Goats are browsers and may eat a variety of plants. They are also agile and inquisitive animals so may gain access to toxic plants if they escape from their enclosure into an ornamental garden or woodland, for example. If plant poisoning is suspected it is important to investigate potential sources such as plants growing in the vicinity, contaminated feed or cuttings to which they may have had access (e.g. been accidentally fed or left in their enclosure). A site investigation may be more useful and quickly identifies possible suspects compared with attempting to identify chewed plant fragments in the rumen or regurgitated rumen content (Harwood, 2021).
Grayanotoxins (e.g. Rhododendrons)
Grayanotoxin poisoning is very common in goats (and sheep). Numerous cases are reported in the literature involving Rhododendron spp. (Figure 1a) (which includes azaleas, Figure 1b) (Casteel and Wagstaff, 1989; Puschner et al, 2001; Pereira et al, 2008; Vargas et al, 2014; Kim et al, 2017) and Pieris species (Figure 1c) (Smith, 1978; Smith, 1979; Hollands and Hughes, 1986; Plumlee et al, 1992; Baert et al, 2005; Eo and Kwon, 2009; Bischoff et al, 2014). Kalmia species (evergreen ornamental shrubs) also contain grayanotoxins. Mortality can be high in goats with grayanotoxicosis; in the 60 field cases described above 22 goats died, a mortality rate of 36.6%.
These plants contain several grayanotoxins in the nectar, flowers, leaves and stems. Poisoning usually occurs when animals access plant cuttings or in adverse weather conditions when hungry animals stray into wooded or garden areas.
Grayanotoxins cause gastrointestinal, cardiovascular and neurological effects. Clinical signs of grayanotoxin poisoning generally occur within 6 hours of ingestion (Puschner et al, 2001) and initial signs are gastrointestinal with severe hypersalivation, regurgitation (which can be severe and projectile) and 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. In experimentally-induced Pieris poisoning in a goat, the animal was given approximately 0.1% of its bodyweight in fresh foliage. It developed classic signs of grayanotoxin poisoning and was euthanased at 29 hours post-ingestion (Smith, 1978).
Effects can be short-lived, often lasting no more than 24 hours becase of the rapid elimination of grayanotoxins (Hikino, 1979), but, in more severe cases recovery may take up to a week and is usually complete. In fatal cases, death is usually a result of respiratory failure and may occur within a few hours of ingestion, but aspiration pneumonia (secondary to regurgitation of ruminal contents) is a risk. Animals can, therefore, recover from the intoxication only to die from complications of aspiration pneumonia (Puschner et al, 2001). Plant material is usually found in the gut on post-mortem examination (Figure 2).
Fetal mummification and abortion have been reported in a goat following Pieris poisoning (Smith, 1979). In another case, normal twins were delivered 48 hours after admission (about a day after onset of effects) in a goat severely poisoned with Pieris (Plumlee et al, 1992). Lactation can cease in goats poisoned by grayanotoxins (Casteel and Wagstaff, 1989), and can take days to recover.
Treatment of grayanotoxin poisoning is supportive and there is no antidote. In valuable animals a rumenotomy with removal of rumen contents may be considered (Plumlee et al, 1992). Activated charcoal (1–3 g/kg) may be given if ingestion was recent and rehydration is usually required as a result of protracted regurgitation, but care should be taken with oral medication because of the risk of aspiration. Atropine (0.15–0.30 mg/kg intramuscularly (IM)) can be given to increase heart rate, if required. Antibiotics may be indicated to prevent secondary infection following aspiration. Intravenous lipid infusion was used in three goats with grayanotoxin poisoning (Bischoff et al, 2014). All the animals recovered within 12 hours of administration although one subsequently died as a result of aspiration pneumonia. In cases reported to the Veterinary Poisons Information Service (VPIS) administration of lipid emulsion appeared to have a positive effect on goats with grayanotoxicosis (VPIS case data).
Cyanogenic glycosides (e.g. cherry laurel)
Many plants contain cyanogenic glycoside compounds, but most cases of poisoning occur following ingestion of plants from the Rosaceae (rose) family, particularly the genus Prunus which includes, cherry laurel (Prunus laurocerasus, Figure 3a) and Portuguese laurel (Prunus lusitanica, Figure 3b).
