THE MERCK VETERINARY MANUAL
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Overview of Poisonings in Poultry

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Also see Toxicology Introduction et seq.

When toxicosis in a poultry flock is suspected based on mortality, on decreased production/growth, or on other clinical signs such as paralysis, the flock owner or veterinarian should maintain and allow access to historical records. These records include use of disinfectants and rodenticides and insecticides on the premises, medications administered in feed and water, and nutritional additives to the feed. Samples to be collected for potential analysis in cases of suspected toxicosis include dead or recently euthanized birds that showed clinical signs, 2 lb (1 kg) of the feed available when the birds were showing clinical signs, and 500 mL of drinking water. For the safety of workers as well as poultry, the grower should have access to material safety data sheets for each chemical used on the premises. Carcasses should be refrigerated as soon as possible for examination by the veterinarian or laboratory diagnostician. Consultation with a toxicologist or laboratory diagnostician before collecting samples is highly recommended.

Aflatoxicosis is one of the most common intoxications in modern poultry production systems. Certain species of Aspergillus and Penicillium can produce aflatoxins in feedstuffs. The production of aflatoxins can occur either in the field where the crops are grown or during storage. Acute aflatoxicosis is characterized by inappetence, ataxia, convulsions, opisthotonos, depression, and death. A gross lesion often seen with acute aflatoxicosis is an enlarged yellow liver. All poultry are susceptible to aflatoxicosis; however, ducks and turkeys are particularly sensitive.

Ammonia gas is produced by the metabolism of uric acid by bacteria that can thrive in wet poultry litter. High ammonia levels often occur during the winter when ventilation is minimized to conserve heat and thus high litter moisture is common. Increased ammonia levels of 25–30 ppm can damage the mucociliary apparatus of the upper respiratory tract, and higher levels (50–75 ppm) can cause decreased feed intake as well as caustic burns to the cornea, which can result in blindness. These birds will often fail to find adequate food and water, resulting in death.

Rodenticides can be safely applied to poultry houses so that rodent baits are sequestered from the flock; however, careless application can result in rodent bait consumption by poultry with usually acute toxic effects. First-generation anticoagulant rodenticides, including warfarin, chlorphacinone, diphacinone, and coumtetralyl, require continual ingestion by rodents to induce toxic effects. Second-generation or single-feed anticoagulants, including brodifacoum, bromadialone, difenacoum, and difethialone, can be acutely fatal to rodents. Clinical signs in poultry are related to the anticoagulant effects and usually observed as sudden death with gross hemorrhagic lesions in one or more body sites, particularly lung, intestine, and peritoneal cavity. These lesions can be confused with flight injury (gamebirds) and trauma from wild animals and dogs. Definitive diagnosis of anticoagulant toxicosis should be based on gross lesions, history of anticoagulant application, and anticoagulant screen on liver of dead birds (available at several USA veterinary diagnostic laboratories).

Clostridium botulinum bacteria produce several exotoxins that are among the most potent toxins known. In ducks and geese, botulism outbreaks commonly occur in the summer months in the vicinity of poorly aerated ponds and lakes. The waterfowl ingest the toxin by eating dead invertebrates from the margins of these lakes or eating maggots on the carcasses of ducks that have already succumbed to the intoxication. In pheasant and broiler flocks, where the timely removal of dead birds has not been practiced, carcasses can also become a source of toxin. The classic clinical sign of botulism intoxication in poultry is paralysis of the muscles of the neck or “limberneck.” The toxin also causes paralysis affecting the legs, wings, and eyelids. Diagnosis of botulism is often based on exclusion of other possible causes, although intestinal contents and blood can be collected for botulism toxin analysis (mouse inoculation assay), which is available at several USA diagnostic laboratories.

Excessive calcium intake in broiler chicks results in urolithiasis and visceral gout (hyperuricemia) with urate deposits on the abdominal viscera and in the joints. Tetanic convulsions can also be seen in chicks consuming excess calcium. Calcium levels >2% will induce these lesions in broilers. Feeding calcium in excess of 3% before the onset of egg production will induce the same lesions in egg-type or meat-type pullets.

