3 CE CE Article CREDITS Lead and Zinc Intoxication in Companion Birds

❯❯ Birgit Puschner, Abstract: Although the toxicity of lead and zinc to birds is widely recognized by veterinarians and bird DVM, PhD, DABVT owners, these metals are frequently found in the environments of pet and aviary birds, and intoxica- tions are common. Clinical signs exhibited by intoxicated birds are often nonspecific, which makes ❯❯ Robert H. Poppenga, early diagnosis difficult. Fortunately, lead and zinc analyses of whole blood and serum or plasma, DVM, PhD, DABVT University of California, Davis respectively, are readily available and inexpensive; elevated concentrations can confirm intoxication. Once diagnosed, intoxication can be effectively treated by (1) preventing further exposure, (2) admin- istering chelating drugs, and (3) providing symptomatic and supportive care. etal intoxication is routinely submitted to the toxicology laboratory of diagnosed in companion birds, the California Animal Health and Food Malthough the diagnosis can pres- Safety Laboratory System involved acci- ent a major challenge to the avian prac- dental exposure to atypical lead sources. titioner. Companion birds are intelligent, In one case, an aviary in a large zoo inquisitive, playful animals with a ten- was contaminated with lead from weld- dency to explore objects with their beak ing activities outside the exhibit, causing and tongue. They are especially fond of intoxication in a group of black parrots.a At a Glance metallic objects, resulting in an increased Over the past 10 to 20 years, an L e a d risk for metal intoxication. Lead and upsurge in zinc poisoning, especially in Page E1 zinc are the metals that most commonly psittacines, has been attributed to the result in clinical disease that requires a more common use of galvanized metal Z i n c Page E6 specific diagnostic workup and intensive for cages and aviaries. This has led to treatment. zinc intoxication being called new wire Comparison of CaNa2EDTA Recognition of the toxicity of lead to disease.2,3 The increased number of doc- and Succimer for the pet and aviary birds and its subsequent umented zinc intoxications may also Treatment of Lead and elimination from their environment has reflect pet bird owners’ and veterinarians’ Zinc Intoxications likely decreased the incidence of expo- increased awareness of the risks associ- Page E7 sure to this metal, although intoxications ated with exposure to galvanized metal. Prevention of Lead and still occur regularly. However, little infor- Unfortunately, there is a relative paucity of Zinc Intoxication in mation is available to judge the actual information in the veterinary and human Companion Birds incidence of lead intoxication in pet and medical literature regarding the treatment Page E10 aviary birds. In one retrospective study of zinc toxicosis. over a 5-year period (1987 to 1992) in Boston, 85 cases of lead intoxication were Lead diagnosed in small companion animals.1 Potential Sources of Exposure Dogs were the most frequently affected Lead is used in an impressive array of species (n = 53), followed by birds (n = products, from industrial items (e.g., tank 20; species were not given). The authors linings, radiation shielding) to common noted a steady decline of cases across consumer products such as paint pigments, species, including birds, over the period inks, ammunition, solder, linoleum, wine of the study. In contrast, a search of our bottle foil, lubricants, bearings, ceramics, diagnostic laboratory database did not plastics, electronic devices, fishing gear, show a decline in lead intoxication in psit- jewelry, and small toys.4,5 Wrappers used tacines between 1995 and 2005. During for imported candy have been found to this period, an average of 13 cases were aPersonal communication, Dr. Jacqueline Jencek, diagnosed per year. Recently, several cases San Francisco Zoo, 2006.

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be printed with lead- Given the number of contaminated inks.6 Lead- The most common variables that can affect contaminated soil can also the toxicity of lead, the be a source of intoxication sources of lead expo- availability of precise for birds.7,8 However, the sure for pet and aviary toxic or lethal doses is most common sources of limited. A chronic cumu- lead exposure for pet and birds kept in home or lative lead dose of 2 mg/ aviary birds kept in home kg/day is reported to be or cage environments are cage environments are toxic for ducks.13 paint (either from direct paint and small, lead- ingestion of lead-based Kinetics paint flakes or secondary containing household The bioavailability of to paint dust contaminat- objects. Birds kept in in­gested lead depends ing the environment) on its form and, to a lesser and small, lead-contain- older homes have an extent, the physiologic ing household objects. state of the animal (e.g., Because lead is toxic increased risk of lead age). Elemental lead is less to children and water- exposure from paint. bioavailable than inor- fowl, several former uses ganic lead salts (e.g., lead for lead have been elimi- acetate) or organic lead nated or curtailed (e.g., paint, gasoline, shot). (e.g., tetraethyl lead). Elemental lead is rela- Lead has not intentionally been added to most tively insoluble in hard, basic water but is paint since 1978, although it has been esti- more soluble in acidic water. Therefore, ele- mated by the Centers for Disease Control and mental lead is more soluble and relatively Prevention that 74% of privately owned US more bioavailable in the acidic fluids of the homes built before 1980 still contain hazard- proventriculus or ventriculus of birds.11 Lead is ous quantities of lead paint.9 Thus, birds kept actively transported across the GI tract through in older homes have an increased risk of lead the same transport mechanism used for cal- exposure from paint. cium absorption.9 This absorption mechanism QuickNotes explains the greater bioavailability of lead in Toxicity immature, rapidly growing animals with an Factors that influ- Few studies have determined the acute or increased need for calcium compared with ence the risk for chronic toxicity of lead in pet birds. Factors that adult animals. Irrespective of its form, ingested lead intoxication influence the risk for lead intoxication include lead is mostly excreted in the feces without include the amount the amount and form of lead ingested, spe- being absorbed. and form of lead cies exposed, dietary factors, size of ingested Approximately 90% of absorbed lead is con- ingested, species lead particles, and amount of grit in the ven- tained in red blood cells; small amounts are exposed, dietary triculus.5 The duration of retention of lead par- bound to albumin or found in plasma as free factors, size of ticles in the GI tract varies among individuals lead. Within red blood cells, lead is associated within a given species and between species; with the cell membrane, hemoglobin, and pos- ingested lead birds that rapidly eliminate lead particles are sibly other cell components.14 Lead is widely particles, and less likely to be intoxicated.10 Bird species that distributed in soft tissue, and bone serves as amount of grit in regurgitate indigestible parts of their diet, such a long-term storage site. The half-life of lead the ventriculus. as raptors, are less likely to be intoxicated by is multiphasic because of its redistribution lead because they more efficiently remove within various compartments of the body.13 lead from their ventriculus.11 For example, the half-life of lead in whole Diets low in protein and calcium increase the blood is approximately 35 days, whereas in toxicity of lead.12 One study examined the tox- brain tissue, it is approximately 2 years. Lead icity of a single size 7½ (2.41-mm) lead shot to can persist in bone for years. Enhanced bone cowbirds. Three of 10 dosed birds on a natural remodeling associated with egg laying or diet containing wild bird seed and cracked corn dietary calcium:phosphorus abnormalities can died within 24 hours, whereas none of the birds increase the release of sequestered lead into fed a pelleted commercial diet died.10 the blood and cause adverse effects. Normal

