Poisonings in Poultry

Aflatoxicosis is an important intoxication encountered in modern poultry production systems, resulting in decreased weight gain, drops in egg production, decreased feed efficiency, and increased morbidity and mortality rates.

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 the following clinical signs:

• inappetence

• ataxia

• seizures

• opisthotonos

• listlessness

• death

A gross lesion often present with acute aflatoxicosis is an enlarged yellow liver.

All poultry are susceptible to aflatoxicosis; however, ducks and turkeys are particularly sensitive.

In cases with chronic exposure, the livers may appear cirrhotic, and birds may develop hydropericardium and ascites. Microscopically, hepatic fibrosis, nodular regeneration, biliary ductular reaction, and hepatic lipidosis can be observed.

Ammonia gas is produced by the metabolism of uric acid through bacteria that can thrive in wet poultry litter. High ammonia concentrations often occur during the winter when ventilation is minimized to conserve heat, and thus high litter moisture is common.

Increased ammonia concentrations of 25–30 ppm (mcg/mL) can damage the mucociliary apparatus of the upper respiratory tract, and higher concentrations (50–75 ppm) can cause decreased feed intake as well as caustic burns and ulceration of the cornea, which can result in blindness (see corneal ulcers photograph). This happens because the alkali ammonium hydroxide is produced when the gas dissolves on liquid interfaces. Affected birds will often fail to find adequate food and water, resulting in death.

Corneal ulcers in ammonia toxicity, pullet

Image

Courtesy of Dr. Robert Porter.

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. Free-ranging backyard poultry may accidentally ingest rodent bait as well.

First-generation anticoagulant rodenticides, including warfarin, chlorphacinone, diphacinone, and coumatetralyl, require continual ingestion by rodents to induce toxic effects. Second-generation or single-feed anticoagulants, including brodifacoum, bromadiolone, difenacoum, and difethialone, can be acutely fatal to rodents.

Clinical signs of toxicosis in poultry are related to the product's anticoagulant effects and are usually observed as sudden death with gross hemorrhagic lesions in one or more body sites, particularly lung, intestine, and peritoneal cavity (see acute hemorrhage photograph). These lesions can be confused with flight injury (game birds) and trauma from wild animals and dogs.

Acute pulmonary and peritoneal hemorrhage, difethialone poisoning, p...

Image

Courtesy of Dr. Robert Porter.

Definitive diagnosis of anticoagulant toxicosis should be based on gross lesions, history of anticoagulant application, and anticoagulant screen on the liver of dead birds (available at several US veterinary diagnostic laboratories).

Bromethalin is a neurotoxic rodenticide and is not anticoagulant. Free-ranging backyard poultry and wild birds can accidentally ingest rodent bait through foraging activity.

Clinical signs include ataxia, seizures, paralysis, and death, depending on the dose ingested.

Gross lesions are usually absent, and cerebral edema with white matter vacuolation is observed microscopically.

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 seizures can also be observed in chicks consuming excess calcium.

Calcium concentrations > 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 (see renal and visceral gout photograph).

Renal and visceral gout (hyperuricemia) as a result of a high-calciu...

Image

Courtesy of Dr. Robert Porter.

Excess vitamin D₃ intake can also cause clinical signs similar to calcium toxicosis. Vitamin D3 is activated by 2 hydroxylation steps—one in the liver and one in the kidney—to become the metabolically active form 1,25-dihydroxycholecalciferol (1,25-D₃). The metabolically active form of vitamin D₃ plays a role in increasing GI calcium absorption, impacts bone formation and resorption, and increases renal tubular calcium resorption.

Vitamin D₃ toxicosis has been reported at≥ 30,000 IU/kg. Toxic effects of excess vitamin D₃ include hypercalcemia and metastatic calcification of soft tissues.

Carbon monoxide (CO) poisoning commonly arises from exhaust fumes when chicks are being transported by truck or from improper ventilation in hatcheries. It can also be the result of carbon monoxide produced by brooders and furnaces that are functioning improperly.

Mortality rates 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 and blood.

Diagnosis can be confirmed by a spectroscopic analysis of the blood.

Citrinin Poisoning in Poultry

See Citrinin Mycotoxicosis in Poultry.

Seeds of Senna obtusifolia, also known as coffee weed and sicklepod, are frequent contaminants of corn and soybeans. The leguminous plant has light green leaves and yellow flowers that hang downwards.

When present at ≥ 2%, they decrease feed intake and lower body weight, increase feed conversion in broilers, and substantially decrease egg production in laying birds.

Clinical signs also include ataxia, leg paralysis, and diarrhea.

At necropsy, lesions may be absent, or pale necrotic muscles may be noted.

