The 1971 Iraq poison grain disaster was a mass methylmercury poisoning incident that began in late 1971. Grain treated with a methylmercury fungicide and never intended for human consumption was imported into Iraq as seed grain from Mexico and the United States. Due to a number of factors, including foreign-language labelling and late distribution within the growing cycle, this toxic grain was consumed as food by Iraqi residents in rural areas. People suffered from paresthesia (numbness of skin), ataxia (lack of coordination of muscle movements) and vision loss, symptoms similar to those seen when Minamata disease affected Japan. The recorded death toll was 459 people, but figures at least ten times greater have been suggested. The 1971 poisoning was the largest mercury poisoning disaster when it occurred, with cases peaking in January and February 1972 and stopping by the end of March.

Reports after the disaster recommended tighter regulation, better labelling and handling of mercury-treated grain, and wider involvement of the World Health Organization in monitoring and preventing poisoning incidents. Investigation confirmed the particular danger posed to fetuses and young children.

Thallium and its compounds are often highly toxic. Contact with skin is dangerous, and adequate ventilation should be provided when melting this metal. Many thallium(I) compounds are highly soluble in water and are readily absorbed through the skin. Exposure to them should not exceed 0.1 mg per m of skin in an 8-hour time-weighted average (40-hour work week). Thallium is a suspected human carcinogen.

Part of the reason for thallium's high toxicity is that, when present in aqueous solution as the univalent thallium(I) ion (Tl), it exhibits some similarities with essential alkali metal cations, particularly potassium (due to similar ionic radii). It can thus enter the body via potassium uptake pathways. Other aspects of thallium's chemistry differ strongly from that of the alkali metals, such as its high affinity for sulfur ligands. Thus, this substitution disrupts many cellular processes (for instance, thallium may attack sulfur-containing proteins such as cysteine residues and ferredoxins). Thallium's toxicity has led to its use (now discontinued in many countries) as a rat and ant poison.

Among the distinctive effects of thallium poisoning are hair loss (which led to its initial use as a depilatory before its toxicity was properly appreciated) and damage to peripheral nerves (victims may experience a sensation of walking on hot coals), although the loss of hair only generally occurs in low doses; in high doses the thallium kills before this can take effect. Thallium was once an effective murder weapon before its effects became understood and an antidote (Prussian blue) discovered. Indeed, thallium poisoning has been called the "poisoner's poison" since thallium is colorless, odorless and tasteless; its slow-acting, painful and wide-ranging symptoms are often suggestive of a host of other illnesses and conditions.

The 1951 Pont-Saint-Esprit mass poisoning, also known as Le Pain Maudit, occurred on 15 August 1951, in the small town of Pont-Saint-Esprit in southern France. More than 250 people were involved, including 50 persons interned in asylums and resulted in 7 deaths. A foodborne illness was suspected, and among these it was originally believed to be a case of "cursed bread" ("pain maudit").

Most academic sources accept ergot poisoning as the cause of the epidemic, while a few theorize other causes such as poisoning by mercury, mycotoxins, or nitrogen trichloride.

An early sign in several animals including cattle, sheep, and guinea pigs is listlessness, which is commonly followed by significant loss of weight and pronounced trembling in the legs and muzzle. These signs often appear several hours after ingestion of white snakeroot. Signs of abdominal pain, polydipsia, and vomiting may be noted. As the effects of the poison progress, signs of constipation, appetite loss, weakness, and difficulty standing and/or walking are usually observed. Complete loss of muscle coordination, stupor, and/or coma precede death. Death usually occurs within 2-10 days of symptom onset. Signs unique to cattle and sheep include peculiar odors found in the breath and urine, breathing difficulties, and over-salivation. Symptoms unique to horses include depression, bloody urine, and choking. In addition to increased heart rate and jugular pulse, swelling around the thoracic inlet in also observed. Horses may also stand with their hind legs wide apart. Symptoms unique to guinea pigs include crouching with half-closed eyes and roughening of the hair. Treatment for milk sickness is typically symptom amelioration, as well as administration of laxatives, sodium lactate, glucose, or hypotonic Ringer’s solution.

