Veterinary · Para-clinical · also MSVE VPT-421
Poisoning by metals, plants, mycotoxins, pesticides, non-protein nitrogen, venoms and pollutants, with residues in food and the antidotes used.
In the exams: AVE Paper 1 toxicology at least 3; SAVC toxicology 10 (plus southern African plant poisonings); ICAR AIEEA-PG 13 Unit IV (poisonous plants, agro-chemicals); ICAR AICE-JRF core group 07
Veterinary toxicology is the study of poisons in animals: where they come from, how they enter and leave the body, what they do to cells and organs, how a poisoning is recognised and proved, and how it is treated and prevented. It also covers residues passing into food and harm to wildlife. A poison (toxicant) is any substance that causes harm at some dose; a toxin is a poison made by a living organism, such as a mycotoxin, a plant toxin or a venom.
Poisoning is common and often a herd event: one batch of mouldy feed, a frosted sorghum crop, a spilled bag of urea or a discarded battery can kill many animals in a day. In companion animals the usual cases are rodenticides, permethrin on cats, xylitol, grapes, slug bait and snake bite. Many cases have legal consequences, so evidence must be collected properly.
This manual moves from principles and general management through each toxicant group to ecotoxicology and residues. Antidotes are described by mechanism; doses are left to the product label and national formulary, because approved products and food-animal rules differ by country.
Paracelsus's principle, that the dose makes the poison, is the foundation of the subject. Toxicity is the inherent capacity of a substance to cause harm; risk is the probability of harm under actual exposure.
Concentrations in feed and water are expressed as parts per million (ppm), which equals mg/kg of feed or mg/L of water, or as parts per billion (ppb, micrograms per kg). One per cent equals 10,000 ppm. To turn a feed concentration into a dose, multiply the concentration by the amount eaten and divide by body weight: a 500 kg cow eating 12 kg of feed containing 50 ppm of a toxicant takes in 600 mg, or 1.2 mg/kg per day.
A graded dose-response describes how the size of an effect in one animal rises with dose. A quantal (all-or-none) dose-response describes the proportion of a population that shows an effect, such as death, at each dose; it is usually sigmoid on a log-dose scale and is linearised by probit analysis. The median lethal dose (LD50) is the dose, statistically derived, that kills 50% of a test population by a stated route in a stated time; LC50 is the equivalent concentration in air or water. A lower LD50 means greater acute toxicity.
The therapeutic index (TI) is LD50 divided by ED50 (the median effective dose); a drug with an LD50 of 50 mg/kg and an ED50 of 5 mg/kg has a TI of 10. The margin of safety is often expressed more cautiously as LD1/ED99, because two curves with the same TI can overlap differently. For chronic exposure, regulators use the no-observed-adverse-effect level (NOAEL) and the lowest-observed-adverse-effect level (LOAEL) from long-term studies.
Lipid-soluble, un-ionised molecules cross membranes readily; this is why organophosphates and organochlorines are absorbed through skin and why weak acids and bases are trapped in compartments where they become ionised (ion trapping). Distribution follows blood flow and binding: lead is stored in bone, organochlorines in fat, cadmium in kidney, fluoride in bone and teeth.
Biotransformation usually makes a poison more water-soluble and easier to excrete. Phase I reactions (oxidation, reduction, hydrolysis, largely by cytochrome P450 enzymes) add or expose a functional group; phase II reactions conjugate it with glucuronic acid, sulfate, glutathione, acetate or amino acids. Sometimes phase I produces a more toxic product, called bioactivation: aflatoxin B1 is converted to a reactive epoxide, parathion to paraoxon, and fluoroacetate is incorporated into fluorocitrate, the classic 'lethal synthesis' that blocks the citric acid cycle.
Excretion is mainly renal and biliary; some poisons undergo enterohepatic recycling, which is why repeated doses of activated charcoal can shorten their stay. Milk and eggs are routes of excretion that matter for food safety: aflatoxin M1, organochlorines and some drugs appear in milk.
Cats have low activity of several UDP-glucuronosyltransferases, so they conjugate phenols, paracetamol (acetaminophen) and many other compounds poorly; they are also highly sensitive to permethrin. Dogs and cats vomit, but horses, ruminants, rabbits and rodents do not vomit effectively, so emesis is not an option in them. Some herding-breed dogs carry a defect in the MDR1 (ABCB1) gene coding for P-glycoprotein, which lets macrocyclic lactones such as ivermectin enter the brain.
Rumen microbes reduce nitrate to nitrite, hydrolyse cyanogenic glycosides to release hydrogen cyanide, and convert urea to ammonia, so ruminants are more susceptible to these three than monogastrics. Horses are exceptionally sensitive to ionophores and yew; sheep are the most sensitive domestic species to copper; young poultry and ducklings are highly sensitive to aflatoxin; pigs are sensitive to zearalenone, salt poisoning with water deprivation, and ochratoxin.
Poisoning is suspected when several animals fall ill suddenly after a change in feed, water, pasture or management, when signs fit a known toxic syndrome, or when an owner reports access to a product. The diagnosis rests on four pillars: history of exposure, compatible clinical signs, compatible lesions, and chemical or biological confirmation. Response to a specific antidote supports the diagnosis but does not prove it.
The history covers numbers at risk, sick and dead; time course; feed, water and pasture changes; treatments, spraying and building work; access to dumps and batteries; and weather.
Samples are chosen for the suspected toxicant but a general set covers most cases: whole blood (EDTA or heparin, depending on the test), serum, urine, stomach or rumen contents, liver, kidney, fat, brain (half fixed, half chilled or frozen), eye or aqueous humour, and representative samples of feed, water, baits and plants. Keep samples chilled or frozen in clean, separate, labelled containers; formalin-fixed tissue is for histopathology, not chemistry. Where litigation is possible, record who collected, sealed and handed over each sample (chain of custody) and keep duplicate samples.
General management follows a fixed order: stabilise, decontaminate, give an antidote if one exists, enhance elimination where possible, and support.
Dermal decontamination means washing with lukewarm water and a mild hand dishwashing detergent, with the handler protected; this is central in permethrin and organophosphate spot-on and dip exposures.
Emesis is useful in dogs and cats within a short time after ingestion of a non-corrosive poison, in an alert animal with a gag reflex. It is contraindicated after corrosives (acids, alkalis) and petroleum distillates (risk of aspiration and further damage), in animals that are seizuring, depressed or already vomiting, and in species that cannot vomit. Apomorphine is commonly used in dogs; alpha-2 agonists such as xylazine or dexmedetomidine are commonly used in cats. Doses: label and national formulary.
Gastric lavage under general anaesthesia with a cuffed endotracheal tube is used when emesis is impossible or unsafe. Activated charcoal adsorbs many organic poisons and reduces absorption; it binds metals, alcohols, xylitol, strong acids and alkalis and many salts poorly. Repeated doses help with poisons that recycle through bile.
Elimination can be enhanced by fluid diuresis, by changing urine pH to trap ionised poisons, and in referral centres by haemodialysis or haemoperfusion.
