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Hepatotoxic Plants


Senecio, Groundsel

Crotalaria, Rattlebox


Blue-Green Algae (Mike)




White Clover











----The most common hepatotoxic plant constituent is Pyrrolizidine alkaloids among the herbs which containing Pyrrolizidine alkaloids are



Alkanna tinctoria (Alkanet, Anchusa)
Borago officinalis (Borage)
Cynoglossum officinale (Hound'stongue)
Eupatorium purpureum (Queen of the Meadow)
Lithospermum officinale (Stoneseed)
Petasites spp. (Butterburr)
Senecio spp. (Liferoot)
Symphytum asperum (Prickly Comfrey)
Symphytum caucasicum (Comfrey)
Symphytum officinale (Comfrey)
Symphytum tuberosum (Comfrey)
Symphytum x uplandicum (Russian Comfrey)
Tussilago spp. (Coltsfoot)

Pyrrolizidine Alkaloids:












High PA doses cause sudden liver failure, but because most poisonings are from contaminated feed, doses usually are low and exposures are long. Clinical liver disease in these animals may not develop until months after exposure. Young animals are most sensitive and there are several reports of fetal and neonatal toxicity without evidence of maternal toxicity. Signs of poisoning are related to liver failure and include weight loss, weakness, sleepiness, yawning, incoordination, neurologic derangement, icterus, photosensitivity, aimless walking, chewing motions and head pressing.


is made by identifying exposure. As most poisonings are caused by contaminated feed, documenting exposure can be difficult. Hay contamination is patchy; often only a few bales from an entire crop may


be bad. Finding the bad bales is difficult, so it often is better to inspect the field.

Though non-specific, good clinical work-ups and post-mortem examinations are helpful to narrow the diagnosis. Classical histologic changes of hepatocellular necrosis, fibrosis, biliary hyperplasia and hepatocyte megalocytosis are suggestive of PA intoxication. However, similar changes may be caused by aflatoxins and other alkalating agents.

In some cases, PA metabolites can be extracted and identified from animal tissues. Current research seeks to improve diagnostics to better identify and predict the outcome to poisoned animals.

As most cases result in liver failure, supportive care is the only treatment. As both contamination rates and PA concentrations within the plant can vary, assessing risk is impossible. Avoiding exposure to any of these plants is recommended:


 Pyrrolizidine alkaloids (PA's) are found in over 240 species, mostly amongst the Asteraceae (Daisy) and Boraginaceae (Borage) families. Hepatotoxicity among PA's varies with minor differences in chemical structure. It is most marked among macrocyclic diesters; these form highly reactive pyrrole intermediates upon metabolism by CYP3A4. Subsequent conjugation of the pyrroles is via glutathione. The reactive pyrrole intermediates form covalent bonds with nucleic acids and disrupt cellular protein synthesis and cell replication which initiates the pathological process. DNA cross linking may also lead to carcinogenesis.

• herbal concern: Evaluation of the risks from ingestion of PA containing herbs is a complex, controversial and unresolved subject. PA's vary in toxicity, not only by distribution in different species of the same genera, but in their distribution in different plant parts (leaf, root etc.) of the same species.

----Regulatory authorities in some countries have proscribed the use of all PA-containing herbs such as Tussilago farfara (Coltsfoot) and Borago officinalis (Borage) despite complete lack of any evidence for toxicity in normal usage,

along with Symphytum spp. (Comfrey) for which there is more compelling evidence of hepatoxicity - with four reports worldwide associating possible VOD with comfrey use at normal dose levels.

-----In the USA, cautions are recommended by AHPA (American Herbal Products Association) to restrict use of PA-containing herbs to external use on unbroken skin and to avoid consumption during pregnancy and nursing.











Overview of interactions:

---- Detoxification of PA's depends initially on the CYP3A4 enzyme subsystem and subsequently on hepatic glutathione (GSH) status. Although age, genetic variation, nutritional status and other factors account for large inter-individual differences, it is known which drugs inhibit CYP3A4 and which drugs are substrates by CYP3A4. Use of these drugs would require an even greater vigilance concerning the concurrent ingestion of PA-containing herbs.

---- Drugs inhibiting CYP3A4 include fluoxetine, itraconazol, fluconazole, ketoconazole, erythromycin, clarithromycin, troleandomycin. See also Grapefruit Juice.
---- Drugs metabolized by CYP3A4 include quinidine, carbamazepine, astemizole, terfanadine, fluoxetine, alprazolam, midazolam, triazolam, diltiazem, nifedipine, cisapride, cyclosporine, lidocaine, lovastatin, lydrocortisone, lexamethsone.
(Bland JS. 1997, 17.)