Seeds, leaves, and stems of many species of Crotalaria contain pyrrolizidine alkaloids that are toxic to chickens. Concentrations > 0.05% in the feed produce signs of toxicosis. At 0.2%, weight gain is decreased markedly; 0.3% causes death in 18 days in commercially raised chickens.

Backyard birds feeding through foraging behavior may develop chronic hepatic lesions. Associated lesions consist of ascites, swelling or cirrhosis of the liver, and hemorrhage. Affected birds may pass yellow urates.

Resistance to the toxin increases with age.

Diazinon is an organic phosphate and cholinesterase inhibitor commonly used to control a variety of insects around poultry houses and is only available as a professional insecticide in a limited number of states.

Diazinon should not be used inside poultry houses. Chickens will consume the diazinon crystals, which results in lacrimation, diarrhea, incoordination, paralysis, dyspnea, and death.

Postmortem lesions include lung edema, fatty liver, proventricular ulceration, and severe enteritis. The diazinon crystals might be evident in the crop and gizzard contents.

Diagnosis can be confirmed by testing the brain for cholinesterase activity.

Dioxin is a fat contaminant of poultry feeds. In young pullets, it decreases growth, delays sexual development, and increases mortality rates. Hatchability is decreased. Turkeys and ducks are less susceptible than chickens.

Signs of intoxication include ruffled feathers, droopiness, and dyspnea.

Associated lesions include ascites and hydropericardium, liver necrosis, subepicardial hemorrhage, and bile duct hyperplasia.

Ethylene glycol is found in antifreeze, transmission fluids, and solvents such as rust remover. Free-ranging chickens can accidentally ingest the liquid from these sources.

Clinical signs include ataxia, seizures, watery feces, dyspnea, and death.

Kidneys may appear enlarged and pale on gross examination. Microscopically, there is renal tubular necrosis, and renal tubules contain rosettes and fan-shaped characteristic crystals of calcium oxalate monohydrate that are birefringent under polarized light. Crystals may also be present in the brain and intestinal tract (see ethylene glycol poisoning photomicrograph).

The minimal lethal dose in poultry is 7–8 mL/kg.

See Ethylene Glycol Toxicosis in Animals.

Ethylene glycol poisoning, chicken

Image

Courtesy of Dr. Carmen Jerry.

Cottonseed meal contains appreciable amounts of gossypol, which produces severe cardiac necrosis and heart failure that results in dyspnea, weakness, anorexia, and death.

When fed to laying hens, gossypol also causes decreased egg production and green egg-yolk discoloration.

Imidacloprid is a neonicotinoid insecticide commonly applied to poultry houses for the control of darkling beetles (Alphitobius diaperinus) before day-old chick placement.

The established LD₅₀ for imidacloprid is 104.1 mg/kg. The established median effective dose 50 (ED₅₀), the dose at which 50% of the population displays neurobehavioral abnormalities, for imidacloprid is 4.62 ± 0.98 mg/kg every 24 hours.

Presumptive cases of imidacloprid toxicosis have been reported in broilers, turkeys, and broiler breeder pullets.

Lead poisoning occurs in free-ranging backyard birds, wild waterfowl, and pigeons. Lead poisoning in poultry usually is caused by consumption of old flakes of lead-based paints and lead containing foreign objects, as well as some lubricants, electronics, and ceramics.

Lead arsenate orchard sprays were widely used until the 1940s, when DDT became available. Lead-based sprays were banned in the US in 1988.

Metallic lead at ≥ 7.2 mg/kg is lethal.

Clinical signs of lead poisoning in poultry include the following:

• lethargy

• inappetence

• emaciation

• thirst

• weakness

• greenish droppings commonly observed within 36 hours

• paralysis

• anemia

• ataxia

As poisoning progresses, the wings may be extended downward. Young birds may die within 36 hours 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. Highest concentrations of lead are found in the liver and kidney; however, there is also accumulation in the blood and bone.

Free-ranging backyard birds with lead intoxication may accumulate lead in eggs.

Mercury poisoning can occur from ingestion of mercurial disinfectants and fungicides, including mercurous chloride (calomel) and bichloride of mercury (corrosive sublimate), although use of both calomel and bichloride has been discontinued and mercurial fungicides have been banned in several countries.

Bioaccumulation of organic mercury from aquatic organisms that are consumed by fish and then fed to poultry may result in mercury poisoning.

Clinical findings are progressive weakness and incoordination. Diarrhea may occur, depending on the amount ingested.

The caustic action of the inorganic form of mercury may produce gray areas in the mouth and esophagus, which usually ulcerate if the bird lives > 24 hours. 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.