Chelators bind metal ions into stable, excretable complexes: calcium disodium EDTA for lead; dimercaprol (British anti-Lewisite, BAL) for arsenic, mercury and lead; succimer (dimercaptosuccinic acid, DMSA) for lead and mercury, mainly in small animals; D-penicillamine for copper and lead; ammonium tetrathiomolybdate for copper in sheep; deferoxamine for iron. The calcium salt of EDTA is used, not disodium EDTA, which causes hypocalcaemia.
Receptor antagonists block the toxic action at its target: atropine blocks muscarinic receptors in organophosphate and carbamate poisoning; digoxin-specific antibody fragments bind cardiac glycosides.
Enzyme reactivators restore a poisoned enzyme: pralidoxime (2-PAM) reactivates acetylcholinesterase inhibited by an organophosphate before 'aging' occurs. Competitive substrates or enzyme inhibitors divert metabolism: ethanol or fomepizole blocks alcohol dehydrogenase in ethylene glycol poisoning; vitamin K1 bypasses the block in the vitamin K cycle caused by anticoagulant rodenticides.
Chemical converters change the poison or its target: sodium nitrite generates methaemoglobin, which binds cyanide as cyanmethaemoglobin; sodium thiosulfate donates sulfur for rhodanese to convert cyanide to thiocyanate; hydroxocobalamin combines with cyanide to form cyanocobalamin; methylene blue reduces methaemoglobin back to haemoglobin in nitrite poisoning; N-acetylcysteine replenishes glutathione in paracetamol poisoning.
Binders and antibodies neutralise the poison before it acts: antivenoms, activated charcoal, Prussian blue for radiocaesium and thallium.
Lead is the commonest metal poisoning of cattle worldwide and is important in dogs, waterfowl and wildlife. Sources include discarded lead-acid batteries, old lead-based paint, putty and linoleum, used engine oil, lead shot and fishing weights, contaminated soil near smelters and mines, and burnt sites where batteries or paint were destroyed.
Lead binds sulfhydryl groups and substitutes for calcium and zinc. It inhibits delta-aminolevulinic acid dehydratase and ferrochelatase in haem synthesis, damages capillary endothelium in the brain (causing cerebral oedema and laminar cortical necrosis), and injures renal tubular cells and peripheral nerves.
In cattle acute poisoning causes blindness, head pressing, bruxism (teeth grinding), muscle tremor, twitching of eyelids and ears, frothing, bellowing, circling and convulsions, often with sudden death in calves; subacute cases show dullness, anorexia, ruminal stasis and blindness. Dogs show gastrointestinal signs (vomiting, abdominal pain, anorexia) and nervous signs (anxiety, seizures, blindness).
Laboratory signs in dogs include nucleated red blood cells out of proportion to anaemia and basophilic stippling of erythrocytes. At necropsy, cattle may show lead objects or flakes in the reticulum and cerebrocortical softening; histologically, acid-fast intranuclear inclusion bodies in renal tubular epithelium are characteristic. Diagnosis is by whole blood lead (lead is carried in red cells, so serum is the wrong sample) and by liver or kidney lead at post mortem.
Treatment removes the source (rumenotomy, endoscopy or surgery for objects; oral magnesium or sodium sulfate to precipitate lead in the gut), chelates absorbed lead with calcium disodium EDTA by slow intravenous infusion in courses separated by rest days, and supports the brain with thiamine, which improves the response in cattle, and anticonvulsants. Succimer given orally is used in dogs and birds.
Arsenic occurs in inorganic forms (trivalent arsenite and pentavalent arsenate) and organic forms.
Trivalent inorganic arsenic binds sulfhydryl groups, especially the lipoic acid of pyruvate dehydrogenase, and blocks cellular respiration; pentavalent arsenate can substitute for phosphate and uncouple oxidative phosphorylation. The main target is capillary endothelium, especially in the gut, causing dilatation, transudation and haemorrhage. Acute poisoning in cattle produces severe colic, profuse watery diarrhoea that may contain mucosal shreds or blood ('rice-water' stools are described in texts), weakness, trembling, collapse and death within hours to a few days.
Organic phenylarsonic compounds (arsanilic acid, roxarsone) were once fed to pigs and poultry as growth promoters and for swine dysentery; their use has been withdrawn in many countries. Overdose causes a different disease, demyelination of peripheral and optic nerves, with incoordination, paresis and blindness in pigs, while the animals keep eating.
Diagnosis in acute cases is by arsenic in liver, kidney, urine or stomach contents. Treatment of inorganic poisoning uses dimercaprol (BAL) by deep intramuscular injection; thioctic acid (lipoic acid) and oral sodium thiosulfate are also used, with fluids and gut protectants.
Mercury toxicity depends on its chemical form. Inorganic mercuric salts are corrosive: ingested, they cause stomatitis, vomiting, bloody diarrhoea and, after absorption, acute renal tubular necrosis. Organic mercury, especially methylmercury and the alkylmercury fungicides once used to dress seed grain, is lipid-soluble, crosses the blood-brain barrier and placenta, and causes a chronic neurological disease with ataxia, blindness, tremor and paralysis, and cerebellar and cerebrocortical neuronal degeneration.
Methylmercury is formed from inorganic mercury by microorganisms in sediments and is concentrated up aquatic food chains (biomagnification).
Diagnosis is by mercury in kidney (inorganic), brain and liver (organic), blood, or feed. Chelators (dimercaprol, succimer) help in inorganic poisoning if given early; they are of little value once organic mercury has damaged neurons.
In the rumen, molybdate and sulfide form thiomolybdates, which bind copper into unabsorbable complexes and, once absorbed, also bind copper in tissues. A high dietary copper to molybdenum ratio therefore favours copper accumulation, and a low ratio (high molybdenum and sulfur) produces copper deficiency.
Sheep are the most susceptible domestic species to copper toxicity because they store copper readily in the liver and excrete little in bile. Chronic copper poisoning is the usual form: copper accumulates in hepatocytes for weeks or months without signs, often from concentrates or mineral mixes formulated for cattle or pigs, from pig or poultry manure spread on pasture, from copper-containing footbaths, or from pastures low in molybdenum. When stress, transport, lactation or reduced feed intake triggers hepatocyte necrosis, copper floods into the blood and causes an acute haemolytic crisis: sudden depression, anorexia, pale then jaundiced mucous membranes, haemoglobinaemia and haemoglobinuria, and death in one to two days. Necropsy shows generalised icterus, a swollen, friable yellow-orange liver, an enlarged dark spleen and dark 'gunmetal' kidneys. Liver copper is the best indicator of body burden; blood copper rises only during the crisis.
Treatment of a flock at risk uses ammonium tetrathiomolybdate given parenterally, or oral ammonium molybdate with sodium sulfate in the feed, to bind and remove copper; D-penicillamine has also been used. Prevention is by formulating sheep rations for sheep.
Molybdenosis (molybdenum-induced copper deficiency) occurs on 'teart' pastures, first described in England, and on soils high in molybdenum. Cattle develop persistent diarrhoea, weight loss and depigmentation of the hair, especially around the eyes ('spectacles').
