Pet Avian Medicine

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Avian Toxicology

jerry LaBonde, MS, DVM*

Exposure to toxins in captive avian species is much less frequent than other free-ranging animals owing to the cage or aviary environment. Birds that have free range of the home and backyard collections of game birds or waterfowl are at greater risk to toxin exposure. However, because of the unique physiology of birds and the life-threatening nature of most toxicities, prompt and well-informed action is necessary. Current research and reportings of pet avian toxicities are broadening the base of information in this area of toxicology. There is, however, much information that needs to be obtained scientifically and clinically concerning avian toxicities. In the past, many lists of potential toxins to pet birds have been extrapolated from human or mammalian toxicities. The majority of reported toxicities in birds are heavy metallic, gaseous, and pharmacologic in nature.

DIAGNOSIS AND MANAGEMENT OF TOXICOSES A fundamental diagnostic and therapeutic approach to a potential avian toxicity aids in the success of the treatment of the bird. Most cases of toxicities presented to the practioner are acutely ill, and the owner is unaware of any toxin exposure. A thorough history from the owner may be the most important information obtained in the diagnosis or suspicion of a toxicosis. Based on the bird's clinical signs, the owner should be questioned concerning toxin exposure. The primary routes by which toxins are absorbed are ingestion, injection, cutaneous, or inhalation. Therefore, any history involving changes in, or the quality of, the bird's environment, diet, and state of health is helpful. Toxicities can be aggravated by age or preexisting illness. Also a history of a lack of response to proper antibiotic therapy may indicate an underlying toxicity. The goals in treating the toxic bird are first to stabilize the patient, which may preclude getting a thorough history from the owner. This should include any emergency procedures as indicated, such as fluids, heat, anticonvulsants, oxygen, or other treatments. After the bird is stable and a history is obtained, a complete evaluation of the patient should be made. It is very important at this time to remember to treat the patient, not the toxin. Stabilizing the bird's physiologic parameters is more important at this time than searching for a specific physiologic antagonist since few exist for most toxins. Because some antidotes have toxic *Avian and Exotic Animal Hospital, Littleton, Colorado Veterinary Clinics of North America: Small Animal Practice-Vol. 21, No. 6, November 1991

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potentials themselvt:s, their use based on an incorrect diagnosis can be detrimental. If the bird is somewhat stable, diagnostic samples can be taken at this time for later analysis. The next five steps in treating the poisoned bird are: (1) Prevent further exposure to the toxicant; (2) delay further absorption of the toxicant; (3) institute physiologic antagonist (antidotal) therapy; (4) facilitate removal of the toxicant; and (5) institute supportive therapy. Prevention of further exposure to a toxicant involves removal of the bird from the source of the toxin. If the toxin is environmental, dietary, or gaseous, removing the bird from the home is preferred. If the toxin is through external contact, frequent washing with a mild liquid hand-washing detergent followed by frequent rinsing is advised. If an acid corrosive is suspected, a sodium bicarbonate paste can be applied to the affec.ted area. Alkali caustic agents can be treated with a 1:4 vinegar solution or lemon juice, followed with frequent rinsing. Avoid use of greasy or oily topical ointments. Ocular treatment involves flushing the eyes with physiologic saline for 20 to 30 minutes. The flushing should be followed with a topical ophthalmic lubricating ointment. To delay absorption of a toxin in the upper gastrointestinal tract, frequent crop or proventricular gavages are indicated. This should be done three to four times with saline or activated charcoal by distending the crop with the fluid and aspirating the contents back out. Pro ventricular gavages must be done carefully by guiding a soft rubber catheter through the crop into the proventriculus. This procedure may require sedation with isoflurane to facilitate passage of the tube. Only birds that are stable enough to handle the isoflurane should be sedated, and an endotracheal tube should be placed to avoid aspiration. A small amount of activated charcoal should be left in the crop. For solid material such as heavy metal objects, an emergency cropotomy may be indicated. The use of emetics in birds is considered unsafe and ineffective. The majority of toxins have no specific antidotal therapy. These physiologic antagonists are discussed with their appropriate toxin. This is also another reason to treat the patient, not the toxin. Cathartics aid in the elimination of toxins and foreign material from the lower digestive tract. Saline cathartics such as sodium sulfate (Glauber's salt) or magnesium sulfate (Epsom salt) are recommended for this purpose (1 g/kg orally). Clinical side effects of repeated doses of saline cathartics have not been determined. Concurrent use with activated charcoal is more effective than the cathartic alone. 4 If the charcoal is to be given in repeated doses, the osmotic or saline cathartic should be given with the first dose or two. Osmotic cathartics include psyllium hydrophilic mucilloid (Metamucil), which can be mixed with activated charcoal, baby food gruel, or mineral oil to hasten toxin removal. Critical assessment of the patient's status should be done once again and appropriate supportive measures implemented. This step often can lead to the success or failure of treatment in the compromised patient. Poison Information Centers Rapid diagnosis and appropriate therapy are critical to the survival of the avian patient suffering acute toxicosis. Proper information on the physiologic effects of specific toxins can be valuable during the course of therapy. Maintaining a reference library on toxicology as well as using local and national poison information centers may accelerate valuable information gathering for the treatment of the bird. There are two primary animal poison information centers in the United States: the Illinois Animal Poison Information Center, Urbana, IL, and the Georgia Animal Poison Information Center, Athens, GA. Certified Regional Poison Control Centers are located in most states and are of valuable help in obtaining information on physiologic

