Mercury toxicosis has been associated with ingestion of seed treated with organic mercurial fungicides.505-507 Topical application or ingestion of inorganic mercurials, used as counterirritants (blistering agents), also can result in toxicosis.505,507,508 If the blistering agents are used concurrently with dimethyl sulfoxide (DMSO), the absorption of the mercury is enhanced and is more likely to cause toxicosis.508
Mercuric ions form covalent bonds with sulfhydryl groups and form mercaptides.507 The kidney is the primary target organ, but mercury also localizes in the GI mucosa. Mercury is excreted by the kidneys, partly by exfoliation of renal tubular epithelium.508 Metallothionein, a metal-binding protein, is synthesized within 48 hours of exposure to mercury. Metallothionein initially may protect the kidney by sequestering mercury; however, as the sequestered mercury is slowly released from the tubular epithelium, renal damage continues.505,508
Acute signs of mercury toxicosis are caused by the corrosive effect of mercury on mucous membranes. Ulceration of the mouth, esophagus, and rest of the GI tract may be followed by diarrhea and anorexia. If the animal survives, acute toxic nephrosis occurs. Anorexia, gastroenteritis, weight loss, nephritis, and alopecia have been reported in animals exposed to chronic, low doses of mercury.507
Clinical pathology testing may reveal elevated creatinine and blood urea nitrogen (BUN), as well as proteinuria, glucosuria, and isosthenuria, depending on the acuteness of the disease. Necropsy findings include an ulcerated and edematous GI tract, with possible intraluminal hemorrhage. The kidneys may be pale and swollen.505,508
Diagnosis of mercury toxicosis is made from history, clinical presentation, and mercury levels within the animal. Mercury concentrations can be measured in liver, kidney, brain, whole blood, and urine. Tissue samples and urine may be frozen after collection.
Chelation therapy can be done using BAL or sodium thiosulfate as for arsenic toxicosis. Remaining topical mercurials should be washed from the animal. Supportive care is necessary for the gastroenteritis and kidney failure. Oliguria indicates a poor prognosis.505,508
Excess dietary sulfate is discussed with copper deficiency in Chapter 32 and with polioencephalomalacia in Chapter 35.
The anticholinesterase insecticides include the organophosphates and the carbamates. Many organophosphate insecticides are used for insect control in crops. Several organophosphates also have been approved for use as insecticides or anthelmintics in domestic animals. Carbamate insecticides are used primarily for crops and other plants. Livestock are usually exposed to these insecticides as a result of drift, accidental ingestion, or improper treatment by owners.509
The mechanism of action of these insecticides is to bind with and inhibit acetylcholinesterase (AChE). As a result, acetylcholine (ACh) accumulates at nerve junctions, and repetitive firing of parasympathetic nerves occurs. Because carbamates bind with ACh on a reversible basis, inhibition of AChE is temporary.509,510 Therefore, carbamates have a shorter duration of action than organophosphate insecticides, which bind irreversibly with AChE.509
Clinical signs are predominantly described by the acronym SLUD: salivation, lacrimation, urination, and defecation. In addition, the animals may have miosis, diarrhea, muscle tremors, seizures, dyspnea, or bloating.509 Death can occur within minutes, depending on the toxicity of the specific compound and the amount of toxicant ingested.511 At postmortem examination, lesions may be minor or absent, depending on the acuteness of death. Pulmonary edema is a frequent finding, because death usually results from increased pulmonary secretions, bronchial constriction, and respiratory paralysis.510
Measuring the cholinesterase activity in brain, retina, or whole blood can be used to make a presumptive diagnosis of toxicosis.512-514 Some laboratories use serum rather than whole blood, depending on the testing method used; therefore it is best to check with the laboratory before submission. Whole blood can reliably be used for cholinesterase evaluation for up to 1 week after collection if the sample is refrigerated.515 Half the brain should be submitted for homogenization because cholinesterase activity varies among regions of the brain.512 Cholinesterase activity in whole blood or brain that is less than 50% of normal for the species being tested indicates excessive exposure to a cholinesterase inhibitor. Cholinesterase activities less than 25% of normal indicates toxicosis, as long as appropriate clinical signs are present.513
An insecticide screen should be performed on GI contents or the liver to identify the insecticide chemical that is involved. These samples should be stored in glass or metal, such as foil, and frozen as soon as possible after collection. If the sample is stored in plastic, the insecticide may leech from the sample into the plastic.
Because carbamates rapidly dissociate from AChE, a diagnosis is often difficult to make based on cholinesterase activity in brain or blood. The activities can be normal or near normal even though the animal has toxicosis.509,510 Because carbamates hydrolyze rapidly, parent compounds may be difficult to detect in ingesta and especially in tissue.509,510 Therefore, when carbamate toxicosis is suspected, multiple samples should be collected and tested as soon as possible.
Treatment for organophosphate toxicosis includes supportive care, activated charcoal, atropine, and oximes. Activated charcoal (1 to 2 lb [0.45 to 0.90 kg] PO for 500-kg animal) should be given even if the route of exposure is not oral, because these insecticides can act systemically even when given topically. If the route of exposure is dermal, the animal should be washed with soap and water to decrease absorption through the skin.513 Atropine competitively inhibits ACh at muscarinic nerve receptors. Therefore, muscarinic effects, but not nicotinic effects, are reduced. Atropine should be given at a dose of 0.10 to 0.25 mg/kg. One fourth of the initial dose is given by IV injection and the rest SC or IM. The dose can be repeated if the clinical signs reappear.513 GI motility should be monitored carefully because atropine can cause ileus, especially in horses. Oximes such as 2-pyridine aldoxime methiodide (2-PAM) can be used as a treatment to release the bond between AChE and an organophosphate. However, oximes are of little benefit after the AChE-organophosphate bond undergoes “aging,” meaning that the bond cannot be broken. The amount and time of “aging” that occurs vary among the different organophosphate compounds.513,516 Recommended doses for 2-PAM are 20 mg/kg IV twice daily517 or 10 to 15 mg/kg SC.518
Treatment of carbamate toxicosis is restricted to atropine, activated charcoal, and supportive care. Oximes such as 2-PAM are contraindicated with carbamate toxicosis because the carbamates bind reversibly, and thus oximes are not needed to release the carbamate from the AChE.509
Most anticholinesterase compounds are rapidly metabolized and excreted.519 Therefore these insecticides do not persist in tissues, and tissue levels are usually low. Animals that survive the toxicosis, however, should be analyzed for residues before consumption.520 Animals that have died from anticholinesterase insecticide toxicosis have been prohibited from being rendered.519
Chlorpyrifos is a chlorinated organophosphorus insecticide used for lice and fly control in cattle. It is applied as a pour-on caudal to the shoulders. This product causes a delayed toxicosis that occurs primarily in bulls and some exotic breeds of cattle. Toxicosis is associated with the testosterone levels in the animal.521 Larger and older bulls are affected more severely. The manufacturer recommends not treating bulls over 8 months old with chlorpyrifos.517 Clinical signs do not occur until at least 2 to 7 days after exposure and include depression, weakness, muscle fasciculations, anorexia, rumen stasis, and rumen distention.517,518,521 The clinical signs typically seen with acute organophosphate toxicosis are usually not present with chlorpyrifos toxicosis.