Symptoms of arsenic poisoning begin with headaches, confusion, severe diarrhea, and drowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation called leukonychia striata (Mees's lines, or Aldrich-Mees's lines) may occur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, vomiting blood, blood in the urine, cramping muscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenic poisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma and death.

Arsenic is related to heart disease (hypertension-related cardiovascular disease), cancer, stroke (cerebrovascular diseases), chronic lower respiratory diseases, and diabetes.

Chronic exposure to arsenic is related to vitamin A deficiency, which is related to heart disease and night blindness.

Inorganic arsenites (arsenic(III)) in drinking water have a much higher acute toxicity than organic arsenates (arsenic(V)). The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.

Convulsive symptoms include painful seizures and spasms, diarrhea, paresthesias, itching, mental effects including mania or psychosis, headaches, nausea and vomiting. Usually the gastrointestinal effects precede central nervous system effects.

The symptoms can be roughly divided into convulsive symptoms and gangrenous symptoms.

Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If exposure occurs over a brief period of time symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.

The most common reason for long-term exposure is contaminated drinking water. Groundwater most often becomes contaminated naturally; however, contamination may also occur from mining or agriculture. Recommended levels in water are less than 10–50 µg/l (10–50 parts per billion). Other routes of exposure include toxic waste sites and traditional medicines. Most cases of poisoning are accidental. Arsenic acts by changing the functioning of around 200 enzymes. Diagnosis is by testing the urine, blood, or hair.

Prevention is by using water that does not contain high levels of arsenic. This may be achieved by the use of special filters or using rainwater. There is not good evidence to support specific treatments for long-term poisoning. For acute poisonings treating dehydration is important. Dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) may be used while dimercaprol (BAL) is not recommended. Hemodialysis may also be used.

Through drinking water, more than 200 million people globally are exposed to higher than safe levels of arsenic. The areas most affected are Bangladesh and West Bengal. Acute poisoning is uncommon. The toxicity of arsenic has been described as far back as 1500 BC in the Ebers papyrus.

A pesticide poisoning occurs when chemicals intended to control a pest affect non-target organisms such as humans, wildlife, or bees. There are three types of pesticide poisoning. The first of the three is a single and short-term very high level of exposure which can be experienced by individuals who commit suicide, as well as pesticide formulators. The second type of poisoning is long-term high-level exposure, which can occur in pesticide formulators and manufacturers. The third type of poisoning is a long-term low-level exposure, which individuals are exposed to from sources such as pesticide residues in food as well as contact with pesticide residues in the air, water, soil, sediment, food materials, plants and animals.

In developing countries, such as Sri Lanka, pesticide poisonings from short-term very high level of exposure (acute poisoning) is the most worrisome type of poisoning. However, in developed countries, such as Canada, it is the complete opposite: acute pesticide poisoning is controlled, thus making the main issue long-term low-level exposure of pesticides.

The exact nature of the poison is still unclear. In the U.S. outbreak, the source of the fish was traced by the Centers for Disease Control and Prevention, and studies of other fish from the same sources showed a hexane-soluble (and hence non-polar lipid) substance that induced similar symptoms in mice; other food-borne poisons commonly found in fish could not be detected. It cannot be inactivated by cooking, as all six CDC cases had consumed cooked or fried fish. Palytoxin has been proposed as a disease model. It has also been suggested that the toxin may have thiaminase activity (i.e. it degrades thiamine, also known as vitamin B1).

Most pesticide-related illnesses have signs and symptoms that are similar to common medical conditions, so a complete and detailed environmental and occupational history is essential for correctly diagnosing a pesticide poisoning. A few additional screening questions about the patient's work and home environment, in addition to a typical health questionnaire, can indicate whether there was a potential pesticide poisoning.