E2 Compendium: Continuing Education for Veterinarians® | January 2009 | CompendiumVet.com FREE Lead and Zinc Intoxication in Companion Birds CE bone turnover does not olevulinic acid synthetase, result in a clinically sig- The clinical signs of δ-aminolevulinic acid dehy- nificant release of lead. dratase (ALAD), copropor- Absorbed lead can be lead intoxication are phyrinogen decarboxylase, eliminated via sloughing primarily related to and ferrochelatase.19 of renal tubular epithelial cells or in bile or pancre- the effects of lead Clinical Signs atic secretions.13 on the nervous, GI, of Intoxication The clinical signs of lead Pathophysiology hematopoietic, and intoxication are primarily Metal ions play many related to the effects of diverse roles in biologic renal systems. The lead on the nervous, GI, systems. They serve as signs vary depending hematopoietic, and renal charge carriers, intermedi­ systems. The signs vary aries in catalyzed reactions, on whether the intoxica- depending on whether and structural elements in tion is acute or chronic. the intoxication is acute the maintenance of pro­tein or chronic, which, in turn, conformation. Disruption depends on the amount and of these functions can affect metal transport, form of lead ingested over time. Chronic intoxi- energy metabolism, apoptosis, ionic conduc- cation is more likely in pet birds as a result of tion, cell adhesion, inter- and intracellular sig- repeated exposure to a source of lead or the slow naling, diverse enzymatic processes, protein degradation and release of lead from ingested maturation, and genetic regulation.15 Lead lead objects. However, death can be acute with- damages cells primarily through its ability to out premonitory signs.20 Signs of intoxication substitute for several metal ions, especially can be nonspecific and limited to regurgitation, calcium and zinc, at their binding sites.15 Lead anorexia, weakness, and weight loss. produces oxidative damage to lipids and pro- Signs related to nervous system impair- teins as a result of iron release, disruption of ment include lethargy, wing droop, leg pare- antioxidant mechanisms, and direct oxidative sis or paralysis, changes in phonation, head damage.15–17 tilt, ataxia, blindness, circling, head tremors, QuickNotes The neurotoxicity of lead is most likely due 11,20 GI signs include regurgita- and seizures. Lead damages cells to such diverse mechanisms as lipid peroxida- tion and decreased motility of the upper GI tion; excitotoxicity (i.e., cell damage secondary tract (esophagus, proventriculus, and ventricu- primarily through its to receptor overstimulation by excitatory neu- lus) resulting in impaction and greenish diar- ability to substitute rotransmitters such as glutamate); alterations rhea that stains feathers around the vent.11,20 for several metal in neurotransmitter synthesis, storage, and Signs related to hematopoietic impairment can ions, especially release; alterations in expression and func- include weakness. Lead causes renal tubular calcium and zinc, at tioning of receptors, such as glutamate and necrosis and renal nephrosis resulting in poly- their binding sites. N-methyl-D-aspartate receptors; interference uria, proteinuria, and hematuria.5 The severity with mitochondrial metabolism and second of clinical signs does not always correlate with messenger systems; and damage to astroglia whole blood lead concentration. and oligodendroglia.15 The mechanism by which lead reduces GI Clinical Pathology motility is not entirely clear, but it does not In cases of chronic exposure, a microcytic, appear to be related to an effect on peripheral hypochromic, regenerative anemia may be nerves or calcium flux. Lead-induced GI relax- present. Characteristic changes noted in mam- ation may be due to stimulation of adenylate malian intoxication, such as basophilic stip- cyclase activity, resulting in increased intracel- pling and cytoplasmic vacuolization of red lular cAMP.18 blood cells, are generally not noted in birds.5 Lead causes anemia by increasing erythro- Serum lactate dehydrogenase (LDH), aspartate cyte fragility, delaying erythrocyte maturation, aminotransferase (AST), and creatine phos- and inhibiting heme synthesis. Heme synthesis phokinase (CPK) activities and uric acid con- is impaired as a result of inhibition of amin- centrations can be elevated.5,20

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Pathology protoporphyrin concentrations are good bio- Acute lead intoxication may not cause gross markers of lead exposure, but these tests are lesions. Splenomegaly can occur secondary to not widely available. increased removal of damaged erythrocytes.5 Postmortem diagnosis depends on a his- Weight loss, air sacculitis, renal or visceral tory of compatible clinical signs, detection of gout, pale musculature or viscera consistent metallic particles or other forms of lead in the with anemia, and muscle and fat atrophy have GI tract, and measurement of liver or kidney been reported.11,21 In raptor species, bile sta- lead concentrations. Reported diagnostic liver sis consistently occurs and is associated with or kidney concentrations vary, but values of an engorged gallbladder; viscous, dark-green 4 ppm wet weight or greater in either tissue bile; a greenish appearance to the liver; and are likely to be significant. There can be sig- bile-stained gastric and intestinal mucosa.11 nificant differences in liver and kidney tissue Histopathologic lesions can include myo- concentrations in the same bird; consequently, cardial necrosis associated with fibrinoid it is often advisable to test both organs. necrosis of arterioles, hepatocellular necrosis, renal tubular necrosis (with or without charac- Case Management teristic intranuclear inclusion bodies in renal Decontamination approaches include the use tubular cells), brain edema, peripheral nerve of emollient laxatives such as mineral oil, bulk degeneration, and necrosis of ventriculus laxatives such as psyllium, or cathartics such as muscles.11,13 Hemosiderosis is a common his- sodium sulfate to promote movement through topathologic finding in some avian species.16 the GI tract.5 In theory, sulfate can bind free This may be secondary to intravascular hemo- lead to form an insoluble and, therefore, unab- lysis or impairment of heme synthesis.16,20 sorbable lead salt.21 However, use of sodium sulfate in combination with chelators such as