Animals with chlorpyrifos toxicosis will have depressed cholinesterase activities in brain and blood. After topical application, chlorpyrifos will undergo systemic distribution and may be detected in blood, rumen contents, fat, and hair for weeks. Animals with chlorpyrifos toxicosis should be washed with detergent and water as soon as possible.517,518,521 Oral treatment with activated charcoal reduces the signs of toxicosis by adsorption of the chlorpyrifos. The manufacturer recommends atropine as an antidote.517 Because most cases involve ruminal stasis and few muscarinic signs, however, atropine may be contraindicated. 517,518 Severity of the rumen stasis often requires removal of rumen contents by a large-bore stomach tube or rumenotomy.518 Pralidoxime (2-PAM) has decreased clinical signs in some animals when given within 4 days of insecticide exposure.517,518
Haloxon is an anthelmintic and toxicosis was reported in the 1970s in sheep that had a familial absence of a plasma A-esterase.522 This enzyme rapidly hydrolyzes haloxon.522 Clinical signs occur 5 to 90 days after exposure and predominantly include hindlimb ataxia or paresis.523 Gross lesions are not evident on necropsy. Microscopically, the white matter of the spinal cord was vacuolated, with swollen axons and increased glial cells.523 Cholinesterase activity can be decreased.522
Haloxon also has been associated with bilateral laryngeal paralysis in Arabian and part-Arabian foals.524 The foals were 23 to 35 days old and had been treated with haloxon every 2 weeks since 2 days of age. The clinical signs were noticeable only when the foals exercised or were stressed. Rhinolaryngoscopy revealed no abductor movement of the arytenoid cartilages.524 Active wallerian degeneration and loss of nerve fibers were seen in the recurrent laryngeal nerves.524 Tracheotomy relieved the dyspnea, and in foals that survived, function of the right arytenoid cartilage returned before the left.524
Chlorinated hydrocarbons are used to control insects and other pests. Examples include DDT, aldrin, heptachlor, and lindane. Although use of several of these products has been banned or restricted, toxicosis in domestic animals still occurs, either from improper use or from exposure to discarded products.525
The mechanism of actions of organochlorines is not completely understood and seems to vary among compounds. Interference with the kinetics of nerve sodium channels and inhibition of γ-aminobutyric acid (GABA) binding are two proposed mechanisms.
Initial clinical signs may include apprehension, hypersensitivity, and a belligerent attitude. Fasciculations of the face and cervical muscles are followed by spasms of the eyelids, forequarters, and finally hindquarters.525 Ataxia, hypersalivation, and diarrhea also have been reported.526 Intermittent convulsions are the major manifestation in most cases.520 Significant gross lesions usually are not found at necropsy.527
Organochlorines accumulate in fatty tissues. Therefore, diagnostic testing should be performed on samples such as brain, fat, milk, and liver.525 The compounds also may be found in whole blood and GI contents. Collected samples should be put in glass or metal containers525 and frozen, with the exception of blood, which should be refrigerated. As with other insecticides, plastic containers should be avoided if possible.
Treatment is mostly symptomatic because no antidote for organochlorine toxicosis exists.525 The animal should be washed with water and detergent if the exposure was dermal.525 Activated charcoal is beneficial if given immediately after oral exposure.525,526 Convulsing animals require treatment with sedatives and muscle relaxants.
Organochlorine residues persist in fat and are excreted in the milk of lactating animals.520 Some of these compounds cross the placental barrier and concentrate in fetal fat.528 Several strategies have been tried to reduce residues as quickly as possible to minimize economic loss. Treatment with compounds such as phenobarbital and butylated hydroxyanisole (BHA) to promote metabolism, cholestyramine to increase excretion, or thyroprotein to increase elimination has not been very successful in livestock.528
At this time, the only successful method of reducing organochlorine residues in livestock is by fat mobilization and removal. One method of accomplishing fat mobilization is by feeding a calorie-restricted diet.526 As the animal loses weight, the fat and organochlorine are mobilized and removed from the body. After removal of the fat, the animal should be fed a high-calorie diet that is free of organochlorine compounds to regain its body fat and decrease the whole-body concentration of the compound. As the body fat decreases, concentration of organochlorine may increase in other tissues as the chemical is mobilized.525 If the diet is too restrictive, the organochlorine mobilization may occur too rapidly, and the animal may develop acute toxicosis.526 The fastest method of reducing organochlorine residues is through milk secretion.528 Residue elimination is fastest during early lactation. Unfortunately, residue reduction may not be economically feasible because of extra costs of feed, labor, and loss of saleable milk.
Paraquat is in the class of bipyridyl herbicides, which act as dessicants by altering enzyme systems and reducing photosynthesis.529 Most concerns about this product occur when it is sprayed on foliage that will later be used for animal consumption or when it accidentally drifts from a sprayed field onto animals or their pasture. Paraquat quickly becomes irreversibly inactivated once it comes into contact with soil.529,530 It is a concern only when the animal ingests a concentrated form of the herbicide or grazes a field that is still wet from paraquat application.
Paraquat is concentrated against a gradient within type I alveolar pneumocytes. The herbicide accepts electrons to form free radicals.529,530 This reaction is catalyzed by nicotinamide adenine dinucleotide phosphate (NADP), reduced from cytochrome P450 reductase (NADPH).529 The result is destruction of cell membranes and subsequent cell death.
Acute signs generally occur 1 to 3 days after ingestion and involve anorexia, depression, and diarrhea. Several days later the animal develops respiratory distress, dyspnea, and pneumomediastinum. Death may be delayed until several weeks after ingestion. Gross and histopathologic lesions primarily consist of progressive lung fibrosis, but may include renal and liver damage.529,530
Treatment should include fuller’s earth or bentonite given orally as soon as possible after exposure and certainly within 24 hours of ingestion.529,530 These products inactivate the paraquat on contact and thus are more effective than activated charcoal. Oxygen therapy reportedly worsens the lung damage.531 Regardless of therapy, the prognosis is poor because of the progressive fibrosis of the lungs.
