Overview of Bracken Fern Poisoning

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 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; 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.

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 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, whereas 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.