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TOXINS Should “Bird-Proof” Their Homes to Provide a Safe and Enjoyable Environment for Their Companion Birds

TOXINS Should “Bird-Proof” Their Homes to Provide a Safe and Enjoyable Environment for Their Companion Birds

irds are curious and frequently investi- gate unusual textures, containers and loca- CHAPTER tions throughout the home. Many of the Bitems that may encounter during these quests can be dangerous. Contact with or consump- tion of certain plants, cleaners, and house- hold disinfectants may cause acute or chronic intoxi- cation. Even some types of provided to birds can be toxic. 37 Most compounds considered toxic to mammals should also be considered toxic to birds. Table 37.1 offers a guide for treatment of intoxication from some common household products. Based on their size and physiology, birds are more prone than mammals to intoxication by some compounds, such as volatile chemicals and fumes. Psittaciformes have a propen- sity to chew on almost anything. All avian clients should “-proof” their homes to provide a safe and enjoyable environment for their companion birds.

Birds should be supervised at all times when out of their enclosures. It has been suggested that the con- sumption of foreign bodies (eg, , , jewelry), over-consumption of grit and coprophagy may all be mediated by (Gerlach H, unpublished). Genevieve Dumonceaux Therefore, birds on a formulated would be ex- pected to chew less on plants, perches and toys than Greg J. Harrison birds on a -based diet. 1031 CHAPTER 37 TOXINS

TABLE 37.1 Normal Household Compounds That May be Toxic to Birds

Agent Toxic Components Clinical Effects Bleaches, pool Chlorine Photophobia, epiphora, coughing, Dilution with or milk orally. Irrigate skin chemicals sneezing, hyperventilation, GI irritation with cool water. GI protectant, demulcent or ulceration Cleaning agents, Ammonia Respiratory tract irritation, immune Fresh air, antibiotics, supportive care accumulated suppression excrement Combustion exhaust Carbon monoxide Somnolence, depression, cyanosis, Fresh air, oxygen, warmth, support (autos, furnaces) death Denture cleaners Sodium perborate Direct irritation, salivation, lacrimation, Irrigate with water, GI protectant, demulcent vomiting, sometimes CNS depression Deodorants Aluminum chloride, Oral irritation and necrosis, hemorrhagic Careful lavage of crop and proventriculus aluminum gastroenteritis, incoordination and chlorhydrate nephrosis Detergents (anionic) Sulfonated or Dermal irritation, vomiting, diarrhea, GI Lavage with water phosphorylated distension, usually not fatal forms, alkaline product Detergents (cationic) Quaternary Vomiting, depression, collapse, coma, Oral milk or activated charcoal. Soap for ammonium with alkyl may cause corrosive esophageal surface areas. Treat and shock as or anyl substituent damage needed groups Drain cleaners Sodium hydroxide, Caustic to skin and mucous membranes, Flush affected areas with water or milk. Do not sodium hypochlorite irritation, inflammation, edema, necrosis, use emetics or lavage. Treat for shock and pain burns in mouth, tongue, pharynx Fireworks Nitrates, chlorates, Abdominal pain, vomiting, bloody feces, Crop or . Use methylene blue or , antimony, rapid shallow respiration, chlorates may ascorbic acid for methemoglobinemia. Treat , strontium, cause methemoglobinemia for specific metal(s) ingested barium, Furniture polish Petroleum, Early CNS depression, disorientation, Prevent aspiration pneumonia. Avoid gastric hydrocarbons, necrosis, mucosal irritation, aspiration or lavage or proceed with caution. Monitor and spirits hydrocarbon pneumonia, hepatorenal treat for pneumonia damage Gasoline, crude oil Petroleum and GI irritation, skin and damage, Wash and skin with mild soap and petroleum distillates aspiration pneumonia water. Vegetable or mineral oil gavage. Antibiotics and supportive care Matches Potassium chloride Gastroenteritis, vomiting, chlorates may Treat symptomatically. Use methylene blue or induce methemoglobinemia with ascorbic acid for methemoglobinemia cyanosis and hemolysis Paint/varnish Benzene, , Dermal irritation, depression, narcosis, See “furniture polish.” Rinse contact areas removers toluene, acetone pneumonia, hepatorenal damage thoroughly with warm water Pencils Graphite GI irritation Demulcent Perfumes Volatile oils Local irritation of skin and mucous If ingested, gastric or crop lavage with weak membranes, pneumonitis, hepatorenal bicarbonate solution. Prevent aspiration. damage with albuminuria, hematuria, Demulcents. Provide plenty of ventilation glycosuria, excitement, ataxia, coma Pine oil disinfectants Pine oil 5-10%, Gastritis, vomiting, diarrhea, followed by If ingested, gastric lavage with caution to phenols 2-6% CNS depression, occasional mild prevent aspiration. Mineral oil. Monitor seizures, phenols may induce nephrosis pulmonary and renal function. Provide fresh air if strong fumes are present Overheated non-stick Polytetrafluoroethylene Sudden death, dyspnea, depression, Fresh air or oxygen, fluids, steroids for cookware, drip pans, pulmonary hemorrhage pulmonary edema, antibiotics, supportive care heat lamps, , ironing board covers Poor grade peanuts, : aflatoxin, Gastrointestinal irritation, dermal Clean feed, antibiotics for secondary peanut waste, moldy ochratoxin, irritation, oral necrosis, secondary infections. Treatment as indicated for clinical grains, corn and corn trichothecenes infections due to immunosuppression syndromes screenings, moldy cheeses, meats

table continued on next page 1032 SECTION FIVE DISEASE ETIOLOGIES

Agent Toxic Components Clinical Effects Therapy

Rodenticides Weakness, dyspnea, hemorrhage, K1 (2.5-5 mg/kg) IM or PO q 24 hr. petechiation, Minimize stress. , treat for 10-14 days. , treat for 21-28 days. , treat for 28-30 days Causes hypercalcemia and renal failure, Activated charcoal, fluid therapy. If vomiting, diarrhea, depression, hypercalcemic, saline diuresis, prednisolone , , polydipsia PO 2 mg/kg q 12 hr, furosemide 2-5 mg/kg q 8- 12 hr, salmon calcitonin SC 4-6 IU/kg q 2-3 hr until stable (mammalian protocol) Rubbing Ethyl alcohol Impaired motor coordination, cutaneous Gastric or crop lavage. Monitor temperature, hyperemia, vomiting, progress to cardiac and pulmonary function peripheral vascular collapse, hypothermia Shampoo Laurel sulfates and Ocular irritation, stimulation of mucous Activated charcoal or kaolin orally triethanolamine production, ingestion causes diarrhea dodecyl sulfate Salt, crackers, chips, Sodium chloride Gastrointestinal irritation, dehydration, Rehydration, offer small amounts of water prepared foods, salt depression, weakness, PU/PD, death frequently. SC, IV or IO fluids, supportive care water, sea sand (as grit) Styptic pencil Potassium aluminum Corrosive due to release of sulfuric acid Oral neutralizer such as magnesium oxide or sulfate during hydrolysis of the salt, oral hydroxide. Do not give bicarbonate orally for necrosis from chewing on pencils acid

Many of the therapeutic recommendations for the above products have been taken from small sources.8,8a,36a,46a

TABLE 37.2 Some Commonly Encountered Toxins and their Potential Effects in Birds19

Alcohol Depression, regurgitation Levamisole Depression, vomiting, ataxia, mydriasis, paralysis, death (hepato- Aminoglycosides Renal tubular necrosis ) Pruritus, polyuria, dyspnea, death Lincomycin Death Atropine Gastrointestinal stasis Medroxyprogesterone Lethargy, obesity, polydipsia, fatty Brodifacoum Death Mercury Depression, hematuria, death Cephaloridine Blindness Metronidazole Death in finches Chloramphenicol Death Niclosamide Death Chlorine Epiphora, upper respiratory signs, Nicotine Depression, dyspnea, coma, death tachypnea Nitrates Anorexia, vomiting, diarrhea, ataxia, Chocolate Vomiting, diarrhea, death convulsions, death Cigarette smoke Dermatitis, sinusitis, pneumonitis Nitrofurazone Ataxia, convulsions, death Copper Anemia, weakness, death Nitrothiazole Death Fatal hemorrhage Polymyxin B Lethargy, ataxia, vomiting, death Cythioate Death Polytetrafluoroethylene Dyspnea, seizures, death Diazinon Death gas Dihydrostreptomycin Paralysis, death Praziquantel Depression, death Dimetridazole Incoordination, ataxia, seizures, death Procaine penicillin Paralysis, death Fenbendazole Depression, ataxia, mydriasis Vomiting, ataxia, convulsions, death Formaldehyde Epiphora, upper respiratory signs, sulfide Death death Sodium chloride Depression, PU/PD, ataxia, Gentamicin Apnea, renal tubular necrosis, death convulsions, death Ivermectin (propylene Weakness, death Ticarcillin Hepatotoxicity glycol formulation) Vitamin D3 Calcification of kidneys and other arsenate Depression, CNS signs, death organs Zinc Depression, vomiting, ataxia, death 1033 CHAPTER 37 TOXINS

Free-ranging birds, particularly Anseriformes, are commonly poisoned through chronic exposure to a contaminated, abused environment. -contami- nated water, air and supplies can affect birds through direct contact or through of com- ponents in the food chain. Often the intoxication is subtle, and accumulate over time (eg, lead in waterfowl, organochlorines in birds of prey).

