Learn the Mushrooms!

Toxic Mechanism:
Gyromitrin is the primary toxin found in mushrooms of the Gyromitra genus—named from Latin for “folded turban,” a reference to their brain-like appearance. Gyromitrin is metabolized into monomethylhydrazine (MMH), a volatile and highly reactive compound also used in rocket fuel.

MMH inhibits pyridoxal phosphate (the active form of vitamin B6), which is essential for the synthesis of GABA (gamma-aminobutyric acid)—the brain’s primary inhibitory neurotransmitter (also the same neurotransmitter responsible for alcohols effect, its usually sedating). Inhibition of GABA production may lead to excitotoxicity, a form of neurotoxicity caused by excessive neuronal activity.

In addition to its effects on the nervous system, MMH causes oxidative damage to hepatocytes and erythrocytes (liver and red blood cells), which can result in liver injury and methemoglobinemia—a state in which hemoglobin is “rusted” (oxidized) and unable to effectively carry oxygen.

Finally, MMH may also exert genotoxic effects by damaging DNA. Chronic exposure has been linked in one French study to an increased incidence of amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease), though this association remains controversial and unproven. The amount of gyromitrin found in any given mushroom can vary by where it growing in the world and even the altitude it is growing at. 

Syndrome:
Symptoms are delayed—typically 6–12 hours after ingestion—as gyromitrin is gradually converted into MMH. The first signs are gastrointestinal: nausea, vomiting, abdominal pain, and diarrhea. Neurologic symptoms like tremor, agitation, and confusion may follow. Seizures are often described in textbooks but are rarely documented in real-world cases. Liver injury is more common. Some cases may also develop methemoglobinemia (rusted hemoglobin).

Treatment:
Care is supportive only and may include:

• Pyridoxine (vitamin B6) administration (to restore GABA production in patients with neurotoxicity)

• Benzodiazepines or barbiturates for seizures (though benzodiazepines may be less effective in GABA depleted states, as they need GABA to work)

• Methylene blue (if clinically significant methemoglobinemia develops)

Where Found:
Gyromitra mushrooms are found throughout the Northern Hemisphere, including Europe, North America, and parts of Asia. They grow in spring near both hardwood and coniferous trees and are frequently mistaken for edible Morchella (true morels). Cooking or parboiling can reduce gyromitrin content but does not guarantee safety.

Toxicologist Notes:
One of the most hotly debated mushrooms. In some countries like Finland, Gyromitra is sold in markets and considered a delicacy (though must be sold with a warning)—while in others it’s banned outright. Toxicity likely varies due to regional differences in gyromitrin levels, species variation, and individual metabolic susceptibility. Some people tolerate it once, only to get sick with repeat exposures. A French study even linked Gyromitra consumption to ALS cases in Montchavin, though this remains unproven.

Game Notes:

• –3 points if paired with morels (easy mix-up) 

• - 1 point if cooked (hard to ensure safety) 

• +7 points if you have the antidote (B6!)

Example Case:
A 42-year-old man presents to the emergency department with severe vomiting, abdominal pain, and confusion. Symptoms began roughly 10 hours after eating sautéed wild mushrooms he foraged with a friend, who remains asymptomatic. The mushrooms were identified as Gyromitra esculenta, which he believed were true morels. Labs reveal elevated liver enzymes (AST 386, ALT 412). His mental status fluctuates, and a mild tremor is noted. Pulse oximetry reads 93% despite normal respiratory exam; co-oximetry confirms 11% methemoglobinemia. He is treated with supportive care, including IV fluids, pyridoxine, and close monitoring. Seizures do not develop. He improves over 48 hours and is discharged with toxicology follow-up.

Toxin: 

Orellanine is a bipyridine toxin found in several species of Cortinarius mushrooms. It causes oxidative stress by generating reactive oxygen species (ROS)—unstable molecules that damage cells. These ROS selectively injure the renal proximal tubules (the part of the kidney that filters and reabsorbs essential nutrients), leading to progressive interstitial nephritis (inflammation and scarring of kidney tissue) and potentially irreversible kidney failure. 

Orellanine is heat-stable—it is not destroyed by cooking, drying, or freezing. Its long biologic half-life (how long it stays in the body) and tendency to accumulate in tissue lead to a very delayed onset of symptoms, often days to weeks after ingestion. This delay makes diagnosis difficult, and there is no known antidote.