Nicarbazin, a chemical coccidiostat, is used in broilers. It should not be fed to layers and breeders because it can cause white discoloration of brown eggs, internal egg quality issues, decreased egg production, and decreased hatchability of eggs depending on the concentration of the drugs and duration of treatment.

The effect is reversible once the nicarbazin is withdrawn. It also may result in decreased heat tolerance in birds exposed to high temperature and humidity.

Nitrofurazone has been used to treat several bacterial diseases in poultry, but it is no longer approved for use in many countries, including the US.

When fed at ≥ 0.022%, nitrofurazone causes hyperexcitability manifested by rapid movements, loud squawking, and frequent falling forward. In turkeys, which are more susceptible to nitrofurazone than are chickens, it produces cardiac dilatation, ascites, and when fed at ≥ 0.033%, death.

The compound 3-nitro-4-hydroxyphenylarsonic acid was used in feed to improve weight gain and feed efficiency.

When improperly mixed or fed at a level 2–3 times as high as 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.

This product has been withdrawn and no longer used in the US.

Ochratoxins are potent nephrotoxic mycotoxins produced from Penicillium viridicatum and Aspergillus ochraceus.

Clinical signs of ochratoxin poisoning in poultry include poor feed conversion, decreased egg production, and diarrhea.

Associated lesions are mostly present in the kidneys, including enlarged kidneys with urate retention grossly; microscopically, renal tubular degeneration and necrosis with cast formation and urate tophi are usually observed. Bone marrow suppression and hepatic necrosis may also occur.

Polychlorinated biphenyl 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 decrease thyroid hormone levels. Concentrations of 50 ppm result in cirrhosis of the liver and ascites in broilers and a decrease in egg production and hatchability in hens.

These compounds may be environmental contaminants, putting free-range birds at risk of poisoning from oil and grease from equipment used in commercial feed manufacture. See Poisoning of Animals by Persistent Halogenated Pollutants (PHPs).

Polyether ionophores facilitate transport of divalent cations across cell membranes to interfere with osmoregulation, resulting in cell rupture.

Toxicosis caused 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.

Turkeys develop more severe disease than chickens. Additionally, these ionophores can interact with certain medications, such as sulfonamides, to cause clinical signs of toxicosis when the ionophore concentration in the feed is normal (see ionophore toxicosis and toxicosis with myodegeneration photographs).

Ionophore toxicosis, turkey

Image

Courtesy of Dr. Robert Porter.

Ionophore toxicosis, myodegeneration, turkey

Image

Courtesy of Dr. Robert Porter.

Examples of ionophores used in poultry include the following:

Polytetrafluoroethylene (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 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 (see pulmonary edema photograph). Mild dyspnea and blood-tinged fluid around the mouth and nares may be noted; however, in many cases, birds are found dead with no premonitory signs.

Massive pulmonary edema and hemorrhage, PTFE poisoning, pheasants

Image

Courtesy of Dr. Robert Porter.

Diagnosis is based on gross lesions, history of using new heat lamps 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 sometimes used as disinfectants and to clean water lines in poultry houses. Turkeys are very susceptible. Concentrations ≥ 150 ppm result in substantial mortality rates.

Clinical signs include decreased water intake, nasal and ocular discharge, facial swelling, and gasping.

Postmortem lesions include caseous ulcers in the oropharynx, upper respiratory tract, commissures of the mouth, crop, esophagus, proventriculus, and gizzard.

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 decreases 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 develop signs of poisoning other than poor hatchability of their eggs.

Starting rations containing 8 ppm have decreased 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 human foods. Sodium arsenite and some of the organic arsenicals, when administered to laying hens with selenium, have increased hatchability.

Some regions have high soil concentrations of selenium, which can accumulate in certain plants. Poultry species that are allowed to free range in these areas could potentially ingest toxic amounts of these plants over time.

The term salt poisoning is misleading. Sodium chloride (ie, table salt) used to be the common source of sodium in a ration, and was thus associated with poisoning. Other sodium sources such as sodium bicarbonate and sodium sesquicarbonate are added to the diet.

The ion responsible for the toxicosis is sodium (Na⁺). Physiologically, water follows the sodium ion gradient, which is why fluid disturbances (edema, ascites) are a clinical sign associated with sodium poisoning.

Birds under 21 days old have increased susceptibility to the toxic effects of sodium. This is related to immature or incompletely developed kidneys and an inability to excrete sodium as efficiently as an older bird.

Increased sodium intake increases plasma osmolality and results in increased intracellular fluid volume. The shift of fluid from intracellular to extracellular results in cellular dehydration and triggers water consumption, exacerbating the problem. Excess sodium has also been demonstrated to increase red blood cell rigidity. Because avian red blood cells, which are nucleated, must deform to move through the pulmonary capillaries, this creates resistance to blood flow through the lungs and contributes to the pathogenesis of ascites with sodium poisoning (see ascites and pulmonary edema photograph).

