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Overview of Bracken Fern Poisoning


Bracken fern (Pteridium aquilinum) is found throughout the world and is among the five most numerous vascular plants. The species includes numerous subspecies and varieties, and plant size varies with frond lengths ranging from 0.5 to 4.5 m. Bracken fern is perennial, with erect deciduous fronds that remain green until they are killed by frost or drought. It spreads primarily through dense rhizome networks and can dominate plant communities, especially those burned or disturbed. Bracken fern may be found in a diversity of sites but is most common in semishaded, well-drained, open woodlands.

A variety of syndromes have been associated with bracken fern poisoning. These syndromes are largely determined by the dose and duration, and also by the species of the poisoned animal.

Enzootic Hematuria:

Enzootic hematuria is the most common result of bracken fern poisoning. It primarily affects cattle and, less frequently, sheep. It is characterized by intermittent hematuria and anemia. Poisoning most often occurs during late summer when other feed is scarce, or when animals are fed hay containing bracken fern. Poisoning requires prolonged exposures; affected livestock must ingest bracken fern for several weeks to years before disease develops.

Affected cattle are weak, rapidly lose weight, and develop pyrexia (106°–110°F [41°–43°C]) once clinical effects manifest. Calves often have difficulty breathing, with pale mucous membranes. Hemorrhages vary from minor mucosal petechia to effusive bleeding, and at times large blood clots form that may be passed in the feces. Coagulation is prolonged, and bleeding may be pronounced and excessive even at small wounds such as small insect bites or minor scratches.

Once animals develop clinical disease, poisoning is almost always fatal. Postmortem examinations usually reveal multiple hemorrhages or bruises throughout the carcass. Necrotic ulcers in the GI tract may be noted. The bladder mucosa often contains small hemorrhages; dilated vessels; or vascular, fibrous, or epithelial neoplasms. Other neoplasms in the upper GI tract of cattle and other species have also been reported. In most cases, mixtures of hemorrhagic and neoplastic lesions are found.

Although not all bracken fern toxins have been completely characterized, the primary cause of enzootic hematuria has been attributed to norsesquiterpene glycosides (ptaquiloside, ptesculentoside, and caudatoside). Ptaquiloside is a potent radiomimetic that initially damages the bone marrow and later is carcinogenic (producing urinary tract neoplasia in ruminants). Both the hemorrhagic syndrome and uroepithelial neoplasms have been reproduced experimentally with bracken fern and ptaquiloside. Although less well characterized, the other norsesquiterpene glycosides, which predominate in some bracken fern populations, probably have similar toxicity and carcinogenicity.

Acute Brackenism or Hemorrhagic Disease:

Acute brackenism occurs when animals ingest high doses over relatively short durations of weeks or months. It is characterized by bleeding. This toxicity is attributed to ptaquiloside's radiomimetic damage to proliferating bone marrow stem cells. This is seen as depletion of bone marrow megakaryocytes followed by panhypoplasia. The leukogram often shows a mixed response. In the initial phases, monocytosis may be pronounced and followed by granulocytopenia and thrombocytopenia. Final phases include marked thrombocytopenia with anemia, leukopenia, and hypergammaglobulinemia. Urinalysis generally shows hematuria and proteinuria. Affected animals have both an increased susceptibility to infection and a tendency for spontaneous hemorrhage.

Lower doses of bracken fern for longer duration are more likely to be carcinogenic. The effects seem cumulative, as animals are exposed repeatedly for years. Often the onset of clinical disease can be delayed for weeks, or even months, after animals have been removed from bracken fern–infested ranges and pastures. The carcinogenic potential of bracken fern and ptaquiloside has been confirmed not only in livestock but also in rats, mice, guinea pigs, quail, and Egyptian toads.

Ptaquiloside is excreted in the urine and milk, and small amounts have also been identified in skeletal muscle and liver of poisoned animals even after a 15-day withdrawal period. Contaminated milk retains toxicity as it has been shown to produce GI neoplasms in rats. Several investigators have suggested ptaquiloside neoplastic transformation may be promoted or enhanced by bovine papillomavirus infection. However this may be a secondary change due to bracken fern–associated myelodysplasia and subsequent immunosuppression that are likely to promote papillomavirus infection.

