- Heavy metal poisonings in birds most commonly occur from ingestion of substances containing lead or zinc.
- Lead that is ingested can be absorbed through the gastrointestinal tract and then taken up by soft tissues and eventually by bone.
- Lead affects all major organs and can cause damage to the gastrointestinal tract, red blood cells, kidneys and liver.
- Clinical signs of heavy metal toxicosis may include non-specific signs of illness, gastrointestinal signs, urinary tract problems and neurological deficits.
- Antemortem diagnosis of heavy metal toxicity relies on blood lead or zinc levels. In some BUT NOT ALL cases, ingested lead will also be visible on survey radiographs.
- Remove heavy metal from the bird’s tissues with a chelation agent such as calcium EDTA.
- Pieces of heavy metal within the digestive tract may also be removed endoscopically, surgically or via gastric lavage.
Heavy metal poisoning in birds most commonly occurs from ingestion of substances containing lead, or less commonly zinc. Acute heavy metal toxicity is occasionally seen in companion parrots that ingest or chew on objects containing metal because of their curious nature and innate desire to forage. Chronic lead poisoning most frequently affects free-ranging wildlife such as ducks, geese, swans and loons (Fig 1). Lead toxicity in wild birds is most commonly seen during migration in the late fall and early spring. In heavily contaminated areas, toxicity may be observed at any time of the year. Lead toxicity also occasionally occurs in upland game birds such as mourning doves (Zenaida macroura), wild turkey (Meleagris gallopavo), pheasants and quail. Lead poisoning has also been reported in small mammals, such as raccoons (Procyon lotor), and raptors, presumably from the ingestion of lead-contaminated prey.
Lead is relatively insoluble. After ingestion, small amounts are absorbed from the gastrointestinal tract and released into the bloodstream. The presence of grit in the ventriculus or gizzard increases the absorption of lead, which is first retained in soft tissues and eventually bone.
Lead causes endothelial damage while also inhibiting enzymes needed for cellular metabolism. Pathologic changes may include:
- Epithelial necrosis in the gastrointestinal system
- Increased erythrocyte fragility
- Bone marrow suppression leading to inhibition of erythrocyte production and function
- Damage to capillaries within the brain resulting in cerebral edema
Lead may be found in many household items (see Box 1):
Although lead shot has been banned for hunting waterfowl in the United States, spent lead shot is still present in waterways. Ingestion of one to three lead shotgun pellets has been reported to be lethal in waterfowl (Beasley 1999).
Clinical signs of lead toxicosis
Birds can present with a variety of clinical signs depending on the rate of toxin exposure. In cases of acute exposure, birds typically show non-specific signs of illness as well as problems associated with the gastrointestinal tract, urinary tract and/or nervous system (Box 2).
|Non-specific signs of illness||Weakness or depression, pallor and anorexia|
|Gastrointestinal signs||Anorexia, crop stasis, vomiting or regurgitation, biliverdinuria and diarrhea (i.e. loose, dark or black stool)|
|Urinary signs||Hematuria or hemoglobinuria, particularly in Amazon parrots (Amazona spp.)|
|Neurologic signs||Twitching, circling, convulsions and/or blindness|
Chronic toxin exposure may be associated with all of the aforementioned signs as well as gradual weight loss.
Diagnosis of lead toxicosis
- A history of exposure to lead should significantly increase the index of suspicion.
- If lead toxicosis is suspected, perform a complete blood cell count or at minimum a packed cell volume. Mild to moderate anemia may be documented; however basophilic stippling is extremely rare in birds (Box 3).
|History of exposure||Mild to moderate anemia|
|Hematology||Mild to moderate anemia (basophilic stippling rare)|
|Survey radiographs||Metallic density|
|Whole blood levels||Lead > 0.2 ppm|
- Survey radiographs are also recommended since some, BUT NOT ALL cases of lead toxicosis will reveal a discrete, metallic density within the gastrointestinal tract (Fig 2). In a survey of mallards (Anas platyrhynchos) dosed with lead shot, only 1.2% had a pellet in their ventriculus at necropsy (Rodriguez 2010).
- Collect heparinized whole blood to measure lead levels. In the presence of clinical signs, blood lead levels above 0.2 ppm are suggestive for lead toxicity. Although portable testing equipment is commercially available, the most direct route for laboratory heavy metal testing is to send a sample to:
- Inhibition of the enzyme, δ-aminolevulinic acid dehydratase (ALAD) also occurs with lead toxicity and ALAD levels may be measured. Aminolevulinic acid dehydratase levels have been described primarily in wildlife studies; ALAD is typically not measured in companion bird care.