Selenium has a narrow margin between requirement and toxicity. In pigs and lambs acute poisoning causes dyspnoea, pulmonary oedema, myocardial necrosis and sudden death. In pigs, subacute to chronic toxicity from excessive feed selenium also causes a symmetrical poliomyelomalacia of the ventral horns of the spinal cord, with paralysis of the hindlimbs or all four limbs, and hoof and hair lesions.
Chronic selenosis in grazing herbivores, called alkali disease in the western USA, results from months of eating forages grown on seleniferous soils. Signs include loss of long hair (the mane and tail of horses, the switch of cattle), lameness, and circular cracks and deformities of the hoof wall that may progress to sloughing of the hoof.
Diagnosis uses blood, liver, kidney, hair or hoof selenium and feed analysis. There is no specific antidote; treatment is removal of the source, correction of mixing errors and supportive care.
Fluorosis is chronic fluoride poisoning. Sources are groundwater naturally high in fluoride (in parts of India, China, the East African Rift Valley and elsewhere), unprocessed rock phosphate used as a mineral supplement, industrial emissions from aluminium smelters, brickworks and fertiliser plants deposited on pasture, and volcanic ash.
Fluoride accumulates in bones and developing teeth. Teeth formed while the animal is exposed, before and during eruption, show mottling, chalky white patches, brown staining, pitting and excessive, uneven wear; teeth already formed are not affected, so the pattern of affected incisors dates the exposure. Bones develop periosteal hyperostosis (exostoses), especially on the metatarsals, metacarpals, mandible and ribs, with lameness, stiffness and reduced feed intake and production.
Diagnosis uses fluoride in urine, bone (for example a rib or tail vertebra biopsy), feed and water, together with dental lesions. There is no antidote that reverses bone or dental changes. Management aims to reduce intake: find safe water, use defluorinated phosphate supplements, and give aluminium or calcium salts, which bind fluoride in the gut and reduce its absorption.
Many plants store cyanide as cyanogenic glycosides, which are harmless until the plant is damaged. Chewing, wilting, frost or trampling brings the glycoside into contact with plant beta-glucosidase, and rumen microbes add their own; the glycoside is hydrolysed to a sugar and a cyanohydrin that releases hydrogen cyanide (HCN). Important plants are sorghum and Sudan grass (dhurrin), cherry, apricot and other Prunus species (prunasin and amygdalin), cassava (linamarin), linseed or flax (linamarin), white clover, arrow grass (Triglochin) and some Acacia and Eucalyptus species. Young, rapidly growing shoots, regrowth after drought or grazing, frost-damaged plants and heavily nitrogen-fertilised plants contain the most. Ruminants are more susceptible than horses and pigs because the rumen releases HCN rapidly.
Cyanide binds the ferric (Fe3+) iron of cytochrome c oxidase (cytochrome aa3), the final enzyme of the electron transport chain, and blocks oxygen use by cells. Haemoglobin stays saturated with oxygen that the tissues cannot use, so venous blood is bright cherry red. Signs appear within minutes of eating a toxic plant: excitement, rapid deep breathing, dyspnoea, salivation, muscle tremor, staggering, convulsions and death, often within an hour; many animals are found dead near the plant. The mucous membranes are bright red, not cyanotic.
The lethal dose of HCN for cattle and sheep is cited in texts at about 2 mg/kg, and forage containing more than about 200 ppm HCN potential is regarded as dangerous; values vary with rate of intake, since slow intake allows detoxification.
Diagnosis: the picrate paper test detects HCN in plant or rumen material in the field; samples of rumen contents, liver, muscle and whole blood must be frozen in airtight containers promptly, because cyanide is lost quickly. Treatment is urgent. Sodium thiosulfate provides sulfur for the enzyme rhodanese, which converts cyanide to relatively harmless thiocyanate excreted in urine, and is safe to give alone. Sodium nitrite, given with thiosulfate, oxidises some haemoglobin to methaemoglobin, which pulls cyanide off cytochrome oxidase to form cyanmethaemoglobin; it must not be used when nitrate poisoning cannot be excluded, because it adds to methaemoglobinaemia.
Nitrate itself is of low toxicity; the problem is nitrite. In the rumen, nitrate is reduced to nitrite and then to ammonia; when nitrate intake is high or sudden, nitrite accumulates, is absorbed and oxidises the ferrous (Fe2+) iron of haemoglobin to the ferric (Fe3+) state, forming methaemoglobin, which cannot carry oxygen. Ruminants, especially cattle, are the most susceptible species; pigs are affected mainly when they drink or eat nitrite directly.
Sources are nitrate-accumulating plants, including oats and oat hay, sorghum, Sudan grass, maize, millet, rape, turnip tops, beet tops and weeds such as pigweed (Amaranthus), lamb's quarters (Chenopodium) and nightshades. Accumulation increases with heavy nitrogen fertilisation, drought, cloudy weather, herbicide treatment and frost, and is highest in the lower stem.
Signs appear within a few hours of eating: rapid, laboured breathing, weakness, trembling, staggering, a fast weak pulse, brown-grey or cyanotic mucous membranes, collapse and death. Blood is chocolate-brown. Methaemoglobin concentrations around 30 to 40% cause signs, and death is likely above roughly 80%; pregnant cows that survive may abort days later. Post mortem nitrate in aqueous humour or ocular fluid is a useful diagnostic sample because it stays stable longer than blood.
Diagnosis: diphenylamine spot test on plant stems in the field, laboratory analysis of forage, water, serum, plasma and aqueous humour. Results may be reported as nitrate (NO3), nitrate-nitrogen (NO3-N) or potassium nitrate (KNO3), and mixing them up is a common error: NO3-N × 4.43 = NO3, and NO3 × 0.226 = NO3-N; KNO3 contains 61% NO3. Guidelines often treat forage with less than about 0.5% nitrate in dry matter as generally safe and more than about 1% as potentially toxic, but the cut-offs vary between laboratories and depend on how the result is expressed.
Treatment is methylene blue by slow intravenous injection. Methylene blue is reduced in red cells, via NADPH-methaemoglobin reductase, to leucomethylene blue, which reduces methaemoglobin back to haemoglobin. It is not approved for food animals in some countries, including the USA, and its extra-label use carries residue obligations; doses by label and formulary.
Soluble oxalates occur in large amounts in Halogeton glomeratus and greasewood (Sarcobatus) in North American rangeland, in soursob and other Oxalis species, in Rumex (docks and sorrel), in beet tops, Amaranthus, and in tropical grasses such as Setaria sphacelata, buffel grass (Cenchrus ciliaris), kikuyu and para grass.
In ruminants, soluble oxalate combines with calcium and magnesium in the blood, causing acute hypocalcaemia, and calcium oxalate crystals precipitate in the renal tubules and vessel walls, causing renal failure. Acute poisoning in hungry sheep and cattle moved onto heavily infested range causes weakness, tremor, recumbency, tetany, coma and death, with calcium oxalate crystals visible in the kidneys histologically.