This poisoning commonly arises from exhaust fumes when chicks are being transported by truck or from improper ventilation in hatchers. Mortality may be high unless fresh air is provided immediately. At necropsy, the beak and face are cyanotic, and a characteristic bright pink color is noted throughout the viscera, particularly the lungs. Diagnosis can be confirmed by a spectroscopic analysis of the blood.

Senna obtusifolia seeds are frequently found in corn and soybeans. When present at ≥2%, they reduce feed intake and lower body weight, increase feed conversion in broilers, and significantly depress egg production in laying birds. Necropsy lesions are absent.

Copper sulfate has been used as a water additive for treatment of crop mycosis (Candida overgrowth) or nonspecific digestive tract disorders in poultry. Copper sulfate in a single dose of >1 g is fatal. The signs are watery diarrhea and listlessness. A catarrhal gastroenteritis and burns or erosions in the lining of the gizzard, accompanied by a greenish, seromucous exudate throughout the intestinal tract, are found at necropsy.

Seeds of many species are toxic to chickens. Concentrations >0.05% in the feed produce signs of toxicosis. At 0.2%, weight gain is reduced markedly; 0.3% causes death in 18 days. Lesions consist of ascites, swelling or cirrhosis of the liver, and hemorrhages. Resistance to the toxin increases with age.

Diazinon is an organic phosphate and cholinesterase inhibitor commonly used for the control of a variety of insects around poultry houses. It should not be used inside poultry houses. Chickens will consume the diazinon crystals, which results in lacrimation, diarrhea, dyspnea, and death. Necropsy lesions include lung edema, fatty livers, and severe enteritis. The diazinon crystals might be seen in the crop and gizzard contents. Diagnosis can be confirmed by testing brain for cholinesterase activity.

Cottonseed meal contains appreciable amounts of gossypol, which produces severe cardiac edema that results in dyspnea, weakness, and anorexia. When fed to laying hens, gossypol also causes egg-yolk discoloration.

Lead poisoning usually is caused by paint or orchard-spray material. Metallic lead in amounts of 7.2 mg/kg body wt is lethal. Signs are depression, inappetence, emaciation, thirst, and weakness. Greenish droppings are commonly seen within 36 hr. As poisoning progresses, the wings may be extended downward. Young birds may die within 36 hr after ingestion. Acute lead poisoning may be diagnosed from the history and necropsy findings of a greenish brown gizzard mucosa, enteritis, and degeneration of the liver and kidney. Chronic poisoning results in emaciation and in atrophy of the liver and heart. The pericardium is distended with fluid, the gallbladder is thickened and enlarged, and urate deposits are usually found in the kidneys. Ingestion of lead shot often occurs in wild waterfowl on heavily gunned feeding grounds. Retention of only a few lead pellets in the gizzard can kill a duck.

Poisoning occurs from mercurial disinfectants and fungicides, including mercurous chloride (calomel) and bichloride of mercury (corrosive sublimate). Clinical findings are progressive weakness and incoordination. Diarrhea may occur, depending on the amount ingested. The caustic action of the chemical may produce gray areas in the mouth and esophagus, which usually ulcerate if the bird lives >24 hr. Catarrhal inflammation of the proventriculus and intestines may occur; if a large amount of mercury is ingested, extensive hemorrhage may occur in these organs. The kidneys are pale and studded with small, white foci. The liver shows fatty degeneration.

This chemical coccidiostat is used in broilers. It should not be fed to layers, because it can cause discoloration and reduced hatchability of eggs (although the effect is reversible once the nicarbazin is withdrawn). It also may result in reduced heat tolerance in birds exposed to high temperature and humidity.

This has been used to treat several bacterial diseases in poultry, but it is no longer approved for use in many countries, including the USA. When fed at 0.022%, it causes hyperexcitability manifest by rapid movements, loud squawking, and frequent falling forward. In turkeys, which are more sensitive to nitrofurazone than are chickens, it produces cardiac dilatation, ascites, and when fed at 0.033%, death.