Syndrome: 

Symptoms begin 2 to 20 days after ingestion, depending on the dose and individual metabolism. Early signs are vague: nausea, fatigue, headache, intense thirst, or flu-like symptoms, which often resolve before more serious effects develop. As the kidneys sustain damage, patients develop decreased urine output (oliguria), flank pain, and elevated creatinine (a marker of kidney function). 

By the time patients seek care, they may have acute kidney injury (AKI) or even anuria (no urine at all). In severe cases, electrolyte imbalances (like high potassium) and uremic symptoms (nausea, confusion, or itching from toxin buildup) occur. Death from kidney failure is possible without treatment.

Treatment: 

No antidote exists. Care is supportive only and may include:

• Early involvement of nephrology (kidney specialists)

• Dialysis (a blood-filtering machine, often required if kidneys no longer working)

• Kidney transplant in severe or irreversible cases

Where Found: 

Cortinarius mushrooms grow in Europe, North America, and Asia, especially in forests with hardwood or coniferous trees. They are most common in late summer and fall and may be mistaken for edible mushrooms, especially by inexperienced foragers. 

Notes: 

Though these mushrooms were once thought to be only in Europe, Cortinarius orellanosus was recently discovered in Michigan when it caused poisoning.  Over a decade later, a cortinarius rubellus poisoning occured in Canada (Quebc). While not published in true peer reviewed literature, the number of experts in consensus as detailed by the report, seems convincing. It is more common than we believed but still rare. It is most famous because the author of The Horse Whisperer, Nicholas Evans, was poisoned along with family members—and eventually required a kidney transplant. Diagnosis is hard: by the time kidney failure appears, patients may not remember eating mushrooms. And even if suspected, there is no hospital test for orellanine—it's a clinical diagnosis based on the timing and history. Many non toxic look alikes exist as well (C. caperatus, C. armillatus, C. violaceus).

Game Notes: 

Delayed onset = more damage. The toxicity builds the earlier it is played and you get more points the more turns it is in play. 

Example case: 

A 29-year-old woman comes to the emergency department with fatigue, low urine output, and flank pain (pain near the lower back, where the kidneys are). Blood tests reveal a creatinine level of 8.6 mg/dL (a marker of kidney function that is severely elevated—normal is ~0.6–1.1), and high potassium levels, which can be dangerous to the heart.

She reports that about 10 days ago, she had mild gastrointestinal (GI) symptoms—nausea and stomach upset—after eating wild mushrooms. She felt better the next day and didn’t think much of it. However, her kidneys were silently being damaged.

She had recently foraged in northern Michigan, and a local mycologist (a mushroom expert) later identified leftover mushrooms as a species of Cortinarius, which can contain orellanine, a toxin known to cause delayed kidney failure.

Despite receiving IV fluids and other supportive care, her kidneys do not recover. She requires hemodialysis (a machine that filters her blood when her kidneys can’t), and she is evaluated for a kidney transplant due to permanent renal (kidney) damage.

Toxic Mechanism:
The main toxins are acromelic acids (ACRO-A and ACRO-B), unusual amino acid derivatives found in Paralepistopis (previously Clitocybe) acromelalga (Japan/Korea) and Paralepistopis amoenolens (France/Morocco). ACRO-A is significantly more potent than ACRO-B. These toxins act as glutamate receptor agonists, primarily targeting kainate-type glutamate receptors on small sensory nerve endings in the skin. (In plain terms: they overstimulate nerve endings that sense pain and heat, leading to burning pain and redness in the extremities.)

The toxins also appear to damage tiny nerve fibers by reducing their blood supply (microvascular ischemia), leading to neuropathic pain. Other molecules in these mushrooms, such as clitidine (a toxic nucleoside), may play a secondary role, but the exact mechanism of human intoxication remains under study.

Syndrome:
This poisoning causes erythromelalgia (intense burning pain with redness and swelling of the hands and feet). Symptoms appear unusually late for mushroom poisoning—24 hours to several days after ingestion. The hallmark is severe paroxysmal pain (sudden bursts, often like electric shocks), especially at night, often leading to insomnia. Pain is worsened by warmth, movement, or pressure, but partially relieved by immersion in cold water. (Patients often sit with their feet in cold water for hours just to get relief.)