Birds of prey and fish-eating birds are particularly susceptible to contaminants in the food chain be- cause of biologic magnification. It is of interest that the health of free-ranging birds is frequently ignored as a sensitive indicator of human-induced damage to our environment. FIG 37.1 Psittacine birds may be exposed to numerous toxins because of their chewing behaviors. In this case, a conure was In addition to human-related toxins, food and water presented with secondary to the consumption of supplies encountered by free-ranging birds may also lead-containing solder used to hold his feeding dish. The case was further complicated by gastrointestinal impaction secondary to the be contaminated by biologic organisms that produce ingestion of pieces of the plastic dish and malnutrition caused by their own toxins, including molds (mycotoxins), bac- a diet of wild bird . Clinicians should carefully evaluate the teria (endotoxins) and certain blue-green algae environment in birds with clinical signs consistent with toxicity. (hepatotoxins).

Birds are generally more susceptible to inhaled toxins When submitting samples for toxicologic analysis, it than mammals because of their rapid metabolic rate, is best to call the laboratory for information on small size, highly efficient respiratory system and low proper sample preparation and shipment. Most labo- body fat content. In comparison, many compounds that ratories request frozen samples (except whole blood), cause intoxication following ingestion by mammals are preferably individually wrapped to prevent cross- relatively nontoxic in companion birds; however, birds contamination. Samples submitted for heavy metal should be restricted from access to compounds known analysis should not be wrapped in foils or contact any to be toxic in mammals (Figure 37.1). metal during shipment. Complete request forms, in- cluding the specific analyses to be run and the spe- Products that produce fumes, fogs or mists are not cies involved, improve the speed and accuracy of the recommended for use in areas where birds are pre- results. sent. Good ventilation should be maintained to pre- vent the accumulation of harmful gases and fumes. Further information on products and chemicals as Some toxins may be absorbed directly through the well as assistance with poisonings is available from skin causing systemic intoxication, while others the National Animal Control Center, Univer- cause localized reactions (eg, nicotine dermatitis). sity of Illinois, College of Veterinary , Ur- Systemic intoxication could occur from birds perch- bana, IL 61801, 1-800-548-2423 (credit cards only, ing on wood or branches treated with preservatives $30 per case) or 1-900-680-0000 ($20 for the first 5 or pesticides. minutes, plus $2.95 for each additional minute [$20 minimum]). This center’s experience is limited when A bird’s response to a toxin may vary depending on dealing with companion birds and they often refer the age, size, health status and plane of nutrition of calls to experienced practitioners. the patient, as well as on the route, duration and quantity of toxin exposure. A malnourished bird is A useful conversion in analysis is 1 ppm = more likely to develop clinical problems from a toxin 100 µg/dl. exposure than is a bird on an adequate diet. A bird suffering from chronic malnutrition is more likely to develop pansystemic diseases following exposure to toxic agents. Table 37.2 lists some compounds that have been associated with toxicity in birds and their principal clinical changes. 1034 SECTION FIVE DISEASE ETIOLOGIES

Ingested Toxins

Lead (Pb) Lead intoxication is one of the most commonly re- ported and clinically recognized poisonings of com- panion and free-ranging birds. Lead is inconspicu- ously included in numerous products found around the home and the precise cause of lead intoxication is frequently undetermined. Table 37.3 offers some ex- amples of possible household sources of lead. The common lead weights used to balance wheels may be an underestimated source of contamination within a bird’s environment. Once ingested, the lead is de- graded by acids in the stomach and absorbed into the bloodstream. Raptors can be exposed to lead by in- gesting carcasses containing lead shot. Unless paints state that they are “lead free” they may still have toxic levels of lead in the drying agent rather than in the base. Lead exposure may also occur through the inhalation of fumes from lead-containing gasoline (Figure 37.2).

Lead deposited in muscle tissue of birds is generally considered to pose minimal health risks; however, lead shot implanted subcutaneously and intramus- cularly in pigeons resulted in decreased levels of delta- aminolevulinic acid dehydratase (ALAD) enzyme ac- tivity, indicating the absorption of lead into the bloodstream.51

TABLE 37.3 Potential Sources of Lead Weights (curtains, penguin Base of light bulbs bird toys, fishing and diving, Linoleum sailing and boating accesso- ries, wheel balances) Contaminated bone meal and dolomite products Bells with lead clappers Leaded gasoline fumes Batteries Glazed ceramics (especially Solder imported products) Lead pellets from shotgun Costume jewelry shells Contaminated cuttlefish bone FIG 37.2 A mature was presented with a history of an Air rifle pellets Plaster acute onset of depression, regurgitation and diarrhea. a) It is a Lead-based paints (var- common but inappropriate practice to obtain only a lateral radio- nishes, lacquers) Stained glass (decorative graph when attempting to detect heavy in the gastrointes- glass) – lead seam Lead-free paints with leaded tinal tract. b) In this case, two metal-density objects that appeared drying agents Seeds for planting (coated to be in the proventriculus and ventriculus were found to be with lead arsenate) hemostatic clips that had been used in a previous laparotomy Hardware cloth Some lubricants (lead nap- incision. Galvanized wire (lead and thalate) zinc) Champagne and wine bottle foils (some) 1035 CHAPTER 37 TOXINS

Lead poisoning and death occurred in an African has been reported as a clinical sign of lead poisoning Grey that was sprayed with an automobile in Amazon and African Grey , but it may not lubricanta to prevent feather picking. The product occur in all cases.72 This finding is thought to be contained 4.5% lead naphthenate and had previously secondary to intravascular hemolysis and is fre- been used to treat a that died with a similar quently misinterpreted as bloody diarrhea.36 Lead clinical progression. Radiographic and clinical pa- poisoning in waterfowl, cranes and pigeons may thology data were unremarkable. The bird’s only cause ileus of the crop, esophagus, proventriculus clinical signs were diarrhea, anorexia and depres- and ventriculus.6 In waterfowl and poultry, lead poi- sion.65 Blood lead levels in the bird were 3.9 µmol/l soning can cause clinical signs similar to those that (78 µg/dl) suggesting lead intoxication. Neither the occur with botulism. Response to therapy product label nor information sheet divulged that it (lead or zinc) or antitoxin (botulism) is suggestive of contained such a high level of lead. a diagnosis (see Chapters 28, 33, 46).

A simple lead testing kitb is available for the detec- Pathology tion of lead in environmental samples. A swab sup- In some cases, hematologic parameters may provide plied with the kit is moistened with a supplied re- an indication of lead intoxication. A hypochromic, agent and rubbed against an item to be tested (eg, regenerative anemia occurs in some affected birds.36 wire, paint). The tip of the swab turns red if lead is Basophilic stippling and cytoplasmic vacuolization of present in the sample. This rapid, in-home test is less red blood cells reported in mammalian lead poison- reliable than tests performed by commercial labora- ing cases are not recognized in avian patients. tories. Elevations of LDH, AST and CPK have been re- Clinical Signs ported. Increased LDH and AST are primarily re- Clinically, lead toxicosis may occur as an acute or a lated to liver damage in birds. High CPK activities chronic problem. Chronic intoxications are most com- may be a result of lead-induced neuronal damage.14 mon in Anseriformes and other free-ranging birds. The chronicity of these problems probably occurs The functional capacity of the renal system should be because the are not evaluated until critically carefully evaluated in birds suspected of having lead ill from prolonged intoxication. The most commonly poisoning. Most commonly used chelating agents reported effect in free-ranging birds is a decrease in have potentially nephrotoxic side effects, and ther- population densities. Because companion birds are apy for heavy metal intoxication should be instituted carefully observed on a daily basis, the non-specific with caution in birds with impaired renal function. signs of acute lead toxicosis are frequently recog- There are no reports detailing serious nephrotoxic nized and birds are presented for medical evaluation. side effects from the use of in companion birds; however, swans that did not re- The presence and severity of clinical signs depends cover from lead poisoning with chelation therapy had on the amount of lead ingested, the surface area of markedly elevated uric acid levels, visceral gout and the particles and the length of time the lead is in the renal nephrosis.6 gastrointestinal tract.19,36 The type and amount of abrasive material in the ventriculus alters the speed Gross necropsy findings in lead-poisoned swans in- of lead digestion and may affect the type of clinical clude and green liver tissue. Histologic presentation.36 lesions are most severe in birds that survive for several weeks. In these birds, necrohemorrhagic en- Once in the bloodstream, lead causes pansystemic teritis secondary to Clostridium perfringens is com- damage, particularly to the gastrointestinal, nerv- mon. Other findings include fibrinoid vascular ne- ous, renal and hematopoietic systems. Clinical signs crosis, renal nephrosis and multifocal myocardial of lead intoxication in psittacine birds may include degeneration.6 lethargy, depression, anorexia, weakness (wing droop, leg paresis), regurgitation, polyuria, diarrhea, emaciation, ataxia, head tilt, blindness, circling, pa- The identification of metallic densities in the gastro- resis, paralysis, head tremors, convulsions and intestinal tract of birds with clinical signs of heavy death.19,35,36 Some birds may die with no clinical signs metal intoxication is suggestive. However, the ab- and in others, the only noted abnormalities may be sence of metal densities in the presence of clinical weakness and chronic weight loss.65 Hemoglobinuria signs does not rule out heavy metal intoxication (Fig- 1036 SECTION FIVE DISEASE ETIOLOGIES

Metal particles usually are visualized in the ven- triculus but may be seen anywhere along the gastro- intestinal tract. In chronic cases involving free-rang- ing birds, eroded pellets have been radiographically documented at necropsy.19 In some cases, the source of lead may be eliminated from the gastrointestinal tract before clinical signs are recognized.

Toxicologic Analysis Several blood tests are available to confirm lead intoxication. They require a small volume of blood, but results require from four days to several weeks. Whole, unclotted blood is the sample of choice for determining lead concentrations because 90% of cir- culating lead is in red blood cells. Lithium heparin is a suitable . EDTA should not be used because this anticoagulant may interfere with test- ing.31 Diagnostic blood levels may vary widely be- tween species.

