Bracken and horsetail are both ancient plants that have long been recognised as poisonous, causing induced avitaminosis B1 in horses. This has multiple effects, as vitamin B1 (thiamine) is an essential vitamin involved in metabolism and in maintaining the myelin of peripheral nerves. This article discusses bracken and horsetail poisoning in horses.
Bracken
The plant
Bracken (Pteridium spp., Figure 1) is a genus of ancient, large, coarse ferns. It is one of the worlds most abundant plants, growing throughout the world (except where it is very cold or very dry). It is found in woods, heaths, sand dunes, neglected pastures, hedgerows, moors and even in walls, and is often dominant over large areas, mainly on light, well-drained acid soils. It is found throughout Britain and Ireland, and is occasionally cultivated in gardens and parks. Bracken has large, highly divided leaves with rhizomes from which the fronds arise at intervals. In the past, the genus was commonly treated as a single species, Pteridium aquilinum, but it is now generally subdivided into about ten species.
Toxic compounds
Bracken contains several toxic compounds, including: carcinogens (sesquiterpenoid glycosides), particularly ptaquiloside; thiaminase, an enzyme; and prunasin, a cyanogenic glycoside. Prunasin is usually present in harmless concentrations (Cooper and Johnson, 1998).
Bracken toxicosis in domestic animals has been well described (Evans, 1989), but causes different clinical syndromes in different species. The thiaminase in bracken can induce avitaminosis B1 in monogastric animals (such as horses and pigs) (Evans, 1976) which is called ‘bracken staggers’. Bracken contains a type I thiaminase which does not destroy thiamine (as type II thiaminase does), but creates a thiamine analogue. This inhibits thiamine-requiring metabolic reactions and has an antithiamine effect, inducing thiamine deficiency (Chick et al, 1985). The highest concentration of thiaminase is in the rhizome (Vetter, 2009) and young fronds, but there is seasonal variation. The concentration in the rhizomes is high in the autumn and winter, declining from January and April and then rising again from May In very young fronds, the concentration is high in April and then declines from May as the aerial parts of the plant unfold. The concentration in the rhizomes in autumn and winter can be 20-30 times higher than in the fronds in June (Evans, 1976). The thiaminase in bracken is destroyed by heating but not by drying (Evans et al, 1951a).
Most cases of bracken poisoning occur in cattle, and acute or subacute poisoning causes acute haemorrhagic syndrome, whereas more chronic exposure causes enzootic haematuria (or enzootic bovine haematuria), which is characterised by tumours of the upper alimentary tract and urinary bladder. A similar condition has been described in deer (Scala et al, 2014). Bracken poisoning in sheep manifests as haemorrhage, cancer and/or retinal neuropathy, which can lead to permanent blindness (Barnett and Watson, 1970).
Circumstances of poisoning
Poisoning only occurs after ingestion of bracken for several weeks (Vetter, 2009), but can occur after ingestion of contaminated hay (Evans et al, 1951a; Wolf et al, 2002), following grazing on bracken when other food sources are unavailable as a result of adverse conditions, or eating bracken used as bedding (Hadwen and Bruce, 1917; Evans et al, 1951a).
Experimental studies
In an early study, it was determined that ingestion of approximately 2.7 kg of bracken can kill a horse in a month (Hadwen and Bruce, 1917). In two adult horses that were fed dried green bracken (10 g/kg/day), clinical signs were consistent with thiamine deficiency and included neutrophilia, changes in ST segments on ECG, apathy, ataxia and nystagmus. The horses died after 108 and 126 days (Fernandes et al, 1990).
In another study by Roberts et al (1949), a 5 year old mare (467 kg) was fed a diet containing 50% dried bracken for 24 days (6.8 kg of bracken daily), followed by a diet of 75% bracken (10.9 kg/day) for 18 days. She ate the food readily and remained well for the first month. Nine days after starting the higher dose, she had depression, anorexia and mild inco-ordination. These became progressively worse and 3 days later she had visible loss of condition, cold extremities, muscle twitching and jerky movements of the head, neck, limbs and tail. She was reluctant to move and swayed from side to side. She was started on thiamine 100 mg subcutaneously twice on the first day and then once daily thereafter. She started to improve the following day and was vastly improved the day after that. After 5 days of treatment (while still on the high dose diet) she appeared well and was able to walk normally. She had marked haematological changes with reduced erythrocytes, packed cell volume and haemoglobin (Roberts et al, 1949).
Horsetail
The plant
Equisetum (Figure 2) is the only living genus in Equisetaceae, a family of vascular plants that reproduce by spores rather than seeds. Horsetails are thought to represent the oldest extant genus of vascular plants and may date back as far as the Triassic period (Vanneste et al, 2015). Equisetum arvense (field horsetail, common horsetail) is an invasive, deep-rooted perennial weed that will spread quickly to form a dense carpet of foliage, crowding out less vigorous plants in beds and borders. Horsetail is a weed of pasture and arable land, particularly in damp areas. Equisetum is native throughout the arctic and temperate regions of the northern hemisphere.
