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Equine plant toxicity: toxic metabolites, internal systems affected and management

Equine plant toxicity: toxic metabolites,  internal systems affected and management

Rebecca Allan, Equine Nutritionist


Approaching the height of summer and increased daylight hours means plants can absorb more energy from sunlight to grow (Jou et al., 2015). Although full-bloom paddocks and gardens are beautiful to see, some plants can have detrimental effects on your horse’s health and wellbeing. All plants have secondary compounds some of which are toxic to animals if consumed in sufficient quantities (James et al., 2005). Equids are monogastric animals making them more susceptible and less able to tolerate toxins than ruminants (Loh et al., 2020). Their physiology combined with their grazing habits of constantly looking for new food material and having strong incisors that enable them to eat plants down to the soil, even eating root material (Webster, 2013), make equids the perfect candidate to become intoxicated by plant sources (Figure 1). Veterinary Investigation Centres in Britain showed that 15-17% of poisoning cases in animals were due to plants, showing just how much of a threat equids are exposed to (Copper & Johnson, 1998). The plants are the causative agents although it is the toxic dosage, and the equine internal systems affected, that influence the severity of the intoxication.


Figure 1. Equine physiology and grazing habitats make them perfect candidates for plant intoxication



The toxic effects that equids experience when ingesting poisonous plants are due to specific toxic compounds present within the plant. Metabolites are known as the substances produced by the plant which can be subdivided into primary and secondary (Pavarini et al., 2012). The primary metabolites are those essential to the plant’s growth and development, whilst secondary metabolites are naturally occurring compounds, functioning as defensive agents, the synthesis of which is influenced by the environment and predators around the plant (Copper & Johnson, 1998; Pavarini et al., 2012). Through studying plant biology, it is thought secondary metabolites are a plant's way to communicate and respond to external stimuli (Pavarini et al., 2012). It is for this reason the poisonous substances present in plants fall under the category of secondary metabolites as they act as a defence mechanism (Copper & Johnson, 1998).

Poisonous plants can be classed biochemically according to their toxic principles, so whether the toxins have been synthesised within the plant or selectively concentrated from the soil (Copper & Johnson, 1998). The toxins which possess a greater threat to equines are grouped into alkaloids, cyanogenic and cardiac glycosides, tannins, and photodynamic substances (Hastie, 2012). The following is a description of these toxins linked to the common poisonous plants in the UK which can be seen in Table 1. Appendix 1 provides a visual guide to these common plants.



Alkaloids are nitrogen-containing secondary metabolites with approximately 20% of plant species containing them, in fact, alkaloids are more likely to poison livestock than any other toxic compound (Pfister et al., 2001; Heinrich et al., 2021) From a biochemical perspective, alkaloids consist of a heterocyclic ring with a nitrogen atom acting as a base, however, this arrangement in structure can vary leading to subtype groups such as piperidine and pyrrolizidine alkaloids amongst others (Copper & Johnson, 1998). Alkaloids are commonly associated with liver damage, central nervous system defects and weight loss, followed by hepatic encephalopathy in extreme cases which are later described (Mair & Love, 2012; Hall et al., 2020).



Poison Hemlock (Conium maculatum) contains several piperidine alkaloids which are prevalent within the plant and probably responsible for its toxicity (Copper & Johnson, 1998). The concentrations at which these alkaloids are present vary with the stage of plant growth and environmental conditions (Matsuura & Fett-Neto, 2015). The leaves are dangerous in the spring whereas the fruit is very dangerous in the autumn (Anadón et al., 2012). Poison Hemlock is often confused with the extremely poisonous Water Hemlock, the main characteristic distinguishing them is that the Water Hemlock has visually distinct partitions in the roots (Panter et al., 2012).

Marsh Horsetail (Equisetum palustre) is a non-flowering, fern-like poisonous plant which contains several compounds leading to its toxic nature. Alongside piperidine alkaloids, it also contains a nicotine alkaloid and thiaminase enzyme (Copper & Johnson, 1998; Cramer et al., 2015). Interestingly, a recent study on cattle revealed that Marsh Horsetail is a major source of piperidine alkaloids, and it is the reason why cattle are exposed to this compound (van Raamsdonk et al., 2015). Horses are reported among the sensitive species to Marsh Horsetail, showing disturbance to their balance if consumed (Cramer et al., 2015).