Whole blood lead levels greater than 20 µg/dl (0.2 ppm; 1.25 µmol/dl) are suggestive, and levels greater than 40 to 60 µg/dl (0.4 to 0.6 ppm; 2.5 µmol/dl) are diagnostic of lead intoxication in psittacine birds when accompanied by appropriate clinical signs (Ta- ble 37.4).19,30 Some birds may have clinical signs and respond to therapy with levels as low as 10 µg/dl. Blood from a normal bird of the same species can be submitted along with that of the ill patient to allow more accurate interpretations of the laboratory re- sults. Higher levels of blood lead have been reported in many avian species with no clinical signs of intoxi- cation.30

In experimentally exposed to lead, peak FIG 37.3 A two-year-old female Rose-breasted Cockatoo was pre- blood concentrations ranged from 44 to 129 µg/dl.36 In sented with dyspnea and weight loss (257 g). Abnormal clinical a study involving zinc toxicosis, the cockatiels in the pathology findings included WBC=48,000 (toxic heterophils), LDH=2791, AST=1562, bile acids=291. The bird was negative for experimental group had a mean of 5 chlamydia by ELISA antigen testing of the excrement. Zinc levels µg/dl.21 In adult Cuban Whistling Tree Ducks, the were 370 µg/dl. Radiographs indicated severe hepatomegaly and blood lead level of one affected bird was 163 µg/dl; an auxiliary mass that was determined by cytology to be a lipoma. One week after initiating therapy with CaEDTA, clinicopathologic compared with the normal value of its mate of 32 findings included AST=901, LDH=1500 and bile acids=613. µg/dl. An affected Eastern Turkey Vulture in that same report had a blood lead level of 320 µg/dl.22 In Mallards and Bald Eagles, values have been reported ure 37.3). In one study involving swans, 25% of lead as high as 500 µg/dl.36 A Blue and Macaw with poisoned birds did not have lead pellets that could be identified by radiographs.6,19 Some intoxications can occur from absorption of lead that is in a nonra- TABLE 37.4 Suggested Normal Blood Lead Levels diodense form (eg, paint chips or gas fumes), or a bird Swan 6 µg/dl can develop clinical signs following the mobilization Mallard 5 – 39 µg/dl of lead stored in the bones months after an initial Canada Goose 10 – 37 µg/dl ingestion has occurred. Pigeon 17 – 81 µg/dl 5 µg/dl Most Psittaciformes <20 µg/dl 1037 CHAPTER 37 TOXINS

lead and zinc poisoning (exposure to galvanized wire) Treatment had a reported blood lead level of 50 µg/dl and a blood Supportive care for heavy metal poisoning may in- zinc level of 1500 µg/dl.40 clude chelation therapy (both oral and IM), intrave- nous lactated Ringer’s, 5% dextrose solution, multi- With the wide range of lead values reported in blood, complex B , dextran, antibiotics, this criterion alone may not be sufficient to diagnose assisted alimentation and prophylactic treatment for 31 36 clinical lead poisoning. Other reports disagree. aspergillosis (waterfowl).6 With a strong suspicion of lead intoxication, therapy should be initiated while awaiting laboratory results. A The prognosis for lead intoxication is guarded if rapid response to therapy lends evidence to a diagnosis chronic exposure has occurred or if the bird has of lead (or other similar heavy metal) poisoning.36 severe CNS signs. In other cases, the response to therapy is dramatic, with most patients responding The inhibition ALAD activity has been used as a to chelation therapy within six hours of administra- reliable and sensitive indicator of exposure to lead in tion. Many hematuric birds can die in this same time 6,19,36 ducks. It also has been recommended as a diag- period. Gastrointestinal stasis and impaction of the nostic tool in other avian species. In cockatiels, ALAD proventriculus is a complicating factor in waterfowl.6 activities less than 86 units were considered indica- tive of lead poisoning.36 In two studies in ducks, lead Chelation therapy is designed to remove lead circu- concentrations of 0.5 ppm in the brain and 200 ppm lating in the bloodstream. Calcium disodium ethyl- in the blood were found to correlate with a 75% ene diamine tetracetate (CaEDTA) or calcium diso- decrease in ALAD activity in the blood.7 dium versenate are commonly used chelation agents. The calcium form of EDTA should be used to reduce Detecting ALAD activity may be of value only in the chances of drug-induced .27 birds with low levels of lead exposure because en- zyme activities failed to decrease in humans and The recommended dosage of CaEDTA is 10-40 mg/kg pigeons with high exposures to lead.31 In swans, twice daily intramuscularly. CaEDTA is poorly ab- ALAD activities could not be used as a prognostic sorbed from the gastrointestinal tract and must be indicator for recovery. Additionally, in swans, as the used parenterally to remove circulating lead in criti- blood levels increased, the ALAD activity was also cally ill patients.36 Chelation therapy should be used found to increase rather than decrease.6 ALAD activ- for the least amount of time that is necessary to ity returned to normal in many birds that were resolve the intoxication. In general, therapy should treated but subsequently died.6 not persist for over ten days without a break in drug administration; however, some clinicians have used Lead interferes with ALAD activity, which reduces CaEDTA until there is no radiographic evidence of heme synthase activity and causes an increase in lead in the gastrointestinal tract (up to 30 days) with protoporphyrin IX concentrations in the blood. Free no clinically apparent side effects.28,36,40 CaEDTA may erythrocytic protoporphyrin (FEPP) and zinc pro- be administered orally at twice the injectable dose toporphyrin (ZPP) levels are considered accurate two to three times daily in asymptomatic birds to 31 methods of detecting lead intoxication in birds. prevent lead from being absorbed.72 CaEDTA must be FEPP levels were found to be suggestive of acute used carefully as it may cause gastrointestinal and toxicity, while ZPP levels were of more value in docu- renal toxicosis.25,36 If evidence of chelation toxicosis is menting chronic lead poisoning. Total protopor- seen (eg, polydipsia, polyuria, proteinuria, hema- phyrin levels were not considered an effective prog- turia), CaEDTA should be discontinued for a period nostic indicator of recovery. of five to seven days. Therapy can then resume if the Blood protoporphyrin levels that exceed 40 ppm are patient is stable. common following lead ingestion. CNS signs occur D- (PA) is an effective lead chelator with levels of 500 ppm. Protophyrin levels drop rap- that can be used orally (55 mg/kg twice daily). It has idly following chelation therapy. Instrumentation used been suggested that PA may increase the gastrointes- to measure protoporphyrin levels in humans must be tinal absorption of lead;30 however, more recent re- altered by removing the filters to compensate for the ports suggest that PA is a superior chelating agent to low levels of zinc protoporphyrin that occur in avian CaEDTA and does not increase absorption.35 Combin- 31,55 erythrocytes. Diagnostic results may be obtained ing CaEDTA and PA for several days until a bird is with one or two microhematocrit tubes of whole asymptomatic followed by the use of PA for three to blood.36 1038 SECTION FIVE DISEASE ETIOLOGIES

TABLE 37.5 Chelating Agents for Heavy Metal from lead poisoning by 35 to 50% when used in conjunction with CaEDTA in swans.6,35 This drug is CaEDTA Beryllium, copper, cerium, iron, zinc, lead experimental and requires a special FDA permit. The BAL () Arsenic, gold, mercury, copper, iron, nickel, experimental dose is 25 to 35 mg/kg BID orally for thorium, zinc, lead five days per week for three to five weeks. D-Penicillamine Copper, mercury, lead, zinc The administration of three to five appropriately six weeks may prove to be the best therapeutic re- sized pieces of grit may help in the removal of metal gime for lead poisoning. Birds should be monitored particles from the ventriculus by reducing their size27 for clinical signs of copper depletion including leth- and facilitating passage, particularly when used in argy, anemia and weight loss. conjunction with psyllium (hemicellulose).40

Dimercaprol (British Anti- - BAL) is the best Activated charcoal is recommended to bind small agent for removing lead from the CNS; however, this lead particles in the gastrointestinal tract and make agent is rarely used because of its low therapeutic them unavailable for absorption. The small animal index and the positive response of most birds to PA or dose for activated charcoal is 2 to 8 g/kg body CaEDTA. The recommended treatment regime is 2.5 weight.46 This should be gavaged as a slurry with mg/kg IM every four hours for two days, then twice water according to manufacturer’s instructions. Acti- daily for up to ten days or until clinical signs resolve vated charcoal will be inactivated if administered (Table 37.5).27 with mineral oil. Activated charcoal may be adminis- tered one to two hours before administration of a Lead-induced seizures can be controlled with diaze- . This allows sufficient time for free heavy pam at 0.5-1 mg/kg intramuscularly two to three metals to be bound to the charcoal before the system times daily as needed.36 The primary therapy for any is purged. heavy metal intoxication is to remove the source of the toxin from the body. Both surgical and nonsurgi- Endoscopic removal of heavy metal particles using cal approaches may be useful, depending on the cir- appropriate forceps30 or gastric lavage can be at- cumstances of an individual case. tempted in stable patients that are of sufficient size to tolerate this procedure.6 This technique is particu- Emollient (mineral oil or peanut butter) larly effective when metal fragments in the ventricu- can be administered to aid in the passage of small lus are too large to pass through the lower gastroin- particles of heavy metal out of the gastrointestinal testinal tract in a reasonable period of time. Lead tract. Other substances that have been used to aid in particles were removed from the gastrointestinal the passage of heavy metal particles include barium tract of swans by eight to twelve hours fol- sulfate, psyllium and corn oil. The comparative effec- lowed by the insertion of a 110 cm tube into the tiveness of these agents has not been determined. ventriculus. The birds were tilted head down at a 45° The use of sodium sulfate (Glauber’s salts) has also angle and warm water was pumped into the ventricu- 16 been recommended for the removal of lead. Addi- lus using a gastric lavage syringe.c The contents were tionally, this agent can be mixed with activated char- filtered through a towel to evaluate the number of coal and used following the ingestion of unknown particles removed. Radiographs of the head, neck toxins for its cathartic and absorptive effects. Sulfate and abdomen were used post-lavage to determine the will bind free lead in the gastrointestinal tract form- presence and location of any remaining lead parti- ing an insoluble lead sulfate that cannot be absorbed cles.6 Occasionally, a proventriculotomy may be nec- (mode of action similar to oral Ca EDTA and PA). essary if other attempts to remove metal particles fail Treated birds will generally develop diarrhea, and (see Chapter 41).56,72 patients must be carefully monitored to prevent de- hydration and severe electrolyte imbalances.16 The sodium sulfate is given as a slurry for up to two doses Zinc (Zn) (in large birds) or until lead is gone from the gut. Zinc is another frequently encountered heavy metal Aluminum sulfate is very irritating to the kidneys and that causes toxicity when ingested by birds. Zinc is not recommended. Magnesium sulfate is not recom- toxicosis should be included in the differential list 16 mended as the released magnesium is depressing. when heavy metal intoxication is suspected. Galva- An experimental chelating agent, dimercapto suc- nized wire and the clips used to construct enclosures cinic acid (DMSA) has been found to improve survival are common sources of zinc. The clinical syndrome 1039 CHAPTER 37 TOXINS