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effects of toxins. These centers may not have specific data on avian toxicities but can supplY: information on principles of toxicity and suggested therapy. Sample Submission and Use of Diagnostic Laboratories The analytic laboratory you choose to use for toxicologic analysis should be consulted before submission of samples. This allows for proper direction in the amounts and types of samples to be submitted. This is critical when submitting samples from avian species since sample size is limited. It also allows the practitioner to submit paired samples if the laboratory does not have a database of normal values in birds. Fresh frozen tissue including the liver, kidney, and brain are generally the most helpful. Submitting crop and gastrointestinal contents can be of benefit in some heavy metal and pesticide toxicities such as lead and metaldehyde, respectively. Make sure that a complete history accompanies the sample, and check with the laboratory before submission.

HEAVY METAL TOXICITIES Lead is the most common toxicity reported in avian species. The soft metal is easily chewed by curious pet birds, and free-ranging fowl have a similar curious nature to ingest metal objects. There are many other forms of lead exposure to which birds are susceptible (Table 1). This list should be reviewed with owners when a case of suspected lead poisoning is presented. Most owners are unaware of these items as potential sources or may assume that the bird would "never chew on that material." The clinical signs of lead toxicity are usually multisystemic, involving hematopoietic, neurologic, and gastrointestinal systems. Physiologic effects of lead intoxication depend on the amount and quration of exposure. Often erythrocytic abnormalities such as premature destruction and decreased production occur. 41 Myocardial degeneration, fibrinoid-vascular necrosis, renal tubular necrosis, and renal nephrosis have been reported. 9 This may explain why in acute cases in Amazon species hematuria is a clinical sign. Neurologic changes include segmental demyelination, competition for calcium at myoneural junctions, and central nervous system edema. Hepatocellular degeneration and testicular disorders can occur as well. 50 · 54 In an acute lead toxicity, the bird usually presents depressed and weak. Gastrointestinal signs are usually the most common clinical signs observed in most species. Clinical signs may include anorexia, weight loss, regurgitation, and diarrhea. Often the regurgitation is due to crop stasis and esophageal or proventricular

Table l. Sources of Lead Lead shot Galvanized wire Lead-based paints Plaster impregnated with lead Lead putty Solder Hardware cloth Foil from some champagne and wine bottles Linoleum Some welds on wrought iron cages

Contaminated feed and bone meal Lead weights (curtain and fishing) Bells with lead clappers Stained glass Tiffany lamps Improperly glazed ceramics Batteries Costume jewelry Mirror backs Bird toys with lead weights Leaded gasoline fumes

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impaction related to myoneural dysfunction. Birds that present with a history of regurgitation should be considered for lead exposure. The diarrhea is typically a dark green-black and pasted to the vent. Other clinical signs that may be observed are wing droop, head tremors, seizures, and blindness. 9 · 37 Polyuria and polydipsia may also be observed, with Amazon Parrots exhibiting hematuria or hemoglobinuria in more severe cases. •• Most birds present with anemia, but this is not always present in acute cases. A tentative diagnosis of lead exposure can be based on clinical signs and history. Hematologic results include heterophilia, hypochromic regenerative anemia, and cytoplasmic vacuolization of red blood cells. Increases in aspartate aminotransferase, creatinine, uric acid, and total protein may also be obsel'ved. 9 • 28 Radiographic examinations (Fig. 1) may reveal metallic densities in the ventriculus, but absence does not rule out lead exposure. Blood or tissue levels of lead can confirm a diagnosis, but the diagnostic laboratory should be consulted first for sample size requirements. Whole blood should be collected in heparinized or sodium citrate tubes. Tissue samples such as liver, kidney, brain, or bone need to be fresh frozen. Blood lead levels above 20 JLg/dL (0. 2 ppm) are suggestive of exposure, and levels above 50 JLg/dL are diagnostic for lead toxicity. Clinical signs are not consistent with lead levels in blood or tissue because of species differentiation, length of exposure, and rate of absorption. Therefore, repeating blood lead level testing is recommended before ending treatment. Other blood constituents such as delta-amino levulonic acid (ALAD) and free erythroprotoporphyrin (FPP) can be monitored as well, but control samples should be submitted when possible for interpretation of results. 9· 28 • 41 · 45 Zinc toxicities present similar to lead toxicoses. The kidneys, liver, and pancreas are the primary target organs. Combination lead and zinc exposures are the most common reported. Zinc is soluble in soft water and organic acids, which results in possible food or water contamination. Common sources of zinc are galvanized containers, galvanized mesh, hardware cloth, and zinc phosphate. 49 Blood and tissue levels reported in macaws suffering from zinc toxicoses have been reported as greater than 200 JLg/dL and 75 ppm, respectively. 43 Serum samples should be submitted in plastic containers because rubber stoppers in blood tubes leach out the zinc from the serum. Iron toxicity is the third most commonly reported heavy metal toxicity in pet birds but is a rare occurrence. Most exposures are due to cast iron food or water bowls with poorly applied or chipping enamel. Clinical signs are usually chronic in nature and include lethargy, anorexia, and emaciation. Treatment The primary goals in the treatment of heavy metal toxicities are chelation, removal of particles from the gastrointestinal tract, and supportive therapy. Chelation therapy forms nontoxic complexes that are excreted in the urine and bile. 33 The chelation takes place in the blood and necessitates multiple treatments because heavy metal concentrations continue to equilibrate from the soft tissue to the bone and blood as blood levels of the heavy metals drop. Treatment periods should be continued until the bird is clinically normal. Then chelation therapy should be held off for a short period of time to allow equilibration from soft tissue before starting therapy again. Birds that present with severe proventricular dilatation, neurologic signs, or hematuria carry a poor prognosis. [Editor's note: The editor's experiences have shown that most Amazons with acute cases of lead poisoning with hematuria respond consistently and recover completely following ethylenediaminetetraacetic acid (EDTA) therapy.] Calcium disodium versenate (CaEDTA) has been the standard treatment for most heavy metal toxicities, but recent work by Degernes 9 and Mautino 39 has

