Welcome to the all-new Vetlearn

  • What’s new on Vetlearn?
  • The latest issues of Compendium and
    Veterinary Technician
  • New CE articles for veterinarians and technicians
  • Expert advice on practice management
  • Care guides on more than 400 subjects
    to give to your clients
  • And more!

To access Vetlearn, you must first sign in or register.


Become a Member

Compendium January 2009 (Vol 31, No 1)

Lead and Zinc Intoxication in Companion Birds

by Birgit Puschner, Robert Poppenga

    CETEST This course is approved for 3.0 CE credits

    Start Test


    Although the toxicity of lead and zinc to birds is widely recognized by veterinarians and bird owners, these metals are frequently found in the environments of pet and aviary birds, and intoxications are common. Clinical signs exhibited by intoxicated birds are often nonspecific, which makes early diagnosis difficult. Fortunately, lead and zinc analyses of whole blood and serum or plasma, respectively, are readily available and inexpensive; elevated concentrations can confirm intoxication. Once diagnosed, intoxication can be effectively treated by (1) preventing further exposure, (2) administering chelating drugs, and (3) providing symptomatic and supportive care.

    Metal intoxication is routinely diagnosed in companion birds, although the diagnosis can present a major challenge to the avian practitioner. Companion birds are intelligent, inquisitive, playful animals with a tendency to explore objects with their beak and tongue. They are especially fond of metallic objects, resulting in an increased risk for metal intoxication. Lead and zinc are the metals that most commonly result in clinical disease that requires a specific diagnostic workup and intensive treatment.

    Recognition of the toxicity of lead to pet and aviary birds and its subsequent elimination from their environment has likely decreased the incidence of exposure to this metal, although intoxications still occur regularly. However, little information is available to judge the actual incidence of lead intoxication in pet and aviary birds. In one retrospective study over a 5-year period (1987 to 1992) in Boston, 85 cases of lead intoxication were diagnosed in small companion animals.1 Dogs were the most frequently affected species (n = 53), followed by birds (n = 20; species were not given). The authors noted a steady decline of cases across species, including birds, over the period of the study. In contrast, a search of our diagnostic laboratory database did not show a decline in lead intoxication in psittacines between 1995 and 2005. During this period, an average of 13 cases were diagnosed per year. Recently, several cases submitted to the toxicology laboratory of the California Animal Health and Food Safety Laboratory System involved accidental exposure to atypical lead sources. In one case, an aviary in a large zoo was contaminated with lead from welding activities outside the exhibit, causing intoxication in a group of black parrots.a

    Over the past 10 to 20 years, an upsurge in zinc poisoning, especially in psittacines, has been attributed to the more common use of galvanized metal for cages and aviaries. This has led to zinc intoxication being called new wire disease.2,3 The increased number of documented zinc intoxications may also reflect pet bird owners' and veterinarians' increased awareness of the risks associated with exposure to galvanized metal. Unfortunately, there is a relative paucity of information in the veterinary and human medical literature regarding the treatment of zinc toxicosis.


    Potential Sources of Exposure

    Lead is used in an impressive array of products, from industrial items (e.g., tank linings, radiation shielding) to common consumer products such as paint pigments, inks, ammunition, solder, linoleum, wine bottle foil, lubricants, bearings, ceramics, plastics, electronic devices, fishing gear, jewelry, and small toys.4,5 Wrappers used for imported candy have been found to be printed with lead-contaminated inks.6 Lead-contaminated soil can also be a source of intoxication for birds.7,8 However, the most common sources of lead exposure for pet and aviary birds kept in home or cage environments are paint (either from direct ingestion of lead-based paint flakes or secondary to paint dust contaminating the environment) and small, lead-containing household objects.

    Because lead is toxic to children and waterfowl, several former uses for lead have been eliminated or curtailed (e.g., paint, gasoline, shot). Lead has not intentionally been added to most paint since 1978, although it has been estimated by the Centers for Disease Control and Prevention that 74% of privately owned US homes built before 1980 still contain hazardous quantities of lead paint.9 Thus, birds kept in older homes have an increased risk of lead exposure from paint.


    Few studies have determined the acute or chronic toxicity of lead in pet birds. Factors that influence the risk for lead intoxication include the amount and form of lead ingested, species exposed, dietary factors, size of ingested lead particles, and amount of grit in the ventriculus.5 The duration of retention of lead particles in the GI tract varies among individuals within a given species and between species; birds that rapidly eliminate lead particles are less likely to be intoxicated.10 Bird species that regurgitate indigestible parts of their diet, such as raptors, are less likely to be intoxicated by lead because they more efficiently remove lead from their ventriculus.11

    Diets low in protein and calcium increase the toxicity of lead.12 One study examined the toxicity of a single size 7½ (2.41-mm) lead shot to cowbirds. Three of 10 dosed birds on a natural diet containing wild bird seed and cracked corn died within 24 hours, whereas none of the birds fed a pelleted commercial diet died.10

    Given the number of variables that can affect the toxicity of lead, the availability of precise toxic or lethal doses is limited. A chronic cumulative lead dose of 2 mg/kg/day is reported to be toxic for ducks.13


    The bioavailability of ingested lead depends on its form and, to a lesser extent, the physiologic state of the animal (e.g., age). Elemental lead is less bioavailable than inorganic lead salts (e.g., lead acetate) or organic lead (e.g., tetraethyl lead). Elemental lead is relatively insoluble in hard, basic water but is more soluble in acidic water. Therefore, elemental lead is more soluble and relatively more bioavailable in the acidic fluids of the proventriculus or ventriculus of birds.11 Lead is actively transported across the GI tract through the same transport mechanism used for calcium absorption.9 This absorption mechanism explains the greater bioavailability of lead in immature, rapidly growing animals with an increased need for calcium compared with adult animals. Irrespective of its form, ingested lead is mostly excreted in the feces without being absorbed.