Other hepatotoxic herbs:
Teucrium chamaedrys (Germander) has been associated with hepatoxicity in humans including at least one fatality, and is restricted in the USA and several other countries. Teucrium is not in general use or available in commerce, although adulteration of other species with Teucrium due to mistaken identification has been reported. Evidence suggests that the relevant diterpenoids are metabolized via CYP3A4.
(De Smet PAGM, et al. 1997, 137.)

Larrea tridentata (Chapparal) was subject of FDA warning following several reports of hepatotoxicity. Controversy surrounded the reports of Chaparral toxicity and four cases reviewed by Watts C, et al. in 1994 were also associated with pre-existing liver conditions.
(McGuffin M, et al.(eds.) 1997, 67.)

Acorus spp. and Asarum spp. both contain beta-asarone, a volatile allylbenzene which can form a hepatotoxic and genotoxic epoxide metabolite when activated by hepatic microsomal enzymes. Adverse reactions of nausea and vomiting have been reported. These herbs are used primarily by professional herbalists: they are considered safe providing therapeutic dose ranges are observed.
(McGuffin M, et al.(eds.) 1997, 134.)
Lantana (Lantana camara Linn)

is a noxious weed that grows in many tropical and subtropical parts of the world. Ingestion of lantana foliage by grazing animals causes cholestasis and hepatotoxicity. Both ruminants and nonruminant animals such as guinea pigs, rabbits, and female rats are susceptible to the hepatotoxic action of lantana toxins. The hepatotoxins are pentacyclic triterpenoids called lantadenes. Molecular structure of lantadenes has been determined. Green unripe fruits of the plan...

Trifolium hybridum (aslike clover –

Alsike clover is one of about 300 Trifolium species that have been associated with phytoestrogenism, slobbers, liver disease and photosensitivity. It is an introduced European plant that is included in some pasture mixes.

Several toxins have been suspected, but none has been proven. Toxicity may be related to environmental conditions and mold or aflatoxin production. Exposures of weeks to months generally are required before animals develop disease.

Three syndromes

Horses are the only species known to be susceptible to poisoning. Three syndromes have been identified.

The first, called "dew poisoning", is characterized by photosensitivity (sunburn), colic and diarrhea, depression or excitation.

The second, called "big liver disease" is severe liver disease or recurrent bouts of liver disease that is seen clinically as icterus, weight loss, CNS depression, anorexia, incoordination, dark and discolored urine and an enlarged fibrotic liver.

The third syndrome is associated with excessive salivation or slobbering, when horses eat clover that is infected with a fungus that causes brown leaf spot. Horses stop slobbering when exposure is discontinued.

Signs of poisoning depend on the syndrome and include anorexia, loss of body condition, jaundice, hepatoencephalopathy (neurologic disease) and death. Signs of other syndromes include sunburn with dermal edema, necrosis and sloughing of skin and possibly excessive salivation.

Treatment includes removing horses from exposure to the plant, treating photosensitivity and supportive care. Recovered animals often are hepatic cripples and more susceptible to liver failure or other liver diseases. It is recommended that alsike clover not be included in pasture seed mixes for horses.

Xanthium spp (Cocklebur).

Cocklebur seeds and seedlings contain a potent toxin called carboxyatractyloside, a plant-growth inhibitor that allows cockleburs to dominate competing plants. In animals, this toxin disrupts cellular metabolism, causing severe liver disease (centrilobular liver necrosis).

Poisoning most often occurs when horses consume feed contaminated with seed or when they eat small seedlings. The minimum lethal dose of seeds is 0.3 percent of body weight. All animals are susceptible to seedling poisoning.

Common signs include neurologic disease related to liver failure, depression, weakness, prostration, abnormal eye position and movements, paddling, convulsions and coma. Other changes include stocking up (swelling and edema of the feet and legs) and vasculitis. Severely poisoned animals generally die or are hepatic cripples that do poorly.

Diagnosis is made by documenting exposure and identifying blood-related changes of liver failure. Microscopic changes in liver cells and blood vessels can be detected in biopsy or post-mortem samples. Stomach or intestinal contents also can be analyzed for carboxyatractyloside.

Treating poisoned horses is symptomatic, with little response, as liver damage is extensive when animals become sick. It is important to mow or remove cockleburs before they form seeds and cause heavy infestations.

Crystalline hepatopathy – Panicum coloratum (Kleingrass), P. virgatum (switchgrass), Tribulus terrestris (puncture vine), Nolinatexana (sacahuiste), Agave lechuguilla (lechugilla).

These plants are native (Nolina, Agave, and Tribulus spp.) and introduced cover crops (Panicum spp.) that can be found across North America. Poisoning is variable and incompletely understood. Likely toxins include saponins (diosgenin and yamogenin) that damage the liver biliary system. Because toxin concentrations vary and poisoning is sporadic, risk is difficult to predict. Some animals never develop disease. Panicum grasses are not very palatable and are poor forages. In most cases, animals must be forced to eat them.