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explored successful, less toxic alternatives. 9 CaEDTA is an effective treatment but must be given parenterally (35 mg/kg intramuscularly two times a day for 5 days, then off for 3 to 4 days, then repeat as needed) in initial treatment owing to poor absorption from the digestive tract and can be nephrotoxic. [Editor's note: Many practitioners, including the editors, use EDTA for 7 to 10 consecutive days routinely without an interim period.] Dimercaprol (BAL) is an effective chelator alone and has been used in combination with CaEDTA successfully. BAL (2.5 mg/kg every 4 hours for 2 days, then twice a day for 10 days or until recovery) has a much broader spectrum for chelation than CaEDTA, but transient toxicities have been reported in mammals. This must be administered parenterally as well. Dimercaptosuccinic acid (DMSA) and D-penicillamine (PA) have been found to be more rapid and effective chelators as well as less toxic than CaE DT A. 9,3 9 The other key advantage to these two drugs is that they are given orally. Effective doses for PA have to be determined but it has been used at 55 mg/kg by mouth twice daily effectively. DMSA is effective at a dose of 25 to 35 mg/kg by mouth twice daily, 5 days a week for 3 to 5 weeks. Deferoxamine is the antidote of choice in humans for iron toxicity, but safety and proper doses have not been determined in birds. CaEDTA and DMSA chelate iron as well. Large metal foreign bodies in the crop or proventriculus can be surgically removed if the patient is stable. soa More often, the particles are too small or are farther down the digestive tract and need to be removed with bulk diets and cathartics (Fig. 1). Radiographic evaluation is recommended every 3 to 4 days to determine efficacy of the bulk diet. Bulk diets and cathartics need to be used with caution if proventricular stasis is present.

Figure l. This 4-year-old Blue Front Amazon ingested lead particles chewed from a medallion of costume jewelry containing lead solder. Note the lead particles in the ventriculus and the distended proventriculus. This bird presented with lethargy, regurgitation, weakness, anemia, and hematuria.

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DRUG AGENTS All substances are poisons. The right dose differentiates a poison and a remedy. PARACELSUS

(1493-1541)

Pharmacologic research and standardization of drug doses in avian species have resulted in fewer reports of unexpected drug reactions. Most drug reactions in birds are due to individual hyperactive responses, species variation, improper route of administration or dosing, and use of medication in drinking water (Table 2). Many new drugs that have not been clinically tested for safety and efficacy are used on birds based on clinical indication.'' Caution must be used when extrapolating treatment regimens from human or animal medications to birds. Unexpected hyperactive responses occur in all species of animals and need to · be treated accordingly. Smaller birds (finches and canaries) and soft bills constitute the majority of reported drug toxicities. This is in part due to an observed tendency for these species to be more susceptible to many medications and improper dosing because of their small size. Daily gram weights are critical when administering medications to small birds, especially with parenteral administration or drugs with a low therapeutic index. It has also been observed that certain drugs, such as ivermectin, are safer to use and just as effective when given subcutaneously or orally rather than parenterally. Excessive or improper use of antibiotics has the potential to cause autointoxication as a result of the drug's adverse effect on normal gastrointestinal flora. This can often lead to conditions such as candidiasis or gramnegative septicemia. Except for a few medications, adding drugs to a bird' s drinking water is not recommended. Many medications are not stable or do not mix well in water and can leave the water with an unpalatable taste. It is difficult to know if the bird is receiving a proper dose, and dosing assumes that the bird is drinking a normal amount. This is not always the case with an ill bird. Other variables to consider are polydipsic or heat-stressed birds, which tend to drink more than expected levels and are prone to overdosing. There are situations when medicating the water is the only practical way to treat a flock of birds or a bird that is critically stressed with handling.