    Approximately 90% of absorbed lead is contained in red blood cells; small amounts are bound to albumin or found in plasma as free lead. Within red blood cells, lead is associated with the cell membrane, hemoglobin, and possibly other cell components.14 Lead is widely distributed in soft tissue, and bone serves as a long-term storage site. The half-life of lead is multiphasic because of its redistribution within various compartments of the body.13 For example, the half-life of lead in whole blood is approximately 35 days, whereas in brain tissue, it is approximately 2 years. Lead can persist in bone for years. Enhanced bone remodeling associated with egg laying or dietary calcium:phosphorus abnormalities can increase the release of sequestered lead into the blood and cause adverse effects. Normal bone turnover does not result in a clinically significant release of lead. Absorbed lead can be eliminated via sloughing of renal tubular epithelial cells or in bile or pancreatic secretions.13


    Metal ions play many diverse roles in biologic systems. They serve as charge carriers, intermediaries in catalyzed reactions, and structural elements in the maintenance of protein conformation. Disruption of these functions can affect metal transport, energy metabolism, apoptosis, ionic conduction, cell adhesion, inter- and intracellular signaling, diverse enzymatic processes, protein maturation, and genetic regulation.15 Lead damages cells primarily through its ability to substitute for several metal ions, especially calcium and zinc, at their binding sites.15 Lead produces oxidative damage to lipids and proteins as a result of iron release, disruption of antioxidant mechanisms, and direct oxidative damage.15-17

    The neurotoxicity of lead is most likely due to such diverse mechanisms as lipid peroxidation; excitotoxicity (i.e., cell damage secondary to receptor overstimulation by excitatory neurotransmitters such as glutamate); alterations in neurotransmitter synthesis, storage, and release; alterations in expression and functioning of receptors, such as glutamate and N-methyl-D-aspartate receptors; interference with mitochondrial metabolism and second messenger systems; and damage to astroglia and oligodendroglia.15

    The mechanism by which lead reduces GI motility is not entirely clear, but it does not appear to be related to an effect on peripheral nerves or calcium flux. Lead-induced GI relaxation may be due to stimulation of adenylate cyclase activity, resulting in increased intracellular cAMP.18

    Lead causes anemia by increasing erythrocyte fragility, delaying erythrocyte maturation, and inhibiting heme synthesis. Heme synthesis is impaired as a result of inhibition of aminolevulinic acid synthetase, d-aminolevulinic acid dehydratase (ALAD), coproporphyrinogen decarboxylase, and ferrochelatase.19

    Clinical Signs of Intoxication

    The clinical signs of lead intoxication are primarily related to the effects of lead on the nervous, GI, hematopoietic, and renal systems. The signs vary depending on whether the intoxication is acute or chronic, which, in turn, depends on the amount and form of lead ingested over time. Chronic intoxication is more likely in pet birds as a result of repeated exposure to a source of lead or the slow degradation and release of lead from ingested lead objects. However, death can be acute without premonitory signs.20 Signs of intoxication can be nonspecific and limited to regurgitation, anorexia, weakness, and weight loss.

    Signs related to nervous system impairment include lethargy, wing droop, leg paresis or paralysis, changes in phonation, head tilt, ataxia, blindness, circling, head tremors, and seizures.11,20 GI signs include regurgitation and decreased motility of the upper GI tract (esophagus, proventriculus, and ventriculus) resulting in impaction and greenish diarrhea that stains feathers around the vent.11,20 Signs related to hematopoietic impairment can include weakness. Lead causes renal tubular necrosis and renal nephrosis resulting in polyuria, proteinuria, and hematuria.5 The severity of clinical signs does not always correlate with whole blood lead concentration.

    Clinical Pathology

    In cases of chronic exposure, a microcytic, hypochromic, regenerative anemia may be present. Characteristic changes noted in mammalian intoxication, such as basophilic stippling and cytoplasmic vacuolization of red blood cells, are generally not noted in birds.5 Serum lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and creatine phosphokinase (CPK) activities and uric acid concentrations can be elevated.5,20


    Acute lead intoxication may not cause gross lesions. Splenomegaly can occur secondary to increased removal of damaged erythrocytes.5 Weight loss, air sacculitis, renal or visceral gout, pale musculature or viscera consistent with anemia, and muscle and fat atrophy have been reported.11,21 In raptor species, bile stasis consistently occurs and is associated with an engorged gallbladder; viscous, dark-green bile; a greenish appearance to the liver; and bile-stained gastric and intestinal mucosa.11

    Histopathologic lesions can include myocardial necrosis associated with fibrinoid necrosis of arterioles, hepatocellular necrosis, renal tubular necrosis (with or without characteristic intranuclear inclusion bodies in renal tubular cells), brain edema, peripheral nerve degeneration, and necrosis of ventriculus muscles.11,13 Hemosiderosis is a common histopathologic finding in some avian species.16 This may be secondary to intravascular hemolysis or impairment of heme synthesis.16,20


    As mentioned, the clinical signs associated with lead intoxication can be nonspecific, making diagnosis difficult. Radiographs may identify metallic objects in the GI tract. However, the absence of metal densities does not rule out metal exposure because the lead may have come from an object that was passed or a nonradiodense form. Diagnosis of lead exposure or intoxication is most directly made by measurement of lead in whole blood samples. Serum and plasma are not appropriate samples for lead analysis because lead associates with red blood cells.