If one is regularly using carbamate and organophosphate pesticides, it is important to obtain a baseline cholinesterase test. Cholinesterase is an important enzyme of the nervous system, and these chemical groups kill pests and potentially injure or kill humans by inhibiting cholinesterase. If one has had a baseline test and later suspects a poisoning, one can identify the extent of the problem by comparison of the current cholinesterase level with the baseline level.

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury, lead and arsenic, all of which appear in the World Health Organisation's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they can bind to and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury, and lead were known to the ancients, but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

The effect of mercury took some time – the latent period between ingestion and the first symptoms (typically paresthesia – numbness in the extremities) was between 16 and 38 days. Paresthesia was the predominant symptom in less serious cases. Worse cases included ataxia (typically loss of balance), blindness or reduced vision, and death resulting from central nervous system failure. Anywhere between 20 and 40 mg of mercury has been suggested as sufficient for paresthesia (between 0.5 and 0.8 mg/kg of body weight). On average, individuals affected consumed 20 kg or so of bread; the 73,000 tonnes provided would have been sufficient for over 3 million cases.

The hospital in Kirkuk received large numbers of patients with symptoms that doctors recognised from the 1960 outbreak. The first case of alkylmercury poisoning was admitted to hospital on 21 December. By 26 December, the hospital had issued a specific warning to the government. By January 1972, the government had started to strongly warn the populace about eating the grain, although dispatches did not mention the large numbers already ill. The Iraqi Army soon ordered disposal of the grain and eventually declared the death penalty for anyone found selling it. Farmers dumped their supplies wherever possible, and it soon got into the water supply (particularly the River Tigris), causing further problems. The government issued a news blackout and released little information about the outbreak.

The World Health Organization assisted the Iraqi government through the supply of drugs, analytical equipment and expertise. Many new treatments were tried, since existing methods for heavy metal poisoning were not particularly effective. Dimercaprol was administered to several patients, but caused rapid deterioration of their condition. It was ruled out as a treatment for this sort of poisoning following the outbreak. Polythiol resins, penicillamine and dimercaprol sulfonate all helped, but are believed to have been largely insignificant in overall recovery and outcomes. Dialysis was tested on a few patients late in the treatment period, but they showed no clinical improvement. The result of all treatments was varied, with some patients' blood mercury level being dramatically reduced, but a negligible effect in others. All patients received periods of treatment interspersed with lay periods; continuous treatment was suggested in future cases. Later treatment was less effective in reducing blood toxicity.

Signs of ethylene glycol poisoning depend upon the time after ingestion. Symptoms usually follow a three-step progression, although poisoned individuals will not always develop each stage.

- Stage 1 (30 minutes to 12 hours) consists of neurological and gastrointestinal symptoms and looks similar to alcohol poisoning. Poisoned individuals may appear to be intoxicated, dizzy, lacking coordination of muscle movements, drooling, depressed, and have slurred speech, seizuring, abnormal eye movements, headaches, and confusion. Irritation to the stomach may cause nausea and vomiting. Also seen are excessive thirst and urination. Over time, the body metabolizes ethylene glycol into other toxins.

- Stage 2 (12 to 36 hours) where signs of "alcohol" poisoning appear to resolve, underlying severe internal damage is still occurring. An elevated heart rate, hyperventilation or increased breathing effort, and dehydration may start to develop, along with high blood pressure and metabolic acidosis. These symptoms are a result of accumulation of organic acids formed by the metabolism of ethylene glycol. Additionally low calcium concentrations in the blood, overactive muscle reflexes, muscle spasms, QT interval prolongation, and congestive heart failure may occur. If untreated, death most commonly occurs during this period.