GASEOUS TOXICOSES Avian species are much more susceptible to gaseous fumes than mammals owing to their unique respiratory system. Fumes that are considered nontoxic to humans or other pets can be lethal to a pet bird. Clients should be advised that any chemical odors or smoke are potentially hazardous to their bird and it is best to avoid exposure or remove the bird from the premises until the odor is not detectable. Many toxicities occur in the kitchen from the burning of foods or the cleaning of appliances such as ovens. Kitchen ventilators or stovetop filters are not adequate to filter smaller, potentially toxic particles from the air and often recycle these toxins. Treatment of toxic inhalation is generally supportive. Pulmonary edema or hemorrhage, owing to pulmonary vascular damage, are observed in many toxicities and should be treated accordingly. 6 · 64 Oxygen therapy and glucocorticosteroids are indicated in most cases. Avoid exciting or stressing birds, and place them in a warmed oxygen chamber. Most deaths occur within the first 2 to 3 hours postexposure. Prevention is the best therapy with all toxic inhalants (Table 3). The most reported gaseous toxicity is polytetrafluoroethylene (PTFE) exposure,

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commonly called polymer fume fever. This toxicity occurs when nonstick cookware or drip pans such as Teflon or Silverstone are exposed to temperatures of 280°C (536°F) or greater. With proper use, the cookware should not exceed 2l0°C even with deep-frying. Problems occur when cookware is left to cook or boil dry, resulting in higher than normal temperatures, which cause the pyrolysis resulting in PTFE toxicosis. Drip pans coated with these nonstick surfaces should be avoided because they can become overheated with normal stove use. The most common clinical sign in birds is acute death, but mild exposures may show dyspnea, ataxia, and pulmonary congestion. 6 • 38 · 64

PESTICIDES Pesticide toxicities usually are due to inappropriate application of rodenticides, insecticides, and, herbicides in or around the bird' s environment. Backyard fowl are capable of bioconcentrating pesticides and chemical fertilizers through chronic lowgraJe exposure from browsing on plants and insects. Owners must be warned that birds can be more sensitive to pesticides than mammals, as is the case with certain organophosphates. 42 Organophosphates and carbamates such as dursban (chlorpyriphos), carbaryl (Sevin dust), diazinon, malathion, dichlorvos, and dieldrin are found in many insecticides or fertilizers. Sensitivity to these compounds depends on species variation, degree of exposure, and whether ingestion has occurred. For example, sevin dust has been used safely in nest boxes. However, if ingestion occurs through food or water contamination, lethal toxicities can occur. 42 Clinical signs observed in birds are similar to those in mammals and are due to inhibition of acetylcholinesterase. Common gastrointestinal signs include anorexia, diarrhea, and crop stasis. Neurologic dysfunction can involve ataxia, tremors, seizures, and paralysis. Other clinical signs may include dyspnea with moist rales and bradycardia. The primary cause of death in a pet bird breeding operation exposed to lethal concentrations of dursban was respiratory failure. 1· 47 • 53 Diagnosis of organophosphate and carbamate toxicities is usually based on history of recent use or exposure. Cholinesterase analysis of whole blood or brain tissue may establish exposure, but additional samples from birds not exposed may be required because most laboratories do not have normal values for birds. Histopathology may give some indication of exposure but is not always consistent. Insecticide identification can be made from suspected food or container sources, gastrointestinal contents, liver, body fat, and skin. The analytic laboratory should be consulted before submission of samples. Atropine (0.2 mg/kg intramuscularly as needed until cessation of clinical signs) and pralidoxime chloride (2-PAM; 10 to 100 mg/kg intramuscularly) are the antidotes of choice for organophosphate and carbamate toxicity. 2-PAM is of benefit within the first 24 hours of exposure and can be used in conjunction with atropine at the lower dose of lO to 20 mg/kg. Both drugs are used until the patient is asymptomatic then as needed. 5 1• 56 Rodenticide toxicities can occur from primary ingestion of inappropriately placed bait or feed contamination and secondary exposure from the consumption of poisoned rodents. 32 • 35 Anticoagulant rodenticides are the most commonly used, such as warfarin, brodifacoum, and indanedione derivatives. Their mechanism of action is interference with vitamin K recycling, thereby depleting clotting factors II, VII, IX, and X. The resulting clinical signs range from depression and anorexia to subcutaneous hemorrhage, bleeding from the nares, and oral petechiation. It is important to identify which anticoagulant has caused the toxicity to determine the length of therapy required. First-generation anticoagulants such as

Table 2. Reported Drug Reactions and Toxicities DRUG

Antibiotics

Antiparasiticals

SPECIES

Aminoglycosides (gentocin, amikacin)

All

Cephalosporins

All

Macrolides (clindamycin, erythromycin, tylosin)

All

Nitrofurazone powder 9.2%

Softbills, lories, grass parakeets

Sulfas (vetasulid)

All

Tetracyclines (oxytetracycline, doxycycline) Trimethoprim-sulfas Quinilones (enerofloxacin, cyprofloxacin)

All

Diazinon

All

Dimetridazole

lvermectin

Pigeons, budgerigars, cockatiels Finches, canaries, quail, pigeons, and young birds Finches, budgerigars

