Quick Reference — All 8 Species
| Mushroom | Toxin | Onset | Severity |
|---|---|---|---|
| Death Cap Amanita phalloides |
Amatoxins (α-amanitin) | 6–24 hr (delayed) | 4 — Potentially Fatal |
| Destroying Angel Amanita ocreata |
Amatoxins (α-amanitin) | 6–24 hr (delayed) | 4 — Potentially Fatal |
| Deadly Galerina Galerina marginata |
Amatoxins (α-amanitin) | 6–24 hr (delayed) | 4 — Potentially Fatal |
| Deadly Webcap Cortinarius rubellus |
Orellanine | 2–3 weeks (extreme delay) | 4 — Potentially Fatal |
| Fly Agaric Amanita muscaria |
Ibotenic acid / Muscimol | 30 min–2 hr (fast) | 3 — Life-Threatening |
| False Morel Gyromitra esculenta |
Gyromitrin (MMH) | 6–12 hr (delayed) | 3 — Life-Threatening |
| Jack-o’-Lantern Omphalotus olivascens |
Illudin S | 30 min–2 hr (fast) | 2 — Serious |
| Panther Cap Amanita pantherina |
Ibotenic acid / Muscimol | 30 min–2 hr (fast) | 3 — Life-Threatening |
Quick reference covers the eight most clinically critical Pacific Coast species. A complete tiered reference with all 16 species is available below.
Death Cap
Amanita phalloides
Severity 4 — Potentially Fatal
Delayed onset 6–24 hr ⚠
🔍 Field Identification Details
Toxin Type
Amatoxins — primarily α-amanitin. Cyclopeptide toxins that inhibit RNA polymerase II, causing cell death in hepatocytes and renal tubular cells.
Onset Time
Gastrointestinal phase: 6–24 hours post-ingestion. Hepatotoxic phase: 24–72 hours. "Honeymoon period" of apparent improvement precedes organ failure at 48–96 hours.
Severity Rating
4 / 4 — Potentially Fatal
Responsible for ~90% of mushroom fatalities worldwide. Lethal dose as low as half a cap (~35g fresh weight).
Responsible for ~90% of mushroom fatalities worldwide. Lethal dose as low as half a cap (~35g fresh weight).
Symptoms by Organ System
Gastrointestinal (6–24 hr)
- Severe nausea, vomiting, watery diarrhea (can be cholera-like)
- Abdominal cramping, dehydration, electrolyte imbalance
Hepatic (24–96 hr)
- Rising AST/ALT — can exceed 10,000 U/L
- Jaundice, coagulopathy (elevated PT/INR)
- Fulminant hepatic failure, hepatic encephalopathy
Renal
- Acute tubular necrosis, oliguria
- Rising creatinine; may require dialysis
Clinical Notes
⚠ Deceptive "Honeymoon Period": After the initial GI phase resolves (24–36 hr), patients often feel substantially better and may be discharged. This is a dangerous false recovery — hepatotoxic phase is just beginning. Admit all suspected Amanita phalloides ingestions regardless of apparent improvement.
⚠ Delayed presentation: The 6+ hour delay between ingestion and GI symptoms is diagnostic — early-onset GI illness within 2 hours strongly suggests a different toxin (e.g. muscarine, illudin). Delayed onset = amatoxins until proven otherwise.
⚠ Urine amanitin testing: Available at some reference labs. Positive confirmation aids diagnosis but should not delay treatment.
⚠ Delayed presentation: The 6+ hour delay between ingestion and GI symptoms is diagnostic — early-onset GI illness within 2 hours strongly suggests a different toxin (e.g. muscarine, illudin). Delayed onset = amatoxins until proven otherwise.
⚠ Urine amanitin testing: Available at some reference labs. Positive confirmation aids diagnosis but should not delay treatment.
Treatment Direction
Immediate: Activated charcoal if <2 hr post-ingestion (or earlier estimated given delayed GI onset). Aggressive IV fluid replacement for dehydration.