Ingestion (and grinding, chewing or crushing) of plant material containing cyanogenic glycosides results in the formation of hydrogen cyanide. Small doses of cyanogenic glycoside compounds can be tolerated because of detoxification mechanisms (the conversion of cyanide to thiocyanates by rhodanese), but ruminants appear to be more susceptible than monogastric animals because of the speed with which ruminal hydrolysis can release hydrogen cyanide.
In the literature cyanogenic glycoside poisoning has been reported in goats after ingestion of black cherry (Prunus serotina, an American species; Gough, 1995; Radi et al, 2004) and crab apple (Malus sylvestris;Shaw, 1986), but most cases involve cherry laurel (Prunus laurocerasus;Caloni et al, 2013; Schmidt et al, 2013; Hahn et al, 2016). Cotoneaster species and Photinia species are common plants that contain low concentrations of cyanogenic glycosides. Although poisoning in goats does not appear to have been reported there are rare cases in other herbivores, e.g. Photinia in sheep (SAC C VS, 2014a) and Cotoneaster in a llama (Grüss and Priymenko, 2009), and they are a potential hazard in goats if a large quantity is ingested.
The onset of poisoning following ingestion of cyanogenic glycosides is very variable and may be rapid (1–2 hours) or delayed; animals can die within a few minutes of onset of clinical features (Knight and Walter, 2003) or several hours later but in many cases sudden death is the presenting sign. Animals observed to develop clinical effects may have ataxia, frothing at the mouth, dilated pupils, hyperventilation, dyspnoea, weakness, tremors, hypotension and collapse. In severe cases there may be coma, convulsions, lactic acidosis, cardiac arrhythmias and pulmonary oedema. Blood and mucous membranes are initially bright red (because of oxygen saturation of haemoglobin); however cyanosis (because of tissue hypoxia) is observed in the terminal stage.
Treatment of cyanogenic glycoside poisoning is aimed at inactivation or removal of cyanide. A rumenotomy with removal of contents could be considered for valuable animals. Activated charcoal can be given (1–3 g/kg). Further management and antidotal therapy depend on the severity of poisoning. The administration of 100% oxygen is the single most important aspect of treatment (if practical), and it should be continued while the animal is receiving antidotal therapy.
Antidotal therapy involves administration of sodium nitrite (22 mg/kg intravenously (IV) as a 1% solution) first and then sodium thiosulphate (660 mg/kg IV as a 25 or 30% solution), where these are available. The dose of sodium thiosulphate can be repeated if required but only one dose of sodium nitrite should be given because of the risk of producing a high concentration of methaemoglobinaemia and exacerbating tissue hypoxia.
Sodium nitrite acts by converting haemoglobin to methaemoglobin for which cyanide has a high affinity; inert cyanmethaemoglobin is produced. Small doses of cyanide are converted to thiocyanate by an enzymatic reaction catalysed by rhodanese, an enzyme widely distributed in body tissues, particularly the liver. The rhodanese system can detoxify large amounts of cyanide but cannot respond quickly enough to prevent death. Sodium thiosulphate increases this reaction and acts by combining with cyanide in the presence of rhodanese to form the relatively non-toxic sodium thiocyanate (Knight and Walter, 2003).
Cardiac glycosides (e.g. oleander)
Cardiac glycosides are found in numerous plants including lily of the valley (Convallaria majalis), foxglove (Digitalis purpurea) and oleander (Nerium oleander). Ingestion of plants containing cardiac glycosides causes gastrointestinal and cardiac effects.
Most cases of cardiac glycoside poisoning in goats seem to involve oleander and both field (Flores Olivares et al, 2019) and experimental studies (Aslani et al, 2007; Barbosa et al, 2008) have been described. A single dose of 110 mg/kg of dried powdered oleander leaves caused abdominal discomfort (manifested by restlessness, bruxism, pawing and humped posture) about 1 hour later. Other signs were ruminal atony, bloat, polyuria, diarrhoea, hypersalivation, depression, weakness, inco-ordination, tachypnoea, convulsions and arrhythmias (bradycardia, tachycardia, atrioventricular (AV) dissociation, ST depression, ventricular tachycardia and ventricular fibrillation). The goats died 4, 13, 25 and 84 hours post-ingestion (Aslani et al, 2007).
The onset of signs from cardiac glycoside poisoning is variable but sudden death is the most common presentation in browsing or grazing animals. Clinical signs usually occur within 6 hours. Death may occur rapidly or 48 hours or longer after ingestion. Death can occur from a single dose or from repeated dosing.