- Stage 3 (24 to 72 hours) kidney failure is the result of ethylene glycol poisoning. In cats, this stage occurs 12–24 hours after getting into antifreeze; in dogs, at 36–72 hours after getting into antifreeze. During this stage, severe kidney failure is developing secondary to calcium oxalate crystals forming in the kidneys. Severe lethargy, coma, depression, vomiting, seizures, drooling, and inappetance may be seen. Other symptoms include acute tubular necrosis, red blood cells in the urine, excess proteins in the urine, lower back pain, decreased or absent production of urine, elevated blood concentration of potassium, and acute kidney failure. If kidney failure occurs it is typically reversible, although weeks or months of supportive care including hemodialysis may be required before kidney function returns.

Milk sickness, also known as tremetol vomiting or, in animals, as trembles, is a kind of poisoning, characterized by trembling, vomiting, and severe intestinal pain, that affects individuals who ingest milk, other dairy products, or meat from a cow that has fed on white snakeroot plant, which contains the poison tremetol.

Although very rare today, milk sickness claimed thousands of lives among migrants to the Midwest in the early 19th century in the United States, especially in frontier areas along the Ohio River Valley and its tributaries where white snakeroot was prevalent. New settlers were unfamiliar with the plant and its properties. A notable victim was Nancy Hanks Lincoln, the mother of Abraham Lincoln, who died in 1818. Nursing calves and lambs may have died from their mothers' milk contaminated with snakeroot, although the adult cows and sheep showed no signs of poisoning. Cattle, horses, and sheep are the animals most often poisoned.

Anna Pierce Hobbs Bixby, called Dr. Anna on the frontier, is credited today by the American medical community with having identified white snakeroot as the cause of the illness. Told about the plant's properties by an elderly Shawnee woman she befriended, Bixby did testing to observe and document evidence. She wrote up her findings to share the discovery in the medical world. The Shawnee woman's name has been lost to history.

Poisoning is a condition or a process in which an organism becomes chemically harmed (poisoned) by a toxic substance or venom of an animal.

Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning.

Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate, or are biomagnified, such as mercury, gadolinium, and lead.

Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.

Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.

Most biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organisms (secondary poisoning), including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, which makes its lethal toxicity specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).

Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.

Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon.

Mushroom poisoning (also known as mycetism or mycetismus) refers to harmful 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 by the fungus. 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.

To prevent mushroom poisoning, mushroom gatherers familiarize themselves with the mushrooms they intend to collect as well as with any similar-looking toxic species. In addition, edibility of mushrooms may depend on methods of preparation for cooking. The edibility or toxicity of some species varies with geographic location.

Lathyrism or neurolathyrism is a neurological disease of humans and domestic animals, caused by eating certain legumes of the genus "Lathyrus". This problem is mainly associated with "Lathyrus sativus" (also known as "Grass pea", "Kesari Dal", "Khesari Dal" or "Almorta") and to a lesser degree with "Lathyrus cicera", "Lathyrus ochrus" and "Lathyrus clymenum" containing the toxin ODAP.

The lathyrism resulting from the ingestion of "Lathyrus odoratus" seeds ("sweet peas") is often referred to as odoratism or osteolathyrism, which is caused by a different toxin (beta-aminopropionitrile) that affects the linking of collagen, a protein of connective tissues.

Lathyrism is mainly due to consumption of Lathyrus sativus ( common name : Khesari ) containing Cyanoalanine(neurotoxin) and mainly causes muscle cramps and excessive consumption may even lead to paralysis

In Chinese alchemy, elixir poisoning refers to the toxic effects from elixirs of immortality that contained metals and minerals such as mercury and arsenic. The official "Twenty-Four Histories" record numerous Chinese emperors, nobles, and officials who ironically died from taking elixirs in order to prolong their lifespans. The first emperor to die from elixir poisoning was likely Qin Shi Huang (d. 210 BCE) and the last was Yongzheng (d. 1735). Despite common knowledge that immortality potions could be deadly, fangshi and Daoist alchemists continued the elixir-making practice for two millennia.

It was first described in 1924 in the vicinity of Königsberg, Germany (now Kaliningrad, Russia) on the Baltic coast, in people staying around the northern part of the Vistula Lagoon (German: "Frisches Haff").

