Bracken Fern Poisoning : Introduction - The Merck Veterinary Manual

Bracken Fern Poisoning : Introduction

Bracken fern ( Pteridium aquilinum [ Pteris aquilina ]) is widely distributed in upland and marginal areas throughout North and South America, Europe, Australia, and Asia. Ingestion of significant quantities produces signs of acute poisoning related to thiamine deficiency in monogastric animals and bone marrow depletion (aplastic anemia) in ruminants. The toxic effects appear to be cumulative and may require 1-3 mo to develop, depending on the species of animal, quantity consumed, time of year, and other factors. Both leaves and rhizomes contain the toxic principles, which vary in concentration with the season. Most acute poisonings are seen after periods of drought when grazing is scarce; however, the plant is toxic even when present as a contaminant in hay, and cases have occurred in stabled animals.

Pteridium aquilinum (bracken fern)

Pteridium aquilinum (bracken fern)

Longterm, low-level consumption has been associated with other clinical syndromes. Enzootic hematuria with hemorrhages or tumors in the bladder is seen in cattle in many areas of the world, and similar tumors have been seen in sheep. Bright blindness with retinal degeneration and hyperreflectivity of the tapetum is found in hill sheep in parts of England, and a similar condition has been recognized in cattle grazing bracken in Wales. Ingestion of bracken fern has been implicated in the occurrence of tumors in the upper GI tract of cattle in areas of Brazil and Scotland.

Some epidemiologic evidence suggests that regular consumption of milk from cattle with access to bracken may be associated with an increased risk of human esophageal or gastric cancer, but this is still under investigation. A greater risk to humans is direct consumption of the fern itself, a practice that continues in various countries throughout the world and is indeed promoted in some North American publications.

Etiology:

Bracken fern contains a number of toxic factors, some of which are not yet fully characterized. Poisoning in nonruminants is due to a thiaminase; the effects are essentially those of vitamin B₁ deficiency, with myelin degeneration of the peripheral nerves. Horses seem to be particularly susceptible, while disease in pigs is rare. Thiamine deficiency is generally not a problem in ruminants because the vitamin is synthesized in the rumen, but polioencephalomalacia ( Polioencephalomalacia: Introduction) associated with impaired thiamine metabolism in sheep has been attributed to consumption of bracken fern and rock or mulga fern ( Cheilanthes sieberi ) in Australia.

The nature of the bone marrow toxin (aplastic anemia factor) to which cattle are particularly susceptible has not been defined, although the compound ptaquiloside has been suggested. The toxin causes death of precursor cells in the marrow so that cells with a shorter life span (the platelets) are affected first. An initial leukocytosis is followed by granulocytopenia and thrombocytopenia with resultant increased susceptibility to infection and tendency to spontaneous hemorrhage.

Bladder tumors, carcinoma of the urothelium, and hemangioendotheliomas in naturally occurring enzootic hematuria suggest that bracken fern may act as a carcinogen. This has been confirmed experimentally—inclusion of bracken fern in the diet of rats, mice, guinea pigs, quail, and Egyptian toads has resulted in tumors at various sites depending on the species and duration of feeding. Identical tumors can be produced by feeding ptaquiloside. Studies suggest that upper GI tract tumors in cattle may be due to the combined action of bracken fern and bovine papilloma virus (BPV). Bracken fern in combination with either BPV types 2 or 4 is believed to cause tumors in cattle. A flavonoid isolated from bracken fern, quercetin, is essential to fully transform bovine cells exposed to BPV type 4 in vitro.

Clinical Findings:

In horses, signs of bracken-induced thiamine deficiency (bracken staggers) include anorexia, weight loss, incoordination, and a crouching stance with back and neck arched and feet placed wide apart. When 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. The rectal temperature is usually normal but may reach 104°F (40°C).

In pigs, signs of thiamine deficiency are less distinct and may resemble heart failure. Affected pigs show anorexia and weight loss. Death can occur suddenly after recumbency and dyspnea.