Other features include erythema (skin redness), edema (swelling), paresthesias (tingling, prickling, or numbness), and sometimes trophic skin injuries like sores between the toes. Fatigue, weakness, and sweating may also occur. Importantly, there are no gastrointestinal symptoms or liver/kidney damage, which distinguishes this from many other toxic mushrooms.

The painful phase can last for weeks. Recovery usually occurs within 1–5 months, but lingering numbness or tingling can persist for years.

Treatment:
No antidote exists. Care is supportive only and may include:

• Cold water immersion provides temporary relief but is not practical long term. 

• Common painkillers like acetaminophen or weak opioids rarely help. Aspirin and morphine have been used with mixed success. The most promising therapy is intravenous nicotinic acid (niacin) at high doses, which has dramatically improved pain and redness in some cases. (Niacin widens blood vessels and reduces oxidative stress in nerves.)

• Other medications (clonazepam, antidepressants, pregabalin) have been tried with inconsistent results. Some patients recover spontaneously, though often after weeks of significant suffering.

Where Found:
Paralepistopis acromelalga grows in Japan and South Korea, typically in bamboo groves in autumn. It resembles edible mushrooms such as Clitocybe gibba or Armillaria mellea, making misidentification easy.

Paralepistopis amoenolens has caused cases in southern France and was first described in Morocco. It grows in cedar forests and alpine valleys and resembles Lepista inversa and Clitocybe gibba.

Game Notes:
A rare mushroom, so very few in the deck, but the most promising treatment seems to be nicotinic acid, grab the antidote to double your points.  

Example Case:

A 35-year-old mountain guide ate mushrooms later identified as Clitocybe amoenolens, mistaking them for edible species. About 24 hours later, he developed severe burning pain in his hands and feet, worsened by heat and movement but partly relieved by cold water. Pain crises occurred every 30 minutes, leading to insomnia, fatigue, swelling, and redness of his ankles. Usual painkillers were ineffective. He was treated with aspirin, clomipramine, and morphine, with partial relief. After six months he still had intermittent pain, and tingling sensations persisted for three years. 

Toxic Mechanism:
No specific chemical toxin has been identified, but Paxillus syndrome is thought to be caused by an immune-mediated reaction (the body’s immune system attacking its own red blood cells). The proposed process is:

• An antigen (a substance that triggers an immune response) in the mushroom causes sensitization (the immune system “remembers” it) in some people after repeated consumption over months or years.

• On subsequent exposure, antibodies (proteins that target the antigen) are released from immune cells and bind to the antigen.

• These antigen–antibody complexes attach to erythrocytes (red blood cells), marking them for destruction (hemolysis).

• This can trigger complement activation (a chain reaction of immune proteins), causing rapid intravascular hemolysis (red cells breaking apart in the bloodstream).

• An IgG antibody against Paxillus involutus extract has been detected in at least one patient, supporting this mechanism.

Syndrome:
A rare, life-threatening reaction to Paxillus involutus, usually after repeated exposure. Begins within 2–3 hours of eating (much faster than amatoxin poisoning) with severe abdominal/back pain, nausea, vomiting, and sometimes diarrhea. This is followed by hemolytic anaemia (immune destruction of red blood cells), causing jaundice (yellowing of skin/eyes from red blood cell products) and red/brown urine. Rapid progression to shock, lactic acidosis, and multi-organ failure is possible.

Treatment:
No antidote—treatment is supportive and aimed at stopping hemolysis, maintaining circulation, and supporting failing organs.

• Anti-shock therapy (IV fluids, vasopressors like noradrenaline if needed)

• Plasma exchange to remove antibodies from the blood—can be lifesaving in severe hemolysis

• Kidney replacement therapy (dialysis) for acute kidney failure

• Liver support (hepatotropic therapy) if liver is affected

• Other measures: sodium bicarbonate for acidosis, hydrocortisone to dampen immune reaction, activated charcoal if ingestion was recent

Where Found:
Widely distributed across the Northern Hemisphere and introduced to South Africa, Australia, and South America. The majority of poisonings are reported from Europe or Turkey, however it it has been reported in parts of North America.

Game Notes:
This is another one where multiple meals seems to be the key to toxicity. One is worth zero but you get more points the more you collect! 