described in birds that ingest zinc from a wire enclo- sample collected from a clinically normal bird of the sure is frequently referred to as “new wire disease.”40 same species and handled identically will assist with The brighter and shinier the wire, the higher the zinc interpreting results. In general, blood zinc levels of level.21 The occurrence of “new wire disease” can be greater than 200 µg/dl (2 ppm) are considered diag- reduced (but not eliminated) by scrubbing the wire nostic for zinc toxicosis.40 In a group of normal cocka- with a brush and mild acidic solution (vinegar).50 tiels, the mean blood zinc level was found to be 163 Galvanized wire may also contain lead.40 Some gal- µg/dl (1.63 ppm). The pancreas proved to be the best vanized coatings contain 99.9% zinc while others are tissue for postmortem zinc level determination. Be- 98% zinc and 1% lead. The white rust associated with fore exposure, the mean pancreatic zinc levels were the galvanized coating is also toxic.21 Galvanized 26.11 µg/g dry weight. The level in zinc-intoxicated containers and dishes are other sources of zinc con- birds ranged from 312.4 µg/g to 2418 µg/g. tamination.27 Pennies minted in the USA since 1982 contain from 96% to 98% zinc that is coated with Calcium EDTA is recommended as an effective copper.1,29,30,40 Monopoly game pieces are made of chelating agent.27,30,40,52 D-penicillamine is also use- 98% zinc.1 ful. Radiographically and clinically, zinc toxicosis cannot be differentiated from lead intoxication. For- A duck from a zoological collection developed an tunately, the therapy is the same for poisonings acute onset of weakness and depression and died caused by either of these . The primary during examination. On necropsy, the ventriculus treatment involves removal of the foreign body. If a contained five tightly stacked, well eroded pennies. bird has ingested galvanized wire, this zinc-coated Some were minted after 1982. Pennies thrown into ferrous metal can be removed using a powerful neo- the duck’s pond by park visitors were the source of dymium-ferro-barium alloy magnet attached to a intoxication. small diameter catheter with a removable, flexible steel grid wire (see Figure 19.13).32 Common signs reported in zinc-intoxicated birds in- clude polyuria, polydipsia, gastrointestinal prob- Fluoroscopy-guided removal is ideal; however, parti- lems, weight loss, weakness, anemia, cyanosis, hy- cles can also be removed by repeatedly passing the perglycemia and seizures.28,30,50,68 Systemic effects apparatus into the ventriculus until no further metal are related to hypoproteinemia-induced damage in particles are removed. The success of the removal the kidneys, gastrointestinal system and pancreas.52 process can be determined with radiographs (Figure There are two cases of zinc depressing fertility, one in 37.4).32 Often, zinc foreign bodies can be removed a male Mallard15 and one in a female Black Bus- with bulk cathartics (sodium sulfate), activated char- tard.30 coal or mineral oil as described for lead. Gastroscopic removal using blunt-jawed forceps has been de- Cockatiels fed the zinc coating from galvanized wire, scribed.32,40 Surgical removal may be necessary if the or white rust from the same wire, developed clinical object cannot be removed with other methods. It may signs that included lethargy, weight loss, greenish be necessary to monitor packed cell volumes peri- diarrhea, ataxia, recumbency and death. This was odically if the bird is anemic. the most common presentation in acute cases. A more chronic clinical course was characterized by intermit- Copper (Cu) tent lethargy, dysphagia and depression. Gross ne- Factors that have been shown to affect the toxicity of cropsy findings were limited to ileus. Histopathologic copper in mammals include dietary zinc and molyb- changes included focal mononuclear degeneration in denum concentrations.46 There are wide differences the liver, and pancreas.21 in how various animal species maintain copper he- mostasis in the body, and birds appear to tolerate Serum concentrations of zinc can be used to confirm higher levels of copper than many mammals. Some a diagnosis. Samples must be properly collected and reports have suggested that water contaminated stored to avoid extraneous contamination. Only glass with antifouling paints can be a source of copper or all-plastic syringes and tubes should be used for intoxication in waterfowl.39 Other sources of copper samples intended for zinc analysis. Rubber stoppers include copper wire, chronic over-supplementation in on serum tubes and the grommets on most plastic the diet, pennies minted before 1982 or any copper- syringes can be a source of zinc contamination.37 coated objects small enough to be ingested. In a warm Serum tubes with royal blue-colored stoppers are climate, copper sulfate used to control algae on a free of zinc and are best for sample handling. A serum 1040 SECTION FIVE DISEASE ETIOLOGIES

FIG 37.4 An adult as presented with an acute onset of depression and regurgitation three days after a lead sinker was placed in the bird’s enclosure as a toy. The metal in the crop, esophagus and proventriculus was removed either by endoscopy or gastric lavage. The bird was given oral D-penicillamine and a bulk laxative (psyllium). Response to therapy was excellent.

pond accumulated over time and caused the intoxica- accumulate mercury, which is then further concen- tion and death of swans. trated in fish-eating birds. An Amazon parrot that consumed the back of a mirror died following a period Clinical abnormalities associated with copper intoxi- of profuse hematuria.34 BAL (and presumably cation have rarely been reported in birds. There have DMSA) and D-penicillamine chelate mercury. been reports of Mute Swans tolerating liver copper residues of up to 1000 mg/kg.13 A Mute Swan with Arsenic (Ar) inanition, anemia and generalized weakness showed Polyuria, polydipsia, feather picking, pruritus, signs of toxicity with liver copper levels in excess of weight loss, dyspnea (air sacculitis), egg binding, 3000 mg/kg and over 50 mg/kg copper in the kid- poor feathering and death occurred in a group of neys.13 Evidence of intravascular hemolysis (which is aviary birds, presumably secondary to the consump- described in mammals) has not been documented in tion of arsenic-contaminated mineral block. Ne- waterfowl.13,39 Postmortem findings following copper cropsy findings included cystic ovaries and adrenal intoxication include anemia and coal-black discolora- gland enlargement. Clinical changes started when a tion of the liver (see Color 20).39 new group of mineral blocks was used in the aviary. These blocks were found to contain 0.5% arsenic, and D-penicillamine increases the renal excretion of cop- all clinical problems in the birds resolved when the per and is the chelating agent of choice for copper mineral blocks were removed.67 toxicosis in mammals. In mammals, a dose of 52 mg/kg/day for six days has been recommended.46 Oil High-quality nutritional support is necessary to pre- Crude oil is extremely toxic, and quantities of 0.3 µl vent chelation and removal of other vital minerals. placed on the outside of eggs caused death in 50% of Supportive care with fluids, warmth and minimal embryos; the embryos that survived had malforma- stress may aid in recovery. In severely anemic birds, tions of the eye, brain and . Generalized edema, blood transfusions may be necessary. In advanced hepatic necrosis, cardiomegaly and splenomegaly cases the prognosis is poor. were noted also.45 Mercury (Hg) is becoming an environmental concern as levels in water continue to rise. Fish 1041 CHAPTER 37 TOXINS

TABLE 37.6 Poisonous Plant Cases Documented in Birds

Avocado Psittaciformes (C,E) Black Locust Budgerigars (E) Clematis Budgerigars (E) Diffenbachia Canaries (E) Foxglove Canaries (E) Lily of the Valley Pigeons (C,E) Lupine Canaries (E) Crown Vetch Budgerigars, cockatiels, (C) Oleander Budgerigars, canaries (E) Parsley Ostriches (C), ducks (E) Philodendron Budgerigars (E) Poinsettia Budgerigars (E) Rhododendron Budgerigars (E) Virginia Creeper Budgerigars (E) Yew Pheasants (C), canaries (E)

C = clinical report; E = experimental FIG 37.5 The pelletized fertilizers found on the surface of the soil in many house plants are more of a threat to companion birds than The state of an animal’s health should be expected to have an impact on its the houseplant itself. These encapsulated products contain high response to ingested plants. The experimental doses used to demonstrate that levels of nitrates that can be rapidly fatal (courtesy of Genevieve some of these plants were toxic are not likely to occur in natural settings. Dumonceaux).

