Heavy Metal Toxicosis
Lead toxicosis is commonly reported in companion birds as well as in free-ranging avian species, especially waterfowl. In pet birds, toxicosis often occurs from ingestion of metal in the home, such as blinds, costume jewelry, mirror backings, bird toys, hardware cloth, and curtain weights. Ingested lead degrades in the ventriculus and then is slowly released into the GI tract and blood. The lead is stored in soft tissues and bone and is slowly excreted over time. Lead toxicosis affects numerous biochemical processes in birds.
Clinical signs vary depending on the amount of lead ingested and may include anorexia, weight loss, regurgitation, diarrhea, depression, ataxia, weakness, seizures, blindness, polyuria, and polydipsia. Amazona spp, Aratinga spp, Eclectus parrots, and some other species may develop hemoglobinuria.
Diagnosis is based on clinical signs, biochemical analysis, hematologic findings, blood lead levels, and diagnostic imaging. Hematologic testing may reveal a microcytic, hypochromic anemia. Increased concentrations of AST, total protein, uric acid, and CK may be present. Radiographs may reveal metallic densities within the GI tract. However, the absence of metal in the GI tract does not exclude toxicosis. A blood level >50 mcg/dL (0.5 ppm) is considered diagnostic of lead toxicosis. Blood lead levels >20 mcg/dL (0.2 ppm) with clinical signs is considered consistent with lead toxicosis. Lead levels of 3–6 ppm or higher are considered significant in tissue (kidney, liver, brain, or bone).
Treatment includes supportive care (fluids, nutrition, etc) and chelating therapy with calcium edetate disodium (Ca EDTA) (30–35 mg/kg, SC or IM, bid) for 3–5 days until asymptomatic (with fluid therapy), followed by oral treatment with dimercaptosuccinic acid (DMSA) (25–35 mg/kg, PO, bid) or, less commonly, d-penicillamine (30–50 mg/kg, PO, bid). Midazolam or diazepam may be necessary for control of seizures. Bulk diets (with psyllium, peanut butter) may assist in removal of lead from the GI tract. In severe cases, flushing of the GI tract under general anesthesia may be necessary. Sources of lead in the environment must be removed.
Lesions associated with lead toxicosis seen on postmortem examination include demyelination of peripheral nerves, vascular necrosis, renal nephrosis, hemosiderosis in multiple organs, and focal areas of vascular damage in the cerebellum.
Zinc toxicosis is frequently reported in pet birds. Sources of zinc include any galvanized toys, chains, mesh, bells, keys, and pennies (post 1982). Galvanized wire contains mainly zinc, but some may also contain lead.
Clinical signs of zinc toxicosis include anorexia, GI disease, weakness, regurgitation, polydipsia, and polyuria. Diagnosis is based on history and clinical signs and an increased blood zinc level. Radiographs may reveal metallic densities within the GI tract. Blood samples for zinc analysis should be collected in glass or all-plastic syringes and tubes. Rubber stoppers on serum tubes and the grommets on some plastic may artifactually increase the zinc levels in the collected sample. Blood zinc levels >2 ppm are diagnostic for zinc toxicosis.
Treatment of zinc toxicosis is similar to lead toxicosis with supportive care, Ca EDTA, DMSA, and d-penicillamine. The source of zinc should be determined if possible and removed from the environment. Zinc is not stored in the bone like lead, so it chelates faster than lead.
Polytetrafluoroethylene (PTFE) gas poisoning occurs commonly in pet birds housed in or near kitchens. The gas is released from nonstick cookware such as Teflon® when the pans are overheated, at temperatures reaching 280°C (536°F). Other sources of PTFE include irons, ironing board covers, some self-cleaning ovens, heating elements from some reverse cycle heat pumps, and some heat lamps. See also Polytetrafluoroethylene (PTFE) and see Etiology.
Often, the only clinical sign is acute death. Other signs depend on the level of exposure and size of the bird. Small birds often die suddenly with minimal exposure. Larger birds may present with dyspnea, wheezing, ataxia, weakness, in respiratory distress, or seizuring. With a large enough exposure, large birds can die acutely. Diagnosis is based on a history of exposure and sudden death, or a history and clinical signs consistent with exposure.
Treatment is supportive with a warm, oxygenated incubator, fluids, NSAIDs, broad-spectrum antibiotics, and diuretics. Prognosis is guarded. Necropsy often reveals severe hemorrhage and congestion of the lungs.
Passive inhalation of tobacco smoke (second-hand smoke inhalation) or contact with tobacco on hands, fingers, hair, or clothes of smokers can lead to chronic respiratory disease and dermatologic problems on the face and feet of pet birds. Clinical signs may include coughing, sneezing, nasal and ocular discharge, dyspnea, conjunctivitis, or feather destructive behavior and mutilation. Ingestion of tobacco products has led to hyperexcitability, seizures, and death. Diagnosis is based on history, clinical signs, and response to treatment.
Treatment will depend on severity of clinical signs. For birds that are dyspneic or showing neurologic signs, supportive care and oxygen may be needed. If the bird has ingested tobacco, activated charcoal may be warranted. Treatment involves removing the bird from the exposure and placing it in a smoke-free environment. Owners who smoke should wash their hands before handling their birds.
Other aerosols, including some carpet fresheners, plastics either melted or burned in a microwave oven, perfumes, deodorizers, votive candles, and new heating duct systems may also be irritating or toxic to caged birds.
Last full review/revision October 2015 by Sharman M. Hoppes, DVM, ABVP (Avian)