In horses, the main problem is chronic: grazing tropical oxalate-rich grasses binds dietary calcium in the gut, causing nutritional secondary hyperparathyroidism ('big head' or 'bran disease'), with enlargement of the facial bones, lameness and loose teeth.
Treatment of acute ruminant cases is intravenous calcium borogluconate with magnesium, given cautiously, and fluids; prevention is avoiding hungry stock on oxalate plants and giving calcium supplements such as dicalcium phosphate on high-oxalate pastures.
Lantana camara is an ornamental shrub from tropical America that has become a serious weed in India, Australia, southern Africa and elsewhere. Its toxic principles are pentacyclic triterpenes, lantadene A and B, found in leaves and unripe fruit.
Lantadenes damage the bile canaliculi and cause intrahepatic cholestasis. Because the cholestatic liver cannot excrete phylloerythrin, a porphyrin formed in the rumen from chlorophyll, this photodynamic pigment accumulates in the skin, absorbs sunlight and damages unpigmented and lightly haired areas: hepatogenous (secondary) photosensitisation. Signs within a day or two include anorexia, ruminal stasis and constipation, jaundice, photophobia, swelling, weeping and later necrosis and sloughing of the muzzle, ears, eyelids and teats, and sometimes ulceration of the tongue.
Lesions are a swollen, yellow-orange or ochre liver, a distended gall bladder, icterus and nephrosis. Treatment is supportive: remove the animals from the plant and from sunlight into shade, give oral activated charcoal (texts describe large doses to bind lantadenes in the rumen), fluids and electrolytes, and treat skin lesions. Other important causes of hepatogenous photosensitisation are sporidesmin in facial eczema of sheep and cattle (New Zealand, Australia, South Africa), and Tribulus terrestris in 'geeldikkop' of sheep in southern Africa; primary photosensitisation, from plant pigments absorbed without liver damage, is caused by hypericin (St John's wort) and fagopyrin (buckwheat).
Bracken (Pteridium aquilinum) grows worldwide on hill land and forest margins. It produces two distinct diseases depending on species. Its thiaminase causes thiamine deficiency in monogastrics: horses fed hay containing bracken develop 'bracken staggers', with incoordination, a crouching stance, tremor and eventually recumbency and convulsions, which respond to thiamine given promptly.
In ruminants the important toxin is ptaquiloside, a norsesquiterpene glucoside that is a radiomimetic, carcinogenic compound. Acute bracken poisoning in cattle, after several weeks of heavy intake, causes bone-marrow aplasia: thrombocytopenia and leucopenia produce a haemorrhagic syndrome with high fever, petechial and ecchymotic haemorrhages on mucous membranes, bloody faeces, bleeding from the nose and injection sites, and death from haemorrhage and secondary infection.
Long-term, lower intake causes bovine enzootic haematuria, the development of haemangiomas and carcinomas of the urinary bladder wall with intermittent haematuria and anaemia, seen in hill cattle in India, Brazil, Europe and elsewhere. Sheep develop 'bright blindness', a progressive retinal degeneration.
Oleander (Nerium oleander) and yellow oleander (Cascabela, formerly Thevetia, species) contain cardiac glycosides, such as oleandrin, that inhibit the sodium-potassium ATPase of cardiac muscle, like digoxin. Signs are gastrointestinal (colic, diarrhoea, vomiting in dogs) and cardiac: bradycardia or tachycardia, heart block and ventricular arrhythmias, with hyperkalaemia in severe cases; sudden death is common. Treatment is decontamination with activated charcoal, antiarrhythmic drugs such as atropine for bradyarrhythmias and lidocaine for ventricular arrhythmias, correction of potassium, and, where affordable, digoxin-specific antibody fragments.
In southern Africa the most important plant poisonings of cattle are caused by bufadienolide cardiac glycosides. Tulp (Moraea species, formerly Homeria) and slangkop (Drimia, formerly Urginea, species) cause acute poisoning with gastrointestinal and cardiac signs, often when hungry or newly introduced cattle eat them. Repeated small doses of cotyledonosides from plakkies and related Crassulaceae (Tylecodon, Cotyledon, Kalanchoe) cause krimpsiekte in small stock, a chronic paretic condition in which sheep and goats tire, lie down with the neck bent, and stand with feet close together. Other southern African syndromes examined for registration include gousiekte, a delayed heart failure of ruminants several weeks after eating certain Rubiaceae (Pachystigma, Fadogia, Pavetta); vermeersiekte (vomiting disease) of sheep caused by Geigeria; and seneciosis, a chronic pyrrolizidine-alkaloid liver disease with megalocytosis caused by Senecio species (also important in Australia, New Zealand and the Americas).
Yew (Taxus species) contains taxine alkaloids that block sodium and calcium channels in cardiac myocytes. Horses are the most sensitive species, and ingestion of clippings, often thrown over a hedge onto a paddock, typically results in sudden death within hours with little warning; cattle, sheep and dogs are also killed.
Mycotoxins are toxic secondary metabolites of fungi growing on crops in the field or in storage. They are not infectious: the disease follows eating the toxin, is not transmitted between animals, and does not respond to antibiotics.
Diagnosis requires analysis of representative feed samples, because mycotoxins are unevenly distributed in hot spots; the sample must be taken from many points in the lot, and the visible mould does not prove the toxin is present, nor does its absence exclude it.
Aflatoxins are produced mainly by Aspergillus flavus and A. parasiticus on groundnuts (peanuts), maize, cottonseed, copra and other crops, especially under warm, humid storage or drought-stressed field conditions. Aflatoxicosis was recognised in 1960 as 'Turkey X disease', in which about 100,000 turkeys died in England after eating contaminated groundnut meal.
Aflatoxin B1 is bioactivated by hepatic cytochrome P450 to aflatoxin B1-8,9-epoxide, which binds DNA and proteins. The result is hepatocellular necrosis in acute cases and, with chronic exposure, fatty change, megalocytosis, bile duct proliferation, fibrosis and liver cancer; aflatoxin B1 is a proven human carcinogen. Susceptibility is highest in ducklings and turkey poults, followed by young pigs, pregnant sows, calves and dogs; adult ruminants are relatively resistant, and sheep are among the most resistant. Acute signs are anorexia, depression, jaundice, haemorrhage (from reduced clotting-factor synthesis) and death; chronic exposure reduces growth, production and resistance to disease.
Lactating animals convert aflatoxin B1 to aflatoxin M1, which is excreted in milk, so dairy feed is regulated more strictly than feed for other stock. Limits for M1 in milk differ, for example 0.05 microgram/kg in the European Union and 0.5 microgram/kg in the USA and under Codex. There is no antidote; management is removing the feed, supportive care, a high-quality protein and antioxidant-supported diet, and binders in feed at risk.