Poisoning signs usually are related to sunburn or photosensitization with elevated blood biomarkers and serum enzymes suggestive of liver disease.

Lesions include severe sunburn with necrosis and sloughing of skin. The photosensitivity cause is liver failure; characteristic microscopic changes of necrosis and bile-duct lesions can be seen in the liver.

It is difficult to predict dose or risk of poisoning, so horses should not be fed monocultures of these forages.

Treatment should include supportive care for both the liver disease and sunburn.



Typically, pyrrolizidine alkaloidosis is a chronic poisoning that results in hepatic failure. It is caused by many toxic plants, most commonly of the genera Senecio , Crotalaria , Heliotropium , Amsinckia , Echium , Cynoglossum , and Trichodesma . These plants grow mainly in temperate climates, but some (eg, Crotalaria spp ) require tropical or subtropical climates. The plants most often implicated are ragwort ( S jacobea ), woolly groundsel ( S redellii , S longilobus ), rattleweed ( Crotalaria retusa ), and seeds of yellow tarweed ( A intermedia ).

Etiology and Pathogenesis

More than 30 toxic factors (alkaloids with a pyrrolizidine base) have been found in the plants. It is likely that their toxic effects are unique. Senecio jacobea contains jacobine; retrorsine, seneciphylline, and monocrotaline are other pyrrolizidine alkaloids frequently incriminated in toxicities.

These plants, which under normal conditions are avoided by grazing animals, may be eaten during drought conditions. Some animals may eat these plants preferentially as roughage when they are available on extremely lush pasture. Animals are also poisoned by eating the plant material in hay, silage, or pellets. Seeds from Crotalaria , Amsinckia , and Heliotropium spp , which have been harvested with grain, have caused the disease in horses, cattle, pigs, and poultry

The toxic alkaloids are metabolized to highly reactive pyrroles, which produce cytotoxic effects on target sites, most commonly the nuclei of hepatocytes. Other target sites may include the epithelial and vascular tissues of the kidneys and lungs. The pyrroles cross-link DNA strands and also unite DNA with nucleoproteins such as actin. These molecular alterations are presumed to create the antimitotic and megalocytic effects characteristic of pyrrolizidine alkalosis.

Clinical Findings:

The clinical signs and hepatic pathology are similar in all animal species regardless of the species of plant involved or the toxic pyrrolizidine alkaloids it contains. Acute intoxication is characterized by sudden death from hemorrhagic liver necrosis and visceral hemorrhages. This is a rare event, as the poor palatability of these plants makes rapid ingestion of large quantities of the toxins uncommon. More chronic exposure is typical, and the liver reflects the cumulative and progressive effects of repeated ingestion of small doses of toxin. Clinical signs may not be seen for several weeks or months after initial exposure. Consumption of the offending plant may even have ceased months earlier. The ongoing hepatic damage in these instances is suspected to be due to the recycling of toxic pyrroles as they are released from one dying cell and taken up by another. Clinical progression may also be altered by concurrent hepatic pathology; a hemolytic crisis may be precipitated in sheep with excessive hepatic copper stores (see copper poisoning



In acute cases, the liver may be enlarged, hemorrhagic, and icteric. In chronic cases, it is atrophied, fibrous, finely nodular, and usually pale with a glistening surface due to fibrous thickening of the capsule. Other livers are markedly icteric. The gallbladder is often edematous and grossly distended with thick, mucoid bile. Edema of the abomasum and segments of the bowel, mesentery, and associated lymph nodes is common, and there may be ascites. In some cases, numerous small hemorrhages are present in the abdominal serous membranes.

Characteristic histologic changes occur in the liver. Irreversible enlargement of individual hepatocytes (megalocytosis) is often seen; it is conspicuous in horses and sheep but less pronounced in cattle. In cattle, marked perivenous fibrosis of sublobular veins is usually present, but this is not a consistent finding in horses and sheep. In all species, increases in connective tissue, both within and around the lobules, are marked. Bile duct hyperplasia is variable but may be the most striking microscopic change seen in some livers. Pigs may show pulmonary congestion, hemorrhage, septal fibrosis, alveolar epithelialization, and emphysema. Renal tubular lining cells and glomerular epithelial cells also may be individually enlarged.