Diagnosis calcium disodium EDTA (CaNa2EDTA) or suc- As mentioned, the clinical signs associated with cimer has not been shown to be more effective lead intoxication can be nonspecific, making than using a chelator alone.21 Administration QuickNotes diagnosis difficult. Radiographs may identify of three to five pieces of grit of a size appro- Diagnosis of metallic objects in the GI tract. However, the priate for the bird species affected has been absence of metal densities does not rule out reported to aid in the passage of metal objects lead exposure or metal exposure because the lead may have from the ventriculus.20 intoxication is most come from an object that was passed or a Early removal of lead objects in the upper directly made by nonradiodense form. Diagnosis of lead expo- GI tract should be strongly considered because measurement of sure or intoxication is most directly made by retention of objects is common. Nineteen of lead in whole blood measurement of lead in whole blood samples. 25 cockatiels (72%) given two #12 lead shot to samples. Serum Serum and plasma are not appropriate sam- induce lead intoxication retained at least one and plasma are not ples for lead analysis because lead associates pellet for 19 days, and 11 of 25 (44%) retained 21 appropriate sam- with red blood cells. at least one pellet for 26 days. Saline lavage Lead analyses are widely available through has been successful in removing lead particles ples for lead analy- veterinary diagnostic laboratories. Fortunately, from the proventriculus or ventriculus of lead- sis because lead small sample sizes can be used; blood sam- intoxicated birds.4,22,23 Endoscopy can be used associates with red ples as small as 20 μL are often suitable. In to remove lead particles entrapped in proven- blood cells. general, any anticoagulant, including EDTA, t r i c u l a r o r v e n t r i c u l a r f o l d s . 23 Proventriculotomy can be used to prevent samples from clotting, may be necessary if other removal attempts although there may be exceptions to this rule. fail. Unfortunately, the removal of small lead It is best to consult the laboratory conducting fragments using such techniques can be dif- the testing before sample collection. Whole ficult and incomplete. blood lead concentrations consistent with lead exposure or intoxication are generally 0.20 Chelation Therapy ppm (20 μg/dL) or greater. There are no “nor- The mainstay of treatment for lead intoxica- mal” background blood lead concentrations in tion is chelation therapy. Several chelators can

pet birds. ALAD activity, blood zinc protopor- effectively bind lead, including CaNa2EDTA, phyrin concentrations, and free erythrocyte succimer, D-penicillamine, and British anti-

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Lewisite. CaNa2EDTA and and succimer were evaluated succimer are currently the The mainstay of in experimentally intoxicated 30 chelators of choice, although treatment for lead domestic pigeons. Doses of no veterinary-approved forms CaNa2EDTA up to 270 mg/kg are available. intoxication is bid (route of administration There is evidence in mam- not indicated) for 15 days were mals that the efficacy of chelation therapy. not lethal, although increases chelation is improved when in uric acid and AST, LDH, thiamine or antioxidants (e.g., ascorbic acid) and CPK activities compared with prechelation 24–26 are used in conjunction with chelators. and control bird (receiving no CaNa2EDTA) This has not been investigated in birds. values were noted. Due to the potential neph-

rotoxicity of CaNa2EDTA, periodic assessment

CaNa2EDTA of renal function during chelation therapy is To avoid calcium chelation and result- recommended. ing hypocalcemia, only the calcium salt of Neurologic signs may initially worsen in birds 21,27 30 EDTA should be used. However, there are treated with CaNa2EDTA. Theoretically, this three significant disadvantages to the use of could be due to CaNa2EDTA-induced mobiliza-

CaNa2EDTA. First, it is potentially nephro- tion of lead from bone. Thus, birds with chronic toxic,20 although nephrotoxicity may be due to lead exposure and potentially higher bone lead 28 the metal chelate and not to CaNa2E D TA it s el f. concentrations may be more likely to be affected Also, renal function may already be impaired in than acutely intoxicated birds. However, this lead-intoxicated birds. Unfortunately, the inci- has not been shown experimentally. dence of CaNa2EDTA-associated nephrotoxic- ity in birds is unknown. Second, CaNa2EDTA Succimer must be administered parenterally because Succimer (dimercaptosuccinic acid, DMSA) is a oral administration enhances the absorption newer chelating agent that has several advan- of lead from the GI tract. However, repeated tages over CaNa2EDTA. It can be given orally, IM injections in birds can cause significant does not increase elimination of other essen- QuickNotes pain and muscle damage. Third, CaNa EDTA tial minerals, and is not nephrotoxic. However, 2 Decontamination chelates important endogenous minerals such oral administration can be a disadvantage in a as zinc. regurgitating bird. Succimer is more effective approaches include the use of emollient CaNa2EDTA can be administered in doses than CaNa2EDTA at removing lead from soft of 10 to 40 mg/kg IM or SC bid.5,20,21 Prolonged tissues,21 and it decreases lead concentrations laxatives such as use is generally interrupted by intervals of no in the central nervous system more rapidly mineral oil, bulk 13 therapy to avoid adverse effects. The recom- than CaNa2EDTA. Succimer can be given at laxatives such as mended protocol is a 5- to 10-day treatment 20 to 40 mg/kg bid without adverse effects, psyllium, or cathar- period followed by a 3- to 5-day “rest” period although 80 mg/kg bid for 26 days was lethal tics such as sodium to allow for a redistribution of tissue and fluid to a significant percentage of cockatiels in one sulfate to promote lead concentrations.29 Assessment of blood experimental study.21 This dose was less toxic lead concentrations at the end of each rest in birds with lead intoxication compared with movement through period should dictate the length of chelation nonintoxicated controls. Unfortunately, days the GI tract. therapy. These follow-up tests should not be to death were not reported in this study. In conducted before the end of the rest period contrast, succimer at doses up to 270 mg/kg because earlier assessment may not allow suf- bid for 15 days was not associated with signifi- ficient time for remaining lead to redistribute cant adverse effects in experimentally intoxi- in the body. The goal is to chelate for the min- cated domestic pigeons.30 The only change imum amount of time necessary to resolve the noted was an initial increase in uric acid that intoxication (based on a decline in blood lead plateaued by day 3 of dosing. to an undetectable concentration). However, Succimer should be given orally by gav-