Levamisole 13.56%

All

Praziquantel 56.8 mg/mL

Finches

Fenbendazole

Macaws All

REACTIONS/TOXICITIES

At higher than recommended doses or in dehydrated birds, these drugs can cause nephrotoxicity and neuromuscular blockade At higher than normal doses or in debilitated young birds, these drugs may cause hepatotoxicity and renal toxicity Have been observed to cause gastrointestinal upset and diarrhea. At doses greater than 40 mg/kg IM of tylosin, anaphylactic-like reactions have been observed in cockatiels At a dose of 1 tsp/gal, ·ataxia, convulsions, and death have been observed. The recommended dose for these birds is '12 tsp/ gal Hypersensitivities and hemorrhagic syndrome have been observed With IM parenteral administration, tissue necrosis and inflammation at injection sites can occur Regurgitation, facial flushing, and depression have occurred Dyspnea and muscle tremors have been observed with injectable doses greater than 70 mg/kg in immature mammals; articular cartilage erosion and lameness have occurred Problems occur when food or water sources are contaminated. Weakness, muscle tremors, and death in young birds may occur When used in drinking water, ataxia, neurologic disorders, and death have been observed When used at 10 mLIL, neurologic signs and death may occur Most toxic reactions involve intrapmscular use in smaller birds. Lethargy, depression, and death can occur When used parenterally or at 10 mL/gal, most species show emesis. Tissue necrosis at injection sites and hepatotoxicity have been reported Depression and death have been reported

Miscellaneous drug reactions

Aventyl HCL (Lilly) Banamine

All All

Calcium

Primarily young birds

Gamma globulin (human)

All

Levothyroxine

Amazons, budgerigars

Medroxy progesterone

All; cockatiels, are most often reported

Mucomyst

All

Phenobarbital

All

Vitamin A4

All

Vitamin D 3

Juvenile macaws are most sensitive

Hyperactivity and agitation have occurred Regurgitation may be observed when used frequently or in high doses Nephrosis, visceral urates, parathyroid dysfunction, al)d retarded growth have been observed Vomiting, weakness, and conjunctival edema have been observed after repeated injections Reactions are individual, but owners should be warned for hyperactivity, aggression, or lethargy A transitory diabetes as well adethargy, obesity, and fatty liver have been observed. Reactions are more common with repeated injections Hypersensitivity reactions have been observed with nebulization therapy. Clinical signs include dyspnea, prolapsed nictitans, and anaphylaxis Excitement or depression may be observed when elixir is used in the drinking water Reactions are due to excessive use. Young birds suffer from osteodystrophy and parathyroid hypertrophy. Adults show a burnt-orange color in the skin, which is prone to drying and cracking Increased soft tissue calcification is the primary underlying problem for most reactions in baby birds. Dietary levels should be monitored closely for both breeding adults and babies

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Table 3. Noxious Inhalants Reported in Pet Birds Most nonstick surfaces (i.e., irons, pots, pans, woks, and drip pans) Leaded gasoline fumes Hair dryer fumes Smoke (any source) Automobile exhaust/carbon monoxide Self-cleaning ovens Bug bombs and pesticide strips and sprays Hair permanents and hair sprays Chemical sprays Glues, paints, and nail polish Ammonia or strong bleach Mothballs (naphthalene, para-dichlorobenzene) Fluoropolymers from spray starch Burning foods and cooking oils

warfarin require multiple ingestions to reach toxic levels and have a shorter halflife. Therefore, treatment may be required only for 5 to 7 days. Second-generation anticoagulants such as brodifacoum can be lethal after a single ingestion. Brodifacoum also has a significantly longer half-life than warfarin and may need prolonged therapy for up to 2 weeks or more. Vitamin K, is the treatment of choice at a dose of 0.2 to 2.2 mg/kg intramuscularly every 4 to 8 hours until stable then daily. 32 Duration of treatment depends on clinical signs and type of anticoagulant exposure. Birds should be rechecked on a regular basis up to 2 weeks posttreatment to assess any recurrence of clinical signs. Other rodenticides that have been reported as causing avian toxicities are crimidine (Castrix), zinc phosphide, and alphachoralose. Recommended treatment for crimidine is pyridoxime and anticonvulsants. Zinc phosphide is treated with supportive therapy and a 5% sodium bicarbonate gavaging solution. Alphachoralose is an avicide that is most commonly seen in pigeons. Anticonvulsant therapy is recommended. 30 Herbicide and fungicide toxicities usually result from bedding or grain contamination. Organomercurial compounds (thiram) are used as grain fungicides and can cause abnormal egg production as well as leg deformities in young birds. Mortalities have been reported from chlorophenol-contaminated bedding. Chlorophenols have been used for termite control and as a herbicide or fungicide. 30

TOXIC PLANTS Inquiries from clients about the toxicity of houseplants appear to dominate most questions related to poisonings in pet birds. Plant toxicoses, however, are rare, and the majority of these result in oral irritations. This may be due to the tendency for birds to chew at plants rather than ingest sufficient amounts to cause clinical conditions. The other factor to consider is that there is a significant species variation between birds and mammals in their sensitivity to toxic properties of plants. Recent clinical studies have shown a wide avian species and individual variation to plants that have previously been reported as toxic. Most reports in birds have been clinical observations and have not addressed the potential of pesticide or herbicide residues as contributing to toxic reactions. Clinical studies in budgerigars have provided useful information on the effects of known toxic plants to birds (Table 4). 26· 29 The most common clinical signs observed

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Table 4. Plant Toxicities in Budgerigars from Clinical Studies* Avocado (Persea americana) Black locust (Robina pseudoacacia) Clematis (Montana rubens) Lily of the valley (C onvallaria majalis) Oleander (Nerium oleander) Philodendron (Philodendron scandens) Poinsettia (Euphorbia pulcherima) Rhododendron (Rhododendron simsii) Yew (Taxus media) Virginia creeper (Parthenocissus quinquefolio) *Data from references 26, 29, and 57.