Chlorophenoxy acid herbicides includes the compounds 2,4-D; 2,4,5-T; and silvex. These herbicides are plant growth regulators, so the mechanism of action is to alter the metabolism of the plant. Therefore they are relatively nontoxic to mammals unless ingested in a concentrated form.529,530 Indirect toxicosis may occur, however, because of the altered metabolism of the sprayed plants. Toxic plants that are normally untouched by grazing animals may become more palatable and result in plant toxicosis after application of some herbicides. In addition, the altered plant metabolism may cause some plants to accumulate higher levels of nitrate or cyanide or increase the level of their inherent toxins.530 Animals should be removed from treated pastures for at least 7 days after application to reduce the occurrence of plant toxicosis.530
Clinical signs of chlorophenoxy acid toxicosis include depression, anorexia, abdominal pain, and diarrhea.529 Weakness is especially profound in the hindlimbs. Gross findings include epicardial hemorrhage and hydropericardium. The liver is swollen and friable. The kidneys may be congested.532
Clorophenoxy acid herbicides are quickly absorbed from the GI tract, but dermal absorption is minimal.533 Treatment consists of activated charcoal and supportive care. The major route of elimination is the urine.533 Neither parent compounds nor metabolites have been found in the milk from orally dosed cattle.533
Triazine herbicides inhibit photosynthesis by blocking electron transport.534 Products in this group of herbicides include atrazine, simazine, and propazine. Livestock should be held from pastures treated with simazine for 30 days and off hay for 60 days.530
Sheep have been reported to exhibit signs of generalized muscle tremors, which progressed to mild tetany and collapse of the hindlegs. Other sheep developed a short, prancing gait.535 Cattle have been reported to develop diarrhea after 12 hours, followed by salivation, ataxia, and stiffness.536 Gross lesions include myocardial degeneration, subcutaneous hemorrhages, and liver congestion. Histopathologic examination demonstrated focal degenerative myocardiopathy and mild nonsuppurative encephalitis.535,536 Rumen papillae are edematous and the reticulum, rumen, and omasum may contain black pigment.536
Triazine herbicides have no antidote, but treatment with activated charcoal once daily for 4 consecutive days after exposure has reportedly decreased lesions and death loss.536
Toxicosis can result from anticoagulant rodenticides when animals ingest baits made with anticoagulants. These products are often incorporated into grains or pellets that are palatable to livestock. Toxicosis also has been reported in horses that have been overdosed with warfarin, which has been used as a treatment for navicular disease and jugular phlebitis.537,538
First-generation compounds such as warfarin were developed originally, but rodents developed a resistance to these over time. The second-generation compounds, such as brodifacoum and bromadiolone, were created for rats that had developed a resistance to the first-generation compounds.539-541 In general, the second-generation compounds are more toxic and have longer half-lives.
All anticoagulant rodenticides function by interfering with vitamin K–epoxide reductase, the enzyme that converts inactive vitamin K to its active form. This interference results in a depletion of active vitamin K and subsequently the vitamin K–dependent clotting factors (II, VII, IX, and X). Factor IX is in the intrinsic coagulation pathway, factor VII is in the extrinsic pathway, and factors II and X are in the common pathway. Therefore, all three pathways are affected.539,540
Clinical signs may not be noticed until 3 to 5 days after ingestion. Affected animals may exhibit melena, epistaxis, hematuria, or excessive bleeding from a wound or injection site.540 Often the hemorrhaging occurs in body cavities, and the animal may show nondescript clinical signs such as depression, weakness, pallor, colic, dyspnea, or fever, depending on the location and extent of hemorrhage.539,540 Sometimes the onset is acute, and the animal dies suddenly from extensive hemorrhage and shock.539 Gross and histopathologic lesions primarily consist of unexplained hemorrhage, which may be generalized or localized.
Warfarin is almost completely absorbed from the GI tract of horses and has a biologic half-life of 13.3 hours, similar to that in other species.538 Warfarin is mostly bound to plasma protein, and only the unbound drug is toxic. Therefore, concomitant use of other protein-bound drugs, such as phenylbutazone, can increase the risk of warfarin-induced hemorrhage.537,542
Diagnosis of anticoagulant toxicosis is based on history, clinical signs, clinical pathology, and response to treatment. The degree of anemia resulting from hemorrhage varies with the time since ingestion of the toxicant and severity of disease. A coagulation panel will reveal prolongation of prothrombin time (PT), partial thromboplastin time (PTT), and activated coagulation time (ACT).540,543 The fibrinogen, fibrinogen degradation products, and platelet count are not directly affected by the anticoagulants.
Determining which anticoagulant rodenticide was ingested is difficult in the live animal. Levels are often too low in blood to be detected. Postmortem detection is most promising in the liver. Although GI contents can be tested, the chemical is often completely absorbed before clinical signs appear or death occurs.
Vitamin K1 is the treatment for all the anticoagulant rodenticides. The duration of treatment, however, depends on the specific compound because the half-life varies considerably. Warfarin has the shortest half-life of the anticoagulants (13.3 hours in the horse).538 The half-lives of the other compounds have not been determined in the horse, but diphacinone has a half-life of 15 to 20 days in humans. Therefore, warfarin toxicosis may require treatment for only a few days, whereas toxicosis from the other compounds may have to be treated for several weeks. Vitamin K1 treatment for an adult horse has been recommended at a dose of 300 to 500 mg SC every 4 to 6 hours.537 The PT should return to normal within 24 hours. To monitor duration of treatment after the animal has stabilized, vitamin K should be discontinued for 48 hours and the PT retested.539 Intravenous injection of vitamin K has been associated with anaphylactoid reactions, and intramuscular injection can aggravate hemorrhage. Oral treatment is advocated for small animals but may be cost-prohibitive for large animals. Vitamin K3 is less expensive but not as effective and will cause renal disease in horses.
Clotting factor synthesis requires 6 to 12 hours; therefore animals may need to be transfused with whole blood if anemic, or with fresh plasma if the anemia is not severe enough to warrant blood transfusion.539 Once the packed cell volume (PCV) begins to decrease, it can continue to decrease at a rapid pace, so it should be monitored regularly. Activated charcoal can be given orally to decrease absorption of rodenticides.