Example Cases:

A 46-year-old man had eaten Paxillus involutus regularly without any problems. About 3 hours after a meal, he developed sudden, severe back pain. His condition quickly worsened, with signs of liver failure, septic shock (dangerously low blood pressure from infection-like inflammation), and disseminated intravascular coagulation—a life-threatening condition where the body forms abnormal blood clots and then bleeds uncontrollably. Despite intensive treatment, he died 4 days later from multi-organ failure. 

Toxic Mechanism:
The main psychoactive compounds are psilocybin and psilocin. Psilocybin is rapidly converted in the body to psilocin, which acts as an agonist (activator) at serotonin 5-HT₂A receptors in the brain. This overstimulates serotonin pathways involved in perception, mood, and thought processing, producing hallucinations, altered sensory experiences, and changes in time perception. Activation of this pathway also appears to increase neuroplasticity (the brain’s ability to form new neuronal connections), which has made psilocybin a promising therapeutic target for mental health disorders such as depression and substance use. It is currently being tested in clinical trials by pharmaceutical companies for potential FDA approval. You can learn more on on going research here from the creator of this game. 

Psilocin’s structure is similar to serotonin, allowing it to cross the blood–brain barrier and bind directly to serotonin receptors. Unlike many poisonous mushrooms, psilocybin-containing species rarely cause direct organ damage—most toxicity comes from central nervous system effects or behavioral risks due to impaired judgment. Though new synsroms are being discovered (see "wood lovers paralysis" below)

Syndrome:
Effects usually begin 20–60 minutes after ingestion, peak at 1–2 hours, and last up to 6–8 hours. Common effects include visual and auditory hallucinations, altered perception of time and space, euphoria, anxiety, and impaired coordination. Physical effects may include nausea, vomiting, dilated pupils, increased heart rate (tachycardia), elevated blood pressure, sweating, and tremors.

In rare cases—especially with very high doses or in individuals with underlying mental health conditions—severe agitation, panic, paranoia, or psychosis can occur. A theoretical risk of serotonin syndrome (dangerous excess serotonin activity) exists, but it has not been documented in the medical literature from psilocybin use. Hallucinogen persisting perception disorder (HPPD), a rare condition with ongoing visual disturbances, has been reported. Uniquely, one case of psilocybe cubensis associated acute kidney injury has also been reported.  

From a toxicology perspective, most emergency visits are due to confusion or unsafe behavior rather than direct toxicity—such as walking into traffic or jumping from heights. “Set and setting” (mental state and environment) are crucial, as these are powerful psychoactive substances. With rising use in the United States, there is also theoretical concern for heart valve disorders with chronic use, similar to other drugs that stimulate serotonin pathways, though this remains unproven. 

There is also a recent phenomeonom that has been discovered when these mushrooms are foraged from trees. "Wood Lovers Paralysis". It is progressive muscle weakness, sometimes leading to difficulty swallowing and breathing. It generally comes on within 4 hours and lasts several hours but is reversible. The mechanism behind this syndrome is unknown but primarily linked to Psilocybe azurescens, Psilocybe cyanescens, and Psilocybe subaeruginosa.

Treatment:
No antidote exists. Care is supportive:

• Reassurance in a quiet, low-stimulation environment

• Benzodiazepines (e.g., lorazepam) for severe anxiety or agitation

• The use of serotonin antagonist drugs to "shut down the trip" has been discussed by researchers. An example of these drugs would be risperidone.

• IV fluids if dehydrated from vomiting or sweating

• Observation until mental status returns to baseline

• Patients with dangerous behavior or psychosis may require temporary hospitalization for safety.

Where Found:
Psilocybin-containing mushrooms occur worldwide, with hundreds of species in the genera Psilocybe, Panaeolus, Gymnopilus, and Pluteus. Common species include Psilocybe cubensis, P. semilanceata (liberty cap), and P. cyanescens (wavy cap). They grow in grasslands, pastures, forest debris, and wood chips. Potency varies widely between species and even between individual mushrooms. 

Game Notes:

One of my favorite game mechanics: whoever collects the most by the end of the game gets +10 points, while everyone else gets –5. Since psilocybin use is associated with increased gratitude (valuing what you have), you can expend two psilocybin cards already in play to double the value of your next card. Just don’t overdo it—or you might lose the race!