When this compound, widely used in feed to improve weight gain and feed efficiency, is improperly mixed or fed at a level 2–3 times higher than normal, it induces a high-pitched chirp and a “duck-walking” stance. Ataxia, neck extension, and paralysis can occur in chickens and turkeys that consume excessive amounts. Clinical signs are usually reversible in a few minutes. Chronic exposure may produce intrahepatic cholangitis.

Residues have been reported in the fatty tissue of chickens and turkeys in excess of the 5 ppm permitted in edible tissue, and in egg products in excess of the permitted 0.5 ppm. PCBs depress egg production and hatchability, and levels of 50 ppm result in cirrhosis of the liver and ascites in broilers and a drop in egg production and hatchability in hens. (Also see Persistent Halogenated Aromatic Poisoning.)

Polyether ionophores facilitate transport of divalent cations across cell membranes to interfere with osmoregulation, resulting in cell rupture. Toxicosis causes by ionophores is relatively common in poultry, because these compounds are commonly administered for the prevention and treatment of coccidiosis and are subject to overdosing and mixing errors. Additionally, these ionophores can interact with certain medications, such as sulfonamides, to cause toxicosis signs when the ionophore concentration in the feed is normal. Examples of ionophores used in poultry are described below.

Lasalocid:

Lasalocid is an anticoccidial compound that has been used in hot summer months, because it increases water consumption. When used at other times of the year, the level of salt in the ration is reduced to prevent excessive water elimination and wet litter problems. If the salt level is reduced too much, it will result in stunting, increased lameness, and a characteristic clinical picture in broilers manifested by the bird walking on its toes. This clinical syndrome has been called lasalocid toxicity when, in reality, it is due to low levels of salt in the feed.

Monensin:

This ionophore coccidiostat is widely used in the broiler industry. At levels >120 ppm it reduces feed intake and weight gain; in layers, egg production is reduced. Signs of toxicity include a characteristic paralysis in which the legs are extended backward. If naive turkeys are switched to a feed that contains monensin, they become paralyzed with the legs extended backward and mortality occurs; no lesions are seen at necropsy.

Narasin:

This ionophore is often administered in combination with the chemical nicarbazone for to prevent coccidiosis in broilers but can be particularly toxic in turkeys (often noted on product label), resulting in flaccid paralysis of the wings and legs. Toxic effects have also been described in broilers simultaneously treated with tiamulin or sulfonamides.

Salinomycin:

Salinomycin is commonly used as an anticoccidial compound in the broiler industry. It is safe when used at 60 g/ton of feed. Toxicities occur when broiler feed containing salinomycin is accidentally fed to naive breeder hens. Clinical signs in these hen flocks include paralysis with the legs extended backward and decreased feed consumption, egg production, and hatchability. Levels of salinomycin >10 g/ton in breeder-hen feed are sufficient to produce these clinical signs. Necropsy lesions are absent in birds with this clinical picture.

PTFE is a synthetic fluoropolymer resin highly resistant to heat and chemically stable with low reactivity. PTFE has been used as nonstick coating for frying pans (Teflon®) and has been used to coat heat lamps and heater filaments that might be used in poultry houses. Although generally heat stable, PTFE heated above 280°C (536°F) can produce aerosolized hydrogen fluoride, carbon fluoride, carbon monoxide, and low-molecular-weight fluoropolymers. PTFE pyrolysis products can cause direct caustic damage to the lung, resulting in marked pulmonary edema and hemorrhage. Birds are often found dead with no premonitory signs. Diagnosis is based on gross lesions, history of using new heating lambs or filaments coated with PTFE, and excluding other possible causes of pulmonary hemorrhage.

Propane is commonly used in poultry facilities as a fuel source to provide heat for young poultry. Chicks are often surrounded by a cardboard brooder ring to provide a safe, warm environment during the first week of life. If a defective heater leaks propane into the brooder ring, the propane gas will displace the lighter air, resulting in asphyxiation of the chicks. On necropsy, these chicks have congested, edematous lungs that sink when placed in formalin.

Quaternary-ammonia-based compounds are widely used as disinfectants. (Also see Antiseptics and Disinfectants.) Turkeys are very sensitive; levels of 150 ppm result in substantial mortality. Clinical signs include reduced water intake, nasal and ocular discharge, facial swelling, and gasping. Necropsy lesions include caseous ulcers at the base of the tongue and commissures of the mouth.