A diagnosis based on history, clinical signs, and gross necropsy findings can usually be confirmed by histologic examination of liver and renal tissue. Chemical analyses of the liver for toxic metabolites are available for confirmation of exposure but are seldom necessary. When hepatic cirrhosis is extensive, hypoalbuminemia and hyperglobulinemia develop. Serum levels of fibrinogen, bilirubin, γ-glutamyltransferase, and glutamate dehydrogenase may be increased, but it should be recognized that the insidious nature of this disease can result in surprisingly mild serum biochemical changes. Other hepatotoxins, such as copper or aflatoxin, as well as infections such as chronic fascioliasis, must be considered before making the diagnosis.

Treatment and Control:

Further intake of toxic plant material must be prevented. Animals showing signs rarely recover, and lesions present in asymptomatic animals may progress and result in further losses over several months.

Because high protein intake may prove harmful, rations high in carbohydrates are indicated. Methionine in 10% dextrose solution, IV, may be of value in treating horses

The diminished ability of the liver to regenerate after pyrrolizidine alkaloid poisoning suggests a guarded prognosis. Preventing further outbreaks by reducing or eliminating contributory factors should be stressed.





  Senecio jacobea                                       Crotalaria spp (rattle weed).












Sheep are commonly used for grazing control of these plants, but this practice carries risks unless sheep destined for early slaughter are used. Biologic control of plants with predator moths, flea beetles, and seed flies has met with variable success. Senecio and related toxic

species in pastures have been controlled satisfactorily by annual herbicide applications, preferably in spring before hay or silage conservation. Measures that enhance destruction of the alkaloids in the rumen of sheep also have shown some promise





Toxic mushroom

Poisonous mushrooms

See also: List of deadly fungi

Three of the most lethal mushrooms belong to the genus Amanita: the death cap (A. phalloides) and destroying angels (A. virosa, and A. bisporiga); and two are from the genus Cortinarius: the deadly webcap (C. rubellus), and the fool's webcap (C. orellanus). Several species of Galerina, Lepiota, and Conocybe also contain lethal amounts of amatoxins. Deadly species are listed in the List of deadly fungi.

The following species may cause great discomfort, sometimes requiring hospitalization, but are not considered deadly.

The mushroom Amanita muscaria, commonly known as "fly agaric"

Mushroom vs. toadstool


Size and age

Yellow, flower pot mushrooms (Leucocoprinus birnbaumii) at various states of development


Human use

The button mushroom (Agaricus bisporus), one of the most widely cultivated mushrooms in the world.

Further information: Ethnomycology


Toxic mushrooms

Main article: Mushroom poisoning

The Panther cap (Amanita pantherina), a toxic mushroom




Toxins and their symptoms



Specific, characterizable, poisonous chemicals, often proteins, with specific biological properties, including immunogenicity, produced by microbes, higher plants, or animals



A group of very potent toxins from Amanita species which cause lethal liver and kidney damage and inhibit some RNA synthesis



Poisonous mushrooms contain a variety of different toxins that can differ markedly in toxicity. Symptoms of mushroom poisoning may vary from gastric upset to life-threatening organ failure resulting in death. Serious symptoms do not always occur immediately after eating; often not until the toxin attacks the kidney or liver, sometimes days or weeks later.

The most common consequence of mushroom poisoning is simply gastric upset. Most "poisonous" mushrooms contain gastrointestinal irritants which cause vomiting and diarrhea (sometimes requiring hospitalization), but no long-term damage. However, there are a number of recognized mushroom toxins with specific, and sometimes deadly, effects:

  • Alpha-amanitin (deadly: causes liver damage 1-3 days after ingestion) – principal toxin in genus Amanita.
  • Phallotoxin (causes gastrointestinal upset) – also found in poisonous Amanitas
  • Orellanine (deadly: causes kidney failure 3 weeks after ingestion) – principal toxin in genus Cortinarius.
  • Muscarine (sometimes deadly: can cause respiratory failure) – found in genus Omphalotus.
  • Gyromitrin (deadly: causes neurotoxicity, gastrointestinal upset, and destruction of blood cells) – principal toxin in genus Gyromitra.
  • Coprine (causes illness when consumed with alcohol) – principal toxin in genus Coprinus.
  • Ibotenic acid and muscimol (hallucinogenic) – principal toxin in A. muscaria, A. pantherina, and A. gemmata.
  • Psilocybin and psilocin (hallucinogenic) – principal toxin in genus Psilocybe.
  • Arabitol (causes gastrointestinal irritation in some people).
  • Bolesatine a toxin found in Boletus satanas

Symptoms of mushroom poisoning vary depending on the toxins involved.