Pyrrolizidine alkaloids (PA) are specifically synthesised in the root of plants and then translocated to all other plant organs (Ober & Hartmann, 1999).

Hound´s Tongue (Cynoglossum officinale) invades pastures and fields, although it is mostly unpalatable to horses therefore most intoxication occurs when hay or forage is contaminated (Copper & Johnson, 1998; Stegelmeier, 2011). It contains four pyrrolidine alkaloids: 7-angelyheliotridine, echinatine, acetylheliosupine and heliosupine, with the latter being 4-6 times more toxic (Pfister et al., 1992). In Europe there was an accident report, whereby Hound´s Tongue was indicated as a potential toxic threat to horses in pasture, specifying the early growth stage of this plant to be the most toxic (Zentek et al.,1999).

Ragwort (Senecio species) is composed of more than 1200 species worldwide with 25 species confirmed poisonous (Anadón et al., 2012). These plants contain a series of PA such as senecioninie, jacidine and jacozine amongst others. In the UK and Belgium, there have been many reported incidents involving the exposure of horses to Tansy Ragwort (Crews & Anderson, 2009; Vandenbroucke et al., 2010).



European Yew (Taxus baccota) is composed of volatile oils in the tree sap acting as irritants together with a complex mixture of taxine alkaloids (Anadón et al., 2012). The taxine is present throughout the Yew but not in the red fruit (Anadón et al., 2012). European Yew poisoning in horses can also occur from ingestion of Yew clippings (Berny et al., 2010).

Nightshade plant species (Solanum species) can also induce toxicity in equines. The Solanum toxins vary from species, although solanine is the common glycoalkaloid across all nightshade species (Norman et al., 2012). Within the UK, Deadly Nightshade and Woody Nightshade are the nightshade variants containing glycoalkaloids affecting horses (Copper & Johnson, 1998; Hastie, 2012).



The term glycoside involves a large group of organic substances which are composed of one or more monosaccharide (sugar) molecules combined with a non-sugar entity, known as aglycone (Copper & Johnson, 1998). Although many plants containing glycosides are not toxic, their toxicity is determined by the aglycone and the properties of the latter enable sub-classification into cyanogenic, goitrogenic, cardiac and saponic glycosides, although not every toxin fits into these groups (Copper & Johnson, 1998).

Buttercups (Ranunculus repens) contain the glycoside ranunculin with the aglycone protoanemonin being the toxic agent which is of a strong oil nature (Majak, 2001; Dalefield, 2017). This is an example of a glycoside containing plant that has not been classified into a category (Copper & Johnson, 1998).



Foxglove (Digitalis purpurea) is a highly toxic plant that contains cardiac glycosides. These glycosides have a specific action on the heart, increasing the contractility of the heart, and slowing down the heart rate. In Foxglove, the toxic agent is termed Digitalis glycosides (also known as Digoxin) (Copper & Johnson, 1998; Kurian, 2015).



Bracken Fern (Pteridium aquilinum) has several harmful constituents. The main concerns that have been identified are cyanogenic glycoside (prunasin) which is often present in harmless quantities, together with the enzyme thiaminase and a carcinogen (ptaquiloside) (Copper & Johnson, 1998). The effects of thiaminase are the primary cause of toxicity in equids as they can cause vitamin B1 deficiency. Although prunasin content in bracken is usually too low to harm animals, the prunasin glycoside metabolises into hydrocyanic acid as the plants are crushed during eating, and death has been reported from animals eating young bracken leaves (Copper & Johnson, 1998).



Tannins are complex phenolic polymers that vary in biological activity and chemical structure. The Oak tree, including the acorns and leaves, contains tannins and is a common cause of tanning poisoning in the UK (Copper & Johnson, 1998). When consumed by horses, the tannins can be broken down by bacteria in the gastrointestinal tract and can give rise to gastroenteritis (Copper & Johnson, 1998; Hastie, 2012).



Photodynamic substances can make non-pigmented or slightly pigmented skin hypersensitive or hyper-reactive to ultraviolet radiation in sunlight (Hastie, 2012). Photodynamic substances become toxic when exposed to light due to their chemical properties, meaning they absorb light wavelengths within the ultraviolet (UV) and visible spectrum (280-700nm) (Collett, 2019). For a compound to be an effective photo toxin it should be absorbed through the gastrointestinal tract or through direct skin contact in sufficient concentrations (Copper & Johnson, 1998).