Ergot alkaloids are produced by Claviceps purpurea in the dark sclerotia (ergot bodies) that replace grains of rye, triticale, wheat, barley and grasses. The alkaloids, such as ergotamine and ergovaline, are alpha-adrenergic and serotonergic agonists and dopamine (D2) agonists. Vasoconstriction produces gangrenous ergotism, with dry gangrene and sloughing of the extremities (feet, tail tip, ear tips) in cattle, especially in cold weather; nervous or convulsive ergotism occurs with some alkaloids. Dopamine agonism suppresses prolactin, causing agalactia in sows and poor udder development.
Tall fescue (Festuca arundinacea, now Lolium arundinaceum) infected with the endophyte Epichloë coenophiala (formerly Neotyphodium) contains ergovaline and related alkaloids. Cattle develop 'summer slump' (hyperthermia, reduced intake and gain, rough coat, seeking shade and water), 'fescue foot' (gangrene of the extremities in cold weather) and fat necrosis. Pregnant mares on infected fescue suffer prolonged gestation, thickened placenta, dystocia, 'red bag' premature placental separation, weak foals, and agalactia; removal from fescue for the last 60 to 90 days of gestation, or treatment with a dopamine D2 antagonist such as domperidone, is recommended by principle.
Zearalenone, produced by Fusarium graminearum and related species on maize and small grains, is an oestrogen analogue that binds oestrogen receptors. Prepubertal gilts show hyperoestrogenism: swelling and reddening of the vulva, vulvovaginitis, enlarged mammary glands and vaginal or rectal prolapse; sows show anoestrus, pseudopregnancy and small litters; boars may show reduced libido.
Other mycotoxins students should know by principle are deoxynivalenol (vomitoxin), which causes feed refusal and vomiting in pigs; T-2 toxin and other trichothecenes, which cause oral and skin necrosis and immunosuppression, especially in poultry; fumonisins from Fusarium verticillioides, which cause equine leukoencephalomalacia (liquefactive necrosis of cerebral white matter) in horses and porcine pulmonary oedema in pigs; ochratoxin A from Aspergillus and Penicillium, which causes nephropathy in pigs and poultry; sporidesmin (facial eczema); and tremorgens such as lolitrem B from endophyte-infected perennial ryegrass, which causes 'ryegrass staggers'.
Organophosphates (OPs), such as chlorpyrifos, diazinon, malathion, dichlorvos and parathion, and carbamates, such as carbaryl, carbofuran, aldicarb, methomyl and propoxur, are insecticides, acaricides and anthelmintics.
Both groups inhibit acetylcholinesterase (AChE), the enzyme that hydrolyses acetylcholine at synapses and neuromuscular junctions. OPs phosphorylate the serine of the enzyme's active site; carbamates carbamylate it. The carbamylated enzyme hydrolyses spontaneously within hours, so carbamate inhibition is reversible and short-lived. The phosphorylated enzyme recovers very slowly and, with time, loses an alkyl group ('aging'), after which it cannot be reactivated and recovery depends on synthesis of new enzyme.
Accumulated acetylcholine causes three groups of signs. Muscarinic signs are salivation, lacrimation, urination, defecation, gastrointestinal hypermotility and colic, bronchoconstriction and bronchial secretion, bradycardia and miosis (remembered as SLUD or DUMBELS). Nicotinic signs are muscle fasciculation, tremor, stiffness, then weakness and paralysis, including of respiratory muscles. Death is usually from respiratory failure caused by bronchial secretion, bronchoconstriction and respiratory muscle paralysis.
Diagnosis: history and signs, and cholinesterase activity in whole blood (live animals) or brain (dead animals; half the brain chilled or frozen), compared with laboratory reference values; activity well below normal (texts commonly cite below about 50% as exposure and below about 25% as consistent with poisoning) supports the diagnosis.
Treatment: atropine blocks muscarinic receptors and is given to effect, until secretions dry and heart rate normalises; it does nothing for nicotinic weakness. Pralidoxime reactivates OP-inhibited enzyme if given before aging, and helps nicotinic signs; it is not used routinely for carbamates. Decontamination is vital: wash the skin, give activated charcoal after ingestion, protect handlers, and ventilate if needed.
Organochlorines include DDT and its analogues (methoxychlor), the cyclodienes (aldrin, dieldrin, endrin, chlordane, heptachlor, endosulfan), and lindane (gamma-hexachlorocyclohexane). Most have been banned or severely restricted under the Stockholm Convention on Persistent Organic Pollutants because they persist in the environment, are stored in fat, bioaccumulate and biomagnify up food chains.
DDT-type compounds keep sodium channels open in neuronal membranes, prolonging depolarisation and causing repetitive firing and tremor. Cyclodienes and lindane antagonise the GABA-A receptor chloride channel, removing inhibition and causing seizures. Acute signs in all species are hyperexcitability, hypersensitivity to stimuli, muscle fasciculation beginning in the face and spreading backwards, abnormal postures, champing of the jaws with frothing, and intermittent or continuous tonic-clonic seizures, often with severe hyperthermia; cattle may be aggressive.
Treatment is decontamination (washing, activated charcoal), anticonvulsants such as diazepam or barbiturates, and cooling. Because residues persist in fat for months, poisoned or exposed food animals present a residue problem; milk and meat testing and withholding decisions follow national rules.
Pyrethrins are natural insecticides from Chrysanthemum (Tanacetum) cinerariifolium flowers; pyrethroids, such as permethrin, cypermethrin, deltamethrin and flumethrin, are synthetic analogues. They slow the closing of voltage-gated sodium channels in nerve membranes, causing repetitive discharges.
Permethrin spot-on and shampoo products formulated for dogs, often at concentrations of 45 to 65%, are toxic to cats, and cats are poisoned by being treated with them or by close contact with a recently treated dog. Their deficient glucuronidation slows permethrin metabolism. Signs begin within hours: hypersalivation, ear and paw flicking, hyperaesthesia, generalised muscle tremor and fasciculation, twitching, ataxia, mydriasis, hyperthermia and seizures; untreated cats may die.
Treatment: stabilise; control tremors with methocarbamol and seizures with diazepam or other anticonvulsants; bathe the cat with mild dishwashing detergent and lukewarm water once it is stable, then dry it and keep it warm, because wet cats become hypothermic; give fluids.
Metaldehyde is a cyclic polymer of acetaldehyde used in slug and snail pellets. Dogs are poisoned most often, because the pellets, sometimes mixed with bran or molasses, are palatable; cats, livestock, horses and birds are also affected.
Signs begin within one to three hours: anxiety, hypersalivation, vomiting, tachycardia, ataxia, continuous muscle tremors and seizures that are not triggered by sound or touch (unlike strychnine), and severe hyperthermia, often above 41°C, which leads to metabolic acidosis, rhabdomyolysis, disseminated intravascular coagulation and multi-organ failure; the syndrome has been nicknamed 'shake and bake'.
There is no antidote. Treatment is aggressive control of tremors and seizures (methocarbamol, diazepam, barbiturates or general anaesthesia), active cooling, intravenous fluids, correction of acidosis, and decontamination by gastric lavage under anaesthesia or by emesis only if the dog is not yet showing signs, followed by activated charcoal.