distribution in the wild.42 It has been proposed that Selenium parrots can consume toxic plants because they care- A shampoo containing selenium sulfide caused fully remove the outer covering, which frequently the death of a budgerigar.19 contains the highest concentration of toxins. Alterna- tively, it has been suggested that the consumption of Nitrates clay by free-ranging birds may serve to absorb some Nitrates are common components of fertilizers and toxic materials and prevent them from passing may cause polydipsia, dyspnea, cyanosis and death through the gastrointestinal mucosa. However, following ingestion. The pelletized form of nitrate- many birds consume potentially toxic plants and only containing fertilizers are particularly hazardous be- macaws have been observed consuming clay. It is cause they resemble seeds and may be readily con- more likely that the ingested plant material is elimi- sumed by birds (Figure 37.5).19 nated before dangerous levels of the toxic component can be systemically absorbed.12 The Cedar Waxwing Plants and the House Finch can safely consume fruit from Clients are frequently concerned when a bird con- the pepper tree (Capsicum annuum) that is toxic to sumes a houseplant; however, plant intoxications are mammals.43 rare (Table 37.6). Free-flying companion birds fre- quently encounter and consume a variety of plants In one study, yew, oleander, Virginia creeper, black found in the home, few of which are at all toxic, some locust, clematis and avocado59 were described as toxic of which are thought to be toxic and some of which to budgerigars when administered by gavage. Many are of unknown toxicity. Determining the amount of other plants that were tested had no harmful effects plant ingested is always difficult, because birds seem under the same testing conditions. In another study, to enjoy shredding leaves more than ingesting them. oleander, lily of the valley, rhododendron, poinsettia There have been few documented cases of plant poi- and philodendron were not found to be major health sonings in birds, and their rapid gastrointestinal hazards for budgerigars.12 transit time is thought to play a role in the low incidence of intoxication. In a similar study involving canaries, oleander, lu- pine, foxglove, yew leaves and diffenbachia were con- The ability of parrots to consume plants and fruits sidered to be highly toxic. Nine other plants that that are deleterious to other animals may have al- have traditionally been considered toxic (parsley, lowed these birds to reach their current widespread hoya [wax plant], rhododendron, black locust, wis- 1042 SECTION FIVE DISEASE ETIOLOGIES

teria, clematis, cherry, pyracintha [fire thorn] and privet) caused no, or only transient, clinical prob- lems. Most canaries that died did so within minutes to hours following the ingestion of the plants.2

Split-leaf philodendrons have been used in some avi- aries in for years with no signs of toxicity. However, in one case, two Amazon parrots that de- stroyed a large split-leaf philodendron had a two- hour course of lethargy and vomiting followed by complete, unsupported recovery.

Cherries, plums and peaches (Prunus spp.) have pits containing seeds that produce cyanogenic glycosides; however, there are no reports of poisoning in birds following the ingestion of these fruits. It has been suggested that may be more common in ruminants because of a rapid enzymatic degradation of the glycoside to free cyanide. Alter- nately, may be more effective in sim- ple-stomached animals.12

Avocados (Persea spp.) have recently been suggested as toxic for companion birds. At one time it was believed that only the pit was a danger; however, some studies suggest that all parts of the avocado, FIG 37.6 Crown Vetch ingestion has been associated with tremors, including the fruit, are toxic to birds.5,18 The toxin in opisthotonos, seizures and death in budgerigars, cockatiels and the avocado has not been described.5 There are sev- lovebirds (courtesy of Michael Lutz). eral varieties of avocados commercially available (eg, Guatemalan, Mexican, Nabal and Fuerte), which ap- mild diuretic may be indicated. Birds have been re- pear to differ in their . In one study ported to die as soon as 9 to 15 hours after consuming involving rabbits, the Guatemalan and Nabal varie- avocado. Some birds died within 10 to 15 minutes ties caused death from pulmonary congestion within after developing signs of respiratory distress without 5 24 hours after ingestion. The Mexican variety was prior clinical signs.18 nontoxic.5 Budgerigars, cockatiels and lovebirds developed Signs of avocado toxicity (Guatemalan and Fuerte tremors, opisthotonus and seizures twelve hours af- varieties) in budgerigars and canaries include cessa- ter consuming crown vetch (Figure 37.6). Eighty per- tion of perching, anorexia, fluffed feathers, increased cent of the birds with clinical signs died despite respiratory rate, outstretched wings and death. At treatment. Deaths in the flocks reached 10% until necropsy, intoxicated birds are in good overall condi- the plant was removed, and no further losses were tion, and the crop and ventriculus may be full of reported.33 The inciting toxin was not confirmed, but ingesta, indicating the acute nature of the toxicity. may be a cyanide. Subcutaneous edema of the pectoral region has been reported in some affected birds, and others will have Oak toxicosis (coast live oak - Quercus agrifola) was pectoral muscles that bulge slightly above the ster- confirmed in a cassowary that consumed the leaves. num with mild pale streaks running parallel to the Clinical changes included anorexia, ataxia, diarrhea, muscle fibers. Histologic lesions have been limited to severe polydipsia and death. Necropsy revealed dif- generalized congestion, especially in the .18 fuse serosal hyperemia, ulcers and hemorrhage in the small intestine. Liver tissue and gastric contents To the authors’ knowledge, a specific treatment regi- tested for tannins showed levels of 178 and 340 ppm men for avocado intoxication in birds has not been respectively, which supported the diagnosis of oak established. Based on clinical signs and postmortem toxicosis.23 findings, activated charcoal and general supportive measures such as oxygen, warmth and perhaps a 1043 CHAPTER 37 TOXINS

Rape seed has been suggested as a hepatotoxin; how- There are no specific for mycotoxicoses. It ever, canary breeders routinely feed soaked rape seed is easier to prevent exposure to mycotoxins than to to breeding canaries and their offspring without a attempt treatment following their ingestion. All problem. Parsley has been shown to cause photosen- foods and seeds available to birds should be clean and sitization and skin lesions in ostriches and experi- fresh. Foods that are dusty, damaged by insects or mentally in ducks.44 have molds present should not be offered to birds. Particular caution should be exercised with poor quality corn and peanuts, as these are common Mycotoxins sources of toxin-producing molds. Some high-quality Mycotoxins are chemical metabolites produced by formulated diets are certified free of mycotoxins. various species of fungi that grow on grains and Treatment involves providing clean food free of foodstuffs. Each fungus has its own light, tempera- molds, supportive care, broad-spectrum antibiotics ture and moisture requirements.74 Some of these and specific for clinical signs. fungi grow on crops in the field during periods of high moisture content (Fusarium spp.). Others grow on There are four main mycotoxins of concern to birds: foods during storage, when moisture contents are aflatoxin B1, ochratoxin A, deoxynivalenol (vomi- relatively low (Aspergillus spp.). Aflatoxin produc- toxin) and the trichothecenes, especially T2 toxin. tion can be decreased by storing food in a low-oxygen, These are all potent mycotoxins that affect different body organs or systems. The molds producing these high-CO2 environment. In areas of the southern United States, where the preferred conditions for toxins can grow on various foods, including grains, aflatoxin production are common (25-30°C, humidity peanuts and peanut products, breads, meats, cheeses 85%), refrigeration of food is often necessary to pre- and cereal grains. Whole kernel peanuts of appar- vent aflatoxin production. ently good quality can harbor high concentrations of aflatoxins.74 Brazil nuts are banned in Austria be- The conditions that induce a fungus to produce toxins cause a -free nut was not available (Ho- may be different than those needed for fungal chleithner M, unpublished). Diagnosis is based on growth; therefore, the fungus can grow without toxin clinical signs, postmortem and histopathologic find- production. Likewise, the toxin can be present after ings, and detecting high quantities of the toxin in the the fungus has stopped reproducing. Clinically, this gastrointestinal contents or the food. However, it is means that the presence of a fungus on a foodstuff difficult to establish a diagnosis of mycotoxicosis in does not necessarily indicate that a toxin is present, birds. Clinical and histologic changes usually mimic nor does its absence mean that food or grain is free of other diseases or may be due to secondary infections. mycotoxins. Often, by the time signs are apparent, the toxin-con- taminated food source has already been consumed The amount of toxin present can vary within any and is not available for evaluation. given batch of grain or feed. Depending on the stor- age methods and size of the stored sample, one area Aflatoxin B1 is a known hepatotoxin. It is produced may have no detectable mycotoxin, while another by Aspergillus spp. and may cause depression, poor may have a very large concentration (known as a “hot growth, anorexia and other signs related to liver spot”). Attempts to determine if mycotoxins are pre- disease. Postmortem changes include an enlarged, sent using light are of little value, because pale liver (probably the result of fatty infiltration), an both false-positive and false-negative results are enlarged spleen, an enlarged pancreas, atrophy of common. the cloacal bursa and less-than-normal body fat de- posits (see Color 20).61 Toxins can enter an avian host through surface-to- skin contact. The effects of mycotoxin exposure can Aflatoxins inhibit protein and nucleic acid synthesis. vary based on the type of toxin and on the species, Microscopic examination shows hepatic cell degen- nutritional state and physiologic status of the pa- eration and bile duct hyperplasia. The kidneys may tient. A stressed bird or one on a poor diet is more have swollen proximal convoluted tubules.41 Antico- likely to be poisoned by a lower dose of mycotoxin agulant activity is altered, and a bird with a pro- than is a healthy, well-fed bird. Ducklings have been longed whole blood clotting time and prothrombin shown to be much more sensitive to aflatoxin than time may be suffering from aflatoxicosis. Gastroin- chicks, indicating species variance in sensitivity.41 testinal hemorrhage is also common. Immunosup- pression through a reduction in alpha and beta 1044 SECTION FIVE DISEASE ETIOLOGIES

globulins has also been linked to afla- toxin exposure. Serum electrophore- sis to detect this IgG pattern may be useful in diagnosing aflatoxicosis.

