Heavy metal toxicoses are commonly reported in companion and free-ranging avian species. Most often toxicosis occurs from
ingestion lead from various sources including fishing and curtain weights, batteries, standard solder, lead pellets, lead-based
paints, hardware cloth and other galvanized wire, foil from wine and champagne bottles, linoleum, Venetian blinds (plastic),
glazed ceramics, plaster, seeds coated with lead arsenate, costume jewelry, mirror backing, leaded gas fumes and some bird
toys. Once the lead is ingested, it is degraded in the stomach (often remaining in the ventriculus) then slowly released into
the gastrointestinal tract and absorbed into the bloodstream. The lead absorbed from the digestive tract is then sequestered
in soft tissues and bone, and excreted by the kidneys over a period of weeks to months.
The toxic effects of lead are numerous due to its ability to disrupt many biochemical processes within the body.
In general, lead toxicosis affects the development of the nervous system by impairing cell-to-cell connections resulting in
alterations in neuronal circuitry and cellular migration. Lead also greatly affects calcium homeostasis and uptake by calcium
membrane channels and substitutes for calcium in calcium-sodium ATP pumps. Lead also blocks the entry of calcium into the
nerve terminals, inhibits calcium uptake in brain mitochondria, and interferes with calcium receptors that are coupled with
second-messenger functions [e.g. calmodulin, protein kinase C (cell division and proliferation, cell-cell communication and
organization of the cytoskeleton)]. Lead-induced Schwann cell degeneration may also lead to segmental demyelination and axonal
degeneration resulting in a peripheral neuropathy.
Photo 1: Lateral radiographic view of a 5-year-old umbrella cockatoo showing heavy metal metallic densities within the lumen
of the ventriculus. Also note the marked distension of the proventriculus, ventriculus and small intestines.
Lead intoxication may cause an anemia (microcytic hypochromic) as a result of decreased life span of the red blood cells and
disruption of heme synthesis. The exact biochemical process is not known; however, the effects are usually accompanied by
inhibition of sodium-potassium dependent ATPases.
A nephropathy associated with lead toxicosis is a common occurrence. The biochemical processes involved in lead toxicity include
a decrease in energy-dependent transport functions including aminoaciduria, glucosuria and ion transport. These changes are
possibly related to leads effect on mitochondrial respiration and phosphorylation.
Lead toxicity can directly or indirectly alter many aspects of bone cell formation. The accumulation of lead in bone occurs
under many of the same mechanisms involved in regulating calcium influx and efflux, including parathyroid hormone, calcitonin
and vitamin D. Lead is also reported to compete with calcium for absorption from the gastrointestinal tract.
In general, acute lead toxicosis is more common in companion avian species while chronic lead toxicosis is seen more often
in free-ranging avian species, especially waterfowl. Interestingly, chickens are reported to be more resistant to lead toxicosis
Clinical signs of lead toxicosis can vary depending upon the amount of lead ingested. However, any bird with a combination
of gastrointestinal and nervous systems signs should have heavy metal toxicosis high on the list of differential diagnoses.
Once the lead enters the circulatory system clinical signs may be pansystemic. Anorexia, weight loss, emaciation, regurgitation,
vomiting, diarrhea, increased gastrointestinal transit time, depression, ataxia and weakness, seizures, blindness, hematuria,
hemoglobinuria, polyuria and polydipsia, and death are all signs associated with lead toxicosis.