The earliest signs of poisoning are hypersalivation, abdominal discomfort, diarrhoea (or constipation), rumen stasis and distension. Animals may appear disorientated with weakness, depression and dullness. An initial diuresis is followed by oliguria and collapse, recumbency and convulsions can occur in severe cases. Cardiac effects are very variable, including irregular pulse, sinus bradycardia (initially) and then tachycardia and arrhythmias. Laboratory findings include hyperkalaemia, hypophosphataemia, acidosis, raised creatine kinase and leucocytosis.
Treatment of cardiac glycoside poisoning is supportive. Repeat dose activated charcoal (1–3 g/kg every 4 hours) may be useful and in valuable animals a rumenotomy could be considered. Analgesia may be required for abdominal discomfort. If possible, the electrolytes, particularly potassium should be checked. Rehydration may be required, but calcium-containing fluids should be avoided as elevated serum calcium concentrations can increase the effect of cardiac glycosides on the myocardium. The blood pressure, heart rate and electrocardiogram should be monitored, if possible.
Atropine (0.15–0.30 mg/kg IM) can be used for bradycardia. Lidocaine (lignocaine) or procainamide have been used in the management of ventricular arrhythmias in other animals but there is no experience of their use in goats with cardiac glycosides poisoning.
Digoxin antibody Fab fragments (DIGIFab®, Protherics Medicines Development Ltd) are an option, but this drug is very expensive. It has been used in dogs with oleander poisoning (Pao-Franco et al, 2017). The antibodies bind to the cardiac glycosides making the molecules unavailable for binding to the sodium-potassium ATP-ase pump. The complex is then excreted in urine. In humans 5–10 vials is recommended for cardiac glycoside toxicity but 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.
Taxane alkaloids (e.g. yew)
Numerous alkaloids have been isolated from various species of yew (Taxus species) (Miller, 1980). The toxic component is taxine, a complex mixture of alkaloids, which produced cardiovascular effects. Taxus species also contain an irritant volatile oil which is present throughout the plant and can cause gastrointestinal irritation and diarrhoea.
In a case report a female goat was found dead with its head in a hay feeder in which cuttings of Japanese yew (Taxus cuspidata) had been placed. More than 200 g of leaves and twigs were found in the rumen at post-mortem examination. A male goat that had also eaten yew developed inappetence and recovered after removal of the clippings (Maxie, 1991). In another case, the rumens of two dead goats contained 2190 and 230 leaves of Taxus species/kg of rumen contents (Coenen and Bahrs, 1994).
All parts of yew are toxic, except the fleshy part of the ‘fruit’ (the aril) (Cooper and Johnson, 1998). Poisoning can occur at any time of the year and plant material is still toxic after drying. Most cases of poisoning in animals occur as a result of accidental ingestion of hedge trimmings or grazing on yew. Yew is not thought to be palatable and is more likely to be ingested in stressed or malnourished animals, or where it has been mixed with a more palatable material, such as grass. A cow, a goat, three sheep and two horses all refused to eat yew clippings when given hay and clover (Alden et al, 1977).
The onset of signs after ingestion of yew is variable; death can occur within 2–36 hours, but usually within 24 hours. Sudden death may occur in animals that have eaten yew. Ataxia, bradycardia, diarrhoea, trembling, weakness, collapse, respiratory distress, recumbency and sudden death (usually as a result of cardiac arrest) occur. Convulsions are rare. Most symptomatic cases are fatal, and death can occur within a few minutes of onset of clinical signs.
There is no specific antidote and treatment of animals with yew poisoning is supportive. A rumenotomy with removal of contents may be considered for valuable animals (Casteel and Cook, 1985). Activated charcoal (1–3 g/kg) can be given. In animals with bradycardia, it should be noted that atropine may be ineffective and will slow peristalsis and delay elimination (Hare, 1998).
Quercus species (oak)
Oak poisoning in animals has been recognised for centuries (Marsh et al, 1919). Goats, like other ruminants, can eat oak and appear to be relatively tolerant but poisoning is occasionally reported, probably as a result of excessive consumption (Çelik and İrak, 2019), although this remains unclear. Poisoning may be more of a risk in some years when the acorn crop is heavy (masting years).