Over the subsequent fifteen years, about 1000 cases were reported in people, birds and cats, usually in the summer and fall, and a link was made with the consumption of fish (burbot, eel and pike). Since that time, only occasional reports have appeared of the condition, mostly from the Soviet Union and Germany.

In 1997, six cases of Haff disease were reported in California and Missouri, all after the consumption of buffalo fish ("Ictiobus cyprinellus").

In July and August 2010, dozens of people contracted rhabdomyolysis after eating "Procambarus clarkii" in Nanjing, China. A month later, the Chinese authorities claimed they were victims of Haff disease.

An outbreak was reported in Brooklyn, New York on 18 November 2011, when two household members were stricken by the syndrome after eating buffalo fish. On February 4, 2014 two cases of Haff Disease were reported in Cook County, Illinois following the consumption of buffalo fish.

A group from Brazil has recently identified a Haff Disease outbreak in Bahia state with 71 cases identified.

Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol. Early symptoms include intoxication, vomiting and abdominal pain. Later symptoms may include a decreased level of consciousness, headache, and seizures. Long term outcomes may include kidney failure and brain damage. Toxicity and death may occur even after drinking a small amount.

Ethylene glycol is a colorless, odorless, sweet liquid, commonly found in antifreeze. It may be drunk accidentally or purposefully in an attempt to cause death. When broken down by the body it results in glycolic acid and oxalic acid which cause most of the toxicity. The diagnosis may be suspected when calcium oxalate crystals are seen in the urine or when acidosis or an increased osmol gap is present in the blood. Diagnosis may be confirmed by measuring ethylene glycol levels in the blood; however, many hospitals do not have the ability to perform this test.

Early treatment increases the chance of a good outcome. Treatment consists of stabilizing the person, followed by the use of an antidote. The preferred antidote is fomepizole with ethanol used if this is not available. Hemodialysis may also be used in those where there is organ damage or a high degree of acidosis. Other treatments may include sodium bicarbonate, thiamine, and magnesium.

More than 5000 cases of poisoning occur in the United States each year. Those affected are often adults and male. Deaths from ethylene glycol have been reported as early as 1930. An outbreak of deaths in 1937 due to a medication mixed in a similar compound, diethylene glycol, resulted in the Food, Drug, and Cosmetic Act of 1938 in the United States which mandated evidence of safety before new medications could be sold. Antifreeze products sometimes have a substance to make it bitter added to discourage drinking by children and other animals but this has not been found to be effective.

, sometimes referred to as , is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, loss of peripheral vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses in the womb.

Minamata disease was first discovered in Minamata city in Kumamoto prefecture, Japan, in 1956. It was caused by the release of methylmercury in the industrial wastewater from the Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local populace, resulted in mercury poisoning. While cat, dog, pig, and human deaths continued for 36 years, the government and company did little to prevent the pollution. The animal effects were severe enough in cats that they came to be named as having "dancing cat fever".

As of March 2001, 2,265 victims had been officially recognised as having Minamata disease (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso. By 2004, Chisso Corporation had paid $86 million in compensation, and in the same year was ordered to clean up its contamination. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims.

A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered two of the four big pollution diseases of Japan.

Various pesticides such as rodenticides may cause secondary poisoning. Some pesticides require multiple feedings spanning several days; this increases the time a target organism continues to move after ingestion, raising the risk of secondary poisoning of a predator.

New species of fungi are continuing to be discovered, with an estimated number of 800 new species registered annually. This, added to the fact that many investigations have recently reclassified some species of mushrooms from edible to poisonous has made older classifications insufficient at describing what now is known about the different species of fungi that are harmful to humans. Thus, contrary to what older registers state, it is now thought that of the approximately 100,000 known fungi species found worldwide, about 100 of them are poisonous to humans. However, by far the majority of mushroom poisonings are not fatal, and the majority of fatal poisonings are attributable to the "Amanita phalloides" mushroom.