In the UK, there are two main plants that cause primary photosensitivity: St John´s Wort (Hypericum perforatum) and Buckwheat (Fagopyrum esculentum). St John´s Wort contains hypericin as the photosensitiser agent, whilst Buckwheat contains the pigment Fagopyrin as the active principle (Copper & Johnson, 1998; Hastie, 2012).


Table 1: Common poisonous plants in the UK, grouped by toxic chemicals, describing their common environment, active principle, and clinical signs (Copper & Johnson, 1998; Lynn & Waldren, 2003; Bergero & Nery, 2008; Hastie, 2012)



Every equine is an individual and their susceptibility to individual poisonous plants will vary. Symptoms resulting from the consumption of toxic plants happen at various speeds and intensities, creating a challenge for both vets and horse owners (Hastie; 2012). Some horses consume toxic plants and only become mildly ill whilst others become severely ill. It is the type of toxin consumed and its quantity that will determine the clinical signs, although they are usually multifactorial (Hastie, 2012). Furthermore, some toxic compounds affect vital organs without any symptomatic warning until the organ is mostly compromised, as is the case for liver disease (Mair & Love, 2012).

The foremost indicator of a toxic event is any meaningful change in your horse’s behaviour. Any inconsistency or uncommon behaviour should be a cause for concern (Sestric & Coates-Markel, 2005; Hastie, 2012). The more common signs are change in appetite, observable physical trauma, digestive changes/upsets, neurological symptoms together with muscle loss and weakness (Hastie, 2012; Stegelmeier & Davis, 2018). The variability in clinical signs is due to the different body systems affected, with some toxins more prevalently affecting certain body systems.

Equine toxicity progresses as follows: the gastrointestinal, cardiovascular, and nervous systems are primarily affected and then as toxin ingestion has developed, further secondary changes can be seen from hepatic (liver) failure and encephalic (brain and nerves) systems (Hastie, 2012). Following on, the physiology of how the bodily systems are affected by toxins is described.



Once a potentially toxic compound is ingested, the initial interaction and damage occur in the gastrointestinal enterocytes (absorption cells lining the intestines), affecting the digestive tract in several ways (Copper & Johnson, 1998; Stegelmeier & Davis, 2018). When chewed, some plants can cause mechanical damage to the digestive tract and cause stomatitis (blistering of tongue, mouth, nose, and developing (Knight & Walter, 2003; Stegelmeier & Davis, 2018).

Colic is the most identifiable clinical symptom when toxic plants are ingested, especially in large quantities, although horse owners may not think the cause is from toxic plants as there are many other reasons from which colic may arise. The potential toxic compound once absorbed may remain unchanged or it may break down spontaneously or undergo enzymatic metabolism (Copper & Johnson, 1998). This could lead to colic which may imitate plant toxicity by three potential actions: acting as a direct irritant to the gastrointestinal system, stimulating the nervous system to act upon the gastrointestinal tract, and by causing obstruction or impaction (Hanson, 2008).

Buttercups contain glycosides together with the highly toxic protoanemonin which affects the gastrointestinal tract (Stegelmeier et al, 2020). Oral irritation is seen as blistered lips and stomatitis which results in increased salivation, then as consumption increases and absorption takes place, gastroenteritis, colic, and diarrhoea can arise with liver disease developing from serious cases (Knight & Walter, 2003; Stegelmeier et al., 2020). Nightshades also affect the digestive tract as they involve the glycoalkaloid toxin solanine which are particularly potent mucosal irritants that commonly cause gastroenteritis, abdominal pain, and diarrhoea (Stegelmeier et al., 2020). However, because most toxins may cause extensive multiple organ damage, it is imperative to understand all the body systems involved in toxicity. After the toxin has been ingested and processed by the gastrointestinal system, the toxin can then also negatively impact the horse’s nervous system together with the cardiac system, with no order preference (Hastie, 2012).



A neuromuscular junction is a highly specialised structure between a motor neuron nerve terminal and a muscle fibre (Cruz et al., 2020). This junction is responsible for converting electrical impulses from the motor neuron to electrical activity in the muscle fibres. However, for muscle function to occur a neurotransmitter known as acetylcholine is required. Acetylcholine crosses the gap from the motor neuron and binds to the receptors on the muscle fibres initiating muscle contraction (Cruz et al., 2020). However, when a toxin affecting neurons (neurotoxin) is involved, this pathway is not completed.