    Lead analyses are widely available through veterinary diagnostic laboratories. Fortunately, small sample sizes can be used; blood samples as small as 20 µL are often suitable. In general, any anticoagulant, including EDTA, can be used to prevent samples from clotting, although there may be exceptions to this rule. It is best to consult the laboratory conducting the testing before sample collection. Whole blood lead concentrations consistent with lead exposure or intoxication are generally 0.20 ppm (20 µg/dL) or greater. There are no "normal" background blood lead concentrations in pet birds. ALAD activity, blood zinc protoporphyrin concentrations, and free erythrocyte protoporphyrin concentrations are good biomarkers of lead exposure, but these tests are not widely available.

    Postmortem diagnosis depends on a history of compatible clinical signs, detection of metallic particles or other forms of lead in the GI tract, and measurement of liver or kidney lead concentrations. Reported diagnostic liver or kidney concentrations vary, but values of 4 ppm wet weight or greater in either tissue are likely to be significant. There can be significant differences in liver and kidney tissue concentrations in the same bird; consequently, it is often advisable to test both organs.

    Case Management

    Decontamination approaches include the use of emollient laxatives such as mineral oil, bulk laxatives such as psyllium, or cathartics such as sodium sulfate to promote movement through the GI tract.5 In theory, sulfate can bind free lead to form an insoluble and, therefore, unabsorbable lead salt.21 However, use of sodium sulfate in combination with chelators such as calcium disodium EDTA (CaNa2EDTA) or succimer has not been shown to be more effective than using a chelator alone.21 Administration of three to five pieces of grit of a size appropriate for the bird species affected has been reported to aid in the passage of metal objects from the ventriculus.20

    Early removal of lead objects in the upper GI tract should be strongly considered because retention of objects is common. Nineteen of 25 cockatiels (72%) given two #12 lead shot to induce lead intoxication retained at least one pellet for 19 days, and 11 of 25 (44%) retained at least one pellet for 26 days.21 Saline lavage has been successful in removing lead particles from the proventriculus or ventriculus of lead-intoxicated birds.4,22,23 Endoscopy can be used to remove lead particles entrapped in proventricular or ventricular folds.23 Proventriculotomy may be necessary if other removal attempts fail. Unfortunately, the removal of small lead fragments using such techniques can be difficult and incomplete.

    Chelation Therapy

    The mainstay of treatment for lead intoxication is chelation therapy. Several chelators can effectively bind lead, including CaNa2EDTA, succimer, D-penicillamine, and British anti-Lewisite. CaNa2EDTA and succimer are currently the chelators of choice, although no veterinary-approved forms are available.

    There is evidence in mammals that the efficacy of chelation is improved when thiamine or antioxidants (e.g., ascorbic acid) are used in conjunction with chelators.24-26 This has not been investigated in birds.


    To avoid calcium chelation and resulting hypocalcemia, only the calcium salt of EDTA should be used.21,27 However, there are three significant disadvantages to the use of CaNa2EDTA. First, it is potentially nephrotoxic,20 although nephrotoxicity may be due to the metal chelate and not to CaNa2EDTA itself.28 Also, renal function may already be impaired in lead-intoxicated birds. Unfortunately, the incidence of CaNa2EDTA-associated nephrotoxicity in birds is unknown. Second, CaNa2EDTA must be administered parenterally because oral administration enhances the absorption of lead from the GI tract. However, repeated IM injections in birds can cause significant pain and muscle damage. Third, CaNa2EDTA chelates important endogenous minerals such as zinc.

    CaNa2EDTA can be administered in doses of 10 to 40 mg/kg IM or SC bid.5,20,21 Prolonged use is generally interrupted by intervals of no therapy to avoid adverse effects. The recommended protocol is a 5- to 10-day treatment period followed by a 3- to 5-day "rest" period to allow for a redistribution of tissue and fluid lead concentrations.29 Assessment of blood lead concentrations at the end of each rest period should dictate the length of chelation therapy. These follow-up tests should not be conducted before the end of the rest period because earlier assessment may not allow sufficient time for remaining lead to redistribute in the body. The goal is to chelate for the minimum amount of time necessary to resolve the intoxication (based on a decline in blood lead to an undetectable concentration). However, 40 mg/kg CaNa2EDTA given IM bid for 21 consecutive days was not associated with adverse effects in experimentally intoxicated cockatiels.21 The subacute toxicities of CaNa2EDTA and succimer were evaluated in experimentally intoxicated domestic pigeons.30 Doses of CaNa2EDTA up to 270 mg/kg bid (route of administration not indicated) for 15 days were not lethal, although increases in uric acid and AST, LDH, and CPK activities compared with prechelation and control bird (receiving no CaNa2EDTA) values were noted. Due to the potential nephrotoxicity of CaNa2EDTA, periodic assessment of renal function during chelation therapy is recommended.

    Neurologic signs may initially worsen in birds treated with CaNa2EDTA.30 Theoretically, this could be due to CaNa2EDTA-induced mobilization of lead from bone. Thus, birds with chronic lead exposure and potentially higher bone lead concentrations may be more likely to be affected than acutely intoxicated birds. However, this has not been shown experimentally.


    Succimer (dimercaptosuccinic acid, DMSA) is a newer chelating agent that has several advantages over CaNa2EDTA. It can be given orally, does not increase elimination of other essential minerals, and is not nephrotoxic. However, oral administration can be a disadvantage in a regurgitating bird. Succimer is more effective than CaNa2EDTA at removing lead from soft tissues,21 and it decreases lead concentrations in the central nervous system more rapidly than CaNa2EDTA.13 Succimer can be given at 20 to 40 mg/kg bid without adverse effects, although 80 mg/kg bid for 26 days was lethal to a significant percentage of cockatiels in one experimental study.21 This dose was less toxic in birds with lead intoxication compared with nonintoxicated controls. Unfortunately, days to death were not reported in this study. In contrast, succimer at doses up to 270 mg/kg bid for 15 days was not associated with significant adverse effects in experimentally intoxicated domestic pigeons.30 The only change noted was an initial increase in uric acid that plateaued by day 3 of dosing.