Bright Blindness:

A less common manifestation of ptaquiloside toxicity is called bright blindness. It is seen clinically as tapetal hyperreflectivity that is most commonly reported in sheep in parts of England and Wales. Affected sheep are permanently blind and adopt a characteristic alert attitude. The pupils respond poorly to light, and ophthalmoscopic examination of sheep with advanced disease reveals narrowing of arteries and veins and a pale tapetum nigrum with fine cracks and spots of gray. Histologically, the lesion is seen as severe atrophy of the retinal rods, cones, and outer nuclear layer that is most pronounced in the tapetal portion of the retina. Affected animals often have many of the other bracken fern–associated lesions such as bone marrow suppression, hemorrhage, immunosuppression, and urinary tract neoplasia.

Bracken Staggers:

Bracken fern poisoning in monogastric animals was first recognized as a neurologic disease when horses consumed contaminated hay. Ingestion at a rate of 20%–25% bracken fern for ≥3 mo may result in bracken staggers. Clinical signs in horses include anorexia, weight loss, incoordination, and a crouching stance while arching the back and neck with the feet placed wide apart. When the horse is forced to move, trembling muscles are noted. In severe cases, tachycardia and arrhythmias are present; death (usually 2–10 days after onset) is preceded by convulsions, clonic spasms, and opisthotonos. These changes are due to bracken fern thiaminases. The resulting disease is similar to vitamin B1 deficiency, and therefore most animals respond to thiamine therapy. Horses seem to be particularly susceptible, while disease in pigs is rare. In pigs, the signs of thiamine deficiency are less distinct and may resemble heart failure. Affected pigs become anorectic and lose weight. Death can occur suddenly after recumbency and dyspnea. Thiamine deficiency is generally not a problem in ruminants, because the vitamin is synthesized in the rumen; however, polioencephalomalacia (see Polioencephalomalacia) associated with impaired thiamine metabolism in sheep has been attributed to consumption of bracken fern and rock or mulga fern (Cheilanthes sieberi) in Australia.

Initial treatment for all species is to discontinue exposure to bracken fern; however, disease can appear weeks after livestock are removed from the fern-infested area. In acutely affected cattle, mortality is usually >90%. Measurement of the platelet count is recommended, because it is the best prognostic indicator for poisoned animals.

Treatment of thiamine deficiency in horses is highly effective if diagnosis is made early. Injection of a thiamine solution at 5 mg/kg is suggested, given initially IV every 3 hr, then IM for several days. Oral supplementation may be required for an additional 1–2 wk, although SC injection of 100–200 mg daily for 6 days has been successful in some cases. Thiamine treatment should also include animals similarly exposed but not yet showing clinical disease, because signs can develop days or weeks after removal from the source of bracken.

Antibiotics may be useful to prevent secondary infections. Blood or even platelet transfusions may be appropriate but require large volumes (2–4 L blood) to effectively treat cattle. Though untested, treatment with granulocyte-macrophage colony-stimulating factor (used to treat aplastic anemia in people) may also be considered.

Poisoning, apart from thiamine deficiency, is essentially untreatable; however, it is most easily controlled by preventing exposure. Bracken fern is usually grazed for want of alternative forages. Most commonly, animals are forced to eat bracken fern when other forage is exhausted in late summer, although some animals may develop a taste for the young tender shoots and leaves. Poisoning can be avoided by improving pasture management to increase production of alternative forage. It has been suggested that alternating bracken fern–contaminated and noncontaminated pastures at 3-wk intervals can minimize poisoning.

Bracken fern growth can be retarded by close grazing or trampling in alternative grazing pasture systems. Bracken fern density can be reduced by regular cutting of the mature plant or, if the land is suitable, by deep plowing. Herbicide treatment using asulam or glyphosate can be an effective method of control, especially if combined with cutting before treatment. Some bracken fern populations contain very low or no ptaquiloside. More work is needed to identify these populations, determine why they are not toxic, and use this information to predict or reduce toxicity.

Initial epidemiologic studies suggest that consumption of milk from cattle with access to bracken increases risk of human esophageal or gastric cancer. Certainly the greater risk to people is direct consumption of bracken fern. Rhizomes have been used to make flour, and the young shoots or croziers are considered a delicacy in many parts of the world. Although preparing and cooking lessens the toxicity of ptaquiloside, it has been identified in these foods. Japanese scientists have shown an association between consumption of bracken crozier and esophageal cancer. Additionally, ptaquiloside has been found as an environmental contaminant in soil and water, and air-borne spores may also present a risk of human exposure. Human exposure through any means should be of concern, because ptaquiloside is a proven carcinogen.

Last full review/revision February 2014 by Bryan L. Stegelmeier, DVM, PhD, DACVP

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