Strychnine is used for mammals such as rats, gophers, moles, squirrels, and coyotes. Strychnine is sold as a powder, as pellets, or as treated seeds that are usually dyed bright green or red. Strychnine poisoning was reported in four horses that had eaten milo treated with it. Use of strychnine is restricted in some states to professionals or registered individuals; however, toxicosis in domestic animals still occurs.544
Strychnine competitively blocks glycine, the transmitter for inhibitory cells (Renshaw cells) of the spinal cord. This lack of inhibition results in rigidity and tetanic convulsions. Clinical signs include sweating, incoordination, recumbency, and tonic clonic seizures that are inducible by loud sounds, touch, or bright light. Signs appear 10 minutes to 2 hours after ingestion. Gross and histopathologic lesions are limited to those attributable to self-induced trauma.544
Diagnosis of strychnine toxicosis is based on clinical signs and detection of the toxicant in urine or serum. Urine is a good diagnostic sample because strychnine is absorbed from the GI tract and excreted in the urine. Stomach contents, liver, kidney, and urine should be collected postmortem and analyzed for strychnine.544
A lethal dose of strychnine can be eliminated in 24 to 48 hours. Because strychnine is an alkaloid, it becomes ionized in the acid of the stomach and is not absorbed until it reaches the intestine. Activated charcoal is a good treatment to prevent further absorption of the toxicant. Seizures should be treated with anticonvulsants and rigidity with muscle relaxants. Animals should be protected from excessive light and sound to reduce the incidence of convulsions.
Zinc phosphide is used to control mice, ground squirrels, rats, and moles. Zinc phosphide is a dark-gray powder that is mixed with grains such as bran, wheat, and oats. Therefore it is palatable to most livestock. The lethal dose for most animals is 20 to 40 mg/kg of body weight.545
Zinc phosphide produces phosphine gas under acidic conditions. Therefore, toxicosis occurs when the rodenticide comes into contact with an acidic stomach. Gastric acidity is an important factor in phosphine gas production. Ruminants should be more resistant because the rumen has a higher pH than a monogastric stomach. Studies show a higher survival rate in dogs that are dosed with zinc phosphide on an empty stomach rather than dosed after a meal when the stomach has a lower pH.545
Zinc phosphide affects the CNS, and clinical signs are similar to those caused by other toxicants, such as strychnine or the anticholinesterase insecticides.545 Gross and histopathologic lesions are not specific, although the GI and pulmonary systems may be red and irritated. Thus, diagnosis is difficult without chemical analysis.
Diagnosis of zinc phosphide toxicosis is based on detecting phosphine gas in the stomach contents. Because the gas dissipates rapidly in air, the collected sample of stomach contents should be placed in an airtight container and frozen immediately.545
Treatment is mostly supportive care following activated charcoal therapy. Food should be withheld until the zinc phosphide has been emptied from the stomach. It may be helpful to add an antacid to the activated charcoal therapy to reduce the amount of phosphine gas produced.
Metaldehyde is a tasteless ingredient used in slug and snail baits and as a solid fuel for some camp stoves.546 Baits may be liquid or dry, but most are dry pellets of metaldehyde mixed with soybeans, rice, oats, sorghum, or apples.546,547 Some baits also contain other toxicants, such as arsenate or insecticides, which can cause concurrent disease. Toxicosis occurs mostly in coastal and low-lying areas where there is a high incidence of snails or slugs.547
The mechanism of metaldehyde toxicosis is unknown.546 It may increase excitatory neurotransmitters or decrease inhibitory neurotransmitters.546,547
Clinical signs can occur immediately or can be delayed for up to 3 hours after ingestion. Affected animals will have convulsions, which may be continuous or intermittent. The animal may have muscle tremors and anxiety and may be hyperesthetic between convulsions. The seizures are not necessarily evoked by external stimuli. Elevated body temperature, up to 43° C (110° F), is a common finding and is probably caused by the excessive muscle activity. Other findings include tachycardia, defective vision, hyperpnea, hypersalivation, ataxia, cyanosis, acidosis, diarrhea, and dehydration. Death usually results from respiratory failure and occurs 4 to 24 hours after ingestion. Gross and histopathologic findings include petechiae and ecchymoses of various organs and subcutaneous edema.548-550
A diagnosis is based on testing for metaldehyde in GI contents or serum.551 Milk samples taken within 24 hours from two affected cows tested negative for metaldehyde.552 No antidote is available.552,553 Administration of oral activated charcoal may prevent further absorption from the GI tract. If the animal is convulsing, tranquilizers should be used to control seizures. Tranquilizers should be allowed to wear off periodically and the convulsive condition reevaluated. Horses have been treated successfully with tranquilizers and mineral oil.554
Animals can become exposed to petroleum hydrocarbons during crude oil spills, pipeline breaks, or careless disposal of automobile or tractor oil. Most cases of petroleum toxicosis occur when the animal’s water supply is contaminated.555
Clinical signs vary but usually include anorexia, depression, GI stasis, bloat, and diarrhea or constipation. Oil may be seen in the feces within days after ingestion. The most common cause of death is aspiration pneumonia after regurgitation of the hydrocarbons. The petroleum product may be seen around the muzzle of the animal. Oil may be found in the GI tract or the lungs at postmortem examination.
Diagnosis of petroleum toxicosis can be made based on history, clinical findings, and detection of hydrocarbons in tissues. The product may be visible on the animal as well as in the GI contents and lungs. A quick method of checking for oil is to place the GI contents or lung in warm water; the oil should float to the top of the water. Samples also can be checked under a black light because many petroleum products will fluoresce yellow or yellow-green. Liver, kidney, lung, and GI contents can be analyzed for hydrocarbons and matched with available source material.555 Collecting suspect source material is especially important because these toxicoses may become legal cases.
The primary aim of treatment is to prevent aspiration pneumonia, which is best achieved by performing a rumenotomy and removing the contaminated ingesta. If surgery is not feasible, activated charcoal should be administered. The charcoal should be followed with a cathartic to enhance removal of the oil. Supportive care is needed for the GI stasis and diarrhea or constipation. Vegetable oil (500 to 1000 mL) may increase the viscosity of the ingested petroleum within the rumen and reduce the occurrence of aspiration pneumonia. The prognosis is generally good unless the animal aspirates or severely bloats.555 Some petroleum products may contain heavy metals such as lead, and a concurrent metal toxicosis can occur.
The most common cause of ethylene glycol toxicosis is ingestion of antifreeze. Although cats and dogs are the species most often affected because of their proximity to available sources, ethylene glycol toxicosis has occurred in cattle and goats.556 Some new brands of antifreeze contain propylene glycol rather than ethylene glycol. Although much less toxic than ethylene glycol, propylene glycol can still cause toxicosis.
