Acute poisoning occasionally occurs in sheep. Two common causes are overdosage of drugs with a narrow therapeutic index, such as closantel, and plant poisoning. Sheep are generally more conservative browsers and not as inquisitive as cattle and goats. Consequently, they generally only eat unfamiliar plants when they are hungry and other forage is unavailable (Angus, 2007). This typically occurs in extreme weather conditions, such as periods of heavy snowfall or drought. Adder bite is also a risk in sheep but is likely underreported.
This article discusses acute poisoning in sheep.
Grayanotoxins
Grayanotoxins are found in Pieris spp. (Figure 1a) and Rhododendron spp. (Figure 1b, which includes azaleas). These plants contain several grayanotoxins in the nectar, flowers, leaves and stems but the main toxin is grayanotoxin I (also known as rhodotoxin, acetylandromedol or andromedotoxin). Grayanotoxins are partial agonists that act on cell membrane sodium channels causing positive inotropic effects resulting in severe weakness, hypotension, dyspnoea and neurological signs.
Poisoning usually occurs when animals are offered cuttings (Casteel and Wagstaff, 1989; Eo and Kwon, 2009), escape from their enclosures (van Leengoed et al, 1983), or in adverse weather conditions when hungry animals stray into wooded or garden areas. Grayanotoxin poisoning is common in sheep and is frequently reported in surveillance reports in the UK (SAC C VS, 2009; Agri-Food and Biosciences Institute (AFBI), 2010; SAC C VS, 2011a; SAC C VS, 2011b; SAC C VS, 2012; AFBI, 2016; SAC C VS, 2015a, b; Animal and Plant Health Agency (APHA), 2016; SAC C VS, 2018).
Clinical signs of grayanotoxin poisoning generally occur within a few hours of ingestion; in an experimental study, signs occurred in 2–4 hours (Armien et al, 1995), but can occur up to 6 hours after ingestion (Puschner et al, 2001). In many cases the first sign that poisoning has occurred is when animals are found dead. Initial signs are gastrointestinal with severe hypersalivation, regurgitation (which can be severe) and signs of abdominal discomfort. Neurological signs (progressive restlessness, ataxia, depression, generalised muscle tremors, dilated pupils) and cardio-respiratory effects (dyspnoea with variation in the pace, intensity and frequency of respiratory movements, episodes of apnoea, bradycardia with cardiac arrhythmia) also occur. There may also be bruxism, hypotension, pyrexia and vocalisation. In the final stages there is increased muscle weakness, flaccid paralysis, coma and convulsions. Aspiration pneumonia (secondary to regurgitation of ruminal contents) is a risk and animals can recover from the intoxication only to die from complications of aspiration pneumonia.
Recovery may take a few days but in more severe cases, it may take up to a week or more (Power et al, 1991). In fatal cases, death is usually a result of respiratory failure and may occur within a few hours of ingestion. Undigested plant material is commonly found in the stomach at post-mortem examination (Gillis et al, 1961; Black, 1991; Power et al, 1991; Ajito et al, 2001; SAC C VS, 2011a; SAC C VS, 2015a, b) and ingesta may also be found in the airways (AFBI, 2010).
Treatment of grayanotoxin poisoning is supportive; there is no antidote. In valuable animals a rumenotomy with removal of rumen contents may be considered (Plumlee et al, 1992). It has been performed in sheep with rhododendron toxicosis; a large volume of leaves was removed and appeared to be an effective intervention in most of the small number of sheep in which it was performed (van Leengoed and van Amerongen, 1983). Activated charcoal (1–3 g/kg) may be given if ingestion was recent, and rehydration is usually required because of protracted regurgitation. Atropine (0.15–0.30 mg/kg intramusularly (IM) in ruminants) can be given to increase heart rate, if required. Antibiotics may be required to prevent secondary infection following aspiration. Although intravenous lipid emulsion administration has been reported in the management of three goats with grayanotoxin poisoning (Bischoff et al, 2014), its use has not been described in sheep. In the goats, all the animals recovered within 12 hours of administration, although one subsequently died as a result of aspiration pneumonia.
Oak (Quercus species)
Oak (Figure 2a) poisoning in animals has been recognised for centuries (Marsh et al, 1919).