Toxic compounds
Equisetum species contain various compounds, but the main compound of concern is thiaminase. Horsetail poisoning in horses resembles bracken poisoning and is a result of an induced thiamine deficiency. It is not clear if the thiaminase in Equisetum is a type I (as in bracken) or type II thiaminase. Both types of thiaminase were detected in Equisetum ramosissimum (Meyer, 1989). Incubation of thiamine solution, oats and brewers yeast (the latter are both natural sources of thiamine) with ground Equisetum has demonstrated that the plant destroys thiamine in vitro (Henderson et al, 1952).
Palustrine and palustridiene are alkaloids in Equisetum palus-trine (Cramer et al, 2015) but their effect in animals is unclear. Mature Equisetum plants contain high concentrations of silica, which makes the plant hard and coarse when dried, but this is not hazardous.
Circumstances of poisoning
As with bracken, poisoning only occurs after ingestion of Equisetum for several weeks. Poisoning may occur follow ingestion of contaminated hay (Lott, 1951) and in horses, this occurs after ingestion of hay containing >20% horsetail (Henderson et al, 1952), but it has been reported with hay containing 5-50% horsetail (Forenbacher, 1952). The higher the concentration of horsetail, the shorter the latent period (Forenbacher, 1952). Poisoning may also occur when other food sources are unavailable owing to adverse conditions (Forenbacher, 1952; Klebesadel and Mitchell, 1964).
Some horses may crave horsetail (Jenkins and Jackman, 1941) and younger, growing animals may be more at risk of toxic effects. The thiaminase in Equisetum is destroyed by heating but not by drying, as in hay (Henderson et al, 1952).
Experimental studies
In an experimental study, three ponies (two Shetland ponies, one German Riding Pony) were fed Equisetum palustre. The material was dried then ground and mixed with the other feed components. The ponies were fed 0, 5, 10 and 22. 6% of Equisetum palustre as a percentage of total dry matter. Feed intake was not reduced, even at the highest dose of 22.6%. Biochemical and haematological parameters remained normal. There was no decline in thiamine blood concentrations, even after ingestion of 22.6% Equisetum palustre for 2 months (Hunsche, 2010).
A 2 year old Clydesdale gelding was given hay (containing 20% Equisetum arvense) that had been responsible for poisoning three horses. The only clinical sign was weight loss until the 32nd day of feeding when he appeared to be slightly ataxic. On the 35th day he seemed anxious and ataxic and was unable to rise on the following day, although he continued to eat and drink. He was given intravenous thiamine on the 36th and 37th day and provided with Equise-iwm-free hay. Treatment was repeated but he became progressively weaker and died on the 40th day (Henderson et al, 1952).
Clinical signs
As stated, poisoning only occurs after ingestion of bracken for several weeks (Hadwen and Bruce, 1917); with horsetail, clinical signs occur after grazing for 2-5 weeks (younger, growing animals become unwell sooner) (Rich and Jones, 1902; Forenbacher, 1952) and the disease generally progresses over 2-8 days (Long, 1924).
Initial signs of thiamine deficiency include ataxia, lack of coordination (known as bracken staggers in bracken poisoning), loss of condition and stumbling. Corneal opacity, blindness (Case 2), sweating (Lott, 1951; Klebesadel and Mitchell, 1964), hypothermia, hypotension and bradycardia (Forenbacher, 1952) have been reported. As the disease progresses there is weakness, inability to stand, nervousness, muscle tremors, coma and convulsions. The appetite remains normal (Hadwen and Bruce, 1917), but paralysis of the lips may make eating difficult (Lott, 1951). If untreated, the horse usually dies of exhaustion (Rich and Jones, 1902; Forenbacher, 1952).
In addition, there may be haemolytic anaemia and haemoglo-binuria (Roberts et al, 1949; Kelleway and Geovjian, 1978; Case 1). Abortion has been reported in horses with bracken poisoning (Wolf et al, 2002).
In post-mortem examination of animals that have died of thiamine deficiency, lesions are generally non-specific (Forenbacher, 1952) and organs such as the liver, brain and lungs may be congested. Haemorrhages of the heart, congested lungs (Diniz et al, 1984), congested ‘nutmeg’ liver, necrosis of the proximal tubular epithelium of the kidney (Henderson et al, 1952), haemorrhagic inflammation of the gastrointestinal tract and degenerative changes in ganglion cells of the cerebral cortex and caudate nucleus (Forenbacher, 1952) have been reported. The stomach and intestines may be empty and may be mottled with haemorrhages (Hadwen and Bruce, 1917).