Ethylene glycol is metabolized in the liver to several metabolic intermediates, especially glycolic acid. This reaction is catalyzed by alcohol dehydrogenase. Glycolic acid results in metabolic acidosis and hyperosmolality in the animal. This metabolite can be excreted or further metabolized into oxalic acid, which combines with ionic calcium and causes hypocalcemia and calcium oxalate formation, especially in kidneys. Ruminants may be more resistant to ethylene glycol toxicosis than monogastrics because the rumen microorganisms can metabolize some ethylene glycol before it is absorbed.556,557
Toxicosis results in an initial inebriation, followed by metabolic acidosis and renal damage.557 Clinical signs in ruminants include ataxia, depression, hypersalivation, and absence of a menace response. These signs progressed to recumbency and clonic-tonic seizures in a pygmy goat.556 Clinical pathology reveals azotemia, metabolic acidosis, and hyperosmolality. Postmortem findings include swollen kidneys and pulmonary edema. Dilated capsular spaces and birefringent crystals are found in renal tubules on histologic examination. These crystals may be arranged in sheaves or rosettes and are typical of oxalate crystals.556
Rumen or stomach contents can be analyzed for ethylene glycol. It is absorbed within 48 hours after ingestion by monogastrics; however, ethylene glycol has been detected in the rumen contents of a goat 4 days after clinical signs began.5 Urine, serum, and ocular fluid can also be analyzed for glycolic acid.
The classic treatment for ethylene glycol toxicosis is 20% ethanol given at 5 ml/kg at 4- to 8-hour intervals. The ethanol binds with the alcohol dehydrogenase so that it is not available to convert ethylene glycol to glycolic acid. This treatment is effective, however, only if initiated within a few hours of ingestion. The effectiveness of ethanol in treating livestock has not been addressed in the literature. Because the ethylene glycol appears to remain in the rumen for several days, treatment with activated charcoal may be beneficial even after the appearance of clinical signs.556
Chlorinated naphthalene has been used in wood preservatives, asphalt roofing, insulating waxes, sealing compounds, and in condensers. Most toxicoses in cattle, however, have been from ingesting lubricating grease used on farm machinery or feed-pelleting machines. Chlorinated naphthalene is no longer used in lubricants, but toxicosis still occurs when animals have access to dumps and salvage yards. The toxic forms are tetra-, penta-, hexa-, hepta-, and octachloronaphthalenes, with the hexa and hepta forms being the most toxic.558
Chlorinated naphthalene interferes with the conversion of carotene to vitamin A. Serum vitamin A levels decrease significantly a few days after exposure and remain decreased for at least 4 weeks.558
Initial clinical signs include weight loss, anorexia, and depression. Excessive salivation and lacrimation occur because of the formation of papular stomatitis and keratinization of the meibomian glands. Several weeks later, nonpruritic thickening and fissuring of the skin occur. Hyperkeratosis involves the withers, neck, head, trunk, and medial thighs; but usually does not involve the lower legs. Diarrhea may occur late in the disease. Postmortem findings include epithelial hyperplasia or metaplasia of the gallbladder, bile ducts, salivary glands, pancreas, and genital tract.558
Diagnosis is based on clinical signs and a low vitamin A level. Suspected source material can be analyzed for chlorinated naphthalene. Treatment with vitamin A may minimize some clinical signs, but treatment of this toxicosis is usually unsuccessful, especially after the appearance of skin lesions.558
Pentachlorophenol (PCP) is used primarily as a wood preservative. Residues have been found in cattle exposed to wood troughs, silos, barns, and fences treated with PCP. Horses have developed toxicosis when bedded on wood shavings that contain PCP.559-561
The primary mechanism of action is uncoupling of oxidative phosphorylation.559,561 PCP is quickly absorbed from the GI tract and excreted in the urine. It is stored mainly in the liver and kidney and acts as a mild hepatotoxin.510 The half-life in cattle is 1.5 days.559
Acute clinical signs in cattle include weight loss, depression, anorexia, intense thirst, and decreased milk production.559,560 Chronic signs in cattle are dyspnea, hyperkeratosis, liver damage, and increased abortion rate.559 Horses have anorexia, dependent edema, weight loss, and alopecia. The skin has cracks and fissures that exude serum. Clinical pathology reveals hepatic changes, anemia, and thrombocytopenia. Horses also may develop colic or recurrent hoof problems.561
Liver, kidney, and serum can be analyzed for PCP. Because of the rapid rate of excretion, serum PCP concentrations may be useful only during acute toxicosis.561 No antidote exists, and treatment is usually unsuccessful. Residues may be a concern, especially from dioxin-related contaminants in the “penta”-treated wood.
Phosphatic fertilizers selectively promote legume instead of grass growth. Therefore these are popular fertilizers for maintaining subterranean clover pastures. The major components of phosphatic or superphosphate fertilizers are calcium pyrophosphate, calcium orthophosphate, calcium sulfate, and sodium fluoride. Toxicosis is believed to be a result of the phosphate and fluoride. It usually occurs after a short pasture has been top-dressed recently.562 The fertilizer is not usually palatable, except to ravenous animals.
Sheep have developed ataxia, bruxism, depression, and diarrhea. Animals will be hypocalcemic, probably because of renal failure. Hyperphosphatemia does not occur until oliguria develops and the animal is near death. Gross lesions include hyperemic GI mucosa, pulmonary edema, and bloody intestinal contents. Histopathologic examination reveals acute proximal renal tubular necrosis.562
Diagnosis is based on history, clinical signs, and lesions. Treatment is limited to supportive care, which is generally successful if the disease is diagnosed early.562
Sodium borate is mildly toxic, and clinical signs may not be seen in ruminants until they consume a near-lethal dose. Toxicosis usually occurs only if animals eat concentrated fertilizer.563 The mechanism of action is unknown, but boron may have a stimulatory effect on serotonergic and dopaminergic neurons.564
Reported clinical signs in cattle include weakness, depression, muscle fasciculations, seizures, and a spastic gait. Most animals develop diarrhea and become dehydrated. Gross and microscopic lesions are not seen.563 Goats that were given a sublethal dose of boron developed anorexia and depression. Seizure-like activity consisted mostly of ear flicking and chomping motions; however, tremors, stargazing, head jerking, and extensor rigidity also were noted.564
Liver, kidneys, and rumen contents can be analyzed for boron content.563 Treatment is limited to supportive care.
