Bracken Fern Poisoning in Animals

Enzootic hematuria, the most common form of bracken fern poisoning, primarily affects cattle and less frequently affects 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 because affected livestock must ingest bracken fern for several weeks to years before disease develops.

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

Once animals develop clinical disease, poisoning is almost always fatal. Postmortem examinations usually reveal multiple hemorrhages or bruises throughout the carcass. There may also be necrotic and hemorrhagic ulcers in the GI tract. 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 ptaquiloside, a norsesquiterpene glucoside. Other toxic and potentially carcinogenic toxins include quercetin, isoquercetin, ptesculentoside, caudatoside, astragalin, and various tannins.

Ptaquiloside is a potent radiomimetic compound that initially damages the bone marrow and later is carcinogenic (primarily producing urinary tract neoplasia in ruminants). Both the hemorrhagic syndrome and uroepithelial neoplasms have been reproduced experimentally with bracken fern and ptaquiloside. High ptaquiloside doses for a few months duration produce the characteristic hemorrhagic disease. This has been attributed to ptaquiloside’s radiomimetic damage to proliferating bone marrow stem cells. This is characterized by depletion of bone marrow megakaryocytes followed by both leukocytic and erythrocytic hypoplasia. The resulting leukogram is often a mixed response. In the initial phase of poisoning there is often pronounced monocytosis followed by granulocytopenia and thrombocytopenia. Final phases include marked thrombocytopenia with anemia, leukopenia, and hypergammaglobulinemia. Urinalysis generally includes hematuria and proteinuria. Affected animals have both an increased susceptibility to infection and a tendency for spontaneous bleeding.

Lower doses of bracken fern for longer duration appear more likely to be carcinogenic. The effects seem to be cumulative as animals are exposed repeatedly for years. Often, the onset of clinical disease is delayed for weeks, or even months, after animals have been removed from bracken fern-infested ranges and pastures. In addition to livestock, the carcinogenic potential of bracken fern and ptaquiloside has been confirmed in rats, mice, guinea pigs, quail, and Egyptian toads.

Ptaquiloside is excreted in the urine and milk of poisoned animals, and contaminated milk 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 presentation 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 funduscopic examination in advanced disease is characterized by 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. Typical poisoning requires relatively high doses of long duration, such as feeding hay with 20%–25% bracken fern contamination for 3+ months. Equine bracken staggers is characterized by anorexia, weight loss, incoordination, and a crouching stance while arching the back and neck and standing with feet placed wide apart. When forced to move, trembling muscles are noted. In severe cases, tachycardia and arrhythmias may occur, and death (usually 2–10 days after onset) is preceded by convulsions, clonic spasms, and opisthotonos. Poisoning has been attributed to bracken fern thiaminases, because clinical disease is similar to vitamin B1 deficiency. Most animals respond with thiamine therapy.

Poisoning in pigs is rare and less distinct, as affected animals become anorexic and lose weight. Often resembling heart failure in the terminal phase, 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, altered thiamine metabolism and polioencephalomalacia in sheep poisoned with bracken fern and rock fern (Cheilanthes sieberi) have been reported in Australia.