Alkaloids are often associated with affecting the action of nerve transmitters (Copper & Johnson, 1998). The alkaloids atropine and scopolamine are competitive antagonists for acetylcholine receptors, therefore interfering with nerve impulses reaching cells, and disrupting muscle contraction (Meriney & Fanselow, 2019). The plant Atropa belladonna, also known as Deadly Nightshade, contains the alkaloids atropine, hyoscine and scopolamine, making it poisonous and hallucinogenic (Passos & Mironidou-Tzouveleki, 2016). Atropine is also the principal alkaloid found in the Deadly Nightshade´s mature fruits. The fruits are similar to berries and are estimated to contain 2mg of atropine, giving them potent toxicity (Passos & Mironidou-Tzouveleki, 2016).

Clinical signs of toxins affecting the nervous systems are imbalance, changes in heartbeat, uneven muscle contraction and weakness (Hastie, 2012; Meriney & Fanselow, 2019).



Cardiac glycosides have a particular effect on the heart, as indicated by their name (Copper & Johnson, 1998). The heart is controlled by electrical impulses which are regulated via sodium-potassium pumps. Sodium is actively transported out of the cells whilst potassium is actively transported into the cells, this balance is crucial for many physiological processes (Pirahanchi et al., 2021). In addition, there is also a sodium-calcium pump regulated by membrane potentials, which generally pumps sodium into the cell and calcium out of the cell, under normal circumstances. Calcium is the molecule involved in the contraction of the cardiac muscle; therefore, this sodium-calcium pump indirectly controls this contraction (Pirahanchi et al., 2021)

When a toxin such as Digoxin found in Foxglove is ingested, this toxin binds to the sodium-potassium pump, inhibiting it and causing an accumulation of sodium intracellularly. This increase in sodium levels disturbs the concentration balance within cells, inhibiting sodiumcalcium exchange, resulting in increased calcium levels within cells (Pirahanchi et al., 2021). Therefore, more calcium is available for cardiac contraction. However, as this increased heart contraction is not a normal physiological response, the body stimulates the Vagus nerve (hearts control mechanism), slowing down conduction between the top and bottom parts of the heart (Pirahanchi et al., 2021), resulting in an abnormal heartbeat as contractile strength has increased and conduction has decreased (Kurian et al., 2015). Prognosis can be positive if the toxin is ingested in low amounts, nevertheless, cardiac glycosides can cause haemorrhaging, diarrhoea, and abdominal pain (Copper & Johnson, 1998; Hall et al., 2020).



After oral ingestion and gastrointestinal absorption, toxins pass to the liver, the major organ in which enzymatic breakdown and detoxification take place (Bergero & Nery, 2008; Carlson, 2015). The term ‘liver disease’ encompasses several pathological conditions that affect the liver’s functions, and it can either consist of a temporary impaired functioning of the liver and/or progress to its failure whereby the liver loses all or most of its functionality (Bergero & Nery, 2008). Pyrrolizidine alkaloid toxicosis is a common cause of liver failure, characterised by liver necrosis and fibrosis (Bergero & Nery, 2008). Several case studies have been reported concerning liver disease in horses after consumption of Ragwort (Senecio spp.) and Hound's Tongue (Cynoglossum officinale), both PA containing plants (Bergero & Nery, 2008)

Following liver damage, cellular lesions can arise whereby hepatic (liver) cells are destroyed (necrosis) or replaced by fibrous connective tissue (fibrosis) (Bergero & Nery, 2008; Mair & Love, 2012). Fibrosis is a typical lesion involved with liver dysfunction and occurs when the rate of cell death (necrosis) exceeds the rate of regeneration, therefore connective tissue replaces parenchymal (functional) tissue on the liver surface, effectively impairing the liver (Wynn, 2009).

The difficulty with liver disease is the non-specific clinical signs, as they often depend on the severity and duration of the disease (Carlson, 2015). Also at least 80% or more of the liver must be damaged for clinical signs to become apparent (Carlson, 2015). Common clinical signs are weight loss, depression, anorexia, and colic, with more liver-specific signs involving hepatic encephalopathy, jaundice, and photosensitivity (Carlson, 2015).



