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,
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 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
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.
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.
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.
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, 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
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
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