40 mg/kg CaNa2EDTA given IM bid for 21 con- age or other direct means (i.e., via syringe), secutive days was not associated with adverse although it has been effective when sprinkled 27 effects in experimentally intoxicated cocka- on food. As with CaNa2EDTA use, the total 21 tiels. The subacute toxicities of CaNa2EDTA length of treatment should be based on clinical

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improvement and deter- protective coating. Until mination of blood lead Sources of zinc in 1982, pennies consisted concentrations. The dos- documented avian mainly of copper (95%) age of succimer in birds with a small amount of should not exceed 40 mg/ zinc toxicoses zinc (4%), but the copper- kg PO q12h. Doses as low clad pennies minted after as 10 mg/kg PO have been include galvanized 1982 contain 97% zinc and suggested as effective.31 wire and cage bars, 2.5% copper.32 Sources of Unfortunately, an opti- zinc in documented avian mal dosing protocol has zinc-contaminated zinc toxicoses include gal- 3 not been determined for drinking water, pennies vanized wire and cage birds. Whole blood lead bars,33 zinc-contaminated concentration should be minted after 1982, drinking water,34 pennies determined after a course minted after 1982,35,36 cage of chelation to assess the cage coatings, cage coatings,37 cage accesso- need for additional ther- accessories, hardware, ries, hardware, and metal- apy. If the concentration lic toys.38 Zinc poisoning is still elevated, another and metallic toys. associated with zinc- course of therapy is indi- coated food containers has 39 cated. As with CaNa2EDTA, 3 to 5 days should been reported in humans but not in birds. be allowed for the remaining lead to redistrib- Additionally, zinc is found in soil and may ute to obtain an accurate assessment of lead be present in high enough concentrations to status. result in avian poisonings. Zinc is also used Clinical improvement is likely to be more in a variety of medical formulations, pigments, rapid (within 24 hours) after succimer admin- wood preservatives, insecticides, and rubber, 30 istration than after CaNa2EDTA. Combining but toxic exposure to any of these sources has

CaNa2EDTA and succimer does not appear not been reported in birds. QuickNotes to be more efficacious than administering CaNa EDTA or succimer alone, based on an Toxicity In birds, a major 2 experimental model of intoxication in cocka- Zinc is an essential metal, and animals and concern is chronic tiels.21 Table 1 compares the advantages and humans regulate zinc effectively. Mammals zinc toxicosis with disadvantages of CaNa2EDTA and succimer. can tolerate dietary loadings greater than resulting anemia. 100 times the minimum recommended daily Supportive Care zinc requirement.40 Dietary zinc require- Symptomatic and supportive care is also criti- me nt s for p et bi rd s h ave no t b e e n e s t abl i she d , cal. Seizure control should be attempted using but most diets for companion birds contain diazepam at 0.5 to 1.0 mg/kg given IM two to between 70 and 110 ppm (mg/kg) of zinc. three times daily or as needed. Midazolam at Research to establish zinc requirements in 0.1 mg/kg IM controlled seizures in an intoxi- birds has focused on chickens and turkeys. cated double yellow-headed Amazon parrot.5 If For example, the dietary zinc requirement diarrhea is present, hydration and electrolyte of young broilers is approximately 35 to 40 status must be monitored and treated appro- ppm (mg/kg).41 priately. Administration of B-complex vitamins If dietary exposure is excessive and homeo- and assisted alimentation should also be con- static mechanisms fail, zinc toxicity can occur. sidered. Fluid support is critical to maintain Zinc toxicosis has been reported in numer- urine output and to replace increased losses fol- ous animal species, including dogs,42 calves,43 lowing the use of a cathartic; lactated Ringer’s chickens,44 and humans.39,45 Definite data on solution can be given subcutaneously. the toxicity of zinc in companion birds are lacking, although limited information is avail- Zinc able for certain species. In chicks, dietary Potential Sources of Exposure concentrations of greater than 2200 ppm (mg/ Metallic zinc is commonly used to galvanize kg) zinc are considered toxic.46 Likewise, in metals such as iron and steel to provide a one study, liver zinc concentrations in mal-

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table 1 Comparison of CaNa2EDTA and Succimer for the Treatment of Lead and Zinc Intoxications

CaNa2EDTA Succimer

Trade names and formulations Calcium Disodium Versenate (3M); Chemet (Sanofi-Synthelabo); 200 mg/mL 100-mg capsules

Routes of administration Slow IV infusion; IM or SC Oral injection Dilution with saline or 5% dextrose needed if given IV

Advantages Rapid absorption Oral administration Can chelate lead and zinc Not nephrotoxic Does not chelate essential minerals such as manganese and copper More rapid clinical improvement in lead intoxication More effective at removing lead from soft tissues

Disadvantages Need for repeated IM or SC Less effective chelation of injections zinc; efficacy uncertain in zinc intoxication Pain at injection site Regurgitation noted in cockatiels Potential nephrotoxicity; need to monitor renal function regularly Potentially narrow margin of safety Chelation of essential minerals such as zinc, manganese, and copper with long-term use Potential to worsen central nervous system signs as a result of lead redistribution

Recommended dosage 10 to 40 mg/kg bid; 5- to 10-day 20 to 40 mg/kg bid; rest period treatment intervals interspersed not essential, but periodic with 3- to 5-day rest periods reassessment of lead and zinc concentration is recommended

Toxicity Doses of up to 270 mg/kg bid 80 mg/kg bid caused death in for 15 days caused increases in cockatiels21 AST, LDH, CPK, and uric acid in 270 mg/kg bid not lethal for domestic pigeons but no other domestic pigeons (some abnormalities30 increase in uric acid)30

AST = aspartate aminotransferase, CPK = creatine phosphokinase, LDH = lactate dehydrogeriase

