Common bracken fern (Pteridium aquilinum) is found globally and is among the five most abundant vascular plants in the world. Because the species includes numerous subspecies and varieties, plant size varies. Frond lengths can range from 0.5 m to 4.5 m (1.6–14.7 feet).
A perennial, bracken fern has erect deciduous fronds that remain green until killed by frost or drought. It spreads primarily through dense rhizome networks and can dominate plant communities, especially those that are burned or disturbed. Bracken fern typically grows in partially shaded, well-drained, open woodlands but can grow in other environments (see bracken fern image with inset).
Courtesy of Dr. Bryan Stegelmeier.
Common bracken fern can cause poisoning in grazing animals when ingested. Poisoning may be more frequent when access to alternative food is limited (eg, during droughts or other times when grazing conditions are poor, as in late summer when pastures are dry). Poisoning can also occur when animals are fed hay contaminated with the fern.
Other ferns species associated with poisoning in grazing animals include Cheilanthes austrotenuifolia (rock fern [see rock fern image]), Cheilanthes sieberi (mulga fern), and Marsilea spp (nardoo ferns [see nardoo fern image]) in Australia. In addition, several bracken species other than common bracken are also implicated in poisoning—namely, Pteridium arachnoideum and Pteridium caudatum in South and Central America; Pteridium esculentum in Australia; and Pteridium semihastatum in northern Australia and Southeast Asia.
Courtesy of Dr. Rhian B. Cope.
Courtesy of Dr. Rhian B. Cope.
The main toxic agents in bracken fern and other ferns are ptaquiloside (a norsesquiterpene glycoside, or illudane-type glycoside) and thiaminases. Thiaminases are present in high concentrations in nardoo ferns; lesser amounts are found in rock ferns and bracken ferns.
Ptaquiloside is most concentrated in bracken rhizomes, leaves, and young, unfolding fronds; however, all parts of bracken fern contain this toxin, and concentrations can vary substantially among the structures of the plant and across seasons and geographical locations.Immaturebracken ferns may be more carcinogenic than mature ferns; however, all stages of plant growth are carcinogenic.
Ptaquiloside is a radiomimetic genotoxin, meaning its effects mimic the effects of ionizing radiation on the bone marrow. Hydrolysis of ptaquiloside leads to the production of pterosin B, either directly or via the generation of pteridienone (an unstable bracken-fern dienone). Pteridienone is a putative DNA alkylating agent. Metabolism of ptaquiloside also produces free radical–associated DNA damage. The net genotoxic effect of ptaquiloside is genetic mutations, clastenogenesis (breakage, rearrangement, or other structural changes in chromosomes), and bone marrow damage.Data suggest that the effects of ptaquiloside may act synergistically with papillomaviruses (1) and Helicobacter pylori (2) during carcinogenesis. Other genotoxic and carcinogenic illudane-type glycosides are present in bracken fern but are less potent and occur in lower concentrations.
The key effects of thiaminase poisoning mimic thiamine deficiency. Fern-associated thiaminase poisoning primarily affects horses and pigs.
Syndromes of Bracken Fern and Other Fern Poisoning
Several clinically distinct syndromes associated with fern toxicosis occur in domestic animals. In some situations, mixed syndromes can occur.
Fern Poisoning–Associated Hemorrhagic Disease and Immunodeficiency Syndrome
Hemorrhagic disease and immunodeficiency syndrome is associated with bracken fern poisoning. In theory, this syndrome could occur in many domestic mammalian species; however, it is mainly observed in cattle, and occasionally in horses. Sheep may be more resistant than other animals, as researchers have been unable to experimentally replicate the condition in sheep. However, rare cases of the syndrome have been reported in sheep in Australia.
Short-term ingestion of large amounts of bracken fern causes bone marrow aplasia, because of the effects of ptaquiloside on bone marrow stem cells. The sequence of hematologic effects relates to the production time of various cellular elements in the bone marrow and their lifespans in blood. Thrombocytopenia and thrombocytopenic hemorrhage occur first, followed by leukopenia. Anemia onset is slower, owing to the longer circulating life of erythrocytes and longer persistence of bone marrow erythroid precursors. Immunodeficiency occurs secondary to leukopenia (particularly neutropenia) and suppression of immune cell proliferation.