are lethargy and regurgitation. Generally most birds that survive the initial toxicity require little or no supportive treatment. Birds should be treated according to their clinical signs and the toxic principal of the plant. Oral or upper gastrointestinal irritation may require soft diets, intestinal protectants (such as activated charcoal or mineral oil), and cathartics. Supportive fluid therapy is useful when indicated. [Editor's note: The most publicized plant toxicity in pet avian medicine remains the avocado controversy. Most practitioners recommend avoiding this food as a psittacine supplement. Some investigators have listed the plant as highly toxic, and others claim it is not toxic at all. 26 The editors have seen at least two cases of sudden death in cockatiels following ingestion of avocado. Until more is known, it is best to avoid using this food.] Only plants that are recommended for aviaries or backyard fowl should be made accessible to birds. It is prudent to prevent access to all plants that may have toxic properties (Table 5). Mycotoxins can be the greatest threat to birds, resulting in acute and severe toxicoses. Usually poorly stored foods such as seed, millet spray, silage, and dog food are the source of mycotoxins. An increase in humidity and heat promotes growth of molds on food. Clinical signs are variable and include acute death of one or more birds in a flock. Diagnosis of mycotoxicity requires identification of the toxin, which can be present without the mold. 16· 27 · 52 • 66

Table 5. Plants That Have Been Reported to Cause Toxic Reactions in Pet Birds, Waterfowl, and Game Fowl* Avocado (Persea americana) Bishops weed (Ammi majus) Black locust (Robina pseudoacacia) Blue-green algae (Microcystis aeruginosa) Burdock (Arctium minus) Camel bush (Trichodesma incanum) Castor bean (Ricinus communis) Clematis (Montana rubens) Coffee bean (Sesbania drumundii) Diffenbachia (Diffenbachia spp) Elephants ear (Colocasia or Alocasia spp) Ergot (Claviceps purpurea) Lily of the valley (C onvallaria majalis) Locoweed (Astragalus emoryanus)

Maternity plant (Klanchoe spp) Milkweed (Asclepias spp) Nightshade (Solanum spp) Oak (Quercus spp) Oleander (Nerium oleander) Parsley (Petroselinum sativum) Philodendron (Philodendron scandens) Poinsettia (Euphorbia pulcheriama) Pokeweed (Phytolacca americana) Precatory bean (Abrus precatoius) Rhododendron (Rhododendron simsii) Tobacco (Nicotiana spp) Virginia creeper (Parthenocissus quinquefolio) Vew (Taxus media)

*Data from references 18, 28, 34, 44, 45, and 60.

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OIL TOXICOSIS Common medical problems associated with environmental or household exposure to oils and petroleum products are hypothermia, diarrhea, dehydration, regurgitation, pneumonia, hypoproteinemia, and hemolytic anemia. All except hypothermia have to do with the ingestion or absorption of the oil. Activated charcoal is recommended as an intestinal absorbent if ingestion is suspected. Hypothermia is the initial primary concern. If the bird is weak and stressed, it must be warmed and stabilized before attempting to wash the oil from the feathers. Failure to do so may stress the bird and result in death. Wrapping the bird in an absorbent diaper prevents preening and soaks up excessive oil. Batliing the bird requires applying a protective ophthalmic ointment in the eyes and using a 4% to 15% solution of a mild detergent. The detergent solution is applied over the bird, and the feathers are stroked in the direction of the feather growth. Do not scrub the feathers. Then the bird is rinsed with warm water (l03°F to 104°F), and the process is repeated as needed until the bird is clean. This may have to be staged over a period of time depending on the physical state of the bird. 10• 36

CHOCOLATE TOXICITY The tendency of pet bird owners to give their bird treats of chocolate is a concern owing to the potential for reactions to the alkaloid theobromine found in chocolate. This usually occurs because the bird ingests a considerable amount of chocolate compared with its body size. Clinical signs include depression and regurgitation in mild cases, progressing to convulsions and death in severe cases. Treatment is directed toward gastrointestinal protectants, cathartics, and supportive therapy.

TOXICITIES RELATED TO FREE-RANGING GAME AND WATERFOWL The curious nature and unrestricted environments of these species exposes them to a variety of potential toxins as well as toxins previously mentioned. Some of the reported toxins include garbage, sodium chloride, nicotine, and ethylene glycol. Fly larvae ingested while feeding on garbage can be contaminated with botulism toxin. Usually within 8 to 24 hours the birds show weakness, lethargy, limber necks, and paralysis of the wings and legs. Rock salt is a common source for toxicity, especially when it has contaminated water or food supplies. Pathologic and clinical effects include cerebral edema and hemorrhage, depression, polydipsia, excitement, torticollis, ataxia, opisthotonus, and hemoglobinuria. Treatment involves diuretics and isotonic fluids. 30 · 61 Nicotine toxicosis is from the ingestion of chewing tobacco and cigarette or cigar butts. Birds may exhibit depression, cyanosis, and dyspnea. Ethylene glycol ingestion is usually fatal when clinical signs are exhibited. Lethargy, ataxia, trembling, watery droppings, and a flaccid neck are typical clinical signs. Post mortem examination may reveal pale, enlarged kidneys with calcium oxalate crystals found in renal tissue. 61