Example Cases:

A 22-year-old man ate several Psilocybe cubensis mushrooms at a music festival. About 45 minutes later, he experienced vivid visual hallucinations, euphoria, and impaired coordination. Two hours in, he became anxious and disoriented, wandering into a restricted area. Security escorted him to onsite medical staff, who noted dilated pupils, elevated heart rate (110 bpm), and mild dehydration. He was given oral fluids, moved to a quiet area, and reassured. Symptoms resolved after about 6 hours, and he was discharged without complications.

Toxic Mechanism:
The primary active compounds in Amanita muscaria (fly agaric) and Amanita pantherina (panther cap) are ibotenic acid (also called pantherine or agarine) and muscimol, concentrated in the red skin and yellow tissue beneath the cap. Ibotenic acid is structurally similar to glutamic acid (an excitatory neurotransmitter) and acts on glutamate receptors, stimulating the central nervous system (CNS). Muscimol is structurally similar to GABA (the brain’s primary inhibitory neurotransmitter) and acts as a potent agonist at GABA A receptors, producing sedative, hypnotic, and psychoactive effects.

Ibotenic acid is rapidly converted into muscimol in the body (and during drying or heating), which is believed to cause most of the symptoms. This conversion also reduces some toxicity while preserving psychoactive effects. Other compounds, such as muscarine (binds acetylcholine receptors, affecting heart rate, sweating, and blood vessels), are present in small but sometimes physiologically relevant amounts. Additional minor constituents include muscazone, choline, acetylcholine, betaine, tropane alkaloids (e.g., atropine, scopolamine), and bufotenine, though their clinical significance is unclear.

Syndrome:
Symptoms usually appear 20 minutes to 3 hours after ingestion and last 8–24 hours (though delirium, psychosis,  and even coma, can sometimes last several days in severe cases) Effects often alternate between CNS stimulation (central nervous system excitation, such as agitation or hallucinations) and CNS depression (drowsiness, confusion, or coma).

• CNS effects: Dizziness, confusion, disorientation, fatigue, euphoria (intense feelings of well-being), anxiety, vivid visual and auditory hallucinations, altered color perception, distortions of space and time, ataxia (impaired balance or coordination), tremors, and myoclonic jerks (sudden muscle twitches). Severe cases can progress to seizures, coma, or respiratory failure (breathing stops or becomes ineffective).

• GI symptoms: Nausea, vomiting, diarrhea, and abdominal pain (less prominent than in many other toxic mushrooms).

• Other physical signs: Flushed face, dry mouth, hyperhidrosis (excessive sweating), pupils that are either dilated (mydriasis) or constricted (miosis), variable heart rate (tachycardia = fast, bradycardia = slow), and blood pressure changes (high or low). Metabolic acidosis (excess acid in the blood) may occur in severe cases.

Treatment:
There is no specific antidote. Management is supportive (focused on treating symptoms and preventing complications) and may include:

• Decontamination: Activated charcoal (binds toxins in the gut to limit absorption) is preferred; older methods included gastric lavage (“stomach pumping”) are reported in cases but almost never performed.

• Supportive care: IV fluids to maintain hydration, correct electrolyte imbalances, and protect the kidneys—especially if seizures cause muscle breakdown (rhabdomyolysis) releasing harmful proteins into the blood.

• Symptom control: Benzodiazepines or barbiturates for agitation, anxiety, or seizures.

• Airway protection: Intubation (placing a breathing tube) and mechanical ventilation in cases of coma or severe breathing problems.

Where Found:
A. muscaria is common across the Northern Hemisphere, often under birch and coniferous trees, and has been introduced to South Africa, Australia, and South America. Found from July–November in Europe, with notable prevalence in Poland and the UK. Recreational use has led to increased regulation in some countries (e.g., Lithuania will classify it as a controlled substance in 2025). A. pantherina has a similarly wide distribution across Asia, Europe, North America, and parts of the Southern Hemisphere. There are variants of these mushrooms just about everywhere (note the "See Also" section below). 

Game Notes:

While some may “forage” these for their reported psychoactive effects, it’s very easy to overdo it—real-life case reports frequently describe severe toxicity (seizures, coma, death). In-game, collect 1 for +7 points, but pick up more than that and you’ll start losing points, as too many land people in intensive care. With the wildly variable content of these psychoactive compounds, even one seems like a gamble in real life, good things its just a game! 