Vitamin K3 is the synthetic vitamin menadione sodium bisulfite. It has been used as a treatment for anticoagulant rodenticide toxicosis, sweet clover (dicumarol) toxicosis, and exercise-induced pulmonary hemorrhage. Its popularity stemmed from being much less expensive than vitamin K1. Studies demonstrate, however, that vitamin K3 is not an effective treatment for sweet clover disease in cattle.565 Furthermore, case reports indicate that vitamin K3 is toxic to horses, even when used at the manufacturer’s recommended dose.566-568
The mechanism for the toxicosis is unknown. Within 4 to 48 hours of administration of vitamin K3, horses become depressed, anorexic, and weak. They may develop muscle stiffness, laminitis, or colic.566 The horses develop renal failure as evidenced by increased BUN and creatinine concentrations. Proteinuria, hematuria, and low specific gravity are found on urinalysis. Serum electrolyte levels are consistent with renal tubular disease: hyponatremia, hypochloremia, and hyperkalemia. Some patients develop hypercalcemia.568 Grossly, the kidneys are enlarged.566 Microscopically, the kidneys have nephrosis with tubular dilation, epithelial degeneration, and necrosis.568 Diagnosis is based on history, clinical signs, and lesions. Treatment should include diuresis and maintenance of serum electrolyte concentrations.567
Propylene glycol is used as a vehicle for drugs with poor water solubility, for treatment of bovine ketosis, and in some new antifreeze products.569 Toxicosis has been reported when cows are overdosed or when horses are accidentally dosed with propylene glycol.569,570
The median toxic dose of propylene glycol in cattle is 2.6 g/kg body weight.570 Ataxia develops in 2 to 4 hours and resolves by 24 hours after dosing. The cattle also become depressed and temporarily recumbent. Serum and cerebrospinal fluid osmolality increase.570
A horse mistakenly given propylene glycol rather than mineral oil developed ataxia and depression in 10 to 15 minutes. The horse also developed pain, excessive salivation, and sweating, but these signs disappeared within 5 minutes. The animal developed rapid, shallow breathing and cyanosis and died of respiratory distress the next day.569 Gross lesions were not seen. Histopathologic findings included myocardial perivascular edema, pulmonary edema, scattered hepatocyte necrosis, and peracute renal infarcts.569
Serum and urine can be analyzed to determine the presence of propylene glycol.569,570 Propylene glycol causes lactic acidosis in humans, which is treated with sodium bicarbonate. This treatment was unsuccessfully used in the horse described here569; if acidosis occurs, however, sodium bicarbonate may be beneficial if the disease is treated early.
Isopropyl alcohol is used as a topical antibacterial agent. When ingested, it is quickly absorbed from the GI tract and metabolized into acetone by the liver through alcohol dehydrogenase. The majority of the acetone is excreted by the kidney and to a lesser extent by the lungs.571
Toxicosis in a horse was reported when 2 L of alcohol was mistaken for mineral oil and administered by nasogastric tube. Initially the horse was depressed and reluctant to move before collapsing and becoming semicomatose. A menace response was not detected, and pupillary light reflexes were slow. Treatment consisted of repeated gastric lavage with 2-L aliquots of warm water, followed by activated charcoal and intravenous fluids. Activated charcoal was repeated the following day, and the horse recovered from the incident. However, the odor of acetone could be detected on the horse’s breath for about 4 days, and acetone was detectable in the horse’s serum during this time.571
This anthelmintic combined with piperazine and carbon disulfide has been used for horses in the past.572,573 Phenothiazine currently is being manufactured for horses in combination with piperazine and trichlorfon. Phenothiazine also has been used in mineral blocks and protein supplements for ruminants.574 Phenothiazine is toxic to both horses and ruminants but causes different diseases.
Phenothiazine causes primary photosensitization in ruminants. The rumen converts phenothiazine to a phototoxin, phenothiazine sulfoxide. This toxic metabolite can be converted by the liver to a nontoxic metabolite, leukophenothiazine; if the liver is overwhelmed, however, toxicosis can occur. Most cases occur in debilitated or young animals that do not have a fully functional liver.574
Clinical signs begin as erythema and edema combined with varying degrees of pruritus, photophobia, and pain. Vesicles and bullae form and progress to oozing, necrosis, and ulceration of the skin. These lesions are usually confined to areas that have white pigmentation or have little hair and are exposed to sunlight. The tail, ears, teats, feet, or ventral surface of the tongue may slough. The skin of black cattle does not usually slough, but these animals can develop epiphora, corneal edema, and blindness because the phototoxin is also secreted in tears and aqueous humor.574,575
Diagnosis is based on the history of phenothiazine consumption and the skin lesions. A skin biopsy may be helpful but usually is not necessary because the lesions are uniquely confined to lightly pigmented skin.
No antidote exists for phenothiazine toxicosis, and treatment is limited to supportive care. Antibiotics may be needed to treat secondary bacterial infections of the skin. Antiinflammatory drugs may be indicated for pain. When prescribing drugs for ruminants with photosensitization, those that can compromise the liver should be avoided. Affected animals should be housed and fed in areas out of direct sunlight to prevent further damage to the skin.
Phenothiazine acts as an oxidant to produce hemolytic anemia in horses. Heinz bodies (precipitated denatured hemoglobin) damage the red blood cell membrane, which results primarily in intravascular hemolysis. Toxicosis has been noted primarily in horses that are in poor condition before exposure to the phenothiazine.576 Primary clinical signs include anorexia, depression, weakness, icterus, anemia, and hemoglobinuria.572,573 Colic, diarrhea, fever, and dependent edema are less frequently reported clinical signs.576 Clinical pathology reveals anemia and elevated indirect bilirubin levels.576
Diagnosis is based on a history of exposure to phenothiazine and ruling out other causes of hemolytic anemia in the horse. Treatment is basically supportive. A blood transfusion may be necessary if the anemia reaches a critical level.576
Nonprotein nitrogen (NPN) products are converted by ruminal microorganisms to ammonia, which is used to form amino acids. Therefore, ruminants can use the nitrogen from NPN for part of their diet rather than the more expensive natural proteins. Urea is the best known source of NPN, and it is also the most toxic.577
Toxicosis can result from overexposure or loss of acclimation to NPN. Too much NPN may be fed to animals because of a miscalculation or by contamination. Urea toxicosis has been reported in cattle that drank from a water source that was contaminated with urea fertilizer.578 Ruminants acclimate to NPN in their diets through the ruminal microorganisms. Animals that have been acclimated to a certain level of NPN in their diets and then go without NPN for more than 1 day can develop toxicosis. Ruminants quickly lose their adaptation to NPN, and toxicosis can occur when urea consumption resumes, even if NPN is fed at the same level as previously.
