Poisoning of livestock in spring is likely to be less common than poisoning in the autumn as foliage and fruits are less readily available. Poisoning can occur with early growth of plants and exposure to herbicides. Early spring may be particularly hazardous when forage is scarce and hungry livestock eat toxic plants they would normally avoid.
Some plants that can cause poisoning in the autumn are also a potential risk in the spring. Hypoglycin A poisoning can occur from ingestion of sycamore seedlings in horses (Bates, 2019a). Grazing on the buds and young leaves of oak is a risk in ruminants, particularly cattle, and is discussed in a previous article (Bates, 2019b).
Poisoning in livestock may be a potential food safety incident, which can have implications for meat and milk and appropriate advice should be sought in these cases. In most cases treatment of poisoning in livestock is supportive and in many cases of poisoning, particularly with plants, the only sign may be sudden death. Access to areas where poisonous plants are known to grow should be restricted.
Glyphosate
Glyphosate is a broad spectrum herbicide and is the most widely used herbicide worldwide. It is commonly used before sowing and also just before harvesting crops. It is an organophosphate herbicide with no anticholinesterase activity. It is widely used because it is of low toxicity, lacks residual soil activity, does not bioaccumulate and is biodegradable. Although exposure in livestock has been reported (Burgat et al, 1998; Cortinovis et al, 2015), glyphosate itself is generally considered of low acute toxicity and some of the effects from glyphosate product exposure are due to the presence of a surfactant, usually polyoxyethylene amine (POEA), present in many liquid preparations which aids adsorption of the herbicide into plants. Cattle, and probably other livestock, do not avoid eating vegetation sprayed with glyphosate (Burgat et al, 1998). Livestock should not be allowed to graze on areas treated with glyphosate for at least 5 days and any poisonous plants should be removed, as some plants become more palatable when sprayed with herbicide.
Clinical signs
Glyphosate products are irritant so may cause hypersalivation, colic, diarrhoea, irritation and swelling of lips. Oral ulceration may occur (Burgat et al, 1998). Salivation, tremor, swelling of the neck and dyspnoea have been reported in sheep after glyphosate exposure (Cortinovis et al, 2015).
Severe cases are rarely reported in livestock but in other animals severe poisoning may cause tachycardia, ataxia, depression, inappetence, pharyngitis, pyrexia, panting, tachypnoea, coughing, bradycardia, twitching and convulsions. Respiratory complications are possible due to the presence of the surfactant in many products. Eye and skin irritation are also possible from spray drift, contact with wet plant material or spills of a glyphosate-containing product. Ingestion of plant material treated with glyphosate is only likely to cause mild signs.
Treatment
Treatment of glyphosate exposure in livestock is symptomatic and supportive. Any contaminated skin or eye should be irrigated.
Bluebells
Bluebells (Hyacinthoides non-scripta) and related species Spanish bluebell (Hyacinthoides hispanica) and Italian bluebell (Hyacinthoides italica), are common spring plants. The bluebell (Figure 1) is native to woods, hedgerows, throughout Britain and Ireland, and the Italian and Spanish bluebells are naturalised in these habitats. All are widely cultivated in gardens and parks.
All parts of these plants contain scillarens, which are cardiac glycosides similar in structure to those of foxglove (Digitalis species) (Cooper and Johnson, 1998). Glycosidase-inhibiting alkaloids have also been described in bluebells and may contribute to the toxic effects (Watson et al, 1997). The cardiac glycosides found in plants are generally precursors (primary glycosides that undergo enzymatic hydrolysis when plant material is dried or damaged to give the active (or secondary) glycosides). The gastrointestinal absorption of many primary glycosides is poor and toxic concentrations are rarely reached following plant ingestion (Frohne and Pfänder, 2005). Cardiac glycosides are negative chronotropes and positive inotropes; therefore, they cause decreased frequency and increased force of contraction of heart muscle. They inhibit sodium-potassium adenosine triphosphatase (Na+K+ATPase) on myocardial cells, preventing outflow of sodium into the extracellular space. The resultant high concentration of sodium within the cell increases the amount of calcium available for release during depolarisation, which increases the force of contraction.
Clinical effects
Clinical signs of bluebell poisoning are expected to be gastrointestinal (abdominal pain, vomiting, diarrhoea) and cardiac (bradycardia, tachycardia, arrhythmias). Signs are likely to start within 6 hours of ingestion, and recovery may take several days.