- Necropsy findings most consistently reported in wild birds include an enlarged gallbladder, impacted proventriculus, and a cracked, peeling ventricular lining, with or without lead shot present. Collect liver and kidney tissue to measure tissue lead levels.
Treatment of lead toxicosis
There are three goals for treatment of heavy metal toxicity:
- Stabilize the patient by providing supportive care such as supplemental heat, fluids to prevent dehydration and medication to stop tremors or seizures.
- Remove heavy metal from bodily tissues with a binding or chelating agent:
- Calcium EDTA (Calcium disodium versenate, 3M Pharmaceuticals) 30-35 mg/kg IM BID x 5 days
- Dimercaptosuccinic acid (DMSA or Succimer) 25 mg/kg PO SID x 10 days. In a study evaluating chelating agents in cockatiels. Although DMSA is administered orally, it may be easier than other chelating agents for bird owners to administer at home, however, DMSA has a narrow margin of safety so this drug should always be used with caution (Denver 2000).
- D-Penicillamine (Cuprimine, Merck) 30 mg/kg PO BID x 7 days minimum
Chelation therapy may not be necessary in cases where prompt removal of the lead source is accomplished. When chelation is started, monitor renal parameters during therapy (Richardson 2006).
- If a source of heavy metal is seen on radiographs, removal of lead from the
gastrointestinal tract via endoscopy, surgery, or gastric lavage may also be indicated. Lubricants such as mineral oil or corn oil, cathartics (i.e. magnesium sulfate), or bulk agents such as peanut butter, psyllium or oral cellulose products may also be used to remove heavy metal from the digestive tract.
Removal of particles with an iron base using a feeding catheter loaded with neodymium-ferro-borium alloy magnets has also been described.
Prevention of lead toxiciosis
Since companion parrots are curious by nature, it can be challenging to prevent chewing and ingestion of undesirable objects. Pet birds should always be supervised during their time outside of the cage, and owners should also remove all known sources of heavy metal or limit exposure to areas with heavy metals (Box 1).
Control of problem areas for wildlife consists of plowing to lessen the availability of spent shot to birds. The use of non-toxic steel or bismuth shot for waterfowl hunting is also now required in the United States. This switch from lead to non-toxic shot has reduced the number of birds dying from lead poisoning in America. The United States and Canada are also considering a ban on lead fishing sinkers.
Zinc is a trace metal or mineral essential for health. Zinc is involved in cell replication and in development of cartilage and bone (McDonald 2006). The primary target organs in zinc toxicity are the kidneys and pancreas.
Sources of zinc
Zinc toxicity usually arises from the ingestion of zinc-coated wire or metallic foreign bodies such as pennies minted after 1983. One penny contains approximately 2440 mg of elemental zinc (Richardson 2006).
Galvanized wire is another common source of zinc intoxication in parrots, especially cheap, imported wire. Aviary birds are often housed in galvanized steel wire cages. Galvanized coatings can contain up to 99.9% zinc, however galvanized wire can also contain lead (Platt 2006). Galvanized dishes should never be used since zinc can leach into the water.
Powder coating is a protective coating for the cage. While formulas differ by manufacturers, most contain no zinc, however some imported powder-coated cages use zinc to expedite setting of powder coating (Richardson 2006).
Zinc can also leach out of zinc-coated iron shot into the environment. Waterfowl can then ingest vegetation and sediments contaminated by zinc (Platt 2006).
A number of websites report that the adhesive in paper towel and toilet paper rolls contains significant amounts of zinc, however this appears to be more urban legend than fact.
Once, when we had a look at the actual zinc content in the glue in those paper rolls, and then “borrowed” the nutritional requirements for zinc in chickens; presuming that the requirements in a parrot would be similar, we were able to show that if a parrot ate toilet paper exclusively with that zinc containing glue, there would still be a need for zinc supplementation to meet the nutritional requirements for the bird. (Speer 2010, Veterinary Information Network)
Clinical signs of zinc toxicosis
As with lead toxicity, signs of zinc toxicity can be vague and non-specific, but clinical signs are often related to disease of the gastrointestinal tract, pancreas, kidneys and/or central nervous system. Although this is a bit controversial and reports are anecdotal, zinc toxicity has also been associated with an “extreme” loss of plumage and feather damaging behavior (Box 5).