The effects of oak poisoning are mainly gastrointestinal and renal, but hepatic effects can also occur. Oak contains tannins, which are polyphenolic biomolecules, as a defence against herbivores. Tannins bind to and precipitate proteins and various other organic compounds including amino acids and alkaloids. Mammalian herbivores produce proline-rich tannin-binding proteins in their saliva as a defensive mechanism against the effects of tannin and other polyphenols in their diet. These salivary proteins bind tannin before it enters the gut and reduces the action of tannin. These proline-rich salivary proteins are found in members of the orders of Rodentia, Lagomorpha and Artiodactyla (Mole et al, 1990). In the gut of herbivores tannins are broken down by gut bacteria to low molecular weight phenolic compounds such as gallic acid and pyrogallol. These compounds are nephrotoxic. Various forms of tannic acid (also a polyphenol) are also found in oak. It is of note that tannic acid alone is not the only substance responsible for the toxic effects observed in animals, since tannic acid administration to sheep (Zhu et al, 1992) and cattle (Plumlee et al, 1998) did not result in signs typical of oak poisoning. The toxicity of oak is not reduced by drying or freezing of plant material (Dollahite et al, 1966). Tannin concentrations vary with the season and year, but the young leaves and immature (green) acorns contain high concentrations.
Gastrointestinal signs following ingestion of oak are a result of damage to the gastrointestinal mucosa and epithelium (Bernays et al, 1989), changes to gut microflora (Samanta et al, 2004) and sub-sequent effects on the digestibility of ingesta (Robbins et al, 1987). Tannins can be absorbed through the damaged gut mucosa and cause tissue destruction in tissues with the highest concentration, that is the liver and kidney (Burrows and Tyrl, 2013). Tannins may lead to increased vascular permeability and subsequent fluid loss, which may be the cause of oedema and fluid accumulation. Damage to the gut is exacerbated by the effects of uraemia (Burrows and Tyrl, 2013).
Although, it is normal for many animals, including sheep, to eat oak and acorns the exact reason why some cases result in poisoning remains unclear. The individual response following ingestion of oak leaves or acorns is very variable. Some animals are severely affected and others not at all. In cattle, for example, prior undernutrition has been shown experimentally to be a factor in subsequent poisoning (Pérez et al, 2011). Some animals may develop a craving for oak and eat immature leaves and acorns directly from the tree.
Cases of poisoning are more common in some years than others because of heavy acorn crops. This is known as masting, where oak trees synchronously product large numbers of acorns. The year 2020 was a big mast year in the UK with a high incidence of poisoning. In sheep, the APHA reported 16 cases diagnosed in 2020 compared with only 10 cases in total (two to three cases/year) recorded over the preceding 5 years. In the cases with post-mortem examination, 70% were adult sheep and 30% were weaned lambs (APHA, 2020).
Typical clinical signs seen in cases of oak poisoning include severe anorexia, depression, lethargy, recumbency, diarrhoea (green/black and watery, or haemorrhagic), abdominal pain and weight loss. Acute kidney injury also occurs. The onset of signs is very variable. In one incident in sheep, the animals died 4–10 days after access and up to 5 days after removal of acorns (Mullins, 1955). Secondary complications (reported in cattle) include bronchopneumonia, gastrointestinal perforation and peritonitis (Spier et al, 1987).
Typical post-mortem findings include black tarry faeces around the perineum, a rumen full of green herbage, including partial acorns and remnants of acorns, severe haemorrhagic enteritis, ascites, pale, grey coloured and fragile kidney (Figure 2b), sub-capsular petechial haemorrhaging in the kidney and tubular changes (Eroksuz et al, 2013; APHA, 2016; APHA, 2020).
Treatment of acorn toxicosis in ruminants is supportive. In cattle, recovery is more likely in animals that do not develop a marked increase in urea concentrations (Dixon et al, 1979). Animals that recover may have elevated urea concentrations for up to 3 weeks after recovery (Holliman, 1985).
A rumenotomy may be considered for valuable animals (Bausch and Carson, 1981). Supplementation of feed with hay, fluid therapy for rehydration and to restore electrolyte imbalances and restoration of ruminal/gut microflora are recommended (Spier et al, 1987). Renal function should be monitored, if practical. Analgesia can be given (although its effectiveness in oak poisoning has not been evaluated in ruminants, and in horses with oak poisoning abdominal pain is often refractory to analgesia). Access to acorns should be prevented by moving animals or fencing off areas containing oak trees.