Recumbency, dullness and depression, rapid, shallow respiration, tachycardia or bradycardia, hypothermia, dehydration, abdominal discomfort, reduced rumen motility and constipation and reduced milk yield may occur in cattle after ingestion of blue-bells (Thursby-Pelham, 1967; Cutler, 2007). Abdominal discomfort, a weak, slow pulse and hypothermia, bloody diarrhoea and anuria were reported in a horse after ingestion of bluebell bulbs (Forsyth, 1979). In pigs bluebell ingestion caused anorexia, ill thrift, pulmonary oedema and dyspnoea, with elevated creatinine and urea concentrations (Payne and Murphy, 2014).
Treatment
Treatment of bluebell poisoning is supportive. Activated charcoal (1–3 g/kg) can be given if ingestion was recent but should not be given in animals with reduced bowel movements or constipation. A good quality diet should be provided with rehydration, if required.
Wild garlic
Allium ursinum (wild garlic, wood garlic, ramsons, Figure 2) is a common woodland plant in the UK. As a member the Allium genus it contains a variety of organic sulphur compounds including n-propyl disulphide. Metabolism of the organosulphoxides causes oxidative damage to haemoglobin which results in sulphaemoglobin and this precipitates then aggregates and binds to cell membranes forming Heinz bodies. Eccentrocytes form due to direct oxidative damage to cell membranes. n-Propyl disulphide also depletes the enzyme glucose-6-phosphate dehydrogenase (G6PD) within erythrocytes which renders them more susceptible to oxidative damage. The damage to erythrocytes and Heinz bodies increases cell fragility and extravascular haemolysis. Erythrocytes containing Heinz bodies are usually removed from the circulation by the recticuloendothelial system, thereby inducing anaemia (Lincoln et al, 1992). There is both intravascular and extravascular haemolysis (Cope, 2005). Cooking, dehydration or spoilage of Allium spp. does not reduce toxicity.
Cattle appear to be particularly susceptible to Allium spp. poisoning but goats and sheep are more resistant (Lincoln et al, 1992; Cooper and Johnson, 1998). While Heinz body formation, anaemia and haemoglobinuria, has been reported in sheep exposed to Allium spp. (James and Binns, 1966; Stevens, 1984), poisoning usually occurs when the animals are fed Allium spp. exclusively or in large quantities (Stevens, 1984; Cooper and Johnson, 1998). It has been suggested that sheep are able to adapt to an onion (Allium cepa) rich diet (Van Kampen et al, 1970; Knight et al, 2000), possibly due to the rapid development of a population of sulphate-reducing rumen bacteria.
In the case of onions, it is advised that calves should not be fed a diet containing more than 25% (as dry matter) onions (Lincoln et al, 1992). Onions should be crushed or chopped and thoroughly mixed with other feedstuff to prevent addictive onion consumption in cattle (they tend to eat onions in preference to other foods, if available). Four Welsh ewes (about 30 kg) were found dead after grazing in woodland carpeted with wild garlic. There was evidence of extensive grazing of leaves and flower heads. Post-mortem findings were anaemia, jaundice and a garlic odour to the rumen contents. Two other ewes were found to be anaemic and were removed. The worst affected died but the other recovered without treatment (Stevens, 1984).
Wild garlic (Allium ursinum) and bluebells often grow together, therefore care should be taken to restrict access to areas where these plants are growing and to ensure adequate forage is available for livestock.
Clinical effects
Onset of Allium spp. poisoning is variable. Signs may occur suddenly within 24 hours if a large quantity has been ingested but it is more common for signs to occur after several days. Signs of haemolysis may be delayed from 1 to 5 days and recovery can take several days but can be longer in severe cases.
The main concern in Allium spp. poisoning is haemolytic anaemia with Heinz body formation. Clinical signs are those generally associated with anaemia, i.e. lethargy, weakness, pale mucous membranes, tachycardia and tachypnoea.
The breath, faeces and urine may smell strongly of onions or garlic. There may be ataxia, dehydration, icteric mucous membranes and recumbency. Milk may taste and smell of onions or garlic, and abortion can occur (Rae, 1999; Aslani et al, 2005).