REFERENCES L Alexander J: Probable diazinon poisoning in peafowl, a clinical description. Vet Rec 113(20):470, 1983

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2. Anderson R, Smiley C: Apparent chlorohexadine toxicity in neonatal psittacines. AFA Watchbird 14(1):43-43, 1987 3. Axelson D: In My Experience. AAV Today 1(5):203, 1987 4. Beasley V, Dorman D: Management of toxicoses. Vet Clin North Am 20(2):307, 1990 5. Bird JE, eta!: Toxicity of gentamycin in red tailed hawks. Am J Vet Res 44(7):1289, 1983 6. Blanford T, et a!: A case of polytetrafluoroethylene poisoning in cockatiels accompanied by polymer fume fever in the owner. Vet Rec 96:175-179, 1975 7. Clipsham R: Cholecalciferol analog toxicity. AFA Watchbird 14(1):38-39, 1988 8. Clipsham R: Hyperactivity with reglan. JAAV 4(1):22, 1990 9. Degernes L, Frank R, Freeman M, et a!: Lead poisoning in trumpeter swans. In Proceedings of Association of Avian Veterinarians Conference, Seattle, 1989, p 144 10. Dein J, Frink L: Rehabilitation of oil contaminated birds. Kirk RW (ed): Current Veterinary Therapy IX. Philadelphia, WB Saunders, 1986, pp 719-722 11. Dorman D: Personal communication, July, 1988, Illinois Animal Poison Information Center, Urbana 12. Ehrich M, Larsen C, Arnold J, eta!: Organophosphate detoxification related to induced hepatic microsomal enzymes with chickens. Am J Vet Res 45(4):755-758, 1984 13. Factor D: l.M.E.-Ivomec toxicity. AAV Newsletter 6(1):28, 1985 14. Fikes J: Organophosphorous and carbamate insecticides. Vet Clin North Am Small Anim Pract 20:353, 1990 15. Flammer K: Avian antibacterial therapeutics. In Proceedings of Association of Avian Veterinarians Conference, Houston, 1988, p 109 16. Fooshee S, Forrester D: Hypercalcemia secondary to cholecalcifero rodenticide toxicosis in two dogs. JAm Vet Med Assoc 196(8):1265, 1990 17. Fowler M: Disinfectant and insecticide usage around birds and reptiles. In Kirk RW (ed): Current Veterinary Therapy VIII. Philadelphia, WB Saunders, 1983, pp 606-611 18. Fowler M: Plant poisonings in small companion animals. St. Louis, Ralston Purina, 1981 19. Fudge A: l.M.E.-contaminated seed. AAV Newsletter 5(1):11, 1984 20. Fudge A: l.M.E.-diazinon toxicity in an aviary. AAV Newsletter 6(2):45, 1985 21. Fudge A, Schmidt R: IME-AAV Today 1(5):208, 1987 22. Gallerstein G: Birdowners Home Health Care Handbook, ed 4. New York, Howell Book House, 1986 23. Gerlach H: IME-dimetridazole toxicity in pigeons. AAV Newsletter 3(4):86, 1982 24. Gerlach G: Sulfa (Vetasulid) hypersensitivity hemorrhagic syndrome. JAAV 14(3):156, 1990 25. Graver G, Mazias T, Hjelle J: The toxicokinetic approach to antidotal therapy. Compendium SA 10(9):1058, 1988 26. Hargis AM, Stauber E, Casteel S, eta!: Avocado (Persea Americana) intoxication in caged birds. JAm Vet Med Assoc 194(1):64, 1989 27. Harris D: !ME-contaminated dog food. AAV Newsletter 5(1):11, 1985 28. Harrison GJ: Toxicology. In Harrison GJ, Harrison LR (eds): Clinical Avian Medicine and Surgery. Philadelphia, WB Saunders, 1986 29. Hoffmann H: Die Wirkung Toxischer Pflanzer in Haltsstoffe Auf Den Wellensittich (Melopsitt Acus Undulatus) Im Appetenzuersuch Und Nach Zwangsverabreichung. Inaugural Dissertation for D.V.M., Hannover, 1980 30. Humphreys DJ: Veterinary Toxicology, ed 3. London, Bailliere Tindal, 1988 31. Kein P, Galey F: The challenge of toxicologic investigation in birds. In Proceedings of Association of Avian Veterinarians Conference, Seattle, 1989, p 139 32. Kenny D, Kinsey M: Brodifacoum toxicity in avian species at the Denver Zoologic Gardens. In Regional Proceedings of American Association of Zoological Parks and Aquariums, 1987 33. Kowalczyk D: Clinical management of lead poisoning. J Am Vet Med Assoc 184(7):858860, 1984 34. LaBonde J: Toxic disorders. In Rosskopf W, Woerpel R (eds): Diseases of Caged and Aviary Birds, ed 3. Philadelphia, Lea & Febiger, 1990 35. Lawrence J, Renny C, Grove R, et a!: Effects of pelletized anticoagulant rodenticides on California quail. J Wildlife Dis 21(4):391-395, 1985 36. Leighton F: Clinical and gross histologic findings in herring gulls and Atlantic puffins that ingested Prudhoe Bay crude oil. Vet Pathol 23:254-263, 1986