Ascites and pulmonary edema, sodium poisoning, turkey poult

Image

Courtesy of Dr. Robert Porter.

The addition of 0.5% salt (NaCl) to the ration of chickens and turkeys is recommended; however, 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 death. 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.

Clinical signs of salt poisoning include dyspnea, lethargy, and distended fluid-filled abdomens. Watery droppings and wet litter are also observed.

Salt concentrations 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 food animals.

Other sources of sodium additions to the water or feed should also be considered in cases where toxicity is suspected. Sodium bicarbonate and sodium sesquicarbonate are other potential sodium sources (see salt poisoning photograph).

Severe ascites with salt poisoning, broiler chick

Image

Courtesy of Dr. Carmen Jerry.

Necropsy findings are not diagnostic; enteritis, ascites, hydropericardium, cystic testicles in young birds, and cardiomegaly with ventricular distention can be observed. Edema of the testicle is pathognomonic of salt toxicity in young birds.

Microscopically, cystic changes in seminiferous tubules of testicles, cerebral edema, and cardiac muscle necrosis may be observed. Analysis of salt concentrations in representative feed and water samples, tissues such as brain, and the combination of gross and microscopic lesions are important in diagnosis of salt toxicosis in poultry.

Sulfonamides have been used for treatment of several bacterial and protozoal infections in some classes of poultry and are usually administered in drinking water because they do not mix well in feed. They also have low solubility in acidic water.

Sulfaquinoxaline, when fed at ≥ 0.25%, results in severe pancytopenia. Hemorrhages are common on the legs, breast muscle, proventriculus, ventriculus and in virtually all abdominal organs. There may be decreased egg production and poor eggshell quality in laying birds. The bone marrow is pale, and the blood is slow to clot.

Poisoning frequently occurs in hot weather when sulfaquinoxaline is provided in drinking water. Water consumption increases rapidly as the temperature increases, which leads to increased drug intake.

Sulfonamide toxicosis usually is responsive to treatment with vitamin K.

Elemental sulfur is applied to the floor after the litter has been removed and is also used in dust baths for treatment of ectoparasites in adult layers and backyard flocks. 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, affected 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 contact dermatitis (see sulfur toxicosis illustration).

Sulfur toxicosis, dermatitis lesions, chickens

Image

Courtesy of Dr. Jenny Nicholds.

Thiram is a fungicide used to treat seed corn. It has been implicated in the development of tibial dyschondroplasia in poultry.

Thiram is toxic to chicks at ≥ 40 ppm and to goslings at ≥ 150 ppm; it causes leg deformities, lameness and weight loss. At 10 ppm, it causes soft-shelled eggs in laying birds, and at 40 ppm, egg production and hatchability are decreased. Turkey poults tolerate up to 200 ppm.

Trichothecenes are mycotoxins produced by fungi, mostly of the Fusarium species. The toxin has a radiomimetic mechanism of action, acting on rapidly dividing cells and producing DNA damage.

Trichothecene toxicosis produces oropharyngeal necrosis and ulceration, stunted feather growth, and feed refusal. Immune suppression may also occur.

Birds may accidentally be fed high concentrations of zinc in rations, or free-ranging birds such as backyard poultry may ingest zinc-containing or zinc-coated metallic objects, as well as some rubber products.

Clinical signs include seizures, green diarrhea, lethargy, hematochezia, pallor, drops in egg production in laying birds, anorexia, and weight loss.

Gross lesions include erosions of the koilin layer of the ventriculus, mottled pancreas, and mild hepatomegaly and renomegaly; however, gross lesions may be absent. Microscopically, there is pancreatic degeneration and atrophy, hepatic necrosis, bile stasis and hemosiderosis, and renal tubular necrosis.

• Hoerr FJ. Mycotoxicoses. In: Swayne DE, Boulianne M, Logue CM, et al, eds. Diseases of Poultry. 14th ed. Wiley; 2019:1330-1348. doi:10.1002/9781119371199.ch31

• Fulton RM. Toxins and Poisons. In: Swayne DE, Boulianne M, Logue CM, et al, eds. Diseases of Poultry. 14th ed. Wiley; 2019:1349-1382. doi:10.1002/9781119371199.ch32

• Fulton RM, Buchweitz JP. Sulfaquinoxaline toxicosis in a juvenile broiler breeder flock. Avian Dis. 2023;67(1):130-133. doi:10.1637/aviandiseases-D-22-00093