  • Alpha-amanitin: For 6-12 hours, there are no symptoms. This is followed by a period of gastrointestinal upset (vomiting and profuse, watery diarrhea). This stage is caused primarily by the phallotoxins[4] and typically lasts 24 hours. At the end of this second stage is when severe liver damage begins. The damage may continue for another 2-3 days. Kidney damage can also occur. Some patients will require a liver transplant.[20] Amatoxins are found in some mushrooms in the genus Amanita, but are also found in some species of Galerina and Lepiota.[8] Overall, mortality is between 10 and 15 percent.[21] Recently, Silybum marianum or blessed milk thistle has been shown to protect the liver from aminita toxins and promote regrowth of damaged cells [22][23], including a study in which 60 patients exposed to death cap poison were given 20 mg/kg of milk thistle seeds per day within 48 hours of consuming the deadly mushrooms. None of the patients died.[24]
  • Orellanine: This toxin causes no symptoms for 3-20 days after ingestion. Typically around day 11, the process of kidney failure begins[4], and is usually symptomatic by day 20. These symptoms can include pain in the area of the kidneys, thirst, vomiting, headache, and fatigue. A few species in the very large genus Cortinarius contain this toxin. People who have eaten mushrooms containing orellanine may experience early symptoms as well, because the mushrooms often contain other toxins in addition to orellanine.[25]
  • Muscarine: Muscarine stimulates the muscarinic receptors of the nerves and muscles. Symptoms include sweating, salivation, tears, blurred vision, palpitations, and, in high doses, respiratory failure.[26] Muscarine is found in mushrooms of the genus Omphalotus, notably the Jack 'o lantern mushrooms. It is also found in A. muscaria, although it is now known that the main effect of this mushroom is caused by ibotenic acid. Muscarine can also be found in some Inocybe species and Clitocybe species, particularly Clitocybe dealbata, and some red-pored Boletes.[8]
  • Gyromitrin: Stomach acids convert gyromitrin to monomethylhydrazine (MMH), a compound employed in rocket fuel. It affects multiple body systems. It blocks the important neurotransmitter GABA, leading to stupor, delirium, muscle cramps, loss of coordination[4], tremors, and/or seizures. It causes severe gastrointestinal irritation, leading to vomiting and diarrhea. In some cases, liver failure has been reported[4]. It can also cause red blood cells to break down, leading to jaundice, kidney failure, and signs of anemia. It is found in mushrooms of the genus Gyromitra[14]. A gyromitrin-like compound has also been identified in mushrooms of the genus Verpa.[13]
  • Coprine: Coprine is metabolized to a chemical that resembles disulfiram. It inhibits aldehyde dehydrogenase (ALDH), which generally causes no harm, unless the person has alcohol in their bloodstream while ALDH is inhibited. This can happen if alcohol is ingested shortly before or up to a few days after eating the mushrooms. In that case the alcohol cannot be completely metabolized, and the person will experience flushed skin, vomiting, headache, dizziness, weakness, apprehension, confusion, palpitations, and sometimes trouble breathing. Coprine is found mainly in mushrooms of the genus Coprinus, although similar effects have been noted after ingestion of Clitocybe clavipes.
  • Ibotenic acid: This organic acid is metabolized to muscimol. The effects of muscimol vary, but nausea and vomiting are common. Confusion, euphoria, or sleepiness are possible. Loss of muscular coordination, sweating, and chills are likely. Some people experience visual distortions, a feeling of strength, or delusions. Symptoms normally appear after 30 minutes to 2 hours and last for several hours. A. muscaria, the "Alice in Wonderland" mushroom, is known for the toxic/hallucinogenic properties caused by ibotenic acid, but A. pantherina and A. gemmata also contain the same compound.[8] While normally self-limiting, fatalities have been associated with A. pantherina,[12] and consumption of a large number of any of these mushrooms is likely to be dangerous.
  • Psilocybin: This compound is converted into psilocin when ingested. Symptoms begin shortly after ingestion. The effects can include euphoria, visual and religious hallucinations, and heightened perception. However, some persons experience fear, agitation, confusion, and schizophrenialike symptoms. All symptoms generally pass after several hours. Some (though not all) members of the genus Psilocybe contain psilocybin, as do some Panaeolus, Copelandia, Conocybe, Gymnopilus, and others. Some of these mushrooms also contain baeocystin, which has effects similar to psilocin.

Some mushrooms contain less toxic compounds and, therefore, are not severely poisonous. Poisonings by these mushrooms may respond well to treatment. However, certain types of mushrooms, such as the Amanitas, contain very potent toxins and are very poisonous; so even if symptoms are treated promptly mortality is high. With some toxins, death can occur in a week or a few days. Although a liver or kidney transplant may save some patients with complete organ failure, in many cases there are no organs available. Patients who are hospitalized and given aggressive support therapy almost immediately after ingestion of amanitin-containing mushrooms have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50-90% mortality rate.[28][29]


Mushroom poisoning

also known as mycetism, refers to deleterious effects from ingestion of toxic substances present in a mushroom. These symptoms can vary from slight gastrointestinal discomfort to death. The toxins present are secondary metabolites produced in specific biochemical pathways in the fungal cells. Mushroom poisoning is usually the result of ingestion of wild mushrooms after misidentification of a toxic mushroom as an edible species. The most common reason for this misidentification is close resemblance in terms of colour and general morphology of the toxic mushrooms species with edible species. Even very experienced wild mushroom gatherers are sometimes poisoned by eating toxic species, despite being well aware of the risks.