    Succimer should be given orally by gavage or other direct means (i.e., via syringe), although it has been effective when sprinkled on food.27 As with CaNa2EDTA use, the total length of treatment should be based on clinical improvement and determination of blood lead concentrations. The dosage of succimer in birds should not exceed 40 mg/kg PO q12h. Doses as low as 10 mg/kg PO have been suggested as effective.31 Unfortunately, an optimal dosing protocol has not been determined for birds. Whole blood lead concentration should be determined after a course of chelation to assess the need for additional therapy. If the concentration is still elevated, another course of therapy is indicated. As with CaNa2EDTA, 3 to 5 days should be allowed for the remaining lead to redistribute to obtain an accurate assessment of lead status.

    Clinical improvement is likely to be more rapid (within 24 hours) after succimer administration than after CaNa2EDTA.30 Combining CaNa2EDTA and succimer does not appear to be more efficacious than administering CaNa2EDTA or succimer alone, based on an experimental model of intoxication in cockatiels.21  TABLE 1 compares the advantages and disadvantages of CaNa2EDTA and succimer.

    Supportive Care

    Symptomatic and supportive care is also critical. Seizure control should be attempted using diazepam at 0.5 to 1.0 mg/kg given IM two to three times daily or as needed. Midazolam at 0.1 mg/kg IM controlled seizures in an intoxicated double yellow-headed Amazon parrot.5 If diarrhea is present, hydration and electrolyte status must be monitored and treated appropriately. Administration of B-complex vitamins and assisted alimentation should also be considered. Fluid support is critical to maintain urine output and to replace increased losses following the use of a cathartic; lactated Ringer's solution can be given subcutaneously.


    Potential Sources of Exposure

    Metallic zinc is commonly used to galvanize metals such as iron and steel to provide a protective coating. Until 1982, pennies consisted mainly of copper (95%) with a small amount of zinc (4%), but the copper-clad pennies minted after 1982 contain 97% zinc and 2.5% copper.32 Sources of zinc in documented avian zinc toxicoses include galvanized wire3 and cage bars,33 zinc-contaminated drinking water,34 pennies minted after 1982,35,36 cage coatings,37 cage accessories, hardware, and metallic toys.38 Zinc poisoning associated with zinc-coated food containers has been reported in humans but not in birds.39 Additionally, zinc is found in soil and may be present in high enough concentrations to result in avian poisonings. Zinc is also used in a variety of medical formulations, pigments, wood preservatives, insecticides, and rubber, but toxic exposure to any of these sources has not been reported in birds.


    Zinc is an essential metal, and animals and humans regulate zinc effectively. Mammals can tolerate dietary loadings greater than 100 times the minimum recommended daily zinc requirement.40 Dietary zinc requirements for pet birds have not been established, but most diets for companion birds contain between 70 and 110 ppm (mg/kg) of zinc. Research to establish zinc requirements in birds has focused on chickens and turkeys. For example, the dietary zinc requirement of young broilers is approximately 35 to 40 ppm (mg/kg).41

    If dietary exposure is excessive and homeostatic mechanisms fail, zinc toxicity can occur. Zinc toxicosis has been reported in numerous animal species, including dogs,42 calves,43 chickens,44 and humans.39,45 Definite data on the toxicity of zinc in companion birds are lacking, although limited information is available for certain species. In chicks, dietary concentrations of greater than 2200 ppm (mg/kg) zinc are considered toxic.46 Likewise, in one study, liver zinc concentrations in mallards reached toxic levels when dietary zinc exceeded 3000 ppm (mg/kg).47 In another study, oral exposure to 16 mg of zinc over a 2-week period resulted in 50% mortality in cockatiels, but even as little as 2 mg of zinc per week proved lethal in some birds.37 Reported cases of naturally occurring zinc poisoning in birds involved ducks,36 a Nicobar pigeon,48 a gray-headed chachalaca,49 macaws,33,38,50 lovebirds,3 and Amazon parrots.34


    In chickens, zinc is absorbed in the proventriculus and small intestine.51 The rate of absorption depends on the amount and form of zinc.52 Once absorbed, zinc is distributed to sites such as the pancreas, liver, kidneys, bones, muscles, brain, retinas, intestinal mucosa, and skin, where it binds to metallothionein, especially in the pancreas, liver, kidneys, intestinal mucosa, and brain. Metallothionein is a low-molecular-weight, cysteine-rich protein that has potent metal-binding capabilities.53 Zinc has a high binding affinity for metallothionein, which may play an integral role in zinc metabolism.54 The major route of excretion is via biliary, pancreatic, and gastroduodenal secretions into feces.


    Zinc is present in more than 200 metalloenzymes and thousands of protein domains.55 It is essential for bone formation, immune function, keratogenesis, reproduction, growth, vision, wound healing, brain development, normal functioning of the central nervous system, and many other physiologic processes.56-58

    Major pathophysiologic mechanisms of zinc are attributed to direct and indirect toxic effects on the GI tract, liver, kidneys, pancreas, red blood cells, and brain, but many of the specific underlying mechanisms have not been established. In acute cases of zinc poisoning, local corrosive effects may occur in the GI tract, followed by damage to the liver, kidneys, and pancreas. Zinc has been shown to cause acute pancreatic, hepatic, and renal failure in birds.