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lards reached toxic levels when dietary zinc iron deficiency leading to reduced heme syn- exceeded 3000 ppm (mg/kg).47 In another thesis and erythropoiesis. The interaction study, oral exposure to 16 mg of zinc over a between zinc and iron may therefore play a 2-week period resulted in 50% mortality in major role in the development of anemia in cockatiels, but even as little as 2 mg of zinc per birds overexposed to zinc. In addition, zinc week proved lethal in some birds.37 Reported limits copper availability46 and decreases tis- cases of naturally occurring zinc poisoning in sue copper and ceruloplasmin concentrations. birds involved ducks,36 a Nicobar pigeon,48 a Decreased ceruloplasmin concentrations can gray-headed chachalaca,49 macaws,33,38,50 love- result in lower availability of iron for hemoglo- birds,3 and Amazon parrots.34 bin synthesis.59 Overall, tissue hypoxia can lead to tissue Kinetics damage in the pancreas, liver, kidneys, and brain. In chickens, zinc is absorbed in the proven- Recently, zinc toxicity has been associated with triculus and small intestine.51 The rate of brain damage that is most likely due to a combi- absorption depends on the amount and form nation of hypoxic and direct toxic effects.60 of zinc.52 Once absorbed, zinc is distributed to sites such as the pancreas, liver, kidneys, bones, Clinical Signs of Intoxication muscles, brain, retinas, intestinal mucosa, and Clinical signs of zinc intoxication in birds are skin, where it binds to metallothionein, espe- varied and nonspecific. They include leth- cially in the pancreas, liver, kidneys, intestinal argy, anorexia, regurgitation, polyuria, poly- mucosa, and brain. Metallothionein is a low- dipsia, hematuria, hematochezia, pallor, dark molecular-weight, cysteine-rich protein that or bright green diarrhea, foul-smelling feces, has potent metal-binding capabilities.53 Zinc paresis, seizures, and sudden death.33–35,37–59 has a high binding affinity for metallothio­ Zinc toxicosis was associated with sudden nein, which may play an integral role in zinc death in 7 of 21 psittacine birds evaluated in metabolism.54 The major route of excretion one study.61 Therefore, any acute death in a is via biliary, pancreatic, and gastroduodenal companion bird should be evaluated for pos- secretions into feces. sible zinc poisoning. Zinc exposure has been suggested as a cause of feather picking, but Pathophysiology there is no evidence to link the two. Zinc is present in more than 200 metalloen- zymes and thousands of protein domains.55 It is Pathology essential for bone formation, immune function, Common findings on gross examination keratogenesis, reproduction, growth, vision, of birds that have died from zinc toxicosis wound healing, brain development, normal include greenish, mucoid feces in the ileum, functioning of the central nervous system, and colon, or cloaca and muscle wasting, espe- many other physiologic processes.56–58 cially of the pectoral muscles. Occasionally, Major pathophysiologic mechanisms of the liver or kidneys are slightly enlarged. No zinc are attributed to direct and indirect toxic other consistent lesions are usually noted on effects on the GI tract, liver, kidneys, pancreas, gross examination. red blood cells, and brain, but many of the In zinc-intoxicated birds, microscopic specific underlying mechanisms have not changes are found in the pancreas, liver, kid- been established. In acute cases of zinc poi- neys, and GI tract. Experimental studies and soning, local corrosive effects may occur in case reports have indicated that the pancreas the GI tract, followed by damage to the liver, is the major target organ of zinc toxicity in kidneys, and pancreas. Zinc has been shown birds. Histologic and ultrastructural pancreatic to cause acute pancreatic, hepatic, and renal lesions include disruption of the normal zymo- failure in birds. gen granules, atrophy of acinar cells, loss of In birds, a major concern is chronic zinc normal architecture, necrotizing pancreatitis, toxicosis with resulting anemia. The toxic the presence of hyaline bodies and other elec- effects of zinc leading to hemolytic anemia tron-dense debris, cellular atrophy and necro- have recently been investigated in mallards.59 sis of individual acinar cells, and interstitial Excess zinc is thought to result in a functional fibrosis.36,61,62 The pancreatic islets are spared.

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Liver lesions vary from assessment of erythrocyte hepatic biliary retention When submitting morphology can aid in the and hemosiderosis to mul- samples for zinc diagnosis of zinc poisoning tifocal, necrotizing hepati- in birds. Observed abnor- tis.37,61 Lesions in the kidneys concentration, malities include a greater include varying degrees number of immature red of acute tubular necrosis, special care must blood cells, hypochromasia, occasionally with secondary be taken to avoid poikilocytosis, and nuclear renal or visceral gout, and abnormalities, such as fusi- moderate interstitial nephri- contact with rubber form, elongated, and irregu- 61 59 tis in addition to nephrosis. products that can be lar nuclei. GI lesions include intestinal Postmortem evaluations hemorrhage, hemorrhagic a source of zinc (e.g., include gross and histologic enteritis, hemorrhagic ven- examinations along with triculitis, ventricular koilin rubber-topped tubes) the determination of zinc degeneration, and, in one and hemolysis. concentrations in fresh liver case, cloacitis.61 samples. Most companion birds have acceptable liver Diagnosis zinc concentrations of 30 to 70 ppm (mg/kg) Diagnosis involves a careful history, correlating wet weight,61 and liver zinc concentrations exposure to items made of zinc with expected of up to 100 ppm (mg/kg) expressed as wet clinical signs, a thorough physical examina- weight are considered nontoxic. Once liver tion, radiography, measurement of serum or zinc concentrations exceed 100 ppm,34 zinc plasma and tissue zinc concentrations, and poisoning may be present and careful histo- blood smear evaluation. The absence of logic evaluation is necessary for a definitive radiographically evident metal densities in diagnosis. the GI tract does not rule out zinc toxicosis in the differential diagnosis because some par- Case Management QuickNotes ticles might not be dense enough to appear. A Unless the patient is severely affected, clinical necropsy with complete histologic evaluation signs may resolve with supportive care once A necropsy with should be performed on all birds that have the source of zinc is removed from the diges- complete histologic died of a potential metal toxicosis. tive tract or from the bird’s environment.34,36 evaluation should In live birds showing clinical signs sug- Removal of metal objects from the upper GI be performed on all gestive of zinc poisoning, serum and plasma tract can be accomplished with lavage, endos- birds that have died samples are considered suitable for zinc deter- copy, or surgery or with the use of emollient of a potential metal 63 5 mination. For most laboratories, sample vol- laxatives or cathartics. In dogs, it has been toxicosis. umes of 50 to 100 µL are sufficient for analysis. shown that plasma zinc concentrations decline Special care must be taken to avoid contact relatively rapidly once further zinc absorption with rubber products that can be a source of is prevented.66 In a puppy with zinc toxico- zinc (e.g., rubber-topped tubes)64 and hemolysis, sis caused by ingestion of four pennies, the which may also increase zinc concentrations. serum zinc concentration decreased from 28.8 Additionally, zinc concentrations in plasma col- ppm to 16.8 ppm within 24 hours after surgi- lected from psittacines show significant diur- cal removal of the pennies. On day 14 after nal variation, with the highest concentrations surgery, the serum zinc concentration had detected in morning samples.65 For most psit- dropped to 3.2 ppm with only supportive care. tacines, the average, physiologic, nontoxic zinc Thus, preventing further absorption of zinc concentration in serum or plasma is at or below should be the primary goal of therapy and, 2 ppm (0.2 mg/dL). Cockatoos and eclectus along with supportive care, may be sufficient parrots tend to have higher physiologic con- for the management of zinc toxicosis. centrations of zinc in serum and plasma, with Removing the source of zinc in a timely acceptable nontoxic concentrations of up to manner or in its entirety is not always pos- 3.5 ppm (0.35 mg/dL) for cockatoos and up to sible. The limitation of endoscopy is that only 2.5 ppm (0.25 mg/dL) for eclectus parrots.61 An larger particles can be removed, while small