To prevent mushroom poisoning, mushroom gatherers need to be very intimately familiar with the mushrooms they intend to collect, including knowledge of the toxic species that look similar to these edible species. Other considerations regard methods of preparation and toxicity of some fungal species that appears to vary with geographic location, raising the potential of mushroom poisoning due to local toxicity of a correctly identified species.


There are many folk traditions concerning the defining features of poisonous mushrooms[1][2]. Unfortunately there are no general identifiers for poisonous mushrooms, and so such traditions are unreliable guides. Use of folk traditions to try to identify edible mushrooms are a frequent cause of mushroom poisoning. Examples of folklore "rules" are:

  • "Poisonous mushrooms are brightly colored." While the toxic/hallucinogenic fly agaric is usually bright red or yellow, the deadly destroying angel is an unremarkable white, and the deadly Galerinas are brown. Some choice edible species (chanterelles, Amanita caesarea, Laetiporus sulphureus, etc.) are brightly colored, while most poisonous species are brown or white.
  • "Insects/animals will avoid toxic mushrooms." Fungi that are harmless to invertebrates can still be toxic to humans; the death cap, for instance, is often infested by insect larvae. Also, animals don't always know to avoid poisonous species.
  • "Poisonous mushrooms blacken silver." None of the known mushroom toxins have a reaction with silver.
  • "Poisonous mushrooms taste bad." People who have eaten the deadly Amanitas reported that they tasted quite good.
  • "All mushrooms are safe if cooked/parboiled/dried/pickled/etc." While it is true that some otherwise inedible species can be rendered safe by special preparation, many toxic species can not be prepared in such a way as to make them edible. Many fungal toxins are not particularly sensitive to heat and so are not broken down during cooking.
  • "Poisonous mushrooms will turn rice red when boiled"[3]. A number of Laotian refugees were hospitalized after eating mushrooms (probably toxic Russula species) deemed safe by this folklore rule.

[edit] Causes of mushroom poisoning

Of the many thousands of mushroom species in the world, only 32 have been associated with fatalities, and an additional 52 have been identified as containing significant toxins.[4] By far the majority of mushroom poisonings are not fatal,[5] but the majority of fatal poisonings are attributable to the Amanita phalloides mushroom.[6]

A majority of these cases are due to "mistaken identity." One way this can happen is that the victim attempts to apply folk knowledge from one area to another geographic area.[3] This is a common occurrence with A. phalloides in particular, due to its resemblance to the Asian "paddy-straw" mushroom, Volvariella volvacea. Both are light-colored and covered with a universal veil when young.

Amanitas can be mistaken for other species, as well, particularly when immature. On at least one occasion[7] they have been mistaken for Coprinus comatus. In this case the victim had some experience in identifying mushrooms, but did not take the time to correctly identify these particular mushrooms until after he began to experience symptoms of mushroom poisoning.


A majority of mushroom poisonings in general are the result of small children, especially toddlers in the "grazing" stage, ingesting mushrooms found in the lawn. While this can happen with any mushroom, Chlorophyllum molybdites is often implicated due to its preference of growing in lawns. C. molybdites causes severe gastrointestinal upset but is not considered deadly poisonous.

A few poisonings are the result of misidentification while attempting to collect hallucinogenic mushrooms for recreational use.[9] In 1981, one fatality and two hospitalizations occurred following consumption of Galerina autumnalis, mistaken for a Psilocybe species.[10] Galerina and Psilocybe species are both small, brown, and sticky, and can be found growing together. However, Galerina contains amatoxins, the same poison found in the deadly Amanita species. Another case reports kidney failure following ingestion of Cortinarius orellanus,[11] a mushroom containing orellanine.

Naturally, accidental ingestion of hallucinogenic species also occurs, but is rarely harmful. Cases of serious toxicity have been reported in small children.[12] Amanita pantherina, while it contains the same hallucinogens as Amanita muscaria (e.g., ibotenic acid and muscimol), has been more commonly associated with severe gastrointestinal upset than its better-known counterpart.[8]

Jack-O-Lantern, a poisonous mushroom sometimes mistaken for a chanterelle.

Chanterelle, edible.