Ammonia that is not used by the ruminal microorganisms is absorbed from the rumen and detoxified by the liver back into urea for excretion. Toxicosis occurs when the microorganisms and the liver are overwhelmed by the level of ammonia.577-579 As the ammonia level increases in the rumen, the ruminal pH increases and creates a shift from charged ammonium ions to uncharged ammonia. The uncharged ammonia is absorbed readily across the rumen wall and increases the ammonia level in the blood.577
Clinical signs begin 30 minutes to 4 hours after ingestion of NPN and include weakness, dyspnea, salivation, bruxism, bloat, and convulsions. Because death can occur in a few hours, some animals may be found dead with no clinical signs observed. The rumen pH will be greater than 8.0 with NPN toxicosis. Rumen pH can decrease with time after death, so the pH should be determined on a recently dead animal.577,579
Diagnosis can be made by analyzing rumen contents, whole blood, or an eye for ammonia. Because ammonia is volatile, the samples should be frozen immediately after collection. Feed material and rumen contents can be analyzed for urea. Urea concentration in the rumen may not be indicative of the amount that was eaten because the microorganisms continue to convert urea to ammonia even after the animal has died. Therefore, a diagnosis should not be based solely on the urea level in the rumen, but in conjunction with the ammonia levels in the animal.
Treatment focuses on decreasing the amount of ammonia absorbed from the rumen. Adult cattle should be given 20 to 30 L of cold water orally to reduce the microorganisms’ ability to convert urea to ammonia. These animals also should receive 2 to 6 L of 5% acetic acid (vinegar) to decrease the pH in the rumen so that ammonia absorption is minimized.577 Rumenotomies can be used to remove the excess NPN source.
To prevent toxicosis, NPN in feed should not exceed 40% of the total nitrogen requirement, and the animals should be acclimated slowly to NPN. Urea should not be fed at a concentration higher than 3% of the grain ration or 1% of the total ration.577
Molasses, hay, and silage can be treated with aqueous or anhydrous ammonia to increase the dietary quality for ruminants. Under certain conditions, these ammoniated feeds can cause “bovine bonkers,” a disease characterized by hyperexcitability. Treatment conditions that predispose to the occurrence of the toxicosis are ammoniating feedstuffs with more than 20% moisture, treating feedstuffs that contain ample soluble sugars, overapplying the ammonia, or treating the forage during high ambient temperatures. High-quality hays, such as wheat, Sudan, alfalfa, orchardgrass, Bermuda grass, fescue, and sorghum, contain high levels of soluble sugars and are more often incriminated in toxicosis than are low-quality hays such as corn stalks, corn silage, and most small grain straws.577
The mechanism of bovine bonkers is not completely understood. Pyrazines and imidazoles are the primary byproducts formed during ammoniation. The two major imidazoles that are formed, 2-methylimidazole (2-me-I) and 4-methylimidazole (4-me-I), cause convulsions in mice, with 4-me-I being more potent. Administration of 4-me-I has experimentally reproduced the disease in a nursing cow without affecting the calf.577 Nursing calves in field cases have developed the disease,580,581 even though the dams did not. However, when orally dosed with 4-me-I, cows developed the disease but the calves did not, despite the imidazole being detected in the milk and colostrum.582 Therefore, more work is needed regarding the mechanism of this disease.
The most striking clinical sign is hyperexcitability, which can occur spontaneously or can be induced by excitement. Animals will suddenly stampede and run in circles or in a straight line while they collide with other animals or with buildings and fences. Other clinical signs include ear twitching, mydriasis, trembling, salivation, increased urination, increased defecation, and bellowing. Gross lesions are not significant other than bruising and broken bones that are self-inflicted.577,580,583
Diagnosis is based on clinical signs and a history of feeding ammoniated feed. Treatment is limited to sedation of animals.581 Thiamine also has been used as a treatment, with variable results.577 It is often not possible to approach an affected animal to treat it without endangering the handler. Most animals recover spontaneously once the ammoniated feed source is removed.
Prevention of ammoniated toxicosis focuses on properly treating the feed. Only poor-quality roughages with low levels of soluble sugars should be ammoniated. The amount of ammonia used should not exceed 3% of the dry weight of the forage. Ammoniate only during cool weather so that the processing temperature of the forage is less than 70° C (158° F).577,580
Ionophore antibiotics are used as coccidiostats and feed additives for poultry and cattle. Ionophores alter the rumen so that a higher level of propionic acid is produced for improved feed efficiency. They also are used to prevent rumen acidosis and emphysema in cattle.584-588 Toxicosis can result from calculation or mixing errors or from use in inappropriate species. Cattle and sheep have been poisoned by ingesting litter from poultry that had been treated with an ionophore.589
Ionophores form lipid-soluble complexes with cations to facilitate transport of the cations across lipid membranes. The monovalent ionophores are monensin, salinomycin, and narasin. Monensin preferentially complexes with sodium ions, whereas salinomycin and narasin preferentially bind with potassium ions. Lasalocid is a divalent ionophore that binds with divalent cations, such as calcium and magnesium ions.585,587
Horses are the most sensitive species to the ionophore antibiotics.586,590 The recommended dose of monensin for cattle can be lethal to a horse. Acute clinical signs in horses include colic, anorexia, weakness, and ataxia.586 Creatinine phosphokinase (CPK) significantly increases within 24 hours; AST and serum ALP activities are increased to a lesser degree.586 Unconjugated serum bilirubin will be slightly but consistently increased. Erythrocyte fragility increases.590 Serum enzymes can be used diagnostically but are poor prognostic indicators.591 If the animal dies peracutely, significant gross lesions may not be present. Acutely affected horses develop degeneration and necrosis of the cardiac muscle and to a lesser degree the skeletal muscles.587
If horses survive the acute episode of toxicosis, they often experience delayed toxicosis because of permanent damage to the heart. These animals have marked cardiac myopathy and fibrosis.588 The most noticeable clinical sign is exercise intolerance, and affected animals may collapse and die during exercise, making them hazardous to use as riding horses.