Laboratory findings of Allium spp. poisoning include haematuria (which may be the presenting sign), evidence of haemolytic anaemia with low packed cell volume (PCV) and Heinz bodies. Red blood cells may be hypochromic, anisochromic and polychromasic with basophilic stippling (Verhoeff et al, 1985). Proteinuria, haemoglobinuria, bilirubinuria and haematuria may occur. Elevated creatine kinase and aspartate aminotransferase (AST) may occur due to muscle damage from recumbency. There may also be elevated liver enzymes, urea and creatinine in some cases.
Treatment
Treatment of Allium spp. poisoning is supportive. Activated charcoal (1–3 g/kg) orally can be given if ingestion was recent. Rehydration may be required but care should be taken if anaemia is severe. If practical, monitoring of haematological parameters for evidence and severity of anaemia, and monitoring of renal and liver function should be undertaken. Antioxidants such as vitamin E, ascorbic acid and acetylcysteine are unlikely to be of benefit in Allium spp. poisoning (Cope, 2005). Supplemental oxygen may also be required in severe cases (Cope, 2005). The use of corticosteroids for this form of haemolysis is controversial. It is argued that their use will prolong the clearing of affected cells by suppression of the recticuloendothelial system, and therefore may not be beneficial (Solter and Scott, 1987).
Hemlock (Conium maculatum)
Hemlock (Figure 3a) grows in damp places, meadows, open woods, river, stream and canal margins, roadsides and disturbed ground throughout much of Britain and Ireland, but is absent from large areas of Scotland. The stems are usually purple-spotted or blotched and hollow (Figure 3b). The unpleasant, foetid odour of Conium maculatum is described as ‘mousy’ or resembling mouse or cat urine. Hemlock is often mistaken for other plants such as wild carrot (Daucus carota), cow parsley (Anthriscus Sylvestris) or wild celery (Apium graveolens). The related plant Cicuta virosa (water hemlock, see below) does not have the purple spotted stem or mousy odour (see below).
The toxicity of C. maculatum has been recognised for centuries. All parts of the plant are toxic (Vetter, 2004) and appear to affect most mammalian species. The main toxic compound is coniine, a piperidine derivative similar in structure and function to nicotine. Four other structurally related alkaloids, N-methyl coniine, conhydrine, γ-coniceine and pseudoconhydrine are present in lower concentrations (Vetter, 2004). Coniine, exerts a nicotinic effect on autonomic ganglia with a characteristic biphasic pattern, an initial stimulant and secondary depressant effect. It also has a curare-like action at the neuromuscular junction, causing flaccid paralysis of the skeletal muscles, which can progress to the respiratory muscles (Bowman and Sanghvi, 1963). The concentration of coniine within the roots, fruit and other plant parts is variable and is thought to be dependent on local climate, geographical location and age of the plant (Bowman and Sanghvi, 1963; Vetter, 2004). γ-Coniceine is present in highest concentration early in the growth season hence the plant is most toxic during the spring (Panter et al, 1988a).
Most animals find C. maculatum unpalatable and will only eat it when other forage it unavailable; however, there are reports of some animals that have actively sought the plant (Panter et al, 1983; Jessup et al, 1986). 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).
The severity of hemlock poisoning varies in different species. In livestock, susceptibility to poisoning following acute ingestion of fresh hemlock decreases among species as follows: cattle > sheep = goats > pigs (Lopez et al, 1999).
Clinical signs
Clinical signs from ingestion of hemlock can occur within a few minutes or 1–3 hours. In some cases, effects can occur later e.g. in an outbreak of poisoning involving contaminated hay effects occurred 36 hours after its introduction (Galey et al, 1992). Recovery can be rapid and occur within a few hours. Death can occur within a few hours of ingestion or up to 2 days later.
Initially, there is central nervous system (CNS) stimulation followed by CNS depression. There may be abdominal pain, hypersalivation, tachycardia, tremors, ataxia, dilated pupils, frequent urination and defecation followed by depression, weakness, rumen stasis, frequent eructation and bloat (in ruminants), bradycardia, vocalisation, collapse, recumbency, temporary blindness (due to third eyelid prolapse), coldness of extremities, rapid, shallow respiration 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 mousey odour (Panter et al, 1988a). Biochemical changes reflect stress, muscle damage and dehydration (Binev et al, 2007).
The alkaloids of hemlock are excreted in the milk of cattle (Panter and James, 1990) and impart an unpleasant taste and smell (Forsyth, 1979). Cessation of milk production has been reported in goats following hemlock ingestion (Copithorne, 1937).