Hepatic encephalopathy (HE) is a condition where the function of the central nervous system is disturbed due to hepatic (liver) insufficiency (Bergero & Nery, 2008). Hepatic encephalopathy is correlated with astrocyte (central nervous system cell type) swelling, acute cytotoxic cerebral swelling, and intracranial hypertension (Divers & Barton, 2018).

Several studies and theories regarding the cause of hepatic encephalopathy exist although only a few have remained the focus of research and shaped the current approach, although all theories are probably related, and the disease is most likely multifactorial (Mair, 1997).

The blood-brain barrier (BBB) protects the brain from a wide range of substances as it forms tight junctions between adjacent endothelial cells of the cerebral capillaries preventing the passage of unknown substances (Skowrońska & Albrecht, 2012). The common derivative amongst all theories revolves around the BBB being compromised due to the liver´s functionality being impaired which then leads to neurological issues (Jones et al., 1984; Maddison, 1992; Bergero & Nery, 2008; Skowrońska & Albrecht, 2012). Together with alterations in the BBB, the liver is also responsible for metabolising amino acids thus if its functionality is impaired by toxins, amino acid metabolism is also altered (Dejong, et al., 2007). This leads to the additional theory of HE, whereby increased levels of Aromatic amino acids develop due to decreased liver functionality which impacts neurological systems as they can act as false neurotransmitters (Bergero & Nery, 2008). It is therefore a combination of these theories that can cause HE.



Bilirubin is a breakdown product of red blood cells which passes through the liver to be excreted (Ravindran, 2020). However, when liver functionality has been impaired, Bilirubin is not excreted as efficiently meaning accumulation in the bloodstream occurs. This clinically manifests as yellow pigmentations that can be seen in non-pigmented skin, mucosal membranes, and the eye's sclera. This condition is known as jaundice or icterus and is commonly associated with liver disease (Ravindran, 2020).



Photosensitivity is a clinical syndrome which develops when animals become abnormally reactive to sunlight due to the presence of a phototoxin or photoallergen in their skin (Figure 2) (Collett, 2019). In farm animals, most cases of photosensitivity are due to phototoxins present in pasture plants or preserved forages (Collett, 2019). There are two types of photosensitivity: primary and secondary.

Primary photosensitivity is associated with the ingestion of plants containing photodynamic compounds which reach the skin after being absorbed by the gastrointestinal tract (Copper & Johnson, 1998). Plants such as St John’s Wort and Buckwheat contain these compounds and illicit such a response. Erythema (skin rash) and oedema of unpigmented skin areas are common, together with blistering of the skin (Mair & Love, 2012). Primary photosensitivity is a painful condition although horses can fully recover if kept out of the sun and by removing the plant source (Mair & Love, 2012).

Secondary photosensitivity develops following liver damage. Phylloerythrin is a bacterial by-product of the breakdown of chlorophyll in plants (Stegelmeier, 2002). Phylloerythrin would be excreted by the liver under normal conditions but when liver functionality is impaired, it accumulates in the blood reaching the capillaries of the skin. The Phylloerythrin compound is then activated by ultraviolet radiation and causes photosensitivity (Stegelmeier, 2002). This photosensitivity is commonly observed in subacute to chronic liver diseases, making it an obvious clinical sign to look out for (Bergero & Nery, 2008).

Taking it all together, many bodily systems are affected by intoxication with some toxins being more prevalent in affecting certain organs. Should there be any suspicion of plant poisoning, immediate veterinary attention must be sought so the problem can be assessed, and the appropriate treatment administered (Hastie, 2012). For more information on treatment of liver disease see Liver disease in horses. What is also essential when an equine poisoning scenario is encountered, and a key step in managing the situation, is preventing further access to the suspected cause of poisoning (Hastie, 2012).


Figure 2. Skin lesion due to secondary photosensitivity on horse’s un-pigmented skin




By identifying the key plants and toxins involved in equine plant toxicity, together with the clinical signs and body systems affected, a management plant can be developed considering the animal’s husbandry, and physiological and behavioural requirements. Equids are notorious for searching for new green forage which may lead to the consumption of toxic compounds (Webster, 2003). Horse owners should be vigilant for poisonous weeds and plants invading their paddocks and these should be eradicated upon identification. Poisonous trees, such as Oak and Yew trees, should be fenced off appropriately to avoid equines consuming them or their fallen leaves, fruits, and seeds (Hastie, 2012).