Ivy (Hedera species)
Ivy (Figure 3) is eaten by many animals, including sheep, without adverse effect (Forsyth, 1979; Metcalfe, 2005). Toxic effects occur when a large quantity is eaten, for example ingestion of cuttings or during conditions when other food is unavailable. All parts of the plant are poisonous, particularly the leaves and fruit. The plant contains various toxins, sometimes referred to collectively as hederin, but it actually contains three types of terpenoid compounds: genins or aglycones (hederagenin and oleanolic acid); their respective monodesmosides which are glycosides (α-hederin and β-hederin); and their respective bidesmosides (hederacosides C and B) (Burrows and Tyrl, 2013).
The main effect of ivy ingestion is irritation to the gastrointestinal mucosa (Burrows and Tyrl, 2013). Signs reported in affected sheep include lethargy, salivation, signs of abdominal pain, incoordination, pyrexia, muscle spasm, recumbency and respiratory distress (Veterinary Poisons Information Service (VPIS) case data). Deaths have occurred in incidents reported to the VPIS.
Treatment of ivy toxicosis in sheep is supportive.
Yew (Taxus species)
Numerous alkaloids have been isolated from the various species of Taxus (Miller, 1980, Figure 4). The toxic component is taxine, a complex mixture of alkaloids such as taxine A, B and C (Hare, 1998). Isotaxine B is an isomer of taxine B and is another important component of the alkaloid element (Wilson and Hooser, 2007).
The main alkaloid toxins in yew are taxine A and taxine B (Ogden, 1988; Wilson et al, 2001; Cope, 2005), with taxine B being more toxic than taxine A and more prevalent in Taxus spp. (Cope, 2005; Orbell, 2006; Wilson and Hooser, 2007; Sula et al, 2013). Taxines are cardiotoxins and they interfere with the ion channels in the myocardial cells (i.e. calcium and sodium channels); their main action is antagonism of calcium channels, affecting atrioventricular (AV) conduction, causing arrhythmias and cardiac arrest (Hare, 1988; Wilson et al, 2001; Sula et al, 2013). Taxine B has negative inotropic effects and also causes hypotension as a result of arterial vasodilation (Cope, 2005). In addition, Taxus spp. contain an irritant volatile oil which is present throughout the plant, and can cause gastrointestinal irritation and diarrhoea (Hare, 1998; Cope, 2005; Sula et al, 2013).
In an experimental study, dried powdered leaves at a dose of 2.5 g/kg bodyweight in sheep caused lethargy, depression, bradycardia and varying intensity of heart sounds. The electrocardiogram (ECG) showed a variety of arrhythmias and abnormalities, including multifocal ventricular tachycardia, idioventricular and idiojunctional rhythm and QRS and T widening. Four sheep died within 4–16 hours after yew administration and three survived (Aslani et al, 2011). Ingestion of yew is only likely to occur when other forage is unavailable. In one study, three Suffolk ewes provided with a full ration of timothy and clover hay did not eat twigs or leaves of Taxus cuspidata (Japanese yew) (Alden et al, 1977). In contrast, some sheep are also reported to browse on yew without harm (Scott, 2010).
In livestock, acute ingestion of yew commonly causes sudden onset collapse and death as a result of cardiac arrest within hours of ingestion, and animals may be found dead (Rae and Binnington, 1995). There may be no clinical effects prior to collapse and death, although ataxia, bradycardia, dyspnoea, trembling/muscle tremors, weakness, lethargy, recumbency, convulsions (rare), diarrhoea, and collapse may occur.
Treatment of yew toxicosis in ruminants is supportive. In animals with suspected ingestion, activated charcoal could be given, mixed with a suitable feed to encourage ingestion (Casteel, 2004). A rumenotomy may be considered for valuable animals, but most die soon after onset of signs. Death may occur so rapidly that yew leaves may be found in the buccal cavity at post-mortem examination (Lovatt et al, 2014). After a rumenotomy and contents removal, replacement with mineral oil, electrolytes and activated charcoal has been suggested as a potentially useful management measure (Wilson et al, 2001; Wilson and Hooser, 2007).
It is also important to avoid any unnecessary stress that may increase susceptibility to arrhythmias in animals with yew toxicosis. For example, where possible, avoid exercise, physical restraint or transportation, and limit handling (Casteel, 2004; Cope, 2005). A combination of intravenous sodium bicarbonate and lipid emulsion was successful in a small case series in humans with yew poisoning (Lanfranchi et al, 2018), but this is unlikely to be practical in most cases of yew poisoning in livestock.