In cattle, acute bracken poisoning causes an acute hemorrhagic syndrome or, in some cases, sudden death. Affected cattle are weak, rapidly lose weight, and are pyrexic (106-110°F [41-43°C]); many have difficulty breathing and have icteric or pale mucosae with petechiae. Clots of blood may be passed in the feces, and there is often bleeding from body orifices. The blood frequently fails to clot normally; where tabanid flies are abundant, the skin of affected cattle is marked by streaks of blood where the insects have fed. The disease is almost always fatal; necropsy reveals multiple hemorrhages throughout the carcass. Necrotic ulcers may be present in the GI tract and bruising in the muscles. Swelling of the larynx and difficulty breathing has been reported in young cattle.

Chronic enzootic hematuria in cattle is characterized by intermittent hematuria and, ultimately, death due to anemia. The bladder contains small hemorrhages, dilated vessels, or tumors, which can be vascular, fibrous, or epithelial. In many cases, a mixture of lesions is found.

Bright blindness in sheep is a progressive retinal atrophy that derives its name from the hyperreflectivity of the tapetum. 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.

Diagnosis:

Equisetum spp (horsetail)

Other plants, such as horsetail ( Equisetum arvense ) and turnip ( Beta vulgaris ), can induce thiamine deficiency. In horses, the condition must be distinguished from other neurologic disorders, including rabies or poisoning due to Crotalaria sp or ragwort ( Senecio jacobea ). Blood thiamine levels decrease from an average normal of 80-100 mg/L to 25-30 µg/L, while blood pyruvate levels increase from a normal of ~20-30 mg/L to 60-80 µg/L; comparison with a sample from an unexposed animal of similar age and type will mitigate problems associated with correlating data from different analytic protocols. In pigs, the signs and lesions may indicate heart failure. Definitive diagnosis is established by demonstrating decreased blood thiamine levels or an increase in blood pyruvate with a decrease in RBC transketolase activity.

The acute hemorrhagic syndrome in cattle is distinctive, but signs may be confused with those of any acute septicemia (including anthrax) or other forms of poisoning such as mycotoxicosis, or poisoning by sweet clover or trichloroethylene-extracted soybean meal. Hematologic examination shows a loss of platelets from the blood, normally accompanied by loss of WBC, and pancytopenia in advanced stages.

Chronic enzootic hematuria must be distinguished from other causes of “red water,” eg, the hemoglobinemia of babesiosis ( Babesiosis: Overview). Occasionally, cases are complicated by coexisting chronic pyelonephritis.

The retinal changes of bright blindness in sheep are characteristic but subtle, so diagnosis requires the exclusion of other causes of blindness, including pregnancy toxemia, infectious keratoconjunctivitis, and cataracts.

Treatment:

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 signs, as they can develop days or weeks after removal from the source of bracken.

In acutely affected cattle, mortality is usually >90%, and the platelet count is the best prognostic indicator. Animals should be removed from contaminated pasture, but it is often difficult to convince farmers that the plant is poisonous because the disease can appear up to 2 wk after livestock are removed from the fern-infested area. Treatment with dl-batyl alcohol to stimulate the bone marrow is of doubtful value. Antibiotics may be useful to prevent secondary infections. Blood or even platelet transfusions from a donor not grazing bracken may be appropriate, but large volumes are required (minimum of 2-4 L blood). Granulocyte-macrophage colony-stimulating factor has been used to treat aplastic anemia in humans.

The other syndromes are essentially untreatable and must be controlled by preventing access to the fern.

Prevention:

Bracken is usually grazed for want of more suitable food, although individual animals may develop a taste for the plant, particularly the young tender shoots and leaves. Early spring (tender bracken shoots) or late summer (poor pasture conditions) are the times when the problem is most often manifest. The disease has been prevented in ruminants and horses by improved pasture management and fertilization or by alternating bracken-contaminated and noncontaminated pasture at 3-wk intervals.

Fern growth can be retarded by close grazing or trampling in alternate grazing pasture systems. In time, a pasture can be freed of bracken using this approach or 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. Biologic control by the use of microorganisms or insects has been considered, but the longterm implications are not clear.