Specific antidote consideration: Silibinin (milk thistle extract, IV) — inhibits hepatocyte uptake of amatoxins. Available via compassionate use in US (contact Poison Control for access). Penicillin G (high-dose IV) may also reduce hepatotoxicity.
Monitoring: Serial LFTs, PT/INR, creatinine every 6–12 hr. Early hepatology and transplant surgery consultation. Liver transplant may be only option in fulminant failure.
Specific antidote consideration: Silibinin (milk thistle extract, IV) — inhibits hepatocyte uptake of amatoxins. Available via compassionate use in US (contact Poison Control for access). Penicillin G (high-dose IV) may also reduce hepatotoxicity.
Monitoring: Serial LFTs, PT/INR, creatinine every 6–12 hr. Early hepatology and transplant surgery consultation. Liver transplant may be only option in fulminant failure.
☏ Poison Control: 1-800-222-1222 — call immediately for case management guidance
Destroying Angel
Amanita ocreata
Severity 4 — Potentially Fatal
Delayed onset 6–24 hr ⚠
🔍 Field Identification Details
Toxin Type
Amatoxins — α-amanitin and phallotoxins. Identical toxin profile to Amanita phalloides. Pure white appearance makes it especially dangerous — no warning coloration.
Onset Time
GI phase: 6–24 hours. Hepatic phase: 24–72 hours. Same biphasic presentation as Death Cap including the deceptive honeymoon period.
Severity Rating
4 / 4 — Potentially Fatal
Symptoms by Organ System
Gastrointestinal (6–24 hr)
- Severe vomiting, profuse watery diarrhea
- Severe dehydration, electrolyte disturbance
Hepatic (24–96 hr)
- Rapid rise AST/ALT, jaundice
- Coagulopathy, encephalopathy
- Fulminant hepatic failure
Renal
- Acute tubular necrosis, renal failure
Clinical Notes
Pacific Coast native — identical to A. phalloides clinically. A. ocreata is endemic to California, Oregon, and Washington and fruits in spring, often under live oak (Quercus agrifolia) and other oaks — when Death Cap activity peaks in fall. The pure white coloration is a major confusion risk; novice foragers mistake it for edible white mushrooms (button mushrooms, puffballs, paddy straw mushroom). Also clinically relevant: the closely related Western Destroying Angel (Amanita elliptoides) occurs in the Pacific Northwest under conifers and carries the same amatoxin profile.
Apply the same treatment protocol as Death Cap. All white Amanita specimens with a cup-shaped volva at the stem base and delayed GI onset should be treated as amatoxin poisoning.
Apply the same treatment protocol as Death Cap. All white Amanita specimens with a cup-shaped volva at the stem base and delayed GI onset should be treated as amatoxin poisoning.
Treatment Direction
Identical to Death Cap (A. phalloides). Activated charcoal, aggressive IV fluids, serial LFTs, hepatology consult, silibinin consideration via Poison Control. Liver transplant evaluation for severe cases.
Deadly Galerina
Galerina marginata
Severity 4 — Potentially Fatal
Delayed onset 6–24 hr ⚠
🔍 Field Identification Details
Toxin Type
Amatoxins (α-amanitin). A small, inconspicuous brown mushroom with amatoxin levels comparable to Amanita phalloides per gram of fresh weight.
Onset Time
GI symptoms: 6–24 hours. Hepatic injury: 24–72 hours. Same biphasic pattern.
Severity Rating
4 / 4 — Potentially Fatal
Symptoms by Organ System
Gastrointestinal
- Nausea, vomiting, diarrhea (delayed 6–24 hr)
Hepatic
- Transaminase elevation, jaundice
- Coagulopathy, hepatic failure
Renal
- Acute tubular necrosis (dose-dependent)
Clinical Notes
The "LBM trap": Galerina marginata is a classic "Little Brown Mushroom" that is commonly confused with edible species — particularly Pholiota species, honey mushrooms (Armillaria), and some oyster mushrooms. It frequently grows in the same habitat as chanterelles and edible species.
Clusters on wood: Grows on dead or decaying wood in dense clusters. Multiple family members may present simultaneously after a shared meal — treat all as amatoxin poisoning.