    In birds, a major concern is chronic zinc toxicosis with resulting anemia. The toxic effects of zinc leading to hemolytic anemia have recently been investigated in mallards.59 Excess zinc is thought to result in a functional iron deficiency leading to reduced heme synthesis and erythropoiesis. The interaction between zinc and iron may therefore play a major role in the development of anemia in birds overexposed to zinc. In addition, zinc limits copper availability46 and decreases tissue copper and ceruloplasmin concentrations. Decreased ceruloplasmin concentrations can result in lower availability of iron for hemoglobin synthesis.59

    Overall, tissue hypoxia can lead to tissue damage in the pancreas, liver, kidneys, and brain. Recently, zinc toxicity has been associated with brain damage that is most likely due to a combination of hypoxic and direct toxic effects.60

    Clinical Signs of Intoxication

    Clinical signs of zinc intoxication in birds are varied and nonspecific. They include lethargy, anorexia, regurgitation, polyuria, polydipsia, hematuria, hematochezia, pallor, dark or bright green diarrhea, foul-smelling feces, paresis, seizures, and sudden death.33-35,37-59 Zinc toxicosis was associated with sudden death in 7 of 21 psittacine birds evaluated in one study.61 Therefore, any acute death in a companion bird should be evaluated for possible zinc poisoning. Zinc exposure has been suggested as a cause of feather picking, but there is no evidence to link the two.


    Common findings on gross examination of birds that have died from zinc toxicosis include greenish, mucoid feces in the ileum, colon, or cloaca and muscle wasting, especially of the pectoral muscles. Occasionally, the liver or kidneys are slightly enlarged. No other consistent lesions are usually noted on gross examination.

    In zinc-intoxicated birds, microscopic changes are found in the pancreas, liver, kidneys, and GI tract. Experimental studies and case reports have indicated that the pancreas is the major target organ of zinc toxicity in birds. Histologic and ultrastructural pancreatic lesions include disruption of the normal zymogen granules, atrophy of acinar cells, loss of normal architecture, necrotizing pancreatitis, the presence of hyaline bodies and other electron-dense debris, cellular atrophy and necrosis of individual acinar cells, and interstitial fibrosis.36,61,62 The pancreatic islets are spared. Liver lesions vary from hepatic biliary retention and hemosiderosis to multifocal, necrotizing hepatitis.37,61 Lesions in the kidneys include varying degrees of acute tubular necrosis, occasionally with secondary renal or visceral gout, and moderate interstitial nephritis in addition to nephrosis.61 GI lesions include intestinal hemorrhage, hemorrhagic enteritis, hemorrhagic ventriculitis, ventricular koilin degeneration, and, in one case, cloacitis.61


    Diagnosis involves a careful history, correlating exposure to items made of zinc with expected clinical signs, a thorough physical examination, radiography, measurement of serum or plasma and tissue zinc concentrations, and blood smear evaluation. The absence of radiographically evident metal densities in the GI tract does not rule out zinc toxicosis in the differential diagnosis because some particles might not be dense enough to appear. A necropsy with complete histologic evaluation should be performed on all birds that have died of a potential metal toxicosis.

    In live birds showing clinical signs suggestive of zinc poisoning, serum and plasma samples are considered suitable for zinc determination.63 For most laboratories, sample volumes of 50 to 100 µL are sufficient for analysis. Special care must be taken to avoid contact with rubber products that can be a source of zinc (e.g., rubber-topped tubes)64 and hemolysis, which may also increase zinc concentrations. Additionally, zinc concentrations in plasma collected from psittacines show significant diurnal variation, with the highest concentrations detected in morning samples.65 For most psittacines, the average, physiologic, nontoxic zinc concentration in serum or plasma is at or below 2 ppm (0.2 mg/dL). Cockatoos and eclectus parrots tend to have higher physiologic concentrations of zinc in serum and plasma, with acceptable nontoxic concentrations of up to 3.5 ppm (0.35 mg/dL) for cockatoos and up to 2.5 ppm (0.25 mg/dL) for eclectus parrots.61 An assessment of erythrocyte morphology can aid in the diagnosis of zinc poisoning in birds. Observed abnormalities include a greater number of immature red blood cells, hypochromasia, poikilocytosis, and nuclear abnormalities, such as fusiform, elongated, and irregular nuclei.59

    Postmortem evaluations include gross and histologic examinations along with the determination of zinc concentrations in fresh liver samples. Most companion birds have acceptable liver zinc concentrations of 30 to 70 ppm (mg/kg) wet weight,61 and liver zinc concentrations of up to 100 ppm (mg/kg) expressed as wet weight are considered nontoxic. Once liver zinc concentrations exceed 100 ppm,34 zinc poisoning may be present and careful histologic evaluation is necessary for a definitive diagnosis.

    Case Management

    Unless the patient is severely affected, clinical signs may resolve with supportive care once the source of zinc is removed from the digestive tract or from the bird's environment.34,36 Removal of metal objects from the upper GI tract can be accomplished with lavage, endoscopy, or surgery or with the use of emollient laxatives or cathartics.5 In dogs, it has been shown that plasma zinc concentrations decline relatively rapidly once further zinc absorption is prevented.66 In a puppy with zinc toxicosis caused by ingestion of four pennies, the serum zinc concentration decreased from 28.8 ppm to 16.8 ppm within 24 hours after surgical removal of the pennies. On day 14 after surgery, the serum zinc concentration had dropped to 3.2 ppm with only supportive care. Thus, preventing further absorption of zinc should be the primary goal of therapy and, along with supportive care, may be sufficient for the management of zinc toxicosis.

    Removing the source of zinc in a timely manner or in its entirety is not always possible. The limitation of endoscopy is that only larger particles can be removed, while small particles may not be visible. In this situation, and in birds showing severe clinical signs, chelation therapy is an important component of treatment for zinc toxicosis.