Diagnosis
In horses, diagnosis of avitaminosis B1 from ingestion of bracken or horsetail is based on history of exposure and characteristic clinical signs of thiamine deficiency.
Prognosis
There is limited information on the prognosis of induced thiamine deficiency after bracken or horsetail poisoning in horses. If the disease is only mild to moderate, a good recovery is expected.
In an outbreak of poisoning in a group of 27 mules 2 months after they were introduced to a bracken-infested pasture, eight mules died and the remainder recovered following removal from the pasture and administration of thiamine (Diniz et al, 1984).
Treatment
Treatment of bracken or horsetail toxicosis is supportive. Animals should be removed from exposure as soon as poisoning is suspected. In mild cases of avitaminosis Bl, removal from exposure may be all that is required.
Administration of thiamine may be required in some cases. It is usually associated with rapid recovery (Jenkins and Jackman, 1941; Lott, 1951; Evans et al, 1951b), generally within 24-48 hours (Forenbacher, 1952). The dosage is 100-1000 mg per horse by intravenous, intramuscular or subcutaneous injection depending on the formulation. Dried yeast has also been given (Forenbacher, 1952). Good nursing care and high-quality feed should be provided. Forage rich in thiamine include wheat germ and rice bran. Affected animals should be monitored for signs of anaemia and a blood transfusion may be required in severe cases (Kelleway and Geovjian, 1978).
Measures for the prevention of bracken and horsetail exposure are outlined in Box 1.
Conclusion
Bracken and horsetail are common plants. They contain thiaminase that can induce an avitaminosis Bl in horses. Signs only occur after weeks of grazing. Initial signs are ataxia and inco-ordination. Treatment is supportive and mildly affected animals recover with removal from the plant, good nursing care and good quality feed. Thiamine supplementation can be given if required.
Case examples
Case 1: Bracken
A 14-month-old Arabian gelding (337.5 kg) was examined for lethargy, anorexia and abdominal distress. He was given an antibiotic, a steroid and analgesia. The pain continued and he passed dark coloured urine. The owner reported he had been eating bracken almost exclusively for the past month, despite feed being provided. He was given thiamine and mineral oil but continued to pass dark urine. He progressed to pyrexia, tachycardia and recumbency and received a blood transfusion with vitamin B complex and iron. He began to improve but had icteric mucous membranes and then developed pyrexia and dark urine again. Blood showed haemolytic anaemia. He was weak by day 4, with pyrexia and icteric mucous membranes, and continued to receive antibiotics and vitamins. On day 6, he developed petite mal convulsions and received acepromazine. He began to improve from day 7 and recovered fully (Kelleway and Geovjian, 1978).
Case 2: Horsetail
Fifty horses were driven to winter pasture, but poor weather resulted in much of the area icing over, forcing the horses to move inland for forage. During a periodic check, 8-10 horses were found dead over a wide area a month later. The remaining horses were moved but two were noted to be behaving abnormally. They showed nervousness, tachypnoea and ataxia, occasionally falling, and perspired heavily. One of the horses, a 14 year old, appeared to have visual impairment. Both horses recovered after a week grazing on good forage. Examination of two dead horses (7 and 8 years old) found an abundance of swamp horsetail (Equisetum fluvia-tile) in their stomachs. Examination of the area showed extensive grazing of the swamp horsetail in preference to the plants present (Klebesadel and Mitchell, 1964).
Box 1.Prevention of bracken and horsetail exposure
- Ensure adequate forage is available
- Prevent access to the plants. If the plants have been slashed, ploughed or burnt there may be regrowth of young stems, or rhizomes may be exposed and spores spread.
Bracken
- Bracken fern density can be reduced by regular cutting, crushing, rolling or deep ploughing, or using herbicides
- Seek specialist advice:
- Legislation may be in place to protect some land areas; bracken is an important habitat for invertebrates, moorlands birds, reptiles and mammals. Some woodland plants grow under bracken
- Steps may be required to protect watercourses and wildlife
- Workers require protection from spores, as they have been shown to cause damage to DNA in vitro (Simán et al, 2000) and may be carcinogenic.
Horsetail
- The plant can be difficult to control owing to its extensive rhizomes and high spore production, silica content and waxy cuticle
- Drainage of excess water, raising the pH, if needed, and increasing fertility of soil aids the growth of forage grasses and makes the environment less favourable for horsetail
- Creating shade by planting trees and shrubs may also help
- Removing stems before cones appear may help reduce spores, but has to be repeated after each regrowth for many years
- Herbicides can also be used.
KEY POINTS
- Both bracken (Pteridium spp.) and horsetail (Equisetum spp.) are ancient plants and have long been recognised as poisonous.
- Both plants contain thiaminase and chronic ingestion causes an induced deficiency of thiamine (vitamin B1).
- Treatment is supportive with prompt removal from exposure.
- Thiamine supplementation may also be provided, if necessary.