As for the plants, there is a naturally increased palatability for plants with lower toxins however this does not guarantee the avoidance of highly toxic plant consumption, although secondary toxic metabolites affect the taste and smell of the plants and negatively impact their palatability (Copper & Johnson, 1998). Horses in overgrazed paddocks, in poor condition or not supplied with enough food, can find toxic plants appealing and are more likely to consume them, meaning it is important that these plants are eradicated from the grazing area.

Toxic plants may be eradicated via the following means:

• Physical removal – carefully remove by digging up the plant and its roots and dispose of appropriately

• Spraying with a herbicide – this method is more invasive, and horses must be removed from the immediate and surrounding area before spraying is carried out. Keeping animals off the area after spraying is also usually required so it is advised to check the herbicide manufacturers' exclusion period before returning animals to the area (Figure 3).

Ornamental garden plants such as Rhododendron, Privet and Yew should also be considered as sources of toxins (Hastie, 2012). These plants may border the grazing area, be encountered whilst hacking, or be consumed if your horse or pony is kept at home with access to your garden.


Figure 3. Spraying with herbicides is one method of controlling undesirable plants in grazing pasture. Ensure any legal requirements for purchase, storage, handling and spraying the product are followed and that animals are removed from the pasture as directed by the herbicide manufacturer.




Consumption of poisonous plants is a cause for concern for any horse owner. Although there is no specific characteristic determining a poisonous plant, they can be grouped based on their toxic components, with alkaloids posing a major threat to equines. The most common clinical signs include altered behaviour, colic, neuronal damage, and muscle loss. Clinical signs are varied due to the various body systems being affected starting at the gastrointestinal tract through to the liver. In severe cases, damage to the liver can cause further issues such as hepatic encephalopathy affecting the central nervous system, together with jaundice and photosensitivity. As soon as a horse experiences a toxic event, veterinary attention is imperative to help manage the horse’s condition and decide the best course of action. Management procedures to minimise toxic events from occurring must be put in place whereby toxic plants should be eradicated once visualised. Thus, enabling horse owners to establish a balance between the mere presence of toxic plants and their over-abundance, keeping horses safe, and free from unfortunate toxic events.



Anadón, A., Martínez-Larrañaga, M.R. & Castellano, V. (2012). Poisonous plants of Europe. In: Veterinary Toxicology: Basic and Clinical Principles, 2nd edition. Elservier: London

Berny, P., Caloni, F., Croubels, S., Sachana, M., Vandenbroucke, V., Davanzo, F. & Guitart, R. (2010). Animal poisoning in Europe. Part 2: Companion animals. Veterinary Journal, 183: 255-259.

Bergero, D. & Nery, J. (2008). Hepatic diseases in horses. Journal of Animal Physiology and Animal Nutrition, 92: 345-355

Carlson, K.L. (2015). Hepatic disease in the horse. In: Sprayberry, K.A. & Robinson, E.N. (eds.). Robinson´s current therapy in equine medicine. 7th edition. Elservier Saunders: USA.

Cooper, M.R. & Johnson, A.W. (1998). Poisonous principles. In: Poisonous plants and Fungi in Britain; Animals and human poisoning. 2nd Edition. The Stationary Office: London

Cramer, L., Ernst, L., Lubienski, M., Papke, U., Schiebel, H.M., Jerz, G. & Beuerle, T. (2015). Structural and quantitative analysis of Equisetum alkaloids. Phytochemistry, 115: 27-37.

Crews, C. & Anderson, W.A.C. (2009). Detection of ragwort alkaloids in toxic hay by liquid chromatography/ time of flight mass spectrometry. Veterinary Records, 165: 568-569

Collett, M. G. (2019). Photosensitisation diseases of animals: Classification and a weight of evidence approach to primary causes. Toxicon: X, 3:100012.

Cruz, P.M.R., Cossins, J., Beeson, D. & Vincent, A. (2020). The neuromuscular junction in health and disease: molecular mechanisms governing synaptic formation and homeostasis. Frontiers in Molecular Neuroscience, 13: 610964

Dalefield, R. (2017). Chapter 24 - Poisonous Plants. In: Kruze, Z. (eds.). Veterinary Toxicology for Australia and New Zealand. Elsevier: UK

Dejong, C.H.C., van de Poll, M.C.G., Soeters, P.B., Jalan, R. & Damink, S.W.M. (2007). Aromatic Amino Acid metabolism during liver failure. The Journal of Nutrition, 137(6): 1579-1585

Hall, A.L., Gornish, E. & Ruyle, G. (2020). Poisonous plants on rangelands. The University of Arizona Cooperative Extension, az1828: 1-10.