The effects of oak poisoning are mainly gastrointestinal in goats, although renal and hepatic effects have been reported in other animals. Abdominal pain, constipation, haemorrhagic diarrhoea and death were reported in goats after ingestion of Quercus floribunda (Katiyar, 1981). In another case, oak ingestion was suspected as the cause of death in four goats and tannic acid was detected in their rumens (Akar and Filazi, 1992). A 2-month-old pygmy goat died after ingestion of cuttings from an oak (Kinde et al, 1989). Anorexia, depression, mucoid diarrhoea and sudden death occurred in goat kids fed oak leaves and acorns. They did not develop kidney injury, but serum calcium, magnesium and iron concentrations were low, and this was attributed to binding of minerals by compounds in the oak (Çelik and İrak, 2019).
Treatment of acorn toxicosis in ruminants is supportive. 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.
Hedera species (ivy)
Ivy (Hedera helix, English ivy) is eaten by many animals without adverse effect (Forsyth, 1979a; Metcalfe, 2005) and it is sometimes given as a ‘tonic’ to livestock (Forsyth, 1979). Few cases of poisoning are reported in goats, but toxic effects may occur when a large quantity is eaten, for example ingestion of cuttings or during conditions when other food is unavailable. 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), particularly in the leaves and fruit.
The main effect of ivy ingestion is irritation to the gastrointestinal mucosa (Burrows and Tyrl, 2013). The most common sign reported in cases in goats reported to the Veterinary Poisons Information Service (VPIS) is diarrhoea, and this can be severe. Management of ivy toxicosis in goats is supportive.
Ligustrum vulgare (common privet)
Poisoning by privet is rare (Burrows and Tyrl, 2013). The toxic principle is unknown, but is usually referred to as a glycoside, ligustrin. All parts of the plant are toxic, particularly the fruit (Cooper and Johnson, 1998). The main effect of privet in cases of poisoning appears to be gastrointestinal irritation (Burrows and Tyrl, 2013).
Some animals appear to be able to tolerate privet and it is also a food source for others e.g. deer (Stromayer et al, 1998). Deaths, however, have been reported in horses (Turner, 1904; Forsyth, 1979b) and cattle (Anon, 1939; Kerr and Kelch, 1999) after ingestion of Ligustrum species. Most cases in animals involve ingestion of clippings or grazing from hedgerows, and effects can occur after ingestion of the leaves or fruit. A goat reportedly ate ‘considerable quantities without apparent harm’ (Forsyth, 1979), but inappetence, bruxism, regurgitation and gut status have been described in cases reported to the VPIS. Management of privet toxicosis in goats is supportive.
Pyrrolizidine alkaloids (e.g. ragwort)
Pyrrolizidine alkaloids are a group of naturally occurring alkaloids produced by plants as a defence mechanism against insect herbivores. Hundreds of pyrrolizidine alkaloids have been identified in over 6000 plants, and many of them are hepatotoxic. The most commonly encountered plant containing pyrrolizidine alkaloids in Europe is Jacobaea vulgaris (previously Senecio jacobaea, ragwort or tansy ragwort, Figure 4), a very common wildflower. Ragwort is subject to legislation in the UK with a code of practice for preventing the spread of the plant. There is no compulsion in these acts for landowners to remove ragwort, although they may be ordered to do so by local authorities or government authorities.
Plants containing pyrrolizidine alkaloids are generally unpalatable but will be eaten if grazing is poor and other forage is unavailable (Emmel and Sanders, 1942) or as a contaminant of feedstuff (Hill et al, 1997). Of note, plants that are dead (Payne and Wright, 2013) or killed with herbicide become more palatable and frosted and dried plants remain toxic (Emmel and Sanders, 1942).
Poisoning with pyrrolizidine alkaloids occurs after chronic ingestion and species susceptibility is variable but goats (and sheep) are relatively resistant, and horses and cattle are more susceptible. This is thought to be because of a protective effect of ruminal flora in these species. J. vulgaris ingestion of 205 and 302% of initial bodyweight is a lethal dose in goats and sheep respectively, compared with 4–8% in cattle and horses. In this study, goats died after 543 days and the sheep after 161 days (Cheeke, 1984). In another study the chronic lethal dose of J. vulgaris in goats ranged from 1.25–4.04 kg/kg of the original bodyweight (Goeger et al, 1982).