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37. Lyman R: Neurologic disorders. In Harrison GJ, Harrison LZ (eds): Clinical Avian Medicine and'Surgery. Philadelphia, WB Saunders, 1986, p 87 38. Lyman R: Polytetrafluoroethylene toxicity. In Harrison GJ, Harrison LZ (eds): Clinical Avian Medicine and Surgery. Philadelphia, WB Saunders, 1986, p 487 39. Mautino M: Avian lead intoxication. In Proceedings of Association of Avian Veterinarians Conference, Phoenix, 1990, p 245 40. McDonald L: Suspected lead poisoning in an Amazon Parrot. Can Vet J 27:131-134, 1986 41. McDonald S: Lead poisoning in psittacine birds. In Kirk RW (ed): Current Veterinary Therapy IX. Philadelphia, WB Saunders, 1986, pp 713-718 42. Mohan R: Dursban toxicosis in a pet bird breeding operation. In Proceedings of Association of Avian Veterinarians Conference, Phoenix, 1990, pp 112-114 43. Morris P, Jensen J, Applehous F, et a!: Lead and zinc toxicosis in a Blue and Gold Macaw caused by ingestion of hardware cloth. In Am Assoc Zoo Vet Proceedings, 1985, pp 13-17 44. Dehme FW, Davis J: Plants poisonous to free living or caged mammals and birds. In Hoff G, Davis J (eds): Non-infectious Diseases of Wildlife. Ames, Iowa State University Press, 1982, pp 8-23 45. Petrak M: Disease of Caged and Aviary Birds, ed 2. Philadelphia, Lea & Febiger, 1982, pp 647-649 46. Poole C: Surgical treatment oflead poisoning in a mute swan. Vet Rec 119:501-502, 1986 47. Porter S, Snead S: Pesticide poisoning in birds of prey. JAAV 4(2):84, 1990 48. Reece R, Barr D, Forsyth W, et a!: Investigations of toxicity episodes involving chemotherapeutic agents in Victorian poultry and pigeons. Avian Dis 29(4):1239-1250, 1985 49. Reece R: Zinc toxicity (new wire disease) in aviary birds. Aust Vet J 63(6):199, 1986 50. Repper D, Drasch R, Grimm G, et a!: Effects of implanted shot of various metals on certain parameters in pigeons. AAV Newsletter 7(2):45, 1986 51. Ritchie B: Organophosphate poisoning in Columbia Iivia. AAV Today 1(1):23, 1987 52. Robinson P, et a!: Waterfowl mortality caused by aflatoxicosis in Texas. J Wildlife Dis 18(3):315, 1982 53. Rosskopf W: Aviculture medical alert. JAAV 1(1):14, 1989 54. Rosskopf W: Hypervitaminosis A in parrots. AAV Today 2(1):35, 1988 55. Rosskopf W, Woerpel R: Heavy metal intoxication in caged birds, part I and II. In Johnston D (ed) Exotic Animal Medicine Practice, The Compendium Collection. Lawrenceville, NJ, Vet Learning Systems, 1986, pp 184-196 55a. Rosskopf W, Woerpel R, eta!: Removal of a lead pellet by gizzardotomy (ventriculotomy) in a green winged macaw. VM/SAC June 1982, pp 969-974 56. Shlosberg A: Treatment of monocrotophos poisoning in birds of prey with pralidoxine iodide. JAm Vet Med Assoc 169:989-990, 1976 57. Shropshire C, Stauber E, Arai M: A Screening Study of Potential Toxic Plants in Budgerigars. Unpublished Paper, Washington State University, 1989 58. Sumner W: IME-D-Con and geese. AAV Newsletter 2(4):22, 1982 59. Tang K, et a!: Vitamin A toxicity: Comparative changes in the bone of the broiler and leghorn chicks. Avian Dis 29(2):416, 1985 60. Taylor M, Perelman B, Kuhin E: Parsley induced photosensitivity in ostriches and ducks. Avian Pathol17:183, 1988 61. Timmins R: !ME-suspect sodium chloride poisoning in an Amazon. AAV Newsletter 4(4):93, 1983 62. Van Vleet JF, Ferrans V: Congestive cardiomyopathy induced in ducklings fed graded amounts offurazolodone. Am J Vet Res 44(1):76, 1983 63. Veit H, et a!: The effects oflead shot ingestion on the testes of adult ringed turtle doves. Avian Dis 27(2):1983 64. Wells R: Fatal toxicosis in pet birds caused by an overheated cooking pan lined with polytetraf!uoroethylene. JAm Vet Med Assoc 182(11):1248-1250, 1983 65. White DH, et a!: Parathion poisoning of wild geese. J Wildlife Dis 13(3):389, 1982 66. White J: Protocol for the rehabilitation of oil affected waterbirds. In Proceedings of Association of Avian Veterinarians, Phoenix, 1990, pp 153-163 67. Wright A: !ME-chocolate toxicity. AAV Today 1(1):12, 1987 68. Wright J: Reports of untoward reactions of birds to pharmaceuticals. JAAV 3(4):190, 1989

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