Whereas the heart is the most affected organ in horses, ionophores damage the cardiac and skeletal muscles more equally in ruminants.587 Clinical signs in feedlot cattle include anorexia, pica, diarrhea, hindlimb ataxia, and dyspnea. These animals have postmortem lesions of hydrothorax, ascites, and pulmonary edema besides hemorrhages and necrosis of the cardiac and skeletal muscles.592 Signs of weakness, increased respiratory rate, nasal discharge, and reddened noses have been reported in dairy calves. Postmortem examination revealed pulmonary edema accompanied by pleural and peritoneal effusions. The hearts had myocardial necrosis.585 Sheep reportedly develop depression, anorexia, diarrhea, and stiffness. CPK and AST activities are increased. Necrosis of the heart and diaphragm has been reported.584
Diagnosis relies on finding appropriate clinical signs and lesions. Currently, analysis for ionophores in tissue or serum is not reliable; however, the feed source can be analyzed for ionophores.587
Antidotes for ionophores are not available.586,587 Mineral oil or activated charcoal may decrease further absorption of the toxicant. Large volumes of intravenous fluids are needed to treat dehydration and shock.586 Serum electrolyte levels should be monitored frequently and fluid electrolytes adjusted accordingly.
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506 Smith R, Morden BB, Ellis LB. Diphenylmercury poisoning in cattle. Can Vet J. 1992;33:135.
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529 Smith EA, Oehme FW. A review of selected herbicides and their toxicities. Vet Hum Toxicol. 1991;33:596.
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534 Duke SO. Overview of herbicide mechanisms of action. Environ Health Perspect. 1990;87:263.
535 Allender WJ, Glastonbury JW. Simazine toxicosis in sheep. Vet Hum Toxicol. 1992;34:422.
536 Kobel W, et al. Protective effect of activated charcoal in cattle poisoned with atrazine. Vet Hum Toxicol. 1985;27:185.
537 Byars TD, Greene CE, Kemp DT. Antidotal effect of vitamin K1 against warfarin-induced anticoagulation in horses. Am J Vet Res. 1986;47:2309.
538 Thijssen HHW, et al. Warfarin pharmacokinetics in the horse. Am J Vet Res. 1983;44:1192.
539 Dorman DC. Anticoagulant, cholecalciferol, and bromethalin-based rodenticides. Vet Clin North Am Small Anim Pract. 1990;20:339.
540 Mount ME. Diagnosis and therapy of anticoagulant rodenticide intoxications. Vet Clin North Am Small Anim Pract. 1988;18:115.
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542 Vrins A, Carlson G, Feldman B. Warfarin: a review with emphasis on its use in the horse. Can Vet J. 1983;24:211.
543 Scott EA, Sandler GA, Byars TD. Warfarin: effects on anticoagulant, hematologic, and blood enzyme values in normal ponies. Am J Vet Res. 1979;40:142.
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549 Sutherland C. Metaldehyde poisoning in horses. Vet Rec. 1983;112:64.
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555 Edwards WC. Toxicology of oil field wastes. Vet Clin North Am Food Anim Pract. 1989;5:363.
556 Boermans HJ, Ruegg PL, Leach M. Ethylene glycol toxicosis in a pygmy goat. J Am Vet Med Assoc. 1988;193:694.
557 Hewlett TP, et al. Ethylene glycol and glycolate kinetics in rats and dogs. Vet Hum Toxicol. 1989;31:116.
558 Panciera RJ, et al. Bovine hyperkeratosis: historical review and report of an outbreak. Compend Cont Educ (Pract Vet). 1993;15:1287.
559 Exon JH. A review of chlorinated phenols. Vet Hum Toxicol. 1984;26:508.
560 Osweiler GD, Van Gelder GA, Zumwalt RW. Toxicologic and residue aspects of pentachlorophenol (PCP). Proc Am Assoc Vet Lab Diagn. 1977;20:159.
561 Kerkvliet NI, et al. Dioxin intoxication from chronic exposure of horses to pentachlorophenol-contaminated wood shavings. J Am Vet Med Assoc. 1992;201:296.
562 East NE. Accidental superphosphate fertilizer poisoning in pregnant ewes. J Am Vet Med Assoc. 1993;203:1176.
563 Sisk DB, Colvin BM, Bridges CR. Acute, fatal illness in cattle exposed to boron fertilizer. J Am Vet Med Assoc. 1988;193:943.
564 Sisk DB, et al. Experimental acute inorganic boron toxicosis in the goat: effects on serum chemistry and CSF biogenic amines. Vet Hum Toxicol. 1990;32:205.
565 Casper HH, et al. Evaluation of vitamin K3 feed additive for prevention of sweet clover disease. J Vet Diagn Invest. 1989;1:116.
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567 Schmitz DG. Toxic nephropathy in horses. Compend Cont Educ (Pract Vet). 1988;10:104.
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573 Blevins DI, Miller CC, Kleckner MD. Effects of a piperazine—carbon disulfide—phenothiazine preparation on hemoglobin and packed cell values of horses. J Am Vet Med Assoc. 1971;159:1260.
574 Rowe LD. Photosensitization problems in livestock. Vet Clin North Am Food Anim Pract. 1989;5:301.
575 Casteel SW, et al. Photosensitization: an investigation and review of the problem in cattle of south Texas. Vet Hum Toxicol. 1986;28:251.
576 McSherry BJ, Roe CK, Milne FJ. The hematology of phenothiazine poisoning in horses. Can Vet J. 1966;7:3.
577 Haliburton JC, Morgan SE. Nonprotein nitrogen—induced ammonia toxicosis and ammoniated feed toxicity syndrome. Vet Clin North Am Food Anim Pract. 1989;5:237.
578 Caldow GL, Wain EB. Urea poisoning in suckler cows. Vet Rec. 1991;128:489.
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580 Henderson J, Dempsey DD. Toxicosis caused by ammoniated hay in calves. Can Vet J. 1991;32:180.
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582 Morgan SE, Edwards WC. Pilot studies in cattle and mice to determine the presence of 4-methylimidazole in milk after oral ingestion. Vet Hum Toxicol. 1986;28:240.
583 Morgan SE, Edwards WC. Bovine bonkers: new terminology for an old problem. Vet Hum Toxicol. 1986;28:16.
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585 Blanchard PC, et al. Lasalocid toxicosis in dairy calves. J Vet Diagn Invest. 1993;5:300.
586 Rollinson J, Taylor FGR, Chesney J. Salinomycin poisoning in horses. Vet Rec. 1987;121:126.
587 Novilla MN. The veterinary importance of the toxic syndrome induced by ionophores. Vet Hum Toxicol. 1992;34:66.
588 Muylle E, et al. Delayed monensin sodium toxicity in horses. Equine Vet J. 1981;13:107.
589 Fourie N, et al. Cardiomyopathy of ruminants induced by the litter of poultry fed on rations containing the ionophore antibiotic, maduramicin. Onderstepoort J Vet Res. 1991;58:291.
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