Cases of pyrrolizidine alkaloid toxicosis are reported in goats in South America after ingestion of Crotalaria retusa. The susceptibility of goats to intoxication by C. retusa was experimentally confirmed by administration of the plant (toxic doses of 5 g/kg, 6 g/kg and 10 g/kg). The clinical signs, post-mortem findings and histopathology in the cases of natural and experimental intoxication by pyrrolizidine alkaloids in goats were similar to those previously described for this toxicosis in sheep. Differences in the clinical picture in goats include colic, as well as bruxism and the lack of jaundice (Lucena et al, 2010; Maia et al, 2013). In one outbreak death occurred within 24–48 hour after the onset of clinical signs (Maia et al, 2013).
The liver is the target organ in pyrrolizidine alkaloid toxicosis but poisoning usually only occurs after weeks, months or even years of exposure. Early signs are insidious and non-specific with anorexia, weight loss and depression. This may be all that is apparent in many cases but there may also be bruxism, salivation, colic, diarrhoea, tenesmus, and more rarely, photosensitivity, ascites, jaundice and dyspnoea.
The neurological signs suggestive of hepatic encephalopathy (head pressing, restlessness and aimless walking, apparent blindness and drowsiness) seen in cattle and horses are usually not seen in sheep and goats with pyrrolizidine alkaloid toxicosis.
Laboratory changes include elevated liver enzymes and bilirubin, hypoalbuminaemia and bilirubinuria and anaemia. Elevated creatine kinase (CK) usually as a result of prolonged recumbency is reported in other animals.
There is usually a long delay between exposure and onset of signs so it can be difficult to identify the offending plant or feed contaminant. There is no specific treatment for pyrrolizidine alkaloid toxicosis and treatment is supportive with nutritional support.
Conium maculatum (hemlock)
Hemlock is a tall, wild plant with purple-spotted or blotched and hollow stem (Figure 5). The leaves have a feathery appearance, with a pungent smell when crushed. The unpleasant, foetid odour of Conium maculatum is described as ‘mousy’ or resembling mouse or cat urine.
The toxicity of C. maculatum has been recognised for centuries and it appears to be toxic to most mammalian species. The toxic chemicals found in this plant are piperidine alkaloids, mainly coniine, and all parts of the plant are toxic (Vetter, 2004). Most animals find the plant unpalatable and will only eat it when other forage it unavailable. Dried plant material is less likely to be toxic as the alkaloids are volatile, although poisoning from hemlock in hay has been reported (Galey et al, 1992). Poisoning occurred in goats hand fed on grass, weeds and plants cut from waste ground, which included C. maculatum. Signs included diarrhoea (sometimes bloody), dullness, inappetence, thirst, hypersalivation, vocalisation, hypothermia, stiffness, tremor, irregular pulse, weakness and cessation of milk production. One animal has convulsions. Four goats died and one survived (Copithorne, 1937).
Onset of toxic effects after ingestion of hemlock may be rapid and can be within a few minutes or 1–3 hours. In some cases, effects can occur later, e.g. if exposure involves contaminated hay. Recovery can be rapid and occur within a few hours.
Initially there is central nervous system stimulation followed by depression. Abdominal pain, hypersalivation, tachycardia, tremors, ataxia, dilated pupils, frequent urination and defecation are followed by depression, weakness, rumen stasis, frequent eructation and bloat, bradycardia, vocalisation, collapse, recumbency, rapid, shallow and then slow and laboured respiration, rhabdomyolysis, impaired renal function, convulsions and ascending muscular paralysis leading to respiratory failure and death. The urine and breath may have a mousy odour (Panter et al, 1988).
Biochemical changes reflect stress, muscle damage and dehydration and include raised liver and muscle enzymes, raised urea and creatinine, dehydration, leucocytosis and hyperglycaemia (Binev et al, 2007).
Hemlock ingestion may cause abortion, and teratogenic effects have been reported from chronic ingestion in ruminants including goats (Panter et al, 1990a,1990b). There is reduced fetal movement resulting in cleft palate and multiple skeletal contracture malformations (arthrogyroposis) with excess flexure of carpal joints, torticollis and scoliosis. In animal studies the longer the duration of signs in the mother the more severe the effects in the offspring (Panter et al, 1990b). The alkaloids of hemlock are excreted in the milk and impart an unpleasant taste and smell (Forsyth, 1979a,b). Cessation of milk production has been reported in goats (Copithorne, 1937).