The trichothecenes, including T2 toxin, are produced by Fusarium spp., which commonly grow on crops in the field. This toxin has corrosive effects on the mucous membranes of the oropharynx, and occasionally the gastrointestinal tract, causing ne- crotic lesions of the hard palate and other oral areas. Lesions can appear within 48 hours of ingestion.58 Trichothecene intoxication in Sand- hill Cranes caused signs including flaccid paralysis of the wing and neck, depression and flying with the head and neck perpendicular (in those birds that could fly). These birds were exposed to waste peanuts FIG 37.7 Birds should not be allowed to consume high-salt foods, chocolate in any form or that contained high levels of tricho- alcoholic beverages (courtesy of Genevieve Dumonceaux). thecenes.71 Peanut farmers are en- couraged to plow ground containing Ethylene Glycol waste peanuts to prevent their consumption by free- ranging birds, particularly Sandhill Cranes. Free-ranging birds may consume ethylene glycol. In gallinaceous birds, consumption of antifreeze has

Trichothecene T2 toxin may also cause contact der- been associated with lethargy, ataxia and polyuria. matitis (from contaminated litter), poor growth and Characteristic calcium oxalate crystals form in the feathering, constrictive lesions of the digits (dry gan- kidneys.28 grene) and occasionally neurologic disorders.71,73 In one study, a high incidence of T2 toxin was reported Harmful Foods in grains heavily damaged by insects.4 Clients frequently share favorite foods with their Histopathology of affected birds may reveal conges- companion birds; however, some of these treats can tion and hyperemia of the gastrointestinal tract, be life-threatening through a single or chronic expo- hemorrhagic myositis, hepatic and renal swelling sure. Chocolate is contraindicated as a treat for any and congestion.71 In chronic cases, evidence of secon- , including birds. Consumption of small quanti- dary infections may be noted. ties of chocolate can result in hyperactivity, vomiting, diarrhea, cardiac arrhythmias, seizures, dark-col- Ochratoxin is produced by species of Aspergillus and ored feces and death. The progression of these effects Penicillium fungi. The toxin has an immunosuppres- can be rapid when large concentrations of the active sive effect and has been associated with air sacculi- ingredients (theophylline and caffeine) are ingested. tis, , CNS signs, hepatotoxicity and A rule of thumb for chocolate toxicity is that the less bone marrow suppression. It has been shown to sugar that is present, the more of the toxic active cause depression of the immunoglobulin-containing ingredients there are in the product. It is best to cells in the lymphoid organs.9 Clinical changes are avoid feeding any type of chocolate to birds (Figure commonly related to secondary infections that take 37.7). Treatment for chocolate toxicosis includes the advantage of a depressed immune system. administration of gastrointestinal protectants and cathartics.

Excessive consumption of sodium chloride can cause polydipsia, polyuria, depression, neurologic excite- 1045 CHAPTER 37 TOXINS ment, tremors, opisthotonos, ataxia and death. Ne- as a herbicide, and there have been some discussions cropsy changes are generally limited to cerebral that it may cause reproductive abnormalities in . edema and hemorrhage.28

Consumption of alcoholic beverages can lead to se- Anthelmintics vere ataxia and death. Additionally, birds may be- Ivermectin in a PG base may cause toxic reactions come intoxicated if compounds containing high levels when administered IM to budgerigars. Oral or topi- of ethanol (STA) are used to clean open wounds. cal administration is safer and equally efficacious. Ivermectin that is diluted in PG and allowed to stand should be mixed thoroughly before administration. Oral administration of a product that was not shaken caused seizures in several canaries and budgerigars. Iatrogenic Intoxications High-dose steroids reversed the clinical signs in these cases. Ivermectin persists in the environment and is excreted unchanged in the urine. Low concen- trations that accumulate in water are extremely Properly administered medications can be life-sav- toxic to crustaceans, and whales may be particularly ing; however, many drugs have a low therapeutic sensitive to this drug. index, and the safest of drugs may be toxic in excess quantities. Pre-existing systemic disease, nutritional Dimetridazole was shown to have a low therapeutic status, state of hydration, drug interactions, carrier index when added to the drinking water of cockatiel agents and species-specific idiosyncracies of a par- chicks. In nestlings (one to eight days old), the recom- ticular therapeutic agent should all be considered mended concentration of 0.1% dimetridazole in the before initiating drug therapy (see Chapter 18). The drinking water caused signs of toxicity including most common cause of iatrogenic drug toxicosis is a weakness, depressed growth rates, tremors and failure to base the dose on an accurate weight. A death. Older nestlings (over eight days old) showed dosing tabled that can be used to quickly and accu- no signs of toxicity at 0.1% concentrations. rately determine drug dosages is commercially avail- able. At 0.5% dimetridazole, older birds developed signs of ataxia, weakness, inactivity, tremors, extensor rigid- There are only a few therapeutic agents approved for ity of the legs and necks, and death. Consistent use in birds; however, many drugs approved for other necropsy findings included multiple hemorrhages, species can be beneficial in the treatment of sick and pale and enlarged, pale kidneys. Treatment of injured avian patients. Administering drugs at the adult cockatiels at the recommended dose appears to proper dose, at an appropriate time interval, through be safe. Dimetridazole should not be used in the a recommended route of administration and with drinking water during the breeding season when consideration for patient-specific contraindications males may consume excess quantities of the drug will minimize the potential for iatrogenic intoxica- and feed it to nestlings, causing toxicosis and death.60 tions. Vetisulid and some other sulfa-containing antibiotics Some drugs given parenterally at the appropriate have been reported to cause hypersensitivity reac- dosage (especially IM) can cause various degrees of tions leading to a hemorrhagic syndrome in gallina- local tissue damage (see Figure 17.4). Many of these ceous birds.17 They may also interfere with renal reactions can be attributed to the carrier in the for- tubular excretion and are contraindicated in dehy- mulation. Injectable products that contain propylene drated or uricemic patients.10 These antimicrobial glycol (PG) or oil as a carrier may cause an abscess or agents should be limited in use to sensitive bacteria toxic reaction. Oral consumption of propylene glycol and the treatment of coccidiosis.17 has not been reported to cause acute signs of toxicity, but the long-term effects of PG used as a food pre- Levamisole hydrochloride (oral) and levamisole servative have not been studied in birds. In , phosphate (injectable) have been used to treat intes- ingestion of PG can cause anemia. Ethoxyquin is tinal parasites in birds. Side effects associated with another food preservative that may have unreported these agents in Psittaciformes and Galliformes in- toxic side effects. This compound was originally used clude regurgitation, ataxia, recumbency, catatonia, dyspnea and death. Effects are immediate, and sur- 1046 SECTION FIVE DISEASE ETIOLOGIES

viving birds are clinically normal within one hour cause clinically recognizable joint abnormalities in a after administration. The dosage range used to study group of psittacine birds from a large aviary.3,26 toxic effects in birds was 22-100 mg/kg. A dose rate of 22 mg/kg was considered effective for some parasites Chloramphenicol, penicillin, tetracycline, and was well tolerated by many genera of aviary oxytetracycline and sulfa drugs may cause deform- birds.54 Regurgitation is the most common side effect ities in embyos and should not be used in hens near associated with oral levamisole administration, and or during the breeding season.45 food and water should be withheld for several hours prior to dosing. Antifungals The parasiticides praziquantel and fenbendazole Antifungal agents can have serious side effects, par- have been reported to cause problems in finches and ticularly with prolonged use. Amphotericin B has pigeons ranging from feather malformations to vom- been associated with acidosis, azotemia, vomiting, iting and death. seizures, , hepatic dysfunction, anemia, and nephrotoxicosis.48 Flucytosine may Antibiotics cause bone marrow depression, anemia, thrombocy- topenia and leukopenia. Decreased renal function Aminoglycosides have a narrow therapeutic index may precipitate gastrointestinal signs and elevate and are nephrotoxic. Gentamicin causes severe renal liver enzymes.48 Amphotericin B used as a sinus flush tubular necrosis and is the most frequently discussed caused a severe granulomatous reaction in an Afri- member of the group. Systemic, topical and ophthal- can resulting in death.66 The toxic side mic canine products can cause nephritis and are effects of these drugs should be considered when generally contraindicated in all companion birds. treating a bird for a fungal infection, and these Amikacin is a safer alternative when an aminogly- agents should be used only when specifically indi- coside is indicated. Renal function should be moni- cated. tored during treatment. Administration of aminogly- cosides into the leg is generally avoided due to the renal portal system of birds. It is speculated that drug administration in the leg muscles may cause Increased awareness of the nutritional needs of birds excessive renal concentrations of the aminoglycoside, and the availability of formulated diets and numer- increasing the potential for nephrotoxicosis. If an ous dietary supplements have created problems as- intoxication is suspected, the antibiotic should be sociated with the consumption of toxic levels of some discontinued and diuresis with physiologic saline nutrients. Of particular concern are vitamins A, D3 should be initiated immediately. (cholecalciferol) and calcium. Many formulated diets contain excess quantities of these nutrients, and fur- Tetracyclines, cephalosporins (especially cephalorid- ther supplementation of these diets with vitamin and 48 ine) and amphotericin B may also cause nephrotoxi- mineral products can result in life-threatening tox- cosis in patients with impaired renal function. icities.