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particles may not be visible. In this situation, common side effect of succimer therapy in and in birds showing severe clinical signs, cockatiels was regurgitation. Therefore, based chelation therapy is an important component on limited information, the dosage of succi- of treatment for zinc toxicosis. mer in birds should not exceed 40 mg/kg PO q12h. While succimer is usually given for 10 Chelation Therapy days, the length of treatment should be based A variety of parenteral chelating agents are on clinical improvement and determination of reported to be effective for chelating zinc. The serum zinc concentrations.

advantages of CaNa2EDTA include its affinity for zinc67 and the fact that it reaches therapeu- Supportive Care

tic systemic levels rapidly. CaNa2EDTA therapy Symptomatic and supportive care is as critical may be indicated to enhance removal of zinc for a bird with zinc toxicosis as it is for a bird in fragile patients for which anesthesia for with lead intoxication. Hydration and electrolyte endoscopy or surgery is too risky. Chelation status must be monitored regularly and treated

therapy with CaNa2EDTA can be commenced appropriately. Lactated Ringer’s solution can be while the bird’s condition is stabilized. given for fluid support. Seizures can be con-

CaNa2EDTA must be administered intramus- trolled with diazepam (0.5 to 1.0 mg/kg IV or IM) cularly, subcutaneously, or intravenously, as or midazolam (0.1 mg/kg IM).5 Administration it is poorly absorbed from the GI tract. The of B-complex vitamins and assisted alimenta-

recommended dose of CaNa2EDTA is 40 mg/ tion should also be considered. 21 kg IM q12h for 5 days. While CaNa2EDTA is a relatively safe agent, renal and GI toxicity Prevention of Lead and Zinc Intoxication may result from long-term therapy.68 In addi- in Companion Birds

tion, a series of CaNa2EDTA chelation therapy The best method of preventing lead or zinc sessions may remove essential minerals, such intoxication is to recognize potential sources as iron or copper.69 These effects can have of exposure and eliminate them from the envi- undesirable clinical consequences, especially ronment. Most reputable bird cage and toy in birds that are deficient in these elements manufacturers avoid the use of lead and zinc before chelation treatment. Thus, it is critical in their products. However, there is always the QuickNotes to monitor essential minerals in birds receiv- potential for products to contain toxic metals. ing CaNa2EDTA to prevent deficiencies. Owners of pet birds should inspect their bird’s The best method Succimer is another heavy metal chela- complete environment, carefully evaluate cage of preventing lead tor that may be a suitable alternative to and toy materials, and remove materials that CaNa EDTA. Use of succimer is relatively new may contain lead or zinc. Questionable mate- or zinc intoxica- 2 21 tion is to recognize to veterinary medicine, although it has been rials should be tested by a veterinary toxicol- used for decades in human medicine for the ogy laboratory before they are given to birds. potential sources of treatment of industrial heavy metal toxicosis exposure and elimi- and childhood lead toxicosis.70 Compared Conclusion nate them from the with other chelators, succimer is fairly spe- Companion birds continue to be exposed to environment. cific for lead, mercury, and arsenic.71 In mice, lead and zinc from their environment, and

succimer is less effective than CaNa 2EDTA but intoxications are frequently reported. Because more effective than D-penicillamine for the of the nonspecific clinical signs associated with treatment of zinc toxicosis.72 The chief advan- lead and zinc intoxication, a comprehensive

tage of succimer over CaNa2EDTA is that it diagnostic workup is required to establish an can be given orally. However, oral adminis- accurate diagnosis. Lead and zinc analyses are tration can be a disadvantage in a regurgitat- routinely available at veterinary toxicology lab- ing bird. oratories, and results are often available within The efficacy and safety of succimer for the hours of sample submission. Once a diagno- treatment of zinc toxicosis has not been inves- sis is reached, treatment should be initiated tigated in birds. A study in cockatiels with as quickly as possible. An important part of lead toxicosis demonstrated that succimer has treatment is prevention of recurrence. Owners a relatively narrow margin of safety (see lead should be advised about the risk of hazardous chelation therapy section for details). The most materials in the birds’ environment.