|Box 5. Clinical signs of zinc toxicity|
Diagnosis of zinc toxicosis
The minimum database in zinc toxicosis may be relatively unremarkable. Mild to moderate regenerative anemia due to erythrocyte loss has been described with zinc toxicity (Box 6). Since zinc toxicosis typically results from chronic exposure to fine metal powder, a metallic density is rarely observed on survey radiographs.
|Box 6. Diagnostic testing for zinc toxicity|
|Hematology||Mild to moderate anemia|
|Whole blood levels||Zinc > 2 ppm|
The normal blood zinc ranges are only weakly understood for a variety of species. Additionally, in a trial following induced zinc toxicity in cockatiels, blood zinc levels were extremely inconsistent as a diagnostic predictor (Howard 1992). Part of the confusion stems from the fact that zinc is an essential nutrient. Normal homeostasis regulates zinc levels based on variations in gastrointestinal content, bioavailability and individual nutritional needs. Significant diurnal variations in zinc values have also been documented in 15 adult psittacine birds (Rosenthal 2005).
Nevertheless in the presence of clinical signs, blood zinc levels exceeding 200 μg/dl (or 2 ppm) are suggestive of toxicity. Collect heparinized whole blood to measure zinc levels. Take care in how the blood sample is drawn and stored to avoid contamination.
- Although microtainers are typically used for companion birds, remember that the
rubber stoppers in red-topped tubes contain zinc. The presence of rubber can cause an artifactual elevation in zinc levels.
- Royal blue-topped tubes are an alternative collection tube to test for zinc and
The pancreas is the tissue of choice for postmortem zinc analysis (Box 7). Liver and kidney samples may also be collected to measure tissue zinc levels.
|Box 7. Pancreatic tissue zinc levels in cockatiels (Dumonceaux 1994)|
|Normal||26.11 μg/gram (dry weight basis)|
Important pathologic lesions seen with zinc toxiciosis include ileus and focal mononuclear degeneration of the liver, kidneys and pancreas (LaBonde 1995). Necrotizing pancreatitis and erosive ventriculitis are other common manifestations. Histologically, the koilin layer is disrupted and there is ulceration of the underlying mucosa and dysplasia of the ventricular glands.
Treatment of zinc toxicosis
The goals for treatment are the same as with lead toxicity. The most important difference is that zinc is not stored in bone, and therefore blood and tissue levels equilibrate faster. This means that the response to chelation therapy is also faster (LaBonde 1995).
Prevention of zinc toxicosis
Scrubbing all new galvanized cage wiring with a mildly acidic solution such as vinegar, then drying carefully, may reduce zinc levels.
Copper toxicosis is rare in birds. Sources of copper include wire, pennies minted before 1982, copper sulfate, anti-fouling paints and possibly copper ammunition (Christian Franson 2011). An important source of acute copper toxicosis in free-ranging waterfowl and other aquatic birds are acid metalliferous water bodies.
Clinical signs of copper toxicosis may include depression, weakness, anemia, convulsions and coma. Black discoloration of the parenchyma is an important gross finding. Common histopathological lesions include proventricular and ventricular necrosis, ventricular hemorrhage and/or congestion, erosion and ulceration of the koilin layer and duodenal hemorrhage (Isanhart 2011).
Like zinc, significant diurnal variations in blood copper levels have been documented (Rosenthal 2005).
Iron toxicosis in companion parrots can result from exposure to cast-iron feeding bowls with chipped enamel. Non-specific signs of illness predominate such as lethargy, emaciation and anorexia. Deferoxamine is the treatment of choice in mammals, but calcium EDTA also works well (LaBonde 1995).
For more information on iron overload, see Iron Storage Disease in Birds.
References and further reading
Altman RB, Clubb SL, Dorrenstein GM, Quesenberry K. Avian Medicine and Surgery. Philadelphia: W.B. Saunders; 1997.
Beasley VR. A Systems Affected Approach to Veterinary Toxicology. Urbana, IL: University of Illinois Press; 1999. Pp. 27-69.
Beyer WN, Franson JC, Locke LN, et al. Retrospective study of the diagnostic criteria in a lead-poisoning survey of waterfowl. Arch Environ Contam Toxicol 35(3):506-512, 1998.
Brown CS, Luebbert J, Mulcahy D, et al. Blood lead levels of wild Steller’s eiders (Polysticta stelleri) and black scoters (Melanitta nigra) in Alaska using a portable blood lead analyzer. J Zoo Wildl Med 37(3):361-365, 2006.