Procaine penicillins have been associated with some can cause osteodystrophy char- toxic reactions in birds (see Chapter 18). A South acterized by thickening of the proliferative-matura- American Black-collared Hawk experienced vomit- tion zone, metaphyseal sclerosis, hyperosteoidosis ing and acute collapse following an intramuscular and decreased numbers of . Parathyroid 48 injection; however, this class of antibiotics is still gland hyperplasia can also occur (see Color 14).63 considered effective and indicated in many bacterial Hypervitaminosis D3 can cause mineralization of infections. Vomiting may be noted following the IM parenchymal organs including the liver, kidneys, or oral administration of doxycycline. stomach, intestines, heart and blood vessels.64 High The popularity of enrofloxacin has been increasing in levels of vitamin D3 cause an increase in serum cal- avian medicine because of its broad spectrum of ac- cium levels, which may affect cardiac conduction and 8 tivity and its good tissue penetration. Abnormalities smooth muscle contractions. Renal calcification in in articular cartilage have been reported in squabs macaws and African Grey Parrots suggests that they dosed at 800 ppm. Only one chick was affected at a may be particularly sensitive to hypervitaminosis D 64 dose of 200 ppm. Enrofloxacin was not shown to and excess calcium consumption. Excessive calcium 1047 CHAPTER 37 TOXINS

can lead to skeletal abnormalities, especially in de- include somnolence, dyspnea, wheezing, incoordina- veloping chicks (see Chapter 3). tion, weakness, respiratory distress and terminal convulsions.69,70 Death usually occurs too rapidly for A thorough dietary history must be included in the treatment to be initiated. general history of any patient presented for evalu- ation. Vitamin injections are often used in debilitated Hemorrhage and congestion of the lungs are the birds. If the patient has been on a formulated diet or usual postmortem findings (see Color 22).69,70 These over-supplemented previously, parenteral admini- lesions are thought to be caused by exposure of the stration of a preparation may cause or respiratory epithelium to inhaled acidic gases.70 Oc- exacerbate a vitamin intoxication problem. casionally, PTFE particles may be recognized his- tologically in some sections. The formulation of the injectable supplement used is important. Injacom 100 is the injectable vitamin sup- With minimal exposure, birds may respond to imme- plement recommended for use in birds. It is water- diate transfer to fresh air, coupled with the admini- soluble and contains 100,000 IU and stration of intratracheal and systemic steroids,

10,000 IU vitamin D3 per milliliter. Regular Injacom broad-spectrum antibiotics, fluids and a warm envi- is an oil-based product containing five times as much ronment to prevent shock, pulmonary edema and

vitamin A and 7.5 times as much Vitamin D3, which bronchopneumonia. increases the potential for toxicosis when adminis- tered to birds. Tobacco Products Birds should never be allowed to consume tobacco products. Ingestion of small quantities of nicotine can cause hyperexcitability, vomiting, diarrhea, sei- Airborne Toxins zures and rapid death. Treatment is supportive and symptomatic.

Passive inhalation of cigarette, cigar and pipe smoke The avian respiratory system is more efficient than can cause chronic ocular, dermatologic and respira- that of mammals. The disadvantage to this efficient tory disease in companion birds (see Chapter 22). system is that it readily extracts harmful gases and Birds that live in homes with smokers will often particles from inhaled air, increasing a bird’s sensi- present with clinical signs including coughing, sneez- tivity to inspired toxins. Administering 100% oxygen ing, sinusitis and conjunctivitis due to continuous to birds for more than 12 hours was found to be fatal irritation of the respiratory system. The clinical with death occuring in four to eight days; exposed signs may resolve without treatment if no secondary birds appeared stressed and uncomfortable as early infectious agents are involved, the clients stop smok- as three days post-exposure.62 ing or the bird is placed in a location where there is no smoke. Secondary bacterial invasion of the dam- aged respiratory epithelium is common and requires Polytetrafluoroethylene Gas therapy; however, therapy for these infections will be Polytetrafluoroethylene (PTFE) gas, released when of little value if the bird is continuously exposed to various non-stick surfaces such as Teflon® overheat smoke. or burn, is a common respiratory toxin in birds. In order to keep pet birds healthy, they should be Potential sources of PTFE gas exposure include non- maintained in well-ventilated, smoke-free environ- stick cookware, drip pans, irons, ironing board cov- ments (Ritchie, BW unpublished). Exposure to secon- ers, the heating elements of some reverse-cycle heat dary smoke from marijuana can cause severe depres- pumps and heat lamps. As these surfaces are heated sion and regurgitation and should be strictly avoided. to above 530°F (280°C), they undergo pyrolysis and PTFE is degraded releasing irritant particles and Nicotine sulfate has been shown to cause severe acidic gases.69,70 skeletal malformation, reduced body weight, torticol- lis, edema, muscular dystrophy and malformation of The lungs are the target organ for PTFE poisoning in the beak, heart and kidneys.45 Pododermatitis has birds. Clinical signs are usually limited to sudden been observed in some birds handled by people who death, but depending on the degree of exposure may smoke routinely. Repeated exposure to the nicotine 1048 SECTION FIVE DISEASE ETIOLOGIES

cation of antibiotic creams and bandaging may be necessary in some cases. When ingestion of cleaning products or disinfectants occurs, the manufacturer’s recommendations for therapy should be followed. If recommendations are not available, then birds in- gesting non-caustic materials should be treated with a mild laxative to speed passage of the solution out of the body. Gentle gavaging or flushing is indicated if a corrosive material has been ingested to prevent perforation of the esophagus or crop.11 Corrosive ma- terials require immediate dilution with water. Eyes or skin areas exposed to corrosives must be rinsed with clean water for at least twenty minutes. Sys- temic poisoning must be treated symptomatically, as FIG 37.8 An adult Amazon parrot was presented with a ten-day history of progressive picking at the feet with scab formation. The there are no antidotes for disinfectant intoxications. bird was fed a formulated diet supplemented with some fresh vegetables. The feet were hyperemic and the feathers were dull Ammonia and bleach are frequently used in house- and appeared tattered, particularly at the ends. The bird had mild hold cleaning, and fumes from these products are epiphora and a serous nasal discharge. Both adult clients were commonly encountered by companion birds. Ammo- heavy smokers. The bird’s ocular, respiratory and foot problems resolved when the clients stopped in the house and nia can be absorbed into the circulation by inhala- washed their hands before handling the bird. tion. In some species, increased blood ammonia con- centrations have been shown to reduce lymphocyte function and alter their mitogenic activity resulting residues on the hands of smokers is thought to cause in a decreased cellular and humoral immune re- this local irritation (Figure 37.8). Macaws may suffer sponse. One study showed that blood ammonia con- a similar dermatitis on the bare cheek patches fol- centration in excess of 1 mg/dl was an indication of lowing repeated contact with a smoker’s hands. toxicity. Even subtoxic concentrations (<1 mg/dl) in Many birds with severe feather picking problems will birds can predispose them to infectious diseases (see resume normal preening behavior when removed Figure 5.3).24 from exposure to cigarette smoke (Ritchie, BW un- published). Ammonia and chlorine vapors can also irritate the epithelial linings of the eyes, conjunctiva, nares and Disinfectants respiratory tract. The resulting inflammation and damage can predispose these surfaces to secondary Disinfecting agents used to clean enclosures and food bacterial and fungal infections. Severe inflammation dishes should be used cautiously in aviaries and from exposure to strong concentrations of ammonia where companion birds are housed. Hatchlings and may impair respiration. Treatment consists of oxy- nestlings are especially prone to respiratory prob- gen therapy, steroids to reduce inflammation and lems associated with chronic exposure to disinfec- broad-spectrum antibiotics to combat secondary bac- tants or their fumes. A standard drain opener that terial infections. contains sodium hypochlorite produced fumes that killed a Goffin’s Cockatoo, African Grey Parrot and a cockatiel within minutes after a Clorox solution was Miscellaneous Aerosols also poured into the sink. Common household aerosol products such as per- fumes, deodorants and cleaning agents may cause Irritation and dermatitis may occur following contact respiratory problems in birds. These problems arise with many concentrated cleaning solutions (phenols, from direct irritation of the respiratory tract by the chlorhexidine and chlorine). All enclosures, nest fluorocarbons and particulates in these aerosols. The boxes or aviary tools that are placed in disinfectants most common effect is inflammation and edema of should be thoroughly rinsed with clean water before the respiratory tract leading to dyspnea. In severe they are in contact with a bird.11 cases, death may occur shortly after a large or direct Direct contact between the bird and cleaning solu- exposure. It is the authors’ recommendation that tions should be avoided. If contact occurs, the area aerosol sprays not be used in areas where companion should be rinsed copiously with sterile saline. Appli- birds may be directly exposed, and definitely not 1049 CHAPTER 37 TOXINS sprayed directly on the bird. Formaldehyde fumes Grossly, this bird’s lungs appeared necrotic, and un- have been associated with epiphora, dyspnea and encapsulated pyogranulomatous nodules that con- death in canaries (see Figure 5.3).19 An ozone gener- tained deposits of pale, amphophilic, refractory crys- ator caused the deaths of some birds in a pet shop. A talline material that displayed birefringence when cockatoo that was in the same room where a suede exposed to polarized light were seen histologically. protector was used developed dyspnea within two Similar toxicities have been described in a rhea, hours, and died five hours after being exposed to the ostrich, turaco, swan, owl, crane, duck, kiwi and fumes from this product. Ring-neck Pheasant.49