Calves weaned onto pasture with bracken fern seem most susceptible to hemorrhagic disease and immunodeficiency syndrome; however, animals of all ages can be affected. Horses occasionally develop the syndrome. In Australia, rock and mulga fern poisonings commonly occur in 2- to 3-month-old calves still feeding from their mothers (via milk and/or grazing during the weaning process) or in young, recently weaned cattle. Rock ferns and mulga ferns grow rapidly after summer rains, and outbreaks of disease can occur approximately 3–4 weeks later.
Clinical signs of hemorrhagic disease and immunodeficiency syndrome in calves can include the following:
depressed affect
"tucked up" and weak appearance
weak, swaying, or stilted gait
swollen joints (secondary to hemorrhage into joint spaces)
ptyalism with bloody or brown-stained saliva
hemorrhages in the oral, nasal, or vaginal mucosa and under the sclera
hematuria
ventral edema
fever (secondary to bacterial infection)
The ptaquiloside in bracken fern can also cause capillary fragility, intestinal ulceration, and laryngeal edema.
Once hemorrhagic disease and immunodeficiency syndrome develops, it is commonly fatal. In cattle, affected animals often die from immunosuppression-associated bacterial infections and bacterial infarcts. Postmortem examination usually reveals diffuse hemorrhage or bruising throughout the carcass. There may also be necrotic and hemorrhagic ulcers in the GI tract.
Fern Poisoning–Associated Bovine Enzootic Hematuria and Gastrointestinal Cancers
Bovine enzootic hematuria and GI cancers are associated carcinogenic consequences of chronic ptaquiloside exposure. Consumption of bracken, rock, or mulga ferns can cause the syndrome. Enzootic hematuria/cancer syndrome predominantly occurs in cattle; however, in theory, it could occur in other species exposed to high levels of ptaquiloside for long periods. The syndrome tends to affect cattle > 3 years old that have consistently consumed small quantities of fern over several years. Enzootic hematuria/cancer syndrome has also occurred in sheep.
Papillomavirus infection and coingestion of quercetin (also present in the ferns) are possible cofactors in this neoplastic syndrome.
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Common clinical signs of bracken fern–associated bovine enzootic hematuria include:
brown to red (blood-tinged) urine (worsening over time)
anemia
pale gingiva
failure to thrive
Mixed enzootic hematuria/cancer and hemorrhagic disease/immunodeficiency syndromes can occur.
Once developed, these forms of fern poisoning are almost always fatal. The bladder mucosa often contains small hemorrhages, dilated vessels, or neoplasia (vascular, fibrous, or epithelial). Bladder tumors ranging from adenomas to hemangiosarcomas are typical and are associated with local inflammation, congestion, and edema. GI cancers are most commonly located in the oral cavity, nasopharynx, esophagus, and rumen.
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Ptaquiloside-associated cancers (esophageal, gastric, and mammary cancers; leukemias) also occur in humans and are caused by consumption ofptaquiloside-contaminated milk (produced by cows ingesting bracken fern) and water (in which bracken ferns are growing).
Fern Poisoning–Associated Retinal Degeneration (Bright Blindness)
Retinal degeneration, also called bright blindness, is a primary retinopathy affecting both retinal rod and cone cells. The syndrome was initially recognized in sheep that grazed on bracken fern in the northern UK. Retinal degeneration in sheep has been replicated experimentally by dosing them with bracken fern powder and, in a separate study, by dosing them with ptaquiloside (3).
Bright blindness can also occur in goats. Rock fern ingestion by calves in Australia has also been associated with sudden blindness and retinal degeneration.
Fern Poisoning–Associated Polioencephalomalacia in Sheep
Polioencephalomalacia (PEM) in sheep has been linked to consumption of nardoo, bracken, and rock ferns, all of which contain thiaminases.
Deaths of sheep after grazing on nardoo fern, which has high thiaminase concentrations, have been detected in Australia for decades. From 1974 to 1975, for example, 2,200 such deaths were recorded in a population of 57,000 sheep across 13 farms in Australia's Gwydir basin. Clinical signs in these sheep were consistent with PEM. Approximately 75% of affected sheep responded positively to treatment with thiamine, 200 mg, IV, every 24 hours until resolution (4). In this epizootic, sheep that were recumbent for > 24 hours were less likely to respond to thiamine treatment.
In a second epizootic in Australia, 30 of 480 sheep that grazed on both bracken and rock ferns for 7 weeks developed PEM (as confirmed by anatomical pathology). In this flock, deaths continued at a rate of three animals per day until thiamine was administered. Thiamine treatment successfully prevented any further deaths (5, 6, 7).