Although usually not fatal, Omphalotus olearius, the "Jack-o-lantern mushroom," is another cause of sometimes significant toxicity.[8] It is sometimes mistaken for a chanterelle. Both are bright orange and fruit at the same time of year, although O. olearius grows on wood and has true gills rather than the veins of a Cantharellus. It containes muscarine, which causes vomiting, diarrhea, salivation, perspiration, and tears. In high doses it can cause respiratory failure. The same toxin occurs in Clitocybe dealbata, which is occasionally mistaken for an oyster mushroom or other edible species.

Toxicities can also occur with collection of morels. Even true morels, if eaten raw, will cause gastrointestinal upset. Therefore morels should always be thoroughly cooked before eating. Verpa bohemica, although referred to as "thimble morels" or "early morels" by some, have caused toxic effects in some individuals. [13] "False morels" or Gyromitra spp., are deadly poisonous if eaten raw. They contain a toxin called gyromitrin, which can cause neurotoxicity, gastrointestinal toxicity, and destruction of the blood cells.[14] The Finns consume the mushroom after parboiling, but it is not known if this renders the mushroom entirely safe, resulting in its being called the "fugu of the Finnish cuisine."

A more unusual toxin is coprine, a disulfiram-like compound which is harmless unless ingested within a few days of ingesting alcohol. It inhibits aldehyde dehydrogenase, an enzyme required for breaking down alcohol. Thus the symptoms of toxicity are similar to being both drunk and "hung over" -- flushing, headache, nausea, palpitations, and in severe cases, trouble breathing. Coprinus species, including Coprinopsis atramentaria, contain coprine. Notably, Coprinus comatus does not[15], but it is best to avoid mixing alcohol with other members of this genus.

Recently, poisonings have been associated with Amanita smithii. These poisonings may be due to orellanine, but the onset of symptoms occurs in 4 to 11 hours, which is much quicker than the 3 to 20 days normally associated with orellanine[16].

In some cases, toxicity can occur even with mushrooms that are widely considered edible.

Paxillus involutus is also indigestible when raw, but is eaten in Europe after pickling or parboiling. However, after the death of the German mycologist Dr Julius Schäffer, it was discovered that the mushroom contains a toxin which can stimulate the immune system to attack its own red blood cells. This reaction is rare, but can occur even after safely eating the mushroom for many years.[17] Similarly, Tricholoma equestre was widely considered edible and good, until it was connected with rare cases of rhabdomyolysis[18].

In the fall of 2004, thirteen deaths were associated with consumption of Pleurocybella porrigens or "angel's wings."[19] These mushrooms are generally considered edible. All the victims died of an acute brain disorder, and all had pre-existing kidney disease. The exact cause of the toxicity was not known at this time.

Cases of idiosyncratic or "unusual" reactions to fungi can also occur. Some are probably due to allergy, others to some other kind of sensitivity. It is not uncommon for an individual person to experience gastrointestinal upset associated with one particular mushroom species or genus.[19] Eating small portions when trying a new mushroom may be used as a precaution to identify individual problems with the new

Table 1. Preliminary diagnoses of mushroom intoxication.

Time of Onset

Type of Poisoning

Nature of Threat

(6-72 h)


Life threatening

(15 min-2 h)

G.I. irritant

Not life threatening*



Not life threatening*



Not life threatening*

*In most cases, however, the patient should be observed and appropriate support therapy provided if necessary.

January 1992


Table 2. Symptomatic diagnoses of mushroom poisonings.

Onset Rapid (15 min-2 h after ingestion)




Nausea and abdominal discomfort,sometimes with diarrhea and vomiting

Unknown toxins from numerous genera

Rapid and complete recovery; serious cases may last 2-3 days and require fluid replacement

Excessive sweating, lacrimation,salivation beginning 15-30 min after ingestion

Muscarine from Clitocybe or Inocybe spp.

Complete recovery within approximately 2 h

Inebriation or hallucinations without drowsiness or sleep

Psilocybin from Psilocybe, Paneolus, Gymnopilus, Conocybe, or Pluteus spp.

Complete and spontaneous recovery within 5-10 h; may take up to 24 h with large doses

Delirium with sleepiness or coma developing within 1 or 2h after ingestion

ibotenic acid/muscimol from Amanita muscaria or A. pantherina

alternating periods of drowsiness and excitement for several h, followed by total recovery

Onset Delayed (6 h-3 days after ingestion)




Feeling of abdominal fullness and severe headache about 6 h after ingestion, vomiting, no diarrhea

Gyromitrin and related hydrazones from Gyromitra esculenta and its relatives

Complete recovery within 2-6 days; may require correction of metabolic acidosis; some deaths have occurred due to liver failure