Ingestion of feeds containing >5 ppm of selenium decreases the hatchability of eggs due to deformities of the embryos, which are unable to emerge from the shell because of beak anomalies. Eyes may be unilaterally hypoplastic or aplastic, and feet and wings may be deformed or underdeveloped. Selenium at 10 ppm, as in seleniferous grains in the laying ration, usually reduces hatchability to zero. Young laying hens entering egg production are more susceptible than older hens.

Mature birds seem to tolerate more selenium in their feed than do pigs, cattle, or horses and do not exhibit signs of poisoning other than poor hatchability of their eggs. Starting rations containing 8 ppm selenium have reduced the growth rate of chicks, but 4 ppm had no noticeable effect. Rations containing as little as 2.5 ppm have resulted in meat and eggs with concentrations of selenium in excess of the suggested tolerance limit in foods. Sodium arsenite and some of the organic arsenicals, when administered to laying hens with selenium, have increased hatchability.

The addition of 0.5% salt (NaCl) to the ration of chickens and turkeys is recommended, but amounts >2% are usually considered dangerous. Rations for chicks have contained as much as 8% without injurious effect, but in poults, rations containing 4% were harmful and levels of 6%–8% have resulted in mortality. The addition of 2% NaCl to the feed, or 4,000 ppm in the water, depresses growth in young ducks and lowers the fertility and hatchability of the eggs in breeding stock.

Salt levels high enough to produce poisoning may be reached when salty protein concentrates (eg, fish meal) are added to rations already fortified with salt or when the salt is poorly incorporated in the feed. Sporadic poisoning also has been reported from accidental ingestion of rock salt or salt provided for other livestock. Necropsy findings are not diagnostic; enteritis and ascites are common. Watery droppings and wet litter often are suggestive of a high salt intake. Edema of the testicle is pathognomonic of salt toxicity in young birds.

Sulfonamides are widely used for treatment of several bacterial and protozoal infections in poultry and are usually administered in drinking water. Sulfaquinoxaline, when fed at 0.25%, results in severe pancytopenia. Hemorrhages are common on the legs, breast muscle, and in virtually all abdominal organs. The bone marrow is pale, and the blood is slow to clot. Toxicity is frequently seen in hot weather when sulfaquinoxaline is provided in drinking water. Water consumption increases rapidly as the temperature increases, which leads to increased drug intake. This toxicity usually is responsive to vitamin K therapy.

Elemental sulfur is often used in broiler houses in an attempt to improve growth rate and feed conversion and to minimize bacterial disease. The compound is applied to the floor after the litter has been removed. Elemental sulfur is also used in dust baths for treatment of ectoparasites in adult layers. If the amount of new litter placed in the house is inadequate, young chicks will come in contact with the sulfur, resulting in conjunctivitis and cutaneous burns, especially under the wings and on the legs. Clinically, the birds appear cold and tend to huddle; in many instances, death will occur due to the birds piling up, causing overheating and suffocation. When sulfur comes into contact with moisture, sulfuric acid is produced, which results in the burns.

Thiram is used to treat seed corn. It is toxic to chicks at 40 ppm and to goslings at 150 ppm; it causes leg deformities and weight loss. At 10 ppm, it causes soft-shelled eggs, and at 40 ppm, egg production and hatchability are reduced. Turkey poults tolerate up to 200 ppm.

A crystalline halogen has been identified as the “toxic fat” factor in some feeds. In young pullets, it reduces growth, retards sexual development, and increases mortality. Hatchability is decreased. Turkeys and ducks are less susceptible than chickens. Signs of intoxication include ruffled feathers, droopiness, and dyspnea. Lesions include ascites and hydropericardium, liver necrosis, subepicardial hemorrhage, and bile duct hyperplasia. Although the amount of toxin varies in feeds from different sources, 0.25%–0.5% fed for 35–150 days produces typical lesions.

Last full review/revision March 2015 by Robert E. Porter, DVM, PhD, DACVP, DACPV

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