    Chelation Therapy

    A variety of parenteral chelating agents are reported to be effective for chelating zinc. The advantages of CaNa2EDTA include its affinity for zinc67 and the fact that it reaches therapeutic systemic levels rapidly. CaNa2EDTA therapy may be indicated to enhance removal of zinc in fragile patients for which anesthesia for endoscopy or surgery is too risky. Chelation therapy with CaNa2EDTA can be commenced while the bird's condition is stabilized. CaNa2EDTA must be administered intramuscularly, subcutaneously, or intravenously, as it is poorly absorbed from the GI tract. The recommended dose of CaNa2EDTA is 40 mg/kg IM q12h for 5 days.21 While CaNa2EDTA is a relatively safe agent, renal and GI toxicity may result from long-term therapy.68 In addition, a series of CaNa2EDTA chelation therapy sessions may remove essential minerals, such as iron or copper.69 These effects can have undesirable clinical consequences, especially in birds that are deficient in these elements before chelation treatment. Thus, it is critical to monitor essential minerals in birds receiving CaNa2EDTA to prevent deficiencies.

    Succimer is another heavy metal chelator that may be a suitable alternative to CaNa2EDTA. Use of succimer is relatively new to veterinary medicine,21 although it has been used for decades in human medicine for the treatment of industrial heavy metal toxicosis and childhood lead toxicosis.70 Compared with other chelators, succimer is fairly specific for lead, mercury, and arsenic.71 In mice, succimer is less effective than CaNa2EDTA but more effective than D-penicillamine for the treatment of zinc toxicosis.72 The chief advantage of succimer over CaNa2EDTA is that it can be given orally. However, oral administration can be a disadvantage in a regurgitating bird.

    The efficacy and safety of succimer for the treatment of zinc toxicosis has not been investigated in birds. A study in cockatiels with lead toxicosis demonstrated that succimer has a relatively narrow margin of safety (see lead chelation therapy section for details). The most common side effect of succimer therapy in cockatiels was regurgitation. Therefore, based on limited information, the dosage of succimer in birds should not exceed 40 mg/kg PO q12h. While succimer is usually given for 10 days, the length of treatment should be based on clinical improvement and determination of serum zinc concentrations.

    Supportive Care

    Symptomatic and supportive care is as critical for a bird with zinc toxicosis as it is for a bird with lead intoxication. Hydration and electrolyte status must be monitored regularly and treated appropriately. Lactated Ringer's solution can be given for fluid support. Seizures can be controlled with diazepam (0.5 to 1.0 mg/kg IV or IM) or midazolam (0.1 mg/kg IM).5 Administration of B-complex vitamins and assisted alimentation should also be considered.

    Prevention of Lead and Zinc Intoxication in Companion Birds

    The best method of preventing lead or zinc intoxication is to recognize potential sources of exposure and eliminate them from the environment. Most reputable bird cage and toy manufacturers avoid the use of lead and zinc in their products. However, there is always the potential for products to contain toxic metals. Owners of pet birds should inspect their bird's complete environment, carefully evaluate cage and toy materials, and remove materials that may contain lead or zinc. Questionable materials should be tested by a veterinary toxicology laboratory before they are given to birds.


    Companion birds continue to be exposed to lead and zinc from their environment, and intoxications are frequently reported. Because of the nonspecific clinical signs associated with lead and zinc intoxication, a comprehensive diagnostic workup is required to establish an accurate diagnosis. Lead and zinc analyses are routinely available at veterinary toxicology laboratories, and results are often available within hours of sample submission. Once a diagnosis is reached, treatment should be initiated as quickly as possible. An important part of treatment is prevention of recurrence. Owners should be advised about the risk of hazardous materials in the birds' environment.

    Downloadable PDF

    1. Morgan RV. Lead poisoning in small companion animals: an update (1987-1992). Vet Hum Toxicol 1994;36(1):18-22.

    2. Doneley R. Zinc toxicity in caged and aviary birds—new wire disease. Aust Vet Pract 1992;22:6-11.

    3. Reece RL, Dickson DB, Burrowes PJ. Zinc toxicity (new wire disease) in aviary birds. Aust Vet J 1986;63:199.

    4. Archambault AL, Timm KI. Treatment of acute lead ingestion in a juvenile macaw. JAVMA 1994;205:852-854.

    5. Riggs SM, Puschner B, Tell LA. Management of an ingested lead foreign body in an Amazon parrot. Vet Hum Toxicol 2002;44:345-348.

    6. Medlin J. Sweet candy, bitter poison. Environ Health Perspect 2004;112:A803.

    7. Lewis LA, Poppenga RJ, Davidson WR, et al. Lead toxicosis and trace element levels in wild birds and mammals at a firearms training facility. Arch Environ Contam Toxicol 2001;41:208-214.

    8. Vyas NB, Spann JW, Heinz GH, et al. Lead poisoning of passerines at a trap and skeet range. Environ Pollut 2000;107:159-166.

    9. Casteel SW. Lead. In: Peterson ME, Talcott PA, eds. Small Animal Toxicology. St. Louis: Elsevier Saunders; 2006:795-805.

    10. Vyas NB, Spann JW, Heinz GH. Lead shot toxicity to passerines. Environ Pollut 2001;111:135-138.

    11. Locke LN, Thomas NJ. Lead poisoning of waterfowl and raptors. In: Fairbrother A, Locke LN, Hoff GL, eds. Noninfectious Diseases of Wildlife. Ames: Iowa State University Press; 1996:108-117.