Example Cases:

A 44-year-old man in Switzerland consumed approximately 0.5 kg of Amanita muscaria, mistaking it for the edible Amanita caesarea (the white surface patches had washed off in heavy rain). About 90 minutes later, he developed dizziness, confusion, and ataxia (loss of coordination), followed by drowsiness and eventual coma. On arrival to the hospital, he had a Glasgow Coma Scale of 5 (indicating deep unconsciousness) but stable vital signs. He was given IV fluids and close monitoring of airway and breathing. His coma persisted for 24 hours before gradually resolving. He was discharged on hospital day 2 with no lasting medical problems. 

Toxic Mechanism:
Muscarine is an alkaloid (naturally occurring plant/fungal compound) and a quaternary ammonium compound that stimulates the parasympathetic nervous system (the branch of the nervous system that promotes “rest and digest” functions). It acts as a muscarinic acetylcholine receptor (AChR) agonist—meaning it binds to and activates muscarinic AChRs. These are G-protein-coupled receptors found throughout the body, controlling functions such as heart rate, digestion, glandular secretions, and smooth muscle tone.

Activation of these receptors causes a cholinergic toxidrome (symptoms of acetylcholine overactivity), including excessive glandular secretions, slowed heart rate, and airway constriction. Muscarine is water-soluble and thermostable (not destroyed by cooking), so cooking does not make contaminated mushrooms safe.

Syndrome:
Symptoms usually begin 30 minutes to 4 hours after eating a muscarine-containing mushroom and generally resolve within 24 hours. Most cases are mild and self-limiting, but severe poisonings can be fatal. The illness is marked by a classic “cholinergic toxidrome,” with profuse sweating—often considered the key sign distinguishing muscarinic mushrooms from other gastrointestinal toxins—alongside nausea, vomiting, and diarrhea, which affect up to 90% of patients. Other hallmark features include hypersalivation (excessive drooling or frothing), lacrimation (excess tearing), bradycardia (slow heart rate), and respiratory effects such as bronchorrhea (excess fluid in the airways), bronchospasm (airway narrowing that causes wheezing or shortness of breath), and miosis (constricted pupils). Patients may also develop abdominal cramps, irritability, exhaustion, lethargy, muscle cramps, blurred vision, ptosis (drooping eyelids), cough, tachypnea (rapid breathing), rhonchi (coarse breath sounds from mucus), and hypotension (low blood pressure). Less commonly, altered mental status, confusion, pulmonary edema (fluid in the lungs), respiratory distress, numbness in the legs, and unexpected drowsiness may occur, despite muscarine’s inability to cross the blood–brain barrier. In some cases, mild elevations in liver enzymes or kidney injury can develop due to dehydration from persistent vomiting and diarrhea. 

Treatment:
Atropine is an effective antidote for severe muscarine toxicity.

• Mild cases: Supportive care only—oral or IV fluids for dehydration and electrolyte correction.

• Moderate to severe cases:

  • Atropine (an anticholinergic drug) given IV to block muscarinic receptors.

  • Fluid resuscitation to correct dehydration and support blood pressure.

  • Continuous monitoring of heart rate, blood pressure, oxygenation, and breathing.

• Decontamination: Activated charcoal may be given if early after ingestion; but given the profuse vomiting that may occur from muscarine, this could be high risk and should be reserved for those who would be deemed to tolerate it (airway protected and minimal nausea) 

• Most patients recover within hours with proper care; death is rare but documented.

Where Found:
Clinically significant muscarine levels occur in several unrelated mushroom groups:

• Most common: Inocybe species and Clitocybe species

  • Examples: Clitocybe dealbata, C. illudens, Inocybe agardhii, I. rimosa, I. erubescens, and many others across North America, Europe, and tropical regions.

• Also found in:

  • Amanita muscaria (first species where muscarine was identified)

  • Entoloma, Omphalotus, Mycena, Boletus, Hygrocybe, Lactarius, and Russula species

• Many muscarinic mushrooms resemble edible varieties and may grow in urban lawns, parks, and wooded areas during rainy seasons.

Game Notes:
These mushrooms hit hard and fast, you get more points as you collect more in the toxin group, but the biggest amplifier is grabbing the antidote, atropine! +2 for each mushroom with atropine!

Example Cases:

An 88-year-old woman ate Clitocybe mushrooms from her yard. Within hours she developed diaphoresis, nausea, vomiting, diarrhea, altered mental status, and respiratory distress. She died within 7 hours; her husband, who ate less, had mild symptoms and survived. Autopsy confirmed Clitocybe ingestion.