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References 1. Morgan RV. Lead poisoning in small companion animals: an toxic metals and organometallic objects. In: Flanagan RJ, Jones AL, update (1987-1992). Vet Hum Toxicol 1994;36(1):18-22. eds. Antidotes. London: Taylor and Francis; 2001:35-93. 2. Doneley R. Zinc toxicity in caged and aviary birds—new wire 29. Howland MA. Antidotes in depth: edetate calcium disodium

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Lead poisoning of waterfowl and raptors. ducks. J Zoo Wildl Med 1994;25:438-445. In: Fairbrother A, Locke LN, Hoff GL, eds. Noninfectious Diseases 37. Howard BR. Health risks of housing small psittacines in galva- of Wildlife. Ames: Iowa State University Press; 1996:108-117. nized wire mesh cages. JAVMA 1992;200:1667-1674. 12. Marn CM, Mirarchi RE, Lisano ME. Effects of diet and cold ex- 38. Van Sant F. Zinc toxicosis in a hyacinth macaw. Proc Ann Conf posure on captive female mourning doves dosed with lead shot. Assoc Avian Vet 1991:255-259. Arch Environ Contam Toxicol 1988;17:589-594. 39. Brown MA, Cova P, Juarez J, et al. Food poisoning involving 13. Gwaltney-Brant S. Lead. In: Plumlee KH, ed. Clinical Veterinary zinc contamination. Arch Environ Health 1964;8:657-660. Toxicology. St. Louis: Mosby; 2004:204-210. 40. Leonard A, Gerber GB. Zinc toxicity—does it exist? J Am Coll 14. Goyer RA, Clarkson TW. Toxic effects of metals. In: Klaassen CD, Toxicol 1989;8:1285-1290. ed. Toxicology: The Basic Science of Poisons. New York: McGraw 41. Nutrient Requirements of Poultry. 9th ed. Washington: National Hill; 2001:811-867. Academic Press; 1994:30-31. 15. Garza A, Vega R, Soto E. Cellular mechanisms of lead neurotox- 42. Ackerman N, Spencer CP, Sundlof SF, et al. Zinc toxicosis in a icity. Med Sci Monit 2006;12:RA57-RA65. dog secondary to ingestion of pennies. Vet Radiol 1990;31:155- 16. Mateo R, Beyer WN, Spann JW, et al. Relation of fatty acid com- 157. position in lead-exposed mallards to fat mobilization, lipid peroxi- 43. Graham TW, Goodger WJ, Christiansen V, et al. Economic dation and alkaline phosphatase activity. Comp Biochem Physiol C losses from an episode of zinc toxicosis on a California veal calf Toxicol Pharmacol 2003;135:451-458. operation using a zinc sulfate-supplemented milk replacer. JAVMA 17. Saxena G, Flora SJ. Lead-induced oxidative stress and hemato- 1987;190:668-671. logical alterations and their response to combined administration of 44. Lu JX, Combs GF. Effect of excess dietary zinc on pancreatic calcium disodium EDTA with a thiol chelator in rats. J Biochem Mol exocrine function in the chick. J Nutr 1988;118:681-689. Toxicol 2004;18:221-233. 45. Murphy JV. Intoxication following ingestion of elemental zinc. J 18. Boyer IJ, Cory-Slechta DA, DiStefano V. Lead induction of Am Med Assoc 1970;212:2119-2120. crop dysfunction in pigeons through a direct action on neural or 46. Stahl JL, Greger JL, Cook ME. Zinc, copper and iron utiliza- smooth muscle components of crop tissue. J Pharmacol Exp Ther tion by chicks fed various concentrations of zinc. Br Poult Sci 1985;234:607-615. 1989;30:123-134. 19. Henritig FM. Lead. In: Goldfrank LR, Flomenbaum NE, Lewin 47. Gasaway WC, Buss IO. Zinc toxicity in the mallard duck. J Wildl NA, eds. Goldfrank’s Toxicologic Emergencies. New York: McGraw- Manag 1972;26:1107-1117. Hill; 2002:1200-1238. 48. Vanderzee J, Zwart P, Schotman AJH. Zinc poisoning in a Nico- 20. Dumonceaux G, Harrison GH. Toxins. In: Ritchie BW, Harrison bar pigeon. J Zoo Anim Med 1985;16:68-69. GJ, Harrison LR, eds. Avian Medicine: Principles and Application. 49. Droual R, Meteyer CU, Galey FD. Zinc toxicosis due to ingestion Delray Beach, Florida: Wingers Publishing; 1994:1030-1052. of a penny in a gray-headed chachalaca (Ortalis cinereiceps). Avian 21. Denver MC, Tell LA, Galey FD, et al. Comparison of two heavy Dis 1991;35:1007-1011. metal chelators for treatment of lead toxicosis in cockatiels. Am J 50. Morris PJ, Jensen J, Applehaus F. Lead and zinc toxicosis in a Vet Res 2000;61:935-940. blue and gold macaw (Ara ararauna) caused by ingestion of hard- 22. Loudis B. Endoscope assisted gastric lavage for foreign body ware cloth. Proc Ann Meeting Am Assoc Zoo Vet 1985:13-17. retrieval. Proc Assoc Avian Vet 2004:83-88. 51. Underwood EJ. Zinc. In: Underwood EJ, ed. Trace Elements 23. Samour J, Naldo JL. Lead toxicosis in falcons: a method for in Human and Animal Nutrition. New York: Academic Press; lead retrieval. Semin Avian Exotic Pet Med 2005;14:143-148. 1977:196-242. 24. Dhawan M, Kachru DN, Tandon SK. Influence of thiamine and 52. Wedekind KJ, Baker DH. Zinc bioavailability in feed-grade ascorbic acid supplementation on the antidotal efficacy of thiol che­ sources of zinc. J Anim Sci 1990;68:684-689. lators in experimental lead intoxication. Arch Toxicol 1988;62:301- 53. Coyle P, Philcox JC, Carey LC, et al. Metallothionein: the multi- 304. purpose protein. Cell Mol Life Sci 2002;59:627-647. 25. Kim JS, Blakley BR, Rousseaux CG. The effects of thiamin on 54. Davis SR, Cousins RJ. Metallothionein expression in animals: the tissue distribution of lead. J Appl Toxicol 1990;10:93-97. a physiological perspective on function. J Nutr 2000;130:1085- 26. Sasser LB, Hall GG, Bratton GR, et al. Absorption and tissue 1088. distribution of lead in thiamin-replete and thiamin-deficient rats. J 55. Prasad AS. Discovery and importance of zinc in human nutri- Nutr 1984;114:1816-1825. tion. Fed Proc 1984;43:2829-2834. 27. Hoogesteijn AL, Raphael BL, Calle P, et al. Oral treatment of 56. Dvergsten CL, Fosmire GJ, Ollerich DA, et al. Alterations in avian lead intoxication with meso-2,3-dimercaptosuccinic acid. J the postnatal-development of the cerebellar cortex due to zinc Zoo Wildl Med 2003;34:82-87. deficiency. II. Impaired maturation of Purkinje cells. Brain Res 28. Flanagan RJ, Jones AL. Agents used to treat poisoning with 1984;318:11-20.