    12. Marn CM, Mirarchi RE, Lisano ME. Effects of diet and cold exposure on captive female mourning doves dosed with lead shot. Arch Environ Contam Toxicol 1988;17:589-594.

    13. Gwaltney-Brant S. Lead. In: Plumlee KH, ed. Clinical Veterinary Toxicology. St. Louis: Mosby; 2004:204-210.

    14. Goyer RA, Clarkson TW. Toxic effects of metals. In: Klaassen CD, ed. Toxicology: The Basic Science of Poisons. New York: McGraw Hill; 2001:811-867.

    15. Garza A, Vega R, Soto E. Cellular mechanisms of lead neurotoxicity. Med Sci Monit 2006;12:RA57-RA65.

    16. Mateo R, Beyer WN, Spann JW, et al. Relation of fatty acid composition in lead-exposed mallards to fat mobilization, lipid peroxidation and alkaline phosphatase activity. Comp Biochem Physiol C Toxicol Pharmacol 2003;135:451-458.

    17. Saxena G, Flora SJ. Lead-induced oxidative stress and hematological alterations and their response to combined administration of calcium disodium EDTA with a thiol chelator in rats. J Biochem Mol Toxicol 2004;18:221-233.

    18. Boyer IJ, Cory-Slechta DA, DiStefano V. Lead induction of crop dysfunction in pigeons through a direct action on neural or smooth muscle components of crop tissue. J Pharmacol Exp Ther 1985;234:607-615.

    19. Henritig FM. Lead. In: Goldfrank LR, Flomenbaum NE, Lewin NA, eds. Goldfrank's Toxicologic Emergencies. New York: McGraw-Hill; 2002:1200-1238.

    20. Dumonceaux G, Harrison GH. Toxins. In: Ritchie BW, Harrison GJ, Harrison LR, eds. Avian Medicine: Principles and Application. Delray Beach, Florida: Wingers Publishing; 1994:1030-1052.

    21. 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 2000;61:935-940.

    22. Loudis B. Endoscope assisted gastric lavage for foreign body retrieval. Proc Assoc Avian Vet 2004:83-88.

    23. Samour J, Naldo JL. Lead toxicosis in falcons: a method for lead retrieval. Semin Avian Exotic Pet Med 2005;14:143-148.

    24. Dhawan M, Kachru DN, Tandon SK. Influence of thiamine and ascorbic acid supplementation on the antidotal efficacy of thiol chelators in experimental lead intoxication. Arch Toxicol 1988;62:301-304.

    25. Kim JS, Blakley BR, Rousseaux CG. The effects of thiamin on the tissue distribution of lead. J Appl Toxicol 1990;10:93-97.

    26. Sasser LB, Hall GG, Bratton GR, et al. Absorption and tissue distribution of lead in thiamin-replete and thiamin-deficient rats. J Nutr 1984;114:1816-1825.

    27. Hoogesteijn AL, Raphael BL, Calle P, et al. Oral treatment of avian lead intoxication with meso-2,3-dimercaptosuccinic acid. J Zoo Wildl Med 2003;34:82-87.

    28. Flanagan RJ, Jones AL. Agents used to treat poisoning with toxic metals and organometallic objects. In: Flanagan RJ, Jones AL, eds. Antidotes. London: Taylor and Francis; 2001:35-93.

    29. Howland MA. Antidotes in depth: edetate calcium disodium (CaNa2EDTA). In: Flomenbaum NE, Howland MA, Goldfrank LR, et al, eds. Goldfrank's Toxicologic Emergencies. 8th ed. New York: McGraw-Hill; 2006:1331-1333.

    30. Mautino M. Therapeutic management of avian lead intoxication. Masters Thesis, ProQuest Information and Learning, Ann Arbor, MI, 1993.

    31. Lightfoot TL, Yeager JM. Pet bird toxicity and related environmental concerns. Vet Clin North Am Exot Anim Pract 2008;11:229-259.

    32. Barceloux DG. Zinc. J Toxicol Clin Toxicol 1999;37:279-292.

    33. Romagnano A, Grinden CB, Degerness L, et al. Treatment of a hyacinth macaw with zinc toxicity. J Avian Med Surg 1995;9:185-189.

    34. Smith A. Zinc toxicosis in a flock of hispaniolan amazons. Proc Ann Conf Assoc Avian Vet 1995:447-453.

    35. Lloyd M. Heavy metal ingestion: medical management and gastroscopic foreign body removal. J Assoc Avian Vet 1992;6:25-29.

    36. Zdziarski JM, Mattix M, Bush RM, et al. Zinc toxicosis in diving ducks. J Zoo Wildl Med 1994;25:438-445.

    37. Howard BR. Health risks of housing small psittacines in galvanized wire mesh cages. JAVMA 1992;200:1667-1674.

    38. Van Sant F. Zinc toxicosis in a hyacinth macaw. Proc Ann Conv Assoc Avian Vet 1991:255-259.

    39. Brown MA, Cova P, Juarez J, et al. Food poisoning involving zinc contamination. Arch Environ Health 1964;8:657-660.

    40. Leonard A, Gerber GB. Zinc toxicity—does it exist? J Am Coll Toxicol 1989;8:1285-1290.

    41. Nutrient Requirements of Poultry. 9th ed. Washington: National Academic Press; 1994:30-31.

    42. Ackerman N, Spencer CP, Sundlof SF, et al. Zinc toxicosis in a dog secondary to ingestion of pennies. Vet Radiol 1990;31:155-157.

    43. Graham TW, Goodger WJ, Christiansen V, et al. Economic losses from an episode of zinc toxicosis on a California veal calf operation using a zinc sulfate-supplemented milk replacer. JAVMA 1987;190:668-671.