Cardiac glycosides
Cardiac glycosides are found in numerous plants including foxglove (Digitalis purpurea, Figure 5a) oleander (Nerium oleander, Figure 5b), hellebores (Helleborus spp, Figure 5c) and lily of the valley (Convallaria majalis, Figure 5d). Poisoning with these plants is less common in sheep compared with oak, pieris and rhododendron, but is occasionally reported (Maclean, 1966).
Some plants such as foxgloves are bitter and so may not be eaten readily, although deer, for example, have been observed to choose to graze foxglove with subsequent toxic effects (Corrigall et al, 1978), therefore a bitter taste may not always provide protection. Dried oleander is reportedly more palatable than fresh material (Butler et al, 2016). Cardiac glycosides inhibit the cellular membrane sodium-potassium adenosine triphosphatase (Na+K+ATPase), causing electrolyte disturbances resulting in changes in the electrical conductivity of the heart. Although therapeutic doses of cardiac glycosides have an antiarrhythmic effect, larger amounts are proarrhythmic.
Sudden death is commonly reported after ingestion of plant material containing cardiac glycosides (Galey, 2004).
Poisoning with foxglove has been reported in sheep, with sudden death in one sheep, and dullness, colicky pain, grunting and frequent urination followed by death in others (Maclean, 1966). In experimental studies with oleander, single doses of 0.25 or 1 g/kg of dried leaves caused restlessness, bruxism, dyspnoea, ruminal distension, hypersalivation, incoordination, limb paralysis and recumbency. Death occurred within 4–5 hours (1 g/kg) or 18–24 hours (0.25 g/kg) after dosing. Post-mortem changes included widespread congestion or haemorrhage, pulmonary congestion, hepatorenal fatty changes and enteritis. Ingestion of 0.06 g/kg daily caused less severe signs with death occurring on days 3, 7 and 14 (Adam et al, 2002). In another experimental study, when fresh leaves of oleander were fed to adult sheep, clinical signs occurred between 1.75 and 7.25 hours after ingestion. The fatal dose was 0.5 to 1 g/kg and death occurred between 6.25 to 53 hours. Clinical signs reported were apathy, anorexia, muscle tremors, tachypnoea, dyspnoea, tachycardia, irregular heart rate, ruminal stasis and acidosis (Armién et al, 1994).
Treatment of cardiac glycoside toxicity is supportive. Activated charcoal (1–3 g/kg repeated 8 hours later) may be useful and analgesia may be required for abdominal discomfort. If possible, the electrolytes, particularly potassium, should be checked. Rehydration may be required, avoiding calcium-containing fluids as elevated serum calcium can increase the effect of cardiac glycosides on the myocardium. Potassium should only be given if hyperkalaemia is absent.
Atropine can be used for atrioventricular block or bradycardia, and lidocaine has been used in the management of ventricular arrhythmias resulting from cardiac glycoside poisoning in other animals and people. Digoxin antibody Fab fragments are an option, but this drug is very expensive. In veterinary medicine, it is recommended that one or two vials are given initially and the effects observed (Gwaltney-Brant and Rumbeiha, 2002). More vials can be given if there is some clinical improvement.
Leylandii or Leyland cypress (x Hesperotropsis leylandii)
Leylandii is a common, fast-growing coniferous tree used for hedging. There is limited information on the toxic effects of leylandii and no cases are described in the literature. There appears to be no characteristic clinical picture, but in cases in sheep reported to the VPIS signs include anorexia, dullness, colic, bruxism, hypothermia, recumbency and sudden death (VPIS case data). Treatment of symptomatic animals is supportive.
Adder bite
The European adder, Vipera berus berus is the only venomous snake native to the UK. It is not found in Ireland. The adder is most commonly found on dry, sandy heaths, sand dunes, rocky hillsides, moorlands and woodland edges. It is a protected species in the UK (Wild-life and Countryside Act 1981 - Variation of Schedule Order 367) and generally only bites when provoked. Bites rarely occur during the winter when the snake is in hibernation and are more likely during the summer months. Not all bites result in envenomation (dry bites).
There are reports of cattle, sheep, goats, pigs and horses bitten by adders (De Luckham, 1944; Prestt, 1971), but detailed clinical descriptions are generally lacking. It is likely that many cases go undiagnosed in sheep and other livestock since the bite is unwitnessed. In a case reported to the VPIS a sheep developed pulmonary oedema and died 24 hours after an adder bite. Puncture wounds were visible and discoloration and swelling around the inside of the lip were observed at post-mortem examination.