Persistent and violent vomiting, abdominal pain, profuse, watery diarrhea beginning around 12 h after ingestion

alpha-, beta-, and gamma-amanitins from Amanita phalloides and its relatives; Galerina autumnalis and its relatives; or Lepiota josserandii and its relatives

Apparent recovery a few hours after onset of symptoms, followed by a symptom-free period of 3-5 days, which precedes a period of jaundice, loss of strength, coma, and often death

Intense, burning thirst and frequent urination beginning 3-14 days after ingestion, followed by gastrointestinal disturbances, headache, pain in the limbs, spasms, and loss of consciousness

Orellanine from Cortinarius orellanus

Recovery (including recovery of renal function) may require several months in less severe cases; death from kidney failure may occur in severe cases

Onset Conditional (within 72 h of ingestion)




Flushing, palpitations, rapid heartbeat, rapid, labored breathing occur within 1/2 to 2 h after consuming alcohol, if alcohol was consumed within 72 h of mushroom ingestion

Coprine in Coprinus atramentarius

Recovery is spontaneous and complete within a few to several hours after onset of symptoms

Table 3. Poisonous Mushrooms and their Edible Look-Alikes.

Mushrooms Containing Amatoxins

Poisonous species


Mistaken for

Amanita tenuifolia (Slender Death Angel)

pure white

Leucoagaricus naucina (Smoothcap Parasol)

Amanita bisporigera (Death Angel)

pure white

Amanita vaginata (Grisette), Leucoagaricus naucina (Smoothcap Parasol), white Agaricus spp. (field mushrooms), Tricholoma resplendens (Shiny Cavalier)

Amanita verna (Fool's Mushroom)

pure white

A. vaginata, L. naucina, white Agaricus spp., T. resplendens

Amanita virosa (Destroying Angel)

pure white

A. vaginata, L. naucina, Agaricus spp., T. resplendens

Amanita phalloides (Deathcap)

pure white variety

Amanita citrina (False Deathcap), A. vaginata, L. naucina, Agaricus spp., T. resplendens

Buttons of A. bisporigera,. A. verna, A. virosa

pure white

Buttons of white forms of Agaricus spp. Puffballs such as Lycoperdon perlatum, etc.

Amanita phalloides (Deathcap)

green = normal cap color

Russula virescens (Green Brittlegill), Amanita calyptrodermia (Hooded Grisette), Amanita fulva (Tawny Grisette), Tricholoma flavovirens (Cavalier Mushroom), Tricholoma portentosum (Sooty Head)

Amanita phalloides (Deathcap)

yellow variety

Amanita caesarea (Caesar's Mushroom)

Amanita brunnescens (Cleft Foot Deathcap)


Amanita rubescens (Blusher), Amanita pantherina (Panthercap)

Galerina autumnalis (Autumn Skullcap)


"Little Brown Mushrooms," including Gymnopilus spectabilis (Big Laughing Mushroom) and other Gymnopilus spp., Armillaria mellea (Honey Mushroom)

Leucoagaricus brunnea (Browning Parasol)


Lepiota spp., Leucoagaricus spp., Gymnopilus spp. and other Parasol Mushrooms and LBM's

Lepiota josserandii, L. helveola, L. subincarnata


Lepiota spp., Leucoagaricus spp., Gymnopilus spp. and other Parasol Mushrooms and LBM's

Mushrooms Producing Severe Gastroenteritis

Chlorophyllum molybdites (Green Gill)


Leucocoprinus rachodes (Shaggy Parasol), Leucocoprinus procera (Parasol Mushroom)

Entoloma lividum (Gray Pinkgill)


Tricholomopsis platyphylla (Broadgill)

Tricholoma pardinum (Tigertop Mushroom)


Tricholoma virgatum (Silver Streaks), Tricholoma myomyces (Waxygill Cavalier)

Omphalotus olearius (Jack O'Lantern Mushroom)


Cantharellus spp. (Chanterelles)

Paxillus involutus (Naked Brimcap)


Distinctive, but when eaten raw or undercooked, will poison some people

January 1992

Medical Care

  • Symptomatic patients may be treated with supportive measures.
  • Start an intravenous (IV) infusion with Ringer lactate or normal sodium chloride solution. The initial rate should be a maintenance rate. Adjust the rate or give bolus infusions to treat dehydration or hemodynamic instability.
  • Begin cardiopulmonary monitoring.
  • Begin monitoring pulse oximetry.
  • Start bronchodilator therapy if the patient is wheezing.
  • Start atropine or glycopyrrolate therapy to manage copious secretions or wheezing.
  • Consider placing a nasogastric (NG) or orogastric (OG) tube to minimize vomiting.


  • Consultation with a mycologist is recommended to identify the mushroom.
  • Psychiatric evaluation may be helpful if the ingestion was intentional or if suicidal intentions are suspected.


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