with mild lymphocytic infiltration.
indoor pets and their tendency to ingest small objects. A Edema of Purkinje cell layer in the cerebellum and mild
proximal renal tubulopathy has been described in a dog neuronal degeneration in the nucleus of mesencephalon
diagnosed with lead intoxication (King, 2016). were seen.
Clinical signs of lead toxicosis vary with the species Lead is also a reproductive and developmental toxi-
involved, duration of exposure, and amount of lead cant and details can be found in other publications (Flora
absorbed. The major systems affected by lead poisoning and Agrawal, 2017).
are the GI system, central nervous system, and hemato- Diagnosis of lead poisoning in animals should be
logical system. Abdominal pain and diarrhea can be made with a combination of history, clinical or
common clinical signs in animals exposed to excess lead. necropsy findings, and lead analysis of tissue.
Anorexia is common as well as vomiting in those species Basophilic stippling of erythrocytes and inhibition of
that are able to. Neurological signs including depression, hemoglobin synthesis are characteristic hematological
weakness and ataxia can progress to more severe clinical features of lead poisoning. From a living animal, whole
signs of muscle tremors or fasciculations, head pressing blood is the best sample for laboratory determination of
(especially in ruminants), blindness, seizure-like activity, lead. The normal background concentration of lead in
and death. Many animals with chronic lead poisoning will the blood of mammals is below 0.1 ppm. Whole blood
show subtle and nonspecific clinical signs such as abdom- lead concentrations above 0.35 ppm, when combined
inal discomfort, vague GI upsets, anorexia, lethargy, with indicative clinical signs in the suspect animal, are
weight loss, and behavior changes. Horses develop acute compatible with a diagnosis of lead toxicosis. Many
lead toxicosis and show clinical signs of laryngeal paraly- authors use a blood lead concentration of 0.6 ppm and
sis and “roaring,” in addition to colic and seizure-like above as diagnostic for lead toxicosis. Postmortem sam-
activity. Evidence suggests that horses may be more sus- ples of choice are kidney and liver with lead concentra-
ceptible to chronic lead toxicosis than cattle. Horses tions above 10 ppm on a wet weight basis being
exposed to a daily intake as low as 1.7 mg/kg body diagnostic for lead toxicosis in domestic species.
weight (approximately 80 ppm Pb in forage dry matter)
were poisoned (Aronson, 1972). A maximum tolerated TREATMENT
dose of 10 ppm lead in dog and cat food products was
determined by the FDA-CVM in response to confusion Acute lead poisoning in animals is usually fatal if the ani-
concerning the misinterpretation of lead analytical results mals are not treated promptly. The treatment approach for
in pet food products (FDA-CVM, 2011). Clinical signs of lead poisoning in animals includes stabilizing and support-
lead toxicosis in avians vary with waterfowl and raptors ing the animal, especially if severe clinical signs are pres-
mainly displaying a chronic wasting disorder with appar- ent, preventing additional exposure to lead, and chelation
ent peripheral neuropathy. Psittacines are more likely to therapy to quickly reduce the body burden of lead. The
display GI problems and neurological abnormalities. exposure history of the animal should be reviewed for
Gross lesions in animals dying of lead poisoning are potential sources of lead and the need for GI decontamina-
often minimal and nonspecific, although lead-containing tion. The use of chelating agents when large amounts of
objects may be visible in the GI tract. Histologically, there lead are present in the GI tract may actually enhance the
may be degeneration and necrosis of the renal tubular epi- absorption of lead into the body. Physical removal of lead-
thelium or the presence of acid-fast inclusion bodies containing objects by surgical means may be necessary
(Hamir et al., 1988; O’Hara et al., 1995). Brain lesions in a with larger objects. The parenteral use of calcium disodium
calf poisoned with lead included multiple focal or laminar ethylenediaminetetraacetic acid (CaEDTA) has been com-
lesions of neuronal necrosis in the cerebral cortex, cauda- monly used for several decades as a chelation agent in
tum, and medial nuclei of thalamus, predominantly at the domestic animals (Kowalczyk, 1984).
tips of gyri in the occipital and parietal lobes. The lesions Although other chelators may be superior, CaEDTA is
spread occasionally to the deeper region of the gyri along still widely used in veterinary medicine, especially in
the sulci (Seimiya et al., 1991). The affected neurons were large animals. CaEDTA is given intravenously (IV) or
shrunken and angular, sometimes triangular in outline with subcutaneously (SQ) and chelates and mobilizes the lead
pale eosinophilic cytoplasm. The nuclei showed pyknosis from bone resulting in a transient increase in blood lead
and rhexis. Edematous dilation of perivascular and peri- levels. This increase in blood lead can increase soft tissue
neuronal spaces with spongiotic state of neuropil was lead levels leading to an exacerbation of clinical signs.
observed from the molecular layer to outer zone of the Preceding CaEDTA usage with a chelator that specifically