Hemlock also causes reproductive effects. Abortion may occur from acute ingestion (Keeler and Balls, 1978; Forsyth, 1979; Swerczek and Swerczek, 2012) and teratogenic effects have been reported from chronic ingestion in cattle (Keeler, 1974; Keeler and Balls, 1978; Keeler et al, 1980), goats (Panter et al, 1990a; Panter et al, 1990b), pigs (Panter et al, 1983; Hannam, 1985) and sheep (Keeler et al, 1980; Panter et al, 1988a). There is reduced fetal movement resulting in cleft palate and multiple contracture skeletal malformations (arthrogyroposis) with excess flexure of carpal joints, torticollis and scoliosis. Bradynathia (abnormal shortness of the lower jaw) has been reported in pigs (Panter et al, 1983). In animal studies the longer the duration of signs in the mother the more severe the effects in the offspring (Panter et al, 1990a). Malformations have also been reported in offspring of asymptomatic mothers (Hannam, 1985). Horses, however, appear to be resistant to the teratogenic effects of coniine (Keeler et al, 1980).
Treatment
There is no antidote for hemlock poisoning and treatment is symptomatic and supportive with rehydration, if required. Careful handling is required to minimise stress, as this may exacerbate the toxic effects. Atropine (0.15–0.30 mg/kg intramuscularly (IM) in ruminants) has been used in some cases for hypersalivation and bradycardia but the effect is temporary. A gastric tube may be required to relieve bloat.
Water hemlock (Cicuta virosa)
Cicuta virosa (water cowbane, water hemlock, Figure 4) is relatively rare in the UK and poisoning incidents are not common. It grows in water and damp, muddy places in East Anglia, Shropshire, Cheshire, southern to central Scotland, and central and northern Ireland. The plant can be difficult to identify, particularly in early spring when only the fleshy roots are present. On cutting the root of Cicuta spp. characteristic chambers are visible and drops of yellowish oil exude which has the odour of raw parsnip (Fleming and Peterson, 1920). The oil quickly oxidizes to a brownish substance (Panter et al, 2007). Roots of the European and American species of Cicuta have been mistaken for wild carrot (Daucus carota), parsnip (Pastinaca sativa), angelica (Angelica sylvestris), artichoke (Helianthus tuberosus), sweet anise (Pimpinella ansium) or sweet potato (Ipomoea batatas).
All parts of the plant are toxic, particularly the root. The main toxin is cicutoxin, a polyacetylene alcohol but the exact mechanism of poisoning is unknown. Cicutoxin affects sodium and potassium channels and delays repolarisation. Prolongation of the action potential at excitatory synapses could promote excitatory activity (Wittstock et al, 1997). Cicutoxin is a powerful CNS stimulant (having similar actions to strychnine) that blocks gammaamino butyric acid A (GABAA) receptors causing neuronal depolarisation resulting in convulsions and death. Cicutoxin may also have cardiopulmonary effects.
The concentration of cicutoxin in the plant varies throughout the year. It is present in greatest concentration between autumn and early winter and is found mainly in the yellow oily juice of the roots. In spring the concentration in leaves and stems increases to concentrations sufficiently high to prove fatal, if ingested in sufficient quantity. Most cases of poisoning occur in the early spring (Fleming and Peterson, 1920), when other plants may be unavailable or less attractive. The tuber is palatable and also most toxic in early spring. As the plant grows toxicity decreases until the flowers and seeds develop, although deaths have been reported from ingestion of mature umbrels and fruits (Panter et al, 2007). Mature leaves in late spring and summer are less hazardous and poisoning generally only occurs in these seasons if the tubers are consumed.
Wet weather may make water hemlock roots more accessible to animals, leading to episodes of poisoning. In early spring the roots may be partially above ground due to winter frost and ice and may be available when other plants have little material available for forage (Fleming and Peterson, 1920).
Clinical signs
Effects of poisoning from water hemlock occur very quickly, usually within 15–60 minutes and death can occur quickly (within 15 minutes; Jenkins and Jackman, 1941) or up to 8 hours after ingestion (Kingsbury, 1964). Animals may be found dead with evidence of a violent terminal struggle. In survivors, recovery can take several days.