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57. Fraker PJ, King LE. Reprogramming of the immune system dur- concentrations of elements: daily fluctuations and clinical implica- ing zinc deficiency.Annu Rev Nutr 2004;24:277-298. tions. J Vet Diagn Invest 2005;17:239-244. 58. Vallee BL, Falchuk KH. The biochemical basis of zinc physiology. 66. Latimer KS, Jain AV, Inglesby HB, et al. Zinc-induced hemo- Physiol Rev 1993;73:79-118. lytic-anemia caused by ingestion of pennies by a pup. JAVMA 59. Christopher MM, Shooshtari MP, Levengood JM. Assessment 1989;195:77-80. of erythrocyte morphologic abnormalities in mallards with experi- 67. Brownie CF, Aronson AL. Comparative effects of Ca-ethylenedi- mentally induced zinc toxicosis. Am J Vet Res 2004;65:440-446. aminetetraacetic acid (EDTA), ZnEDTA, and ZnCaEDTA in mobiliz- 60. Dineley KE, Votyakova TV, Reynolds IJ. Zinc inhibition of cellu- ing lead. Toxicol Appl Pharmacol 1984;75:167-172. lar energy production: implications for mitochondria and neurode- 68. Moel DI, Kumar K. Reversible nephrotoxic reactions to a com- generation. J Neurochem 2003;85:563-570. bined 2,3-dimercapto-1-propanol and calcium disodium ethylene- 61. Puschner B, St Leger J, Galey FD. Normal and toxic zinc con- diaminetetraacetic acid regimen in asymptomatic children with centrations in serum/plasma and liver of psittacines with respect to elevated blood lead levels. Pediatrics 1982;70:259-262. genus differences. J Vet Diagn Invest 1999;11:522-527. 69. Powell JJ, Burden TJ, Greenfield SM, et al. Urinary excretion of 62. Wight PAL, Dewar WA, Saunderson CL. Zinc toxicity in the essential metals following intravenous calcium disodium edetate: fowl—ultrastructural pathology and relationship to selenium, lead an estimate of free zinc and zinc status in man. J Inorg Biochem and copper. Avian Pathol 1986;15:23-38. 1999;75:159-165. 63. Kosman DJ, Henkin RI. Plasma and serum zinc concentrations. 70. Ellis MR, Kane KY. Lightening the lead load in children. Am Fam Lancet 1979;1:1410. Phys 2000;62:545-554, 559-560. 64. Minnick PD, Braselton WE, Meerdink GL, et al. Altered serum 71. Graziano JH. Role of 2,3-dimercaptosuccinic acid in the treat- element concentrations due to laboratory usage of vacutainer tubes. ment of heavy metal poisoning. Med Toxicol 1986;1:155-162. Vet Human Toxicol 1982;24:413-414. 72. Llobet JM, Domingo JL, Corbella J. Antidotes for zinc intoxica- 65. Rosenthal KL, Johnston MS, Shofer FS, et al. Psittacine plasma tion in mice. Arch Toxicol 1988;61:321-323.

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1. Lead toxicity in birds is influenced by all c. Measurement of lead in whole blood 8. Which statement is true regarding the of the following except the samples is critical for a diagnosis of diagnosis of zinc intoxication in birds? a. form of lead ingested. lead intoxication. a. There is no need to handle serum or b. bird’s diet. d. Measurement of lead in feathers is a plasma samples with special care when c. quantity of grit in the ventriculus. useful way to assess lead exposure. evaluating zinc concentrations. d. length of the bird’s small intestine. b. Nontoxic serum and plasma zinc 5. Which intervention is not generally indi- concentrations are the same for all 2. Which statement regarding the kinetics cated when treating a lead-intoxicated psittacines. of absorbed lead is incorrect? bird? c. Zinc concentrations in plasma are high- a. Lead is actively absorbed from the GI tract. a. remove lead objects that remain in the est in morning samples. b. Lead in the blood is primarily associated GI tract at the time of presentation d. Toxic zinc concentrations have not been with red blood cells and not plasma. b. initiate chelation therapy with either established for birds.

c. Bone serves as a long-term storage succimer or CaNa2EDTA depot for lead. c. control seizures using benzodiazepines 9. Which mechanism is known to contribute d. Once absorbed, lead has a half-life of such as diazepam or midazolam to the development of anemia in birds approximately 2 weeks. d. administer blood transfusions to correct with chronic zinc intoxication? nonregenerative anemia a. Excess zinc decreases copper availabil- 3. Which organ or system is not a primary ity, leading to decreased ceruloplasmin target for lead damage? 6. What is the most common source for zinc concentrations. a. central nervous system poisoning in birds? b. Zinc inhibits heme synthesis by interfer- b. liver a. wood preservatives ing with ALAD. c. hematopoetic system b. zinc-coated food containers c. Zinc increases erythrocyte fragility. d. GI system c. galvanized cage material d. Zinc delays erythrocyte maturation. d. pennies minted before 1982 4. Which statement is true regarding the 10. Which statement is true with regard to diagnosis of lead intoxication in birds? 7. Acute zinc poisoning in birds does not the use of succimer in birds? a. Basophilic stippling is a common finding result in a. Succimer must be given IV or IM. on blood smears from intoxicated birds. a. anemia. b. Succimer is given orally. b. Gross and microscopic postmortem b. corrosive effects in the GI tract. c. Succimer is nephrotoxic. lesions are pathognomonic for lead c. pancreatic damage. d. Succimer is not recommended as a intoxication. d. liver damage. chelator for metal toxicoses.

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