Leaks in natural gas lines may cause subtle respira- tory signs in birds, even when no odors are detected by the clients. With more serious leaks, sudden death can occur. When birds are presented with respiratory Insecticides problems or weakness of unknown etiology, careful questioning concerning the home environment may help determine if a leaking gas line could be a con- tributing factor. Kerosene fumes may also be toxic to Exposure to high concentrations of pesticides can birds, and combustible space heaters should not be lead to nonspecific signs of poisoning including gas- used in homes containing companion birds. trointestinal problems, tremors, weakness, dyspnea, seizures or sudden death. Chronic low-grade expo- Carbon monoxide (CO) is an odorless, colorless, sure to pesticides may induce more subtle clinical tasteless gas produced by combustion engines and signs that are more difficult to attribute to a toxin some furnaces. Birds maintained in poorly venti- exposure. These exposures may cause immunosup- lated, heated areas, or transported in poorly venti- pression and increased susceptibility to disease, de- lated vehicles (especially in car trunks) are at high creased reproductive activity or generalized un- risk of CO poisoning. Carbon monoxide competes thriftiness (Figure 37.9). with oxygen for hemoglobin binding sites in the blood. The affinity of hemoglobin for CO is about 250 The most commonly used household insecticides con- times greater than its affinity for oxygen in mam- tain pyrethrins, carbamates and organophosphates. mals. Binding of CO to hemoglobin decreases the While pyrethrins and carbamates are occasionally ability of oxygen to dissociate from hemoglobin, re- used as pesticides in association with birds, these sulting in hypoxia. Carbon monoxide poisoning can agents are nonetheless toxic, especially following in- occur when birds are placed in a confined area where halation or contact with high concentrations. Pesti- the gas cannot escape. cides may be absorbed through the skin following secondary contact with treated surfaces. Addition- Birds suffering from CO poisoning may die acutely ally, many insecticides contain carriers that can be and have bright red, apparently well oxygenated irritating to the skin and respiratory tract mucosa.11 blood and pink- or red-colored tissues. Other signs of Ingestion of foods contaminated with common agri- CO poisoning include depression, somnolence and culture pesticides could be a source of intoxication in dyspnea. birds. All grain products, fruits and vegetables that If CO poisoning is suspected, fresh air should be are not certified organic have levels of pesticides that provided immediately, and emergency care should have been determined to be acceptable (“safe” is a include the administration of 90 to 95% oxygen in a relative term) for human consumption. The effects of cool, dark, stress-free environment. Oxygen toxicosis constant exposure of birds to these toxins has not been determined. can occur if a bird is exposed to O2 levels of 90% to 100% for prolonged periods.62 If absolutely necessary, dusting powders containing Pulmonary silicosis caused chronic dyspnea and pyrethrins or carbamates (eg, 5% Sevin) can be used death in a Blue and Gold Macaw. The bird was with some margin of safety on birds.11 These com- exposed to the silicone through peat moss used as pounds are not absorbed through the skin and are nesting material. In humans, a silicone/sulfur ratio more likely to penetrate the feathers than sprays; of over 0.3 is considered indicative of silicosis. The however, excessive preening (ingestion) or inhalation ratio in this Blue and Gold Macaw was 9.07.49 of the dusts can lead to systemic intoxication that is dose-related. 1050 SECTION FIVE DISEASE ETIOLOGIES

FIG 37.9 A Scarlet Macaw that was housed ten feet from a cyclic (every 30 minutes) pyrethrin mister was presented for regurgitation and severe weight loss (590 g). Radiographs indicated ileus, microcardia and microhepatia. Note the gastric distension of an empty cranial gastrointestinal tract and a full crop. The bird did not respond to supportive care. A perforating proventricular ulcer and liver were demonstrated at necropsy (see Color 19).

Clients can minimize a bird’s exposure to insecticides chromatography can be used to determine tissue by providing clean water and residue-free foods. If concentrations of these compounds.47 fresh fruits and vegetables are provided, they should be thoroughly rinsed in clean water to remove any Organophosphates insecticides used by the grower. Care must be exer- cised when pesticides and other volatile chemicals Clinical signs of organophosphate toxicity are caused are used in and near a bird’s area. Any materials by inhibition of acetylcholinesterase. Organophos- used for perches should be thoroughly scrubbed and phate poisoning in raptors appears clinically differ- rinsed before being placed into the bird’s enclosure. ent than is typically described for mammals. Raptors are frequently contaminated by consuming poisoned Most potential contaminants are difficult to detect, starlings or grackles.47 Clinical signs include ataxia, and it is best to err on the side of caution. The effects spastic nictitans, a detached attitude, inability to fly of modern petro-chemicals on companion birds can and occasionally convulsions. If present, convulsions only be postulated using the statistics that suggest are characterized by rigid paralysis, tightly clinched their impact on the declining migratory bird popula- talons, rapid respiration, alivation, twitching of mus- tions in North and South America. cles and anascaria.

Organochlorines Scoliosis, lordosis (shortening or contortion of the axial skeleton) and severe edema were described in The use of some organochlorines (DDT and DDE) embryos exposed to parathion. Diazinon caused in- have been banned in the United States and other complete ossification and stunting. Carbaryl, countries, yet reports of poisoning in native species methomyl and permethrin were considered rela- persist.47 Migratory birds may be exposed in other tively nontoxic to embryos.45 countries that still use DDT produced in the United States. Poisoned birds may develop signs of convul- Dichlorvos (DDVP, Vapona) is a commonly used or- sions, blindness (pupils may or may not respond to ganophosphate that is impregnated in insect repel- light), ataxia, anemia and hypoproteinemia. Gas lant strips. It is best for birds not to be exposed to any inhaled toxins; however, if a dichlorvos insecticide 1051 CHAPTER 37 TOXINS

must be used, it should be placed in a well ventilated cases lung edema and hemorrhage may occur. A de- room of appropriate size. Direct oral exposure should finitive postmortem diagnosis can be made by tissue be avoided. Smaller species (eg, canaries, finches) are analysis of the liver, kidneys, body fat and gastroin- more sensitive to the vapors than budgeri- testinal contents for insecticide residues. Brain choli- gars and larger psittacine birds.11 In addition, higher nesterase activity can be used to determine if the ambient temperatures increase the risk of intoxica- bird’s death was due to an organophosphate intoxica- tion.11 Other sources of avian exposure to organo- tion; clinical analysis of tissues may not always be phosphates include flea collars, contaminated fruit reliable due to the rapid metabolism of these insecti- limbs and frequently treated baseboards. There have cides.38 Any tissues to be analyzed for insecticide been reports of birds being poisoned by consuming residues or acetylcholinesterase activity should be food that was stored in containers in which dichlor- submitted frozen in separate containers. vos strips had been placed to control insects. A mite protector (para-chlormetazymol) placed in a con- Treatment for organophosphate toxicosis includes tainer of finch seeds was thought to have caused the supportive care (supplemental heat, fluids and diaze- death of a finch. Seven of 15 canaries and finches died pam to control seizures). Atropine is indicated for when moth balls were enclosed in a container that cholinergic signs (0.2 to 0.5 mg/kg one-fourth dose IV 47,53 held their seed mix.23 The toxic ingredients in these or IM every three to four hours). Pralidoxime products are naphthalene and para-dichlorobenzene, hydrochloride (2-PAM) is antidotal for organophos- respectively. phate intoxications. 2-PAM was administered to King Pigeons with good results at 10 mg/kg IM.53 The Pyrethrins have perhaps the lowest degree of toxicity recommended range for mammals is 10 to 100 mg/kg. in birds and warm-blooded mammals. They are often Steroids may be beneficial for the treatment of pul- combined with the synergist piperonal butoxide to monary edema or shock. For maximum effectiveness, enhance insecticidal activity.11 antidotal therapy must be initiated within 24 hours of exposure. Organophosphates irreversibly bind to acetylcholinesterase. The more binding that is al- General Considerations lowed to occur, the less effective the will be. Birds suffering insecticide intoxication can manifest symptoms similar to those observed in mammals Carbamates including sudden anorexia, incoordination, weak- ness, ataxia, muscle tremors, diarrhea, convulsions, Carbamates’ mode of action, induced clinical signs respiratory difficulty and bradycardia.23,34,53 Sudden and methods of diagnosis and treatment are the death is usually due to respiratory failure from a same as for organophosphates, although 2-PAM is single high-dose exposure.38 Other less obvious signs contraindicated. Over 2,000,000 bird deaths are esti- of exposure include reductions in hatchability and mated to occur annually in the United States as a egg production. These clinical changes are more com- result of the granular carbamate, carbofuran.47 mon in breeding populations chronically exposed to pesticides.38 While taking a history, clients should Rodenticides always be questioned about their use of insecticides in and around (outside open windows) the home. Most rodenticides are of the anticoagulant variety. The first-generation products (warfarin) are less A tentative diagnosis of insecticide poisoning is usu- toxic and require longer periods of exposure than the ally possible with a history of recent exposure and newer generation products (brodifacoum). Clinical appropriate clinical signs. Whole blood acetylcholi- signs of toxicity include depression, anorexia, pete- nesterase activity can be used to confirm a diagnosis chiation, epistaxis and subcutaneous hemorrhage. of organophosphate intoxication. This test is fre- The antidote is vitamin K1. Some rodenticides con- quently available in human pediatric laboratories. A tain cholecalciferol or bromethalin and are poten- sample from an unexposed bird should be included to tially more difficult to treat than the anticoagulant serve as a control. In quail dusted with carbaryl, types. poisoning has been reported in plasma cholinesterase activities were depressed up quail and aviary birds when the poison is carried into 20 to 27% within six hours. the bird’s food or water by contaminated rodents. Secondary poisonings of raptors from consumption of There are usually no gross postmortem changes as- poisoned rodents (brodifacoum - Talon) have also sociated with insecticide poisoning, although in some been reported.19 1052 SECTION FIVE DISEASE ETIOLOGIES

Products Mentioned in Text a. Bardahl Super Spray, Bardahl, Durdrecht, The Netherlands b. Leadcheck kits or swabs, Hybrivet Systems, Inc., Framingham, MA c. Edlich Gastric Lavage Kit, Monoject, Sherwood Medical, St. Louis, MO d. Formulator,© Wingers Publishing, Inc, Lake Worth, FL

References and Suggested Reading

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