Heavy metal toxicoses in pet birds: Watch for combination of gastrointestinal and nervous systems signs



Jan 01, 2006

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.

Nervous system

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.
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.

Hematologic effects

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.

Urinary system

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.

Musculoskeletal system

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 than waterfowl.

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.