Hanson, G. (2008). The toxicity of plants in equines: A modern three-point approach to disseminating information (PhD Thesis). University of Idaho: USA

Hastie, P.S. (2012). Poisons and Poisoning (Toxicology). In: Ivens, P. (eds.). The BHS Veterinary Manual. 2nd Edition. Kenilworth Press: UK

Heinrich, M., Mah, J., & Amirkia, V. (2021). Alkaloids used as medicine: Structural Phytochemistry Meets Biodiversity. Molecules. 26(7):1836.

James, L.F., Gardner, D.R., Lee, S.T., Panter, K.E., Pfister, J.A., Ralphs, M.H., & Stegelmeier, B.L. (2005). Important poisonous plants on rangelands. Rangelands, 27:3-7.

Jones, E. A., Schafer, D. F., Ferenci, P., & Pappas, S. C. (1984). The GABA hypothesis of the pathogenesis of hepatic encephalopathy: current status. The Yale Journal of Biology and Medicine, 57(3): 301–316.

Jou, J. H., Lin, C. C., Li, T. H., Li, C. J., Peng, S. H., Yang, F. C., Thomas, K., Kumar, D., Chi, Y., & Hsu, B. D. (2015). Plant Growth Absorption Spectrum Mimicking Light Sources. Materials, 8(8):5265–5275.

Knight, A.P. & Walter, R.G. (2003). Plants affecting the digestive system. International Veterinary Information Service, B0503.1102: 1-42.

Kurian, M. (2015). The Effect of Digitalis on the Heart – An Update. Journal of Pharmaceutical Sciences and Research, 7(10): 861 – 863.

Loh, Z. H., Ouwerkerk, D., Klieve, A. V., Hungerford, N. L., & Fletcher, M. T. (2020). Toxin Degradation by Rumen Microorganisms: A Review. Toxins, 12(10):664.

Lynn, D.E. & Waldren, S. (2003). Survival of Ranunculus repens L. (Creeping Buttercup) in an Amphibious Habitat. Annals of Botany, 91(1):75-84.

Maddison, J.E. (1992). Hepatic encephalopathy. Current concepts of the pathogenesis. Journal of Veterinary Internal Medicine, 6(6):341-353

Mair, T.S. (1997). Ammonia and encephalopathy in the horse. Equine Veterinary Journal, 29(1): 1-2

Mair, T. S. & Love, S. (2012). Chapter 22 - Metabolic Diseases and Toxicology. In: Schumacher, J., Smith, R. & Frazer, G.S. (eds.). Equine Medicine, Surgery and Reproduction. 2nd Edition. Elsevier Ltd: China.

Mair, T. S., & Love, S. (2012). Gastroenterology: Hepatic and intestinal disorders. Equine Medicine, Surgery and Reproduction, PMC7150257: 49–65.

Majak, W. (2001). Review of toxic glycosides in rangelands and pasture forages. Journal of Range Management, 54(4): 494-498.

Marcella, K. (2011). Stomatitis and excessive salivation in horses. Doctor of Veterinary Medicine 360, 42(4).

Matsuura H.N. & Fett-Neto A.G. (2015) Plant Alkaloids: Main Features, Toxicity, and Mechanisms of Action. In: Gopalakrishnakone P., Carlini C., Ligabue-Braun R. (eds.). Plant Toxins. Toxicology. Springer: Netherlands.

Meriney, S.D. & Fanselow, E.E. (2019). Chapter 16: Acetylcholine. In: Synaptic Transmission, Elsevier: UK

Norman, T.E., Chaffin, M.K., Norton, P.L., Coleman, M.C., Stoughton, W.B. & Mays, T. (2012). Concurrent Ivermectin and Solanum spp. Toxicosis in a Herd of Horses. Journal of Veterinary Internal Medicine, 26: 1439-1442.

Ober, D., & Hartmann, T. (1999). Homospermidine synthase, the first pathway-specific enzyme of pyrrolizidine alkaloid biosynthesis, evolved from deoxyhypusine synthase. Proceedings of the National Academy of Sciences of the United States of America, 96(26): 14777–14782.

