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(Stegelmeier et al. 1996; Stegelmeier 2011). Houndstongue contains 4 pyrrolizidine alkaloids: 7-angelylheliotridine, echinatine, heliosupine and acetylheliosupine. Heliosupine is the most abundant and toxic alkaloid in the plant (Pfister et al. 1992). Pyrrolizidine alkaloids are bioactivated in the liver into metabolites called pyrroles which are cumulative hepatotoxins (Stegelmeier 2011; Panter et al. 2012). Hepatic changes vary from fulminant necrosis to chronic hepatic fibrosis depending on the amount of pyrrolizidine alkaloids ingested (Stegelmeier 2011). Horses may show no clinical signs for several months after houndstongue ingestion. However, liver damage may progress and horses may develop clinical liver failure with photosensitivity, icterus and increased susceptibility to hepatic lipidosis or ketosis (Stegelmeier 2011). In Europe, a possible case of horse poisoning resulting from consumption from a young pasture containing houndstongue in its rosette stage has been reported. Tympany and colic were observed in the affected horses (Zentek et al. 1999).


Senecio jacobaea (tansy ragwort) Tansy ragwort (Fig 2) is a widespread invasive weed belonging to the Compositae family found throughout much of Europe. In the UK and in Belgium, tansy ragwort is one of the most frequent causes of horse poisoning by plants (West 1996; Crews and Anderson 2009; Vandenbroucke et al. 2010). Cases of equine poisoning by Senecio spp. are also increasingly common in France (Passemard and Priymenko 2007). The compounds responsible for the toxicity of tansy ragwort are a series of pyrrolizidine alkaloids including seneciphylline, senecionine, jacozine, jacobine, jacoline and jaconine (Crews and Anderson 2009). Poisoning occurs when seedlings are consumed accidentally along with other forage, when horses graze on poor pastures, or when hay is contaminated with dried plant parts (Crews and Anderson 2009; Vandenbroucke et al. 2010). Poisoning is characterised by hepatic insufficiency, secondary photosensitisation and CNS derangement due to elevated blood ammonia from reduced liver function. Clinical signs may appear after several weeks or even months after ingestion of the plant and include hyperexcitability, anorexia, depression, diarrhoea, jaundice, constipation, ataxia, head pressing and aimless walking (Anadón et al. 2012; Panter et al. 2012). Once affected, the


prognosis is generally poor (Botha and Naudé 2002; Anadón et al. 2012). In the UK fatal hepatic encephalopathy typical of tansy ragwort toxicosis has been reported in horses. Circumstantial evidence implicated the pasture as the source of the toxic alkaloids (Giles 1983). More recently, the presence of ragwort in the hay fed to horses showing diarrhoea and increased liver enzyme activities was determined by the detection of ragwort alkaloids using liquid chromatography/time-of-flight mass spectrometry (Crews and Anderson 2009).


Other alkaloid-containing plants


Astragalus spp. and Oxytropis spp. (locoweeds) Locoweed is the species of the Astragalus and Oxytropis genera (Fabaceae family) that contains the toxin swainsonine, an indolizidine alkaloid, and induces a neurological condition called locoism (Panter et al. 2012). Locoweed is a perennial flowering plant available worldwide which remains toxic throughout the season (Panter et al. 2012; Chenchen et al. 2014). Locoweed is palatable to horses, which appear to be particularly susceptible to locoweed poisoning (Pfister et al. 2007). Clinical signs develop after weeks of ingesting locoweed and include depression, proprioceptive deficit, high stepping gait, staggering, intention tremor, excitement and emaciation followed by death if continued consumption is allowed (Pfister et al. 2007; Panter et al. 2012). Other signs include reproductive failure, birth defects (bowed limbs) and abortion (Panter et al. 2013). To the authors’ knowledge, there is only one report of swainsonine intoxication involving an European horse (Nollet et al. 2008) where the horse showed signs of excitement, exaggerated fright reactions, trembling and mild ataxia. Renal tubular damage was also diagnosed based on uraemia, potassium abnormality, high urinary level of γ-glutamyltransferase and metabolic alkalosis (Nollet et al. 2008). Poisoning by swainsonine was confirmed by the presence of the toxin in the serum sample taken from the horse about 12 h after the beginning of clinical signs (Nollet et al. 2008).


Fig 2: Senecio jacobaea (tansy ragwort). Photograph by C. Cortinovis.


© 2015 EVJ Ltd


Colchicum autumnale (meadow saffron) Meadow saffron is an autumn flowering plant from the Colchicaceae family widely found in Europe. It grows mostly in damp meadows in areas ranging from lowland to mountain districts (Sundov et al. 2005). All parts of the plant are toxic. The main toxic compound is the alkaloid colchicine, which binds to the cell protein tubulin, thus disrupting spindle formation and arresting mitosis in metaphase (Sundov et al. 2005; Kupper et al. 2010). Poisoning may occur when the fresh plant is ingested in pastures or when it contaminates hay or silage, since colchicine is able to withstand storage and drying (Anadón et al. 2012). Clinical signs appear 48 h after ingestion and because of the rapid turnover of the intestinal epithelial cells, they are predominantly related to the digestive tract (colic, abdominal pain, diarrhoea, fetid faeces with tenesmus) (Kupper et al. 2010; Anadón et al. 2012). Death occurs from cardiorespiratory collapse (Anadón et al. 2012). In Europe, several cases of horse poisoning by meadow saffron have been reported in Germany (Kamphues and Meyer 1990; Wolf et al. 2009). Colic was the most common clinical sign observed in affected horses (Kamphues and Meyer 1990; Wolf et al. 2009).


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