A majority of these cases are due to mistaken identity. 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.

"Amanita"s can be mistaken for other species, as well, in particular when immature. On at least one occasion they have been mistaken for "Coprinus comatus". In this case, the victim had some limited 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.

The author of "Mushrooms Demystified", David Arora cautions puffball-hunters to beware of "Amanita" "eggs", which are "Amanita"s still entirely encased in their universal veil. "Amanita"s at this stage are difficult to distinguish from puffballs. Foragers are encouraged to always cut the fruiting bodies of suspected puffballs in half, as this will reveal the outline of a developing "Amanita" should it be present within the structure.

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 for 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. In 1981, one fatality and two hospitalizations occurred following consumption of "Galerina autumnalis", mistaken for a "Psilocybe" species. "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", a mushroom containing orellanine.

It is natural that accidental ingestion of hallucinogenic species also occurs, but is rarely harmful when ingested in small quantities. Cases of serious toxicity have been reported in small children. "Amanita pantherina", while containing 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.

Although usually not fatal, "Omphalotus" spp., "Jack-o-lantern mushrooms," are another cause of sometimes significant toxicity. They are sometimes mistaken for chanterelles. Both are bright-orange and fruit at the same time of year, although "Omphalotus" grows on wood and has true gills rather than the veins of a "Cantharellus". They contain toxins known as illudins, which causes gastrointestinal symptoms.

Bioluminescent species are generally inedible and often mildly toxic.

"Clitocybe dealbata", which is occasionally mistaken for an oyster mushroom or other edible species contains muscarine.

Toxicities can also occur with collection of morels. Even true morels, if eaten raw, will cause gastrointestinal upset. Typically, morels are thoroughly cooked before eating. "Verpa bohemica", although referred to as "thimble morels" or "early morels" by some, have caused toxic effects in some individuals. "Gyromitra" spp., "false morels", are deadly poisonous if eaten raw. They contain a toxin called gyromitrin, which can cause neurotoxicity, gastrointestinal toxicity, and destruction of the blood cells. The Finns consume "Gyromitra esculenta" after parboiling, but this may not render 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 that 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 hung over—flushing, headache, nausea, palpitations, and, in severe cases, trouble breathing. "Coprinus" species, including "Coprinopsis atramentaria", contain coprine. "Coprinus comatus" does not, but it is best to avoid mixing alcohol with other members of this genus.

Recently, poisonings have also been associated with "Amanita smithiana". 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.

"Paxillus involutus" is also inedible 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 that 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. Similarly, "Tricholoma equestre" was widely considered edible and good, until it was connected with rare cases of rhabdomyolysis.

In the fall of 2004, thirteen deaths were associated with consumption of "Pleurocybella porrigens" or "angel's wings". In general, these mushrooms are 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 and the deaths cannot be definitively attributed to mushroom consumption.

However, mushroom poisoning is not always due to mistaken identity. For example, the highly toxic ergot "Claviceps purpurea", which grows on rye, is sometimes ground up with rye, unnoticed, and later consumed. This can cause devastating, even fatal effects, which is called ergotism.

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.

Diarrhetic shellfish poisoning (DSP) is one of the four recognized symptom types of shellfish poisoning, the others being paralytic shellfish poisoning, neurotoxic shellfish poisoning and amnesic shellfish poisoning.

As the name suggests, this syndrome manifests itself as intense diarrhea and severe abdominal pains. Nausea and vomiting may sometimes occur too.

DSP and its symptoms usually set in within about half an hour of ingesting infected shellfish, and last for about one day. A recent case in France, though, with 20 people consuming oysters manifested itself after 36 hours. The causative poison is okadaic acid, which inhibits intestinal cellular de-phosphorylation. This causes the cells to become very permeable to water and causes profuse, intense diarrhea with a high risk of dehydration. As no life-threatening symptoms generally emerge from this, no fatalities from DSP have ever been recorded.