First-generation compounds, such as warfarin and coumatetralyl, need repeated feeding to kill rodents; second-generation compounds, such as brodifacoum, bromadiolone, difenacoum and difethialone, and the indandiones, such as diphacinone and chlorophacinone, are more potent, have much longer half-lives, and are effective after a single feed. Bait concentrations are low, commonly 0.005% (50 ppm) for many second-generation baits, so an animal must eat a substantial amount of bait for a large dose; the calculation is bait mass = toxic dose (mg) ÷ concentration (mg per g of bait).
These compounds inhibit vitamin K epoxide reductase (VKOR), preventing the recycling of vitamin K1 epoxide to the active hydroquinone needed to carboxylate clotting factors II, VII, IX and X. Existing factors are used up according to their half-lives; factor VII has the shortest half-life, so the prothrombin time (PT) prolongs first, typically within 36 to 72 hours, while clinical bleeding is usually delayed three to five days or more after ingestion. Signs are those of haemorrhage into body cavities and tissues: weakness, pale mucous membranes, dyspnoea from haemothorax or pulmonary haemorrhage, coughing, haematomas, lameness from haemarthrosis, epistaxis, melaena and haematuria.
Diagnosis is by prolonged PT (and later activated partial thromboplastin time), a normal platelet count, response to vitamin K1, and detection of the rodenticide in blood or liver; PIVKA (proteins induced by vitamin K absence) tests are also used. Treatment of a recent ingestion is emesis and activated charcoal, followed either by vitamin K1 or by checking the PT at 48 to 72 hours and treating only if it is prolonged. Vitamin K1 (phytonadione) is given orally with a fatty meal for a course that depends on the compound: about a week or more for first-generation compounds and commonly four weeks or longer for second-generation compounds; the PT is rechecked 48 to 72 hours after the last dose, and treatment is extended if it is prolonged. Vitamin K3 (menadione) is ineffective and nephrotoxic in horses and is not used. Bleeding animals need fresh frozen plasma or fresh whole blood to supply factors at once, because vitamin K1 takes hours to allow new factor synthesis.
Bromethalin uncouples oxidative phosphorylation in the central nervous system, causing loss of ATP, failure of sodium-potassium pumps, and cerebral and spinal cord oedema with intramyelinic vacuolation. High doses cause a convulsant syndrome within hours (tremor, hyperexcitability, hyperthermia, seizures); lower doses cause a paralytic syndrome over days, with hindlimb ataxia and paresis progressing to depression. There is no antidote; decontamination with repeated activated charcoal (it recirculates in bile), control of oedema and seizures, and nursing are the treatment.
Cholecalciferol (vitamin D3) baits cause hypercalcaemia and hyperphosphataemia through increased intestinal absorption and bone resorption, leading to mineralisation of kidneys, blood vessels, stomach and heart, and acute kidney injury. Signs begin one to three days after ingestion: vomiting, polyuria and polydipsia, depression, and cardiac arrhythmias. Treatment uses saline diuresis, furosemide, corticosteroids, and agents that lower calcium, such as calcitonin or a bisphosphonate, with serial calcium and renal monitoring for weeks.
Zinc phosphide and aluminium phosphide release phosphine gas in the acid stomach. Phosphine causes vomiting (the vomit may smell of garlic or rotten fish), abdominal pain, dyspnoea, pulmonary oedema, shock, seizures and death. Phosphine vomited or released during lavage can poison staff, so decontamination is done in a well-ventilated place.
Strychnine antagonises the inhibitory neurotransmitter glycine at postsynaptic receptors in the spinal cord and medulla, so motor neurons fire unchecked. Signs start within minutes to two hours: stiffness, then violent tetanic extensor seizures ('sawhorse' stance, opisthotonos) set off by sound, touch or light, with periods of relaxation between; death is from respiratory paralysis.
Sodium fluoroacetate (compound 1080) is used for vertebrate pest control in Australia and New Zealand and elsewhere under restriction. It is converted to fluorocitrate, which inhibits aconitase and blocks the citric acid cycle. Dogs are extremely sensitive and develop frenzied running, howling, vomiting and seizures, while herbivores show mainly cardiac signs such as arrhythmias and sudden death.
Urea and other non-protein nitrogen (NPN) sources, such as ammonium salts and biuret, are fed to ruminants because rumen microbes use ammonia to make microbial protein. Urea contains 46.6% nitrogen, so each kilogram supplies the nitrogen of about 2.9 kg of crude protein (46.6 × 6.25 = 291%). A frequently taught guideline is that urea should not exceed about 1% of total ration dry matter or about 3% of the concentrate, with gradual adaptation; recommendations vary.
Rumen urease hydrolyses urea rapidly to ammonia. When ammonia forms faster than microbes can use it, rumen pH rises, more ammonia is in the un-ionised form (NH3), which crosses the rumen wall readily, and the liver's capacity to convert it to urea is exceeded. Signs appear within 20 to 60 minutes: restlessness, muscle tremors especially of the face and ears, frothy salivation, frequent urination and defecation, abdominal pain, bloat, bellowing, incoordination, rapid breathing, tetanic spasms and death, often within a few hours. Rumen pH above about 7.5 and a smell of ammonia in rumen contents support the diagnosis; rumen fluid and blood samples must be frozen promptly because ammonia is volatile.
Treatment is to give cold water and dilute acetic acid (vinegar) through a stomach tube. Acid lowers rumen pH so that ammonia becomes the ionised ammonium ion (NH4+), which is poorly absorbed; cold water slows urease activity and dilutes the rumen. Horses are relatively tolerant of urea because they have little urease in the upper gut, but are susceptible to ammonium salts; monogastrics generally are sensitive to free ammonia.
Ionophores (monensin, lasalocid, salinomycin, narasin, maduramicin) are carboxylic polyether antibiotics used as coccidiostats in poultry and as growth promoters or feed-efficiency and bloat-control agents in cattle in countries that allow them. They form lipid-soluble complexes with cations and move them across membranes, disturbing sodium, potassium and calcium gradients; calcium overload in mitochondria leads to necrosis of cardiac and skeletal muscle.
Horses are the most sensitive species, far more than cattle or poultry; toxicity has followed feeding of cattle or poultry feed to horses and mill contamination of horse feed. Signs in horses begin within hours to days: anorexia, colic, sweating, restlessness, weakness, ataxia, recumbency, tachycardia, arrhythmias, myoglobinuria and sudden death; survivors may develop chronic heart failure months later from myocardial fibrosis. In pigs and poultry, tiamulin (and some other drugs) given together with ionophores inhibits their metabolism and produces toxicity at normal ionophore doses.
There is no antidote. Treatment is removal of feed, activated charcoal, fluids and strict rest, with cardiac monitoring; recovered horses should be assessed before returning to work.