There is no antidote for hemlock poisoning and treatment is symptomatic and supportive. Activated charcoal (1–3 g/kg) can be used, depending on the clinical condition of the animal. Atropine can be used for hypersalivation and bradycardia, but the effect is temporary. A gastric tube may be required to relieve bloat. Careful handling is recommended to minimise stress, as this may exacerbate the toxic effects.
KEY POINTS
- Goats may be poisoned when they gain access to poisonous plants.
- This may occur through browsing/grazing or being accidentally fed poisonous plants, either as cuttings or through contamination of feed.
- Grayanotoxin (e.g. Rhododendron species, Pieris species) and cyanogenic glycoside (e.g. Prunus species) poisoning are common in goats.
- Treatment of plant poisoning is supportive with rehydration, activated charcoal and cardiac support.
Leylandii or Leyland cypress (× 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. In cases in goats reported to the Veterinary Poisons Information Service signs include gastrointestinal effects and sudden death (VPIS case data). Treatment of symptomatic animals is supportive. Activated charcoal (1–3 g/kg) can be given.
Buxus sempervirens (box)
Box is an evergreen shrub or small tree that is widely cultivated particularly as an ornamental hedge plant and is often used to edge flower beds and for hedges and topiary. Although the plant has a disagreeable odour and unpalatable taste and poisoning is not common it has been reported in numerous animals including goats. In one case, poisoning was diagnosed in 4-month-old kids where one was found dead and the other showed signs of abdominal pain and died soon afterwards. Two further kids died over the next 24 hours. At post-mortem examination the first kid had haemorrhages in the diaphragmatic lung lobes and the second was diarrhoeic. In both cases box leaves were identified in the rumen (SAC C VS, 2014b).
The toxin in box was believed to be an alkaloid, ‘buxine’, but this is now recognised to be a complex group of over 135 steroidal alkaloids rather than a single substance (Atta-ur-Rahman et al, 1988, 1999; Loru et al, 2000; Zhang et al, 2015). The mechanism of action of the alkaloids has not been determined.
Clinical effects from ingestion of box can occur within 24 hours of access to plant material with death often occurring soon after onset of signs. Box ingestion can cause abdominal discomfort which can be severe, diarrhoea which can be bloody, ataxia and recumbency. In more severe cases a stiff gait or hind-limb paralysis and difficulty swallowing as a result of oropharyngeal paralysis may also occur. Death occurs from respiratory failure.
There is no antidote for box poisoning and treatment is symptomatic and supportive. Activated charcoal (1–3 g/kg orally) can be given, depending on the clinical condition of the animal, and analgesia for abdominal pain.
Further considerations
Food safety should be considered with all poisoning incidents and products withheld from the food chain until a risk assessment has taken place. This will involve identification of the source/hazard, determination of the exposure pathway and identification of the animals poisoned or at risk of poisoning. Food safety authorities (in the UK this is the Animal and Plant Health Agency (APHA) — see Box 1) should be contacted early in the investigation to prevent contaminated material entering the food chain. Advice on the management of poisoning can be obtained from a poisons information service. Cases can be reported retrospectively to help build our knowledge of plant poisoning in goats.
Box 1.Further advice
- Veterinary Poisons information Service (VPIS) — 24 hour treatment advice for veterinary professionals Telephone 020 73 055 055 (charges apply) Website www.vpisglobal.com Email: info@vpisglobal.com You can report a case of poisoning via the website https://vpisglobal.com/report-a-case/
- Animal and Plant Health Agency (APHA) — for farm-related toxicology advice including incidents with food safety implications in the UK APHA/Defra Rural Services Helpline 03000 200 301 (England); 0300 303 8268 (Wales), find the appropriate Field Office for Scotland https://www.gov.uk/government/organisations/animal-and-plant-health-agency/about/access-and-opening
Conclusions
As herbivores, goats are at risk of plant poisoning, and it is important to prevent access to areas where hazardous plants grow. Clippings of poisoning plants should be disposed of safely to prevent accidental ingestion. Common plant poisonings in goats involve grayanotoxins and cyanogenic glycosides but they are at risk from ingestion of other poisonous plants. Treatment of plant poisoning in goats is generally supportive with administration of activated charcoal, rehydration and monitoring of vital signs. Few practical antidotes are available for the management of poisoning in goats and prevention is key. Advice on the management of poisoning is available from poisons information services.