The exact composition of adder venom is unknown and there are seasonal, individual and geographical differences. The venom is a complex mixture of high molecular weight proteins, mainly proteases, peptide hydrolases, hyaluronidase and phospholipases (Siigur et al, 1979; Calderón et al, 1993; Samel et al, 2006).
Hypovolaemia and local oedema result from an increase in vascular permeability, caused initially by the release of pharmacologically active substances, such as histamine, serotonin, bradykinin and prostaglandins, and later as a direct result of venom on heart and blood vessels. Local haemorrhage is rare and a result of cytolytic and haemolytic factors. Vasoactive substances (histamine, serotonin, prostaglandins) cause systemic vasodilation leading to hypovolaemia and hypotension. Cardiac effects may be a result of impaired circulation and poor perfusion of the myocardium, because of coronary spasm and hypovolaemia (Pelander et al, 2010). Myocardial damage may cause reduced contractility resulting in hypotension. The venom has a myotoxic effect as evidenced by biochemical indicators of skeletal muscle damage (e.g. creatine kinase concentration) and histological examination (Calderón et al, 1993). Renal effects are probably a result of increased glomerular permeability and decreased absorption of proteins as a result of tubular injury (Palviainen et al, 2013). Hypovolaemic shock, hypotension myoglobinuria, haemoglobinuria and disseminated intravascular coagulation (DIC) may contribute to renal effects. Hepatic effects may be a result of direct cytotoxic effects of the venom or indirectly as a result of vascular damage and ischaemia (Lervik et al, 2010). Hypoproteinaemia is mainly a result of hypoalbuminaemia and increased vascular permeability, causing plasma leakage and the resulting oedema.
A bite from an adder can cause rapid onset localised, painful swelling. Puncture wounds may be visible (two punctures about 1 cm apart) and may weep bloody exudate. Local swelling is usually the first sign noted, and it typically progresses over the next 2 days. Other potential signs include hypersalivation, depression, tachycardia, tachypnoea, pyrexia, generalised muscle spasms, and reduced gut sounds with colic. There may be lameness after a bite on the leg, and cellulitis may occur. Hypotension and shock may be noted.
Coagulopathy, haematological, renal, hepatic and cardiac effects can occur following adder envenomation. This is no information on fatality rate in ruminants following adder bite, but in dogs, death occurs in 3–4.6% of cases, and occurs after 5–7 days in dogs that receive no antivenom (Bratberg and Flesja, 1973).
Treatment of adder bite in livestock is supportive. The spread of local swelling should be monitored, and analgesia provided. The bite site should be monitored for signs of tissue necrosis. Fluid therapy is important to protect the kidneys, ensure adequate hydration, and correct hypovolaemia and haemoconcentration. There is no role for steroids in the treatment of adder bites (except in rare cases of anaphylactic reactions to antivenom). The initial swelling is not an inflammatory response but a result of the cytotoxic effect of the venom. Antibiotics are probably only required if infection occurs.
Adder antivenom could be considered in sheep, if required, but in most cases may be impractical or too expensive. It should be considered where there is significant swelling or any systemic signs such as coagulopathy, evidence of myocardial damage or shock. The optimal dose of antivenom in large animals has not been established, but the dose of antivenom is the same irrespective of the size of the victim as the dose is designed to counteract the venom of one bite.
Closantel
Closantel is a halogenated salicylanilide licensed in sheep for the treatment of fluke infestation. It is thought to act by uncoupling oxidative phosphorylation in the mitochondrial membrane of parasite cells and disrupting the synthesis of adenosine triphosphate (ATP). It has a narrow therapeutic index, so it is essential animals are weighed accurately to ensure correct dosing.
In overdose closantel causes optic neuritis and retinal degeneration. In some cases, blindness may be the only sign reported (Button et al, 1987; Rao et al, 2018). Other signs of toxicosis include anorexia, depression, ataxia, circling, laboured respiration, recumbency, pyrexia (uncommon), weakness, hypotonia, opisthotonus and convulsions. Urine may be green because of the presence of bilirubin, and liver enzymes may be elevated. Signs can start hours to days after overdosage and a higher dose may result in a more rapid onset of signs (Crilly et al, 2014).