Fern Poisoning–Associated Acute Cardiopulmonary Failure in Sheep
Although sheep are less susceptible than cattle to hemorrhagic disease and immunodeficiency syndrome, sheep poisoned by rock and mulga ferns can develop a syndrome of sudden collapse during mustering (roundup). Affected sheep exhibit the following clinical signs:
fever
respiratory distress
black diarrhea
hematuria
Hematologic and coagulation test results may be normal. Anatomical pathology findings can include the following:
pulmonary edema
patchy cardiomyopathy
enlarged, congested kidneys
It is not known if this syndrome is responsive to thiamine treatment.
Fern Poisoning–Associated Neurocardiac Syndrome in Pigs and Horses
Consumption of bracken fern and nardoo fern by pigs and horses is associated with a thiamine deficiency–like neurological syndrome that also has features of acute myocardial failure. The syndrome has been attributed to poisoning by thiaminases present in both types of fern.
In horses, the condition is commonly called bracken staggers. Bracken staggers usually occurs with consumption of relatively large amounts of fern over a long period of time—eg, eating hay with 20–25% bracken fern contamination for ≥ 3 months. Clinically, the disease resembles thiamine deficiency, and clinical signs include the following:
anorexia
weight loss
incoordination
crouching stance while arching the back and neck
wide-based stance
muscle trembling when forced to move
in severe cases, tachycardia and arrhythmias
in severe cases, death (usually 2–10 days after onset), preceded by seizures, clonic spasms, and opisthotonos
Thiaminase-associated neurocardiac syndrome in pigs is less common. Affected pigs become anorectic and lose weight. In its terminal phase, the syndrome in pigs resembles heart failure, and deaths can appear to be sudden, after a short period of recumbency and dyspnea.
In both horses and pigs, the syndrome responds to thiamine treatment (though often only partially). For this reason, it is assumed to be due to thiaminase poisoning. Partial responsiveness to thiamine treatment suggests that other fern toxins may be involved.
Fern Poisoning–Associated Developmental Toxicosis
Ptaquiloside is maternotoxic and embryotoxic in laboratory species.
Diagnosis of Bracken Fern and Other Fern Poisoning
Diagnosis of bracken fern and other fern poisoning is predominantly based on the following:
history
clinical observations
response to thiamine treatment (in cases of thiaminase-associated poisoning)
hematologic evaluation
necropsy findings
presence of bracken or other ferns in pasture, in combination with poor grazing conditions (lack of alternative food and feed)
Ptaquiloside concentrations in food and feed, meat, milk, urine, and rumen contents can be measured; and pterosin B, a major metabolite of ptaquiloside, can be detected in blood and urine. However, both ptaquiloside and pterosin B are rapidly cleared from systemic circulation in cattle, so the timing of sample collection relative to toxin exposure is important.
The presence of fern in rumen contents at necropsy can also be detected.
Prevention and Control of Bracken Fern and Other Fern Poisoning
Because bracken and other fern poisoning, apart from resultant thiamine deficiency, is essentially untreatable, it is best controlled by preventing exposure. Most poisonings occur when animals have no option but to eat ferns because other forages are exhausted (eg, in late summer). However, some animals can develop a taste for the young, tender shoots and leaves.
Poisoning can be avoided by removing animals from areas where ferns are present and improving pasture management to increase alternative forage growth. It has been suggested that alternating between fern-contaminated and uncontaminated pastures at 3-week intervals can minimize poisoning.
Control of bracken fern and other fern growth may include some or all of the following:
effective pasture management and improvement
combining cultivation with cropping before the establishment of a competitive pasture
fern slashing
fern rolling and crushing
burning (only as a supplemental measure)
chemical control
Effective pasture management and improvement promotes the growth of other pasture species that will outcompete toxic ferns.
Combining cultivation with cropping over 2–3 consecutive years, before establishment of a competitive pasture, helps control fern growth.
Slashing ferns in late spring or early summer, when new fronds have just unfurled, can be effective. Follow-up slashing should occur approximately 4 weeks later. Approximately three cuts a year from late spring to early autumn gives the best results. Slashing should be repeated for ≥ 3 consecutive years.
Rolling and crushing ferns, which damages the fronds, is quicker and less expensive than slashing but less effective.
Burning bracken and other ferns is not effective on its own. The ferns regenerate quickly after burning, because fire does not damage the rhizomes. Furthermore, burning may make the plants more toxic, as new fronds may have higher concentrations of ptaquiloside.