Xylitol is a sugar alcohol used as a sweetener in sugar-free chewing gum, sweets, baked goods, some peanut butters and oral-care products. In dogs, unlike humans, it is a potent stimulus for insulin release, causing hypoglycaemia within 30 to 60 minutes (sometimes delayed up to 12 hours with some products), with vomiting, weakness, ataxia, collapse and seizures. Larger doses cause acute hepatic necrosis and liver failure with coagulopathy over one to three days. Doses commonly cited are above about 0.1 g/kg for hypoglycaemia and above about 0.5 g/kg for liver failure, though liver failure has been reported at lower doses. Treatment is emesis if the dog is not yet hypoglycaemic, intravenous dextrose, frequent blood glucose checks for at least 12 to 24 hours, and monitoring of liver enzymes and clotting, with liver-protective care.
Grapes, raisins, sultanas and currants cause acute kidney injury in some dogs, with no clear dose-response and unpredictable individual susceptibility. Tartaric acid has been proposed as the toxic principle, but this is not fully established. Signs are vomiting within hours, then anorexia, lethargy, abdominal pain and oliguric or anuric renal failure over one to three days. Because no safe dose is known, any ingestion is treated: emesis, activated charcoal, intravenous fluid diuresis for 48 to 72 hours and monitoring of creatinine and urine output.
Other common small-animal poisonings, examined mainly by principle, are chocolate (theobromine and caffeine, methylxanthines that antagonise adenosine receptors and cause vomiting, restlessness, tachyarrhythmias and seizures; dark and cooking chocolate contain much more theobromine than milk chocolate), onions and garlic (Allium species, oxidative damage with Heinz-body haemolytic anaemia, cats more sensitive), lilies (Lilium and Hemerocallis, acute kidney injury in cats from very small amounts), ethylene glycol (calcium oxalate nephrosis; ethanol or fomepizole must be given early), paracetamol in cats (methaemoglobinaemia, facial oedema; N-acetylcysteine), NSAIDs (gastric ulceration and kidney injury) and macrocyclic lactones in MDR1-defective dogs.
Corrosives destroy tissue on contact. Acids (sulfuric, hydrochloric, some descaling agents) cause coagulation necrosis, which forms an eschar that limits penetration. Alkalis (sodium hydroxide, drain cleaners, some dishwasher detergents, cement and lime) cause liquefaction necrosis, which penetrates deeply and continues after contact, so alkali burns of the oesophagus are often worse than they look at first. Other irritants include phenols and coal-tar products (cats are especially sensitive), cationic detergents, and petroleum distillates such as kerosene, which are easily aspirated and cause chemical pneumonitis.
Signs of ingested corrosives are salivation, pawing at the mouth, oral ulcers (which may be absent even when the oesophagus is burned), dysphagia, vomiting, abdominal pain and, later, oesophageal stricture.
Management: do not induce emesis, which re-exposes the oesophagus and risks aspiration; do not give activated charcoal, which does not bind corrosives and obscures endoscopy; do not try to neutralise an acid with an alkali or the reverse, because the reaction produces heat. Dilute promptly with small volumes of water or milk if the animal can swallow.
Venomous snakes of veterinary importance belong mainly to two families. Elapids (cobras, kraits, mambas, coral snakes, and most Australian venomous snakes such as brown snakes and tiger snakes) typically have neurotoxic venoms: postsynaptic toxins block nicotinic acetylcholine receptors, and presynaptic toxins (such as beta-bungarotoxin of kraits) destroy nerve terminals. Signs are ptosis, dilated pupils, weakness, dysphagia, flaccid paralysis and respiratory failure, often with little local swelling. Vipers (true vipers such as Russell's viper, saw-scaled vipers and puff adders) and pit vipers (rattlesnakes in the Americas) have predominantly cytotoxic and haemotoxic venoms, with enzymes that cause marked local swelling, pain, bruising and tissue necrosis, and procoagulant and anticoagulant components that cause venom-induced consumption coagulopathy, bleeding, hypotension and acute kidney injury. In South Asia the 'big four' of human snake bite are the Indian cobra, common krait, Russell's viper and saw-scaled viper; livestock and dogs are bitten by the same snakes.
First aid is to keep the animal calm and still and transport it quickly. For elapid bites on a limb, a pressure-immobilisation bandage is used in Australia to slow lymphatic spread. Tourniquets, cutting, suction and ice are harmful and are not used. The 20-minute whole-blood clotting test (blood left undisturbed in a clean glass tube; failure to clot at 20 minutes indicates coagulopathy) is a simple field test for viper and some elapid envenomation.
Antivenom, made from the serum of immunised horses or sheep, neutralises circulating venom; it is the only specific treatment. Anaphylactic and anaphylactoid reactions can occur, so it is given slowly with adrenaline available. Supportive care includes fluids, analgesia (opioids rather than NSAIDs when there is coagulopathy), ventilation for paralysis, blood products, wound care and tetanus protection in horses.
Bees, wasps, hornets and fire ants inject venoms containing melittin, phospholipase A2, hyaluronidase, histamine and other amines. A previously sensitised animal may develop anaphylaxis within minutes, with vomiting, collapse, hypotension and, in dogs, hepatic congestion and haemorrhagic diarrhoea because the liver is the dog's main shock organ. Treatment of anaphylaxis is adrenaline, fluids and oxygen, with antihistamines and corticosteroids as adjuncts; remove bee stings by scraping rather than squeezing the venom sac.
Other animal toxins that appear in examinations include toad poisoning in dogs (Rhinella marina, the cane toad, and Bufo species), whose parotoid secretions contain bufadienolides and cause hypersalivation, red gums, arrhythmias and seizures, treated by flushing the mouth and cardiac support; pine processionary caterpillars (Thaumetopoea pityocampa) in southern Europe, whose urticating hairs cause tongue swelling and necrosis in dogs; blister beetles (Epicauta, containing cantharidin) in alfalfa hay, which cause colic, oral and urinary tract ulceration and hypocalcaemia in horses; and scorpion and spider envenomation in regional contexts.
Cyanobacteria (blue-green algae) bloom in warm, still, nutrient-rich water, often in late summer, and wind can concentrate them along shorelines where livestock and dogs drink or swim. Microcystins (from Microcystis and others) and nodularin are hepatotoxins that inhibit protein phosphatases and cause acute hepatic necrosis, haemorrhage into the liver, and death within hours to days. Anatoxin-a, a nicotinic agonist, causes rapid neuromuscular signs, tremor, paralysis and death within minutes; guanitoxin (formerly anatoxin-a(s)) is a natural organophosphate-like cholinesterase inhibitor.
Salt poisoning, more accurately sodium ion toxicosis with water deprivation, occurs when pigs or poultry are deprived of water (frozen or broken drinkers) while eating normal salt levels, or when salty water, whey or brine is fed. Brain sodium rises and, when water becomes available and animals drink freely, water moves into the brain and causes cerebral oedema. Pigs show thirst, constipation, blindness, deafness, head pressing, wandering, and intermittent seizures with the head pulled back and 'dog sitting'; eosinophilic perivascular cuffing in the cerebral cortex (eosinophilic meningoencephalitis) is characteristic in pigs.