Denver MC, Tell LA, Galey, FD, et al. Comparison of two heavy metal chelators for treatment of lead toxicosis in cockatiels. Am J Vet Res 61(8):935-940, 2000.
Christian Franson J, Lahner LL, Meteyer CU, Rattner BA. Copper pellets simulating oral exposure to copper ammunition: Absence of toxicity in American kestrels (Falco sparverius). Arch Environ Contam Toxicol Apr 22 2011 [Epub ahead of print].
Harrison GJ, Lightfoot TL. Clinical Avian Medicine. Palm Beach: Spix Publishing, Inc; 2006.
Hoogesteijn AL, Raphael BL, Calle P, et al. Oral treatment of avian lead intoxication with meso-2,3-dimercaptosuccinic acid. J Zoo Wildl Med 34(1):82-87, 2003.
Howard BR. Health risks of housing small psittacines in galvanized wire mesh cages. J Am Vet Med Assoc 200(11):1667-174, 1992.
Hunt WG, Parish CN, Orr K, Aguilar RF. Lead poisoning and the reintroduction of the California condor in northern Arizona. J Avian Med Surg 23(2):145-150, 2009.
Isanhart JP, Wu H, Pandher K, et al. Behavioral, clinical, and pathological characterization of acid metalliferous water toxicity in mallards. Arch Environ Contam Toxicol 61(4):653-667, 2011.
Kerr R, Holladay S, Jarrett T, et al. Lead pellet retention time and associated toxicity in northern bobwhite quail (Colinus virginianus). Environ Toxicol Chem 29(12):2869-2874, 2010.
LaBonde J. Toxicity in pet avian patients. Seminars in Avian and Exotic Pet Medicine 4(1):23-31, 1995.
Macintire DK, Drobatz KJ, Haskins SC, Saxon WD. Manual of Small Animal Emergency and Critical Care Medicine. Ames: Blackwell Publishing; 2006. Pp. 270-271.
Martinez-Haro M, Green AJ, Mateo R. Effects of lead exposure on oxidative stress biomarkers and plasma biochemistry in waterbirds in the field. Environ Res 111(4):530-538, 2011.
McDonald D. Nutritional considerations Section I. In: Harrison GJ, Lightfoot TL (eds). Clinical Avian Medicine. Palm Beach, FL: Spix Publishing; 2006. Pp. 102-103.
Olson GH and Orosz SE. Manual of Avian Medicine. St. Louis: Mosby Inc; 2000.
Platt SR. Evaluating and treating the nervous system. . In: Harrison GJ, Lightfoot TL (eds). Clinical Avian Medicine. Palm Beach, FL: Spix Publishing; 2006. P. 510.
Richardson JA. Implications of toxic substances in clinical disorders. In: Harrison GJ, Lightfoot TL (eds). Clinical Avian Medicine. Palm Beach, FL: Spix Publishing; 2006. Pp. 713-715.
Ritchie BW, Harrison GJ, Harrison LR. Avian Medicine: Principles and Applications. Lake Worth: Wingers Publishing, Inc; 1994.
Rodriguez JJ, Oliveira PA, Fidalgo LE, et al. Lead toxicity in captive and wild Mallards (Anas platyrhynchos) in Spain. J Wildl Dis 46(3):854-863, 2010.
Rosenthal KL, Johnston MS, Shofer FS, Poppenga RH. Psittacine plasma concentrations of elements: daily fluctuations and clinical implications. J Vet Diagn Invest 17(3):239-244, 2005.
Speer B. Are toilet paper rolls a potential source of zinc poisoning? Veterinary Information Network. June 26, 2010. Available at http://www.vin.com/Members/boards/discussionviewer.aspx?FirstMsg=1&LastMsg=20&DocumentId=4550946. Accessed on November 15, 2011.
Stauber E, Finch N, Talcott PA, Gay JM. Lead poisoning of bald (Haliaeetus leucocephalus) and golden (Aquila chrysaetos) eagles in the U.S. inland Pacific northwest region—an 18-year retrospective study: 1991-2008. J Avian Med Surg 24(4):279-287, 2010.
Wynee J, Stringfield C. Treatment of lead toxicity and crop stasis in a California condor (Gymnogyps californianus). J Zoo Wildl Med 38(4):588-590, 2007.
Pollock C, Chow C. Heavy metal poisoning in birds. May 13, 2011. LafeberVet Web site. Available at https://lafeber.com/vet/heavy-metal-poisoning-in-birds/