Closantel-induced blindness is permanent in most cases, but recovery (in 3 to 4 weeks) has occurred in some animals with less severe signs. Ophthalmoscopic examination shows fixed dilated pupils, loss of pupillary light reflex, absent menace reflex, nystagmus, oedema (papilloedema and swelling of the optic disc), retinal atrophy and degeneration. Other potential causes of blindness in sheep are listed in Box 1.
Box 1.Differential diagnoses of blindness in sheep
- Ceroid lipofuscinosis
- Bright blindness (chronic bracken ingestion)
- Trauma leading to bilateral retinal detachment
- Hypovitaminosis A
- Infectious keratoconjunctivitis
- Polioencephalomalacia
- Focal symmetrical encephalomalacia
- Pregnancy toxaemia
Toxic effects have not been reported in lambs born to mothers with closantel toxicosis (Van Cauteren et al, 1985; Hannon et al, 2014). This is likely a result of high protein binding of the drug since albumin has limited ability to cross the placenta.
The toxic effects of closantel are thought to be because of disruption of cells with tightly packed layers of cell membrane (such as photoreceptors, Schwann cells and oligodendrocytes) resulting in retinopathy, myelinic oedema and white matter vacuolation, respectively (Crilly et al, 2014). The myelenic oedema is thought to cause swelling of the optic nerve, which is then subject to compression in the bony confines of the optic canal resulting in axon disruption and neuronal loss (Gill et al, 1999).
Individual response is variable following closantel overdosage, and may be influenced by factors such as body condition, plasma protein concentrations and parasite load. In some individuals, toxic effects occur at the therapeutic dose (10 mg/kg oral and 2.5 or 5 mg/kg IM) with more severe signs at doses of >10 mg/kg. Toxic effects in sheep have been reported at doses of less than 1.5 times the therapeutic dose (Crilly et al, 2014), a 2.5 times overdose (Watt and Bunker, 2016), and a 10 times overdose, but not after a two or four times overdose (Rivero et al, 2015). The oral and intramuscular LD50 of closantel in sheep is >40 mg/kg for both routes. Signs of toxicity in these studies included anorexia, laboured respiration, recumbency, weakness and blindness, which occurred about 7 days after dosing. After lethal doses there was hypotonia and quadriplegia prior to death (Marsboom, 1976).
In a toxicity study where sheep were given 10 or 40 mg/kg orally or 5 or 20 mg/kg IM at 4 week intervals for 10 doses, transient hypersalivation and diarrhoea occurred in animals given 40 mg/kg orally. There was muscle irritation at injection sites for both IM doses. Closantel did not cause any deaths at these doses (Marsboom et al, 1977; Van Cauteren et al, 1985).
Treatment of closantel overdosage is supportive. Repeat dose activated charcoal (1–3 g/kg 4 hourly) can be given as an absorbent as the drug is excreted in the bile. Ophthalmological examination is recommended to monitor optic damage, but there is no specific treatment for ocular effects. Anti-inflammatory drugs such as steroids may be useful to reduce the inflammatory response. The effectiveness of steroids in the closantel toxicosis is unclear. Systemic steroids were reportedly successful in a human case (but it is not clear if there would have been improvement in time anyway, without the use of steroids) (Kumar et al, 2019). Steroids were ineffective in another human case, but that may have been because of late treatment (10 days post-ingestion) (Tabatabaei et al, 2019).
Conclusion
Plant poisoning in sheep may occur if they are hungry and other forage it not available, for example in poor weather. Poisoning may also result when there is an abundance of acorns, as occurs periodically (so called mast years). Adder bite can also occur in sheep, although it is likely to be underreported. Overdosage of drugs with a narrow therapeutic index, such as closantel, may result in toxic effects. Management of poisoning in sheep is generally supportive with removal from the source, and rehydration and analgesia if required. A poisons information service can be contacted for specific treatment advice. In the UK cases can be reported via the VPIS website (https://www.vpisglobal.com/report-a-case/).
KEY POINTS
- Plant poisoning may occur in sheep when other forage is unavailable.
- Grayanotoxins in pieris and rhododendron are common causes of acute poisoning in sheep.
- Oak poisoning may also occur, particularly in years when the acorn crop is heavy.
- Adder bite is probably under recognised and underreported in sheep.
- Acute closantel poisoning is a risk when animals are not accurately weighed, as it has a narrow therapeutic index.