    44. Lu JX, Combs GF. Effect of excess dietary zinc on pancreatic exocrine function in the chick. J Nutr 1988;118:681-689.

    45. Murphy JV. Intoxication following ingestion of elemental zinc. J Am Med Assoc 1970;212:2119-2120.

    46. Stahl JL, Greger JL, Cook ME. Zinc, copper and iron utilization by chicks fed various concentrations of zinc. Br Poult Sci 1989;30:123-134.

    47. Gasaway WC, Buss IO. Zinc toxicity in the mallard duck. J Wildl Manag 1972;26:1107-1117.

    48. Vanderzee J, Zwart P, Schotman AJH. Zinc poisoning in a Nicobar pigeon. J Zoo Anim Med 1985;16:68-69.

    49. Droual R, Meteyer CU, Galey FD. Zinc toxicosis due to ingestion of a penny in a gray-headed chachalaca (Ortalis cinereiceps). Avian Dis 1991;35:1007-1011.

    50. Morris PJ, Jensen J, Applehaus F. Lead and zinc toxicosis in a blue and gold macaw (Ara ararauna) caused by ingestion of hardware cloth. Proc Ann Meeting Am Assoc Zoo Vet 1985:13-17.

    51. Underwood EJ. Zinc. In: Underwood EJ, ed. Trace Elements in Human and Animal Nutrition. New York: Academic Press; 1977:196-242.

    52. Wedekind KJ, Baker DH. Zinc bioavailability in feed-grade sources of zinc. J Anim Sci 1990;68:684-689.

    53. Coyle P, Philcox JC, Carey LC, et al. Metallothionein: the multipurpose protein. Cell Mol Life Sci 2002;59:627-647.

    54. Davis SR, Cousins RJ. Metallothionein expression in animals: a physiological perspective on function. J Nutr 2000;130:1085-1088.

    55. Prasad AS. Discovery and importance of zinc in human nutrition. Fed Proc 1984;43:2829-2834.

    56. Dvergsten CL, Fosmire GJ, Ollerich DA, et al. Alterations in the postnatal-development of the cerebellar cortex due to zinc deficiency. II. Impaired maturation of Purkinje cells. Brain Res 1984;318:11-20.

    57. Fraker PJ, King LE. Reprogramming of the immune system during zinc deficiency. Annu Rev Nutr 2004;24:277-298.

    58. Vallee BL, Falchuk KH. The biochemical basis of zinc physiology. Physiol Rev 1993;73:79-118.

    59. Christopher MM, Shooshtari MP, Levengood JM. Assessment of erythrocyte morphologic abnormalities in mallards with experimentally induced zinc toxicosis. Am J Vet Res 2004;65:440-446.

    60. Dineley KE, Votyakova TV, Reynolds IJ. Zinc inhibition of cellular energy production: implications for mitochondria and neurodegeneration. J Neurochem 2003;85:563-570.

    61. Puschner B, St Leger J, Galey FD. Normal and toxic zinc concentrations in serum/plasma and liver of psittacines with respect to genus differences. J Vet Diagn Invest 1999;11:522-527.

    62. Wight PAL, Dewar WA, Saunderson CL. Zinc toxicity in the fowl—ultrastructural pathology and relationship to selenium, lead and copper. Avian Pathol 1986;15:23-38.

    63. Kosman DJ, Henkin RI. Plasma and serum zinc concentrations. Lancet 1979;1:1410.

    64. Minnick PD, Braselton WE, Meerdink GL, et al. Altered serum element concentrations due to laboratory usage of vacutainer tubes. Vet Human Toxicol 1982;24:413-414.

    65. Rosenthal KL, Johnston MS, Shofer FS, et al. Psittacine plasma concentrations of elements: daily fluctuations and clinical implications. J Vet Diagn Invest 2005;17:239-244.

    66. Latimer KS, Jain AV, Inglesby HB, et al. Zinc-induced hemolytic-anemia caused by ingestion of pennies by a pup. JAVMA 1989;195:77-80.

    67. Brownie CF, Aronson AL. Comparative effects of Ca-ethylenediaminetetraacetic acid (EDTA), ZnEDTA, and ZnCaEDTA in mobilizing lead. Toxicol Appl Pharmacol 1984;75:167-172.

    68. Moel DI, Kumar K. Reversible nephrotoxic reactions to a combined 2,3-dimercapto-1-propanol and calcium disodium ethylenediaminetetraacetic acid regimen in asymptomatic children with elevated blood lead levels. Pediatrics 1982;70:259-262.

    69. Powell JJ, Burden TJ, Greenfield SM, et al. Urinary excretion of essential metals following intravenous calcium disodium edetate: an estimate of free zinc and zinc status in man. J Inorg Biochem 1999;75:159-165.

    70. Ellis MR, Kane KY. Lightening the lead load in children. Am Fam Phys 2000;62:545-554, 559-560.

    71. Graziano JH. Role of 2,3-dimercaptosuccinic acid in the treatment of heavy metal poisoning. Med Toxicol 1986;1:155-162.

    72. Llobet JM, Domingo JL, Corbella J. Antidotes for zinc intoxication in mice. Arch Toxicol 1988;61:321-323.

    aPersonal communication, Dr. Jacqueline Jencek, San Francisco Zoo, 2006.

    References »

    NEXT: Letters — The Curious Case of the Cat with the Munchies

    CETEST This course is approved for 3.0 CE credits

    Start Test


    Did you know... Metaldehyde is the active ingredient in many commercial slug and snail baits and is extremely attractive to dogs due to its palatability and appearance.Read More

    These Care Guides are written to help your clients understand common conditions. They are formatted to print and give to your clients for their information.

    Stay on top of all our latest content — sign up for the Vetlearn newsletters.
    • More