Chemical control of bracken and other ferns is effective when applied in late spring to late autumn, when most fronds are fully unfurled. Herbicide application is most effective in late autumn. Animals should not be allowed to graze for at least 6 months after application, nor should follow-up controls be used for at least 6 months, as sprayed ferns may take several months to die. Ferns should not be slashed or rolled for at least 8–12 months before using chemical controls. Use of recommended spray adjuvants can help herbicides penetrate fronds. Animals are still at risk for poisoning if they continue to graze on ferns, even if the ferns have been treated with herbicide. Chemical control is usually most effective when combined with a pasture resowing program.
Treatment of Bracken Fern and Other Fern Poisoning
Thiamine administration
Antimicrobial treatment
Blood or platelet transfusions
Bracken fern and other fern poisoning, apart from resultant thiamine deficiency, is essentially untreatable. For this reason, prevention is of utmost importance.
Thiaminase-associated syndromes are responsive, to some degree, to treatment with thiamine. However, in many cases animals are often too badly affected for treatment to be successful. Accordingly, affected animals should be euthanized early when appropriate.
In horses, treatment of bracken fern–induced thiamine deficiency is highly effective if diagnosis is made early. Animals exposed to ferns but not yet showing clinical signs should also receive thiamine treatment, because signs can develop days or weeks after animals have been removed from the source of bracken fern.
Antimicrobials can be administered to prevent secondary infections. Blood or even platelet transfusions may be appropriate but require large volumes to effectively treat cattle (2–4 L blood).
Key Points
At least two toxins found in ferns are of veterinary importance: ptaquiloside and thiaminases.
Ptaquiloside is radiomimetic and genotoxic.
Several clinically distinct syndromes are associated with fern poisoning; however, overlapping syndromes can occur.
Ptaquiloside-associated poisonings are often fatal, and there is no treatment; removing animals from the source of ptaquiloside exposure and providing safe feed are essential for prevention and control.
Thiaminase-associated syndromes are treatable in some cases, if diagnosed and treated early in the disease process.
For More Information
Aranha PCDR, Rasmussen LH, Wolf-Jäckel GA, Jensen HME, Hansen HCB, Friis C. Fate of ptaquiloside—a bracken fern toxin—in cattle. PLoS One. 2019;14(6):e0218628.
McKenzie R. Australia's Poisonous Plants, Fungi and Cyanobacteria: A Guide to Species of Medical and Veterinary Importance. CSIRO; 2020.
Vetter J. The norsesquiterpene glycoside ptaquiloside as a poisonous, carcinogenic component of certain ferns. Molecules. 2022;27(19):6662.
Also see pet owner content regarding bracken fern poisoning.
References
Medeiros-Fonseca B, Abreu-Silva AL, Medeiros R, Oliveira PA, Gil da Costa RM. Pteridium spp. and bovine papillomavirus: partners in cancer. Front Vet Sci. 2021;8:758720. doi:10.3389/fvets.2021.758720
Gomes J, Magalhães A, Michel V, Amado IF, et al. Pteridium aquilinum and its ptaquiloside toxin induce DNA damage response in gastric epithelial cells, a link with gastric carcinogenesis. Toxicol Sci. 2012;126(1):60-71. doi:10.1093/toxsci/kfr329
Watson WA, Terlecki S, Patterson DS, Sweasey D, Herbert CN, Done JT. Experimentally produced progressive retinal regeneration (bright blindness) in sheep. Br Vet J. 1972;128(9):457-469. doi:10.1016/s0007-1935(17)36785-4
McCleary BV, Kennedy CA, Chick BF. Nardoo, bracken and rock ferns cause vitamin B1 deficiency in sheep. Agricultural Gazette of New South Wales. 1980;91(5):40-43.
Clark IA, Dimmock CK. The toxicity of Cheilanthes sieberi to cattle and sheep. Aust Vet J. 1971;47(4):149-152. doi:10.1111/j.1751-0813.1971.tb02124.x
Chick BF, Carroll SN, Kennedy C, McCleary BV. Some biochemical features of an outbreak of polioencephalomalacia in sheep. Aust Vet J. 1981;57(5):251-252. doi:10.1111/j.1751-0813.1981.tb02680.x
Beckett RJ. Rock Fern Toxicity in Sheep and Cattle. Doctoral thesis. University of Sydney; 1984.