Panter, K.E., Gardner, D.R., Lee, S.T., Pfister, J.A., Ralphs, M.H., Stegelmier, B.L. & James, L.F. (2012). Poisonous plants of the United States. In: Gupta, R.C., Veterinary Toxicology: Basic and Clinical Principles. 2nd edition. Elsevier Inc: USA

Passos, I.D. & Mironidou-Tzoueleki, M. (2016). Hallucinogenic plants in the Mediterranean countries. In: Preedy, V.R. (eds.). Neuropathology of drug addictions and substance misuse. Volume 2. Elsevier: Kings College London

Pavarini, D.P., Pavarini, S.P., Niehues, M. & Lopes, N.P. (2012). Exogenous influences on plant secondary metabolite levels. Animal Feed Science and Technology, 174 (1-4): 5-16.

Pfister, J.A., Molyneux, R.J. & Baker, D.C. (1992). Pyrrolizidine alkaloid content of houndstongue (Cynoglossum officinale L.). Journal of Range Management, 45: 254-256.

Pfister, J.A., Panter, K.E., Gardner, D.R., Stegelmier, B.L., Ralphs, M.H. & Molyneux, R.J. (2001). Alkaloids as anti-quality factors in plants on western U.S. rangelands. Journal of Range Management, 54: 447-461.

Pirahanchi, Y., Jessu, R. & Aeddula, N.R. (2021). Physiology, Sodium Potassium Pump. StatPearls Publishing, 30725773.

Ravindran, R. (2020). Jaundice. Hepatobiliary Surgery, 38(8):446-452

Divers, T.J. & Barton, M.H. (2018). Disorders of the liver. In: Reed, S.M., Bayly, W.M. & Sellon, D.C. (eds.). Equine Internal Medicine. 4th Edition. Elservier: USA

Sestric, E. & Coates-Markle, L. (2005). Keeping your horse healthy. Oregon State University Extension Service Bulletin, EC-1472:1-5.

Skowrońska, M. & Albrecht, J. (2012). Alterations of blood-brain barrier function in hyperammonaemia: an overview. Neurotoxicity Research, 21(2):236-244

Stegelmeier, B.L. (2002). Equine Photosensitization. Clinical Techniques in Equine Practices, 1(2): 81-88

Stegelmeier, B.L. (2011). Pyrrolizidine alkaloid – Containing Toxic Plants (Senecio, Crotalaria, Cynoglossum, Amsinckia, Heliotropium, and Echium spp.). Veterinary Clinics of North America: Food Animal Practice, 27(2): 419-428.

Stegelmeier, B.L. & Davis, T.Z. (2018). Toxic Causes of Intestinal Disease in Horses. In: Stämpfli, H., Schoster, A. & Divers, T.J. Recent Advances in the Diagnosis and Management of Equine Gastrointestinal Diseases. Volume 34, Elsevier: USA.

Stegelmeier, B.L., Davis, T.Z. & Clayton, M.J. (2020). Plants containing Urinary tract gastrointestinal, or miscellaneous toxins that affect livestock. Veterinary Clinics of North America: Food Animal Practice, 36(3):701-713

Vandenbroucke, V., van Pelt, H., de Backer, P. & Croubels, S. (2010). Animal poisoning in Belgium: A review of the past decade. Vlaams Diegeneeskund. Tijdschr, 79: 259-268.

Van Raamsdonk, L.W., Ozinga, W.A., Hoogenboom, L.A., Mulder, P.P., Mol, J.G., Groot, M.J., van der Fels-Klerx, H.J. & de Nijs, M. (2015). Exposure assessment of cattle via roughages to plants producing compounds of concern. Food Chemistry, 189:27-37.

Webster, J. (2013). Audits of animals in agriculture. In: Animal Husbandry Regained, The place of farm animals in sustainable agriculture. Taylor and Francis Group: USA.

Wynn, T. (2008) Cellular and molecular mechanisms of fibrosis. The Journal of Pathology, 214 (2):199–210.

Zentek, J., Aboling, S. & Kamphues, J. (1999). Accident report: Animal nutrition in veterinary medicine actual cases: Houndstongue (Cynoglossum officinale) in pasture – A health hazard to horses. Deutsche Tierarztliche Wochenschrift, 106(11):475-477.


Appendix 1: Common plants in the UK poisonous to equids