Other water-borne problems are nitrate from shallow wells contaminated by manure, septic systems or fertiliser; high sulfate, which contributes to polioencephalomalacia in cattle through rumen hydrogen sulfide and induces copper deficiency; fluoride and arsenic from geological sources; lead from old pipes; high total dissolved solids (salinity), which reduce intake and production; and petroleum, pesticide or industrial contamination.
Ionising radiation (X-rays, gamma rays, alpha and beta particles, neutrons) removes electrons from atoms and damages DNA directly and through free radicals from water. The absorbed dose is measured in gray (Gy, one joule per kilogram); the equivalent and effective doses, which weight for type of radiation and tissue sensitivity, in sievert (Sv); and radioactivity in becquerel (Bq, one disintegration per second).
Whole-body exposure to high doses causes the acute radiation syndrome, which has three overlapping forms as dose rises: haematopoietic (marrow failure with infection and haemorrhage over weeks), gastrointestinal (loss of intestinal epithelium, diarrhoea, dehydration and sepsis within days) and neurovascular (collapse within hours).
Radioiodine (I-131, half-life about 8 days) concentrates in the thyroid and passes quickly into milk; after three half-lives (about 24 days) one-eighth remains. Radiocaesium (Cs-137, half-life about 30 years) behaves like potassium and accumulates in muscle, and persists in soils, especially acid, organic soils, and in mushrooms, lichens and the animals that eat them, such as reindeer and upland sheep. Strontium-90 (half-life about 29 years) behaves like calcium and deposits in bone and milk. After Chernobyl (1986) and Fukushima (2011), countermeasures included housing animals on uncontaminated feed, restrictions on milk and meat, stable iodine to block thyroid uptake in people, and hexacyanoferrate (Prussian blue) compounds given to ruminants in feed, boluses or salt licks to bind radiocaesium in the gut and increase its faecal excretion.
Key terms: persistence is how long a compound resists breakdown in the environment; bioaccumulation is the build-up of a compound in an organism faster than it is eliminated; biomagnification is the rise in concentration at each step up a food chain, so that top predators carry the highest loads.
DDE inhibits calcium deposition in the eggshell gland of birds of prey and fish-eating birds, producing thin shells that break during incubation; population crashes of peregrine falcons, bald eagles, ospreys and pelicans in the mid-twentieth century were reversed after DDT bans.
The most important veterinary example is diclofenac and Gyps vultures in South Asia. From the 1990s, populations of white-rumped, long-billed and slender-billed vultures in India, Pakistan and Nepal fell by more than 95%. Vultures that fed on carcasses of cattle treated with diclofenac shortly before death developed acute kidney failure and visceral gout. India, Pakistan and Nepal banned veterinary diclofenac in 2006; meloxicam was shown to be safe for Gyps vultures and is the recommended alternative, while some other NSAIDs, such as ketoprofen and aceclofenac (which is metabolised to diclofenac), are also considered unsafe for vultures.
A residue is any parent compound or metabolite of a drug, pesticide or contaminant that remains in edible tissues, milk, eggs or honey.
Safety limits come from toxicology. The acceptable daily intake (ADI) is the amount a person can ingest daily over a lifetime without appreciable risk; it is usually the NOAEL from the most sensitive long-term animal study divided by a safety (uncertainty) factor, typically 100 (10 for differences between species and 10 for differences between individuals), and larger when data are weak. A NOAEL of 10 mg/kg per day with a factor of 100 gives an ADI of 0.1 mg/kg per day. The maximum residue limit (MRL, called tolerance in the USA) is the highest legally permitted concentration in a food, set so that intake from a standard food basket stays below the ADI. The withdrawal period (withholding time) is the time after the last dose before an animal may be slaughtered or its milk or eggs used, set so that residues fall below the MRL; it applies to the approved dose, route and species, and extra-label use requires a longer, conservatively set withdrawal period under national rules.
Internationally, the Joint FAO/WHO Expert Committee on Food Additives (JECFA) evaluates veterinary drug residues and the Codex Alimentarius Commission adopts MRLs; national and regional authorities set their own, and they differ. Some substances have no ADI because no safe level can be set and are prohibited in food animals in many jurisdictions; chloramphenicol and nitrofurans are standard examples.
Learn the handful of mechanisms that explain most poisonings: sulfhydryl binding by metals, cytochrome oxidase block by cyanide, methaemoglobin from nitrite, acetylcholinesterase inhibition, GABA and glycine antagonism, vitamin K cycle inhibition and bioactivation by P450. Then attach species, source, signs, lesions, sample and antidote to each. Practise unit conversions (ppm, ppb, per cent, nitrate versus nitrate-nitrogen) and dietary-intake-to-dose calculations until they are automatic, because examiners and farmers both give numbers in mixed units. Know which species cannot vomit and why cats and sheep are special.
At five years you are the person who takes the call about a dog that ate rodent bait or a group of cattle found dead by a sorghum paddock. The daily decisions are whether to induce emesis, whether to start vitamin K1 or check the PT at 48 to 72 hours, how long to treat, and which samples to freeze before the carcasses are removed. In food animals you advise on salvage, withholding and reporting, and you warn clients about seasonal hazards: frosted sorghum, drought nitrate, cattle feed reaching horses, permethrin products near cats, and blue-green algae in late-summer dams.
A senior clinician or state veterinarian manages outbreaks and their consequences. That means investigating herd poisonings systematically, preserving a chain of custody when a feed mill, spray contractor or neighbour may be liable, deciding with regulators whether exposed animals can enter the food chain, and designing prevention: ration formulation for sheep versus cattle, nitrate and mycotoxin testing programmes, safe urea feeding, and control of toxic weeds such as Lantana. Senior veterinarians also sit on residue monitoring, pesticide registration and wildlife protection bodies, where the diclofenac-vulture story is the reference case.
Research questions include the still-unclear mechanisms (grape and raisin nephrotoxicity, metaldehyde), mycotoxin co-exposure and low-dose chronic effects, biomarkers and rapid field tests, the genetics of species and breed sensitivity (MDR1, glucuronidation, copper handling), ptaquiloside and papillomavirus in bovine cancers, and One Health links such as aflatoxin M1 in milk, groundwater arsenic and fluoride, antimicrobial residues and resistance, and pharmaceutical effects on wildlife. A senior scientist also evaluates risk for regulators, deriving NOAELs, ADIs and MRLs and judging the quality of toxicity data.
Antidote doses are given by principle, not by number, except where a standard figure is stated with its caveat; use the product label and the national formulary. Approval of antidotes for food animals, and the residue rules that follow extra-label use, differ by country and are not tabulated. Diagnostic thresholds (blood lead, liver copper, cholinesterase activity, forage nitrate and HCN, water quality) vary between laboratories and authorities and are given only as commonly cited orientation values. Regional plant poisonings are covered in depth only for southern Africa; Indian, South American and Australian regional plants beyond those named, marine and aquaculture toxicology, avian and exotic species toxicology, drug adverse reactions in detail, and occupational toxicology are outside this edition. Mechanisms still debated (metaldehyde, grape and raisin toxicity, blind staggers) are stated as uncertain.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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