Initial effects of water hemlock ingestion include anxiety, hypersalivation, abdominal discomfort, dilated pupils, ataxia, tremor and twitching. Bloat may occur in ruminants. This is followed by bruxism, grand mal convulsions alternating with periods of relaxation and resulting in pyrexia. There may also be a running motion of the legs. The convulsions become more frequent and prolonged. They are violent resulting in lacerations of the tongue, lips and cheeks. There may also be vocalisation, bradycardia or tachycardia, hypotension, coma and metabolic acidosis. Death occurs from cardiopulmonary arrest. Rhabdomyolysis and acute renal failure are reported complications in humans (Carlton et al, 1979).
Biochemical changes in animals with water hemlock poisoning reflect stress and muscle damage from convulsions and include raised liver and muscle enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase) and hyperglycaemia. These changes are minimal in animals that die quickly (<1 day) (Panter et al, 2007).
Treatment
Management of water hemlock poisoning is supportive. Activated charcoal may be given (1–3 g/kg), depending on the condition of the animal. Rumenotomy could be considered for valuable ruminants. Anticonvulsants will be required in severe cases, but diazepam is often ineffective and barbiturates may be required.
Grayanotoxins
Grayanotoxins are found in the spring flowering plants Rhododendron (which includes azaleas, Figure 5a) and Pieris spp. (Figure 5b). 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. Receptor binding results in a modified sodium channels that undergo slow opening. The activated cells maintain a persistent excitation and depolarisation and calcium influx is facilitated. Excitable cells in the nerves and muscle are maintained in a state of depolarisation (Seyama and Narahashi, 1981). The sodium-channel effects of grayanotoxins have positive inotropic effects and cause severe weakness, hypotension, dyspnoea and neurological signs.
Poisoning usually occurs when animals are offered cuttings or in adverse weather conditions when hungry animals stray into wooded or garden areas. Numerous cases are reported in the literature; most involve goats (Smith, 1979; Casteel and Wagstaff, 1989; Plumlee et al, 1992; Puschner et al, 2001) and sheep (Casteel and Wagstaff, 1989; Black, 1991; Power et al, 1991; Anon, 1995), and more rarely, cattle (Lothian, 1924) and equines (Forsyth, 1979; Thiemann, 1991). Camelids have also been poisoned with grayanotoxins (Gillis et al, 1961; Miller, 1981; Crawford, 1999). In many cases the first sign that poisoning has occurred is when animals are found dead.
Clinical signs
Clinical signs of grayanotoxin poisoning generally occur within 6 hours of ingestion (Puschner et al, 2001). Initial signs are gastrointestinal with severe hypersalivation, regurgitation (which can be severe and projectile particularly in goats and cattle (Forsyth, 1979)) 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. 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.
Elevated creatine kinase and alanine aminotransferase (ALT) (due to muscle damage) have been reported in equines. Findings reported in other species are non-specific with leucocytosis, anaemia, metabolic acidosis and evidence of dehydration (Plumlee et al, 1992; Pearson et al, 1996).
Effects can be short-lived, often lasting no more than 24 hours due to the rapid elimination of grayanotoxins (Hikino, 1979). In more severe cases, however, recovery may take up to a week and is usually complete. In fatal cases, death is usually due to respiratory failure and may occur within a few hours of ingestion.
Lactation can cease in goats poisoned by grayanotoxins (Casteel and Wagstaff, 1989), and can take days to recover.
Treatment
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 due to protracted regurgitation. Atropine (0.15–0.30 mg/kg IM in ruminants) can be given to increase heart rate, if required. Antibiotics may be required to prevent secondary infection following aspiration. Intravenous lipid emulsion was used in three goats with grayanotoxin poisoning (Bischoff et al, 2014). All the animal recovered within 12 hours of administration although one subsequently died due to aspiration pneumonia.
Conclusion
Poisoning in the spring is a risk in livestock, particularly when other forage is scare and early plant growth is available. This includes rhododendrons and pieris, bluebells, wild garlic, hemlock and water hemlock. Unpalatable plants that would normally be avoided may be grazed by hungry animals when other forage is unavailable. Poisoning may also occur from exposure to herbicides such as glyphosate, which can be used before sowing of plant crops. Treatment of poisoning in livestock is supportive.
KEY POINTS
- Poisoning in the spring may occur from glyphosate herbicide exposure or ingestion of toxic plants.
- Poisoning with spring plants may occur when other forage is scare.
- Hungry livestock will eat unpalatable plants if other forage is unavailable.
- Livestock with signs of poisoning should be managed supportively with removal from exposure and provision of good quality forage.