Clusters on wood: Grows on dead or decaying wood in dense clusters. Multiple family members may present simultaneously after a shared meal — treat all as amatoxin poisoning.
Treatment Direction
Same protocol as Death Cap. Activated charcoal if early. Serial liver function monitoring. Silibinin and penicillin G considered via Poison Control. Hepatology and transplant surgery consult for elevated LFTs.
Deadly Webcap
Cortinarius rubellus (syn. C. speciosissimus)
Severity 4 — Potentially Fatal
Extreme delay: 2–3 weeks ⚠
🔍 Field Identification Details
Toxin Type
Orellanine — a bipyridine N-oxide toxin that generates free radicals in renal tubular cells, causing progressive nephrotoxicity. No known antidote.
Onset Time
2–3 weeks for renal symptoms. Mild flu-like prodrome possible at 3–5 days. Extreme delay means ingestion is often not reported and diagnosis is missed.
Severity Rating
4 / 4 — Potentially Fatal
Leading cause of mushroom-induced renal failure requiring transplant in Europe.
Leading cause of mushroom-induced renal failure requiring transplant in Europe.
Symptoms by Organ System
Early (3–5 days — subtle)
- Nausea, headache, malaise, myalgia
- Polydipsia, polyuria (early tubular dysfunction)
Renal (2–3 weeks)
- Oliguria progressing to anuria
- Rising creatinine and BUN — rapidly progressive renal failure
- Flank pain, hematuria
- Irreversible renal failure requiring dialysis or transplant
Systemic
- Nausea, vomiting, weight loss in subacute phase
Clinical Notes
⚠ Critical diagnostic challenge: The 2–3 week delay means the patient has typically forgotten about the mushroom meal by the time renal failure presents. Take a dietary history going back 3–4 weeks in any unexplained acute renal failure — ask specifically about foraged or wild mushrooms.
⚠ No GI phase: Unlike amatoxin poisoning, there is no early gastroenteritis to trigger medical attention. Orellanine poisoning often presents directly as established renal failure.
Orellanine is excreted in urine and detectable by HPLC but this is not widely available clinically.
⚠ No GI phase: Unlike amatoxin poisoning, there is no early gastroenteritis to trigger medical attention. Orellanine poisoning often presents directly as established renal failure.
Orellanine is excreted in urine and detectable by HPLC but this is not widely available clinically.
Treatment Direction
No specific antidote. Activated charcoal is unlikely to be useful given extreme delay. Supportive care: aggressive hydration, monitor renal function closely. Nephrology consultation immediately. Dialysis for renal failure. Renal transplant may be required for irreversible injury. High-dose steroids are sometimes used (evidence limited).
Fly Agaric
Amanita muscaria
Severity 3 — Life-Threatening
Fast onset: 30 min–2 hr
🔍 Field Identification Details
Toxin Type
Ibotenic acid and muscimol — isoxazole derivatives. Ibotenic acid is a glutamate receptor agonist; muscimol is a GABA-A agonist. Together produce a dissociative / hallucinogenic toxidrome. Also contains muscarine in small amounts.
Onset Time
30 minutes to 2 hours. Fast onset is key diagnostic indicator.
Severity Rating
3 / 4 — Life-Threatening
Rarely fatal in adults; high risk in children and elderly from respiratory depression and seizures.
Rarely fatal in adults; high risk in children and elderly from respiratory depression and seizures.
Symptoms by Organ System
Neurological (primary)
- Confusion, agitation, delirium
- Hallucinations (visual, auditory), euphoria
- Ataxia, dysmetria, dizziness
- Seizures (especially in children)
- CNS depression, sedation, coma (severe)
Gastrointestinal
- Nausea, vomiting (early phase)
Autonomic (if muscarine component)
- Mild salivation, lacrimation, diaphoresis
Clinical Notes
Isoxazole toxidrome — distinct from muscarine (cholinergic) toxidrome. CNS effects dominate. Patients may appear intoxicated or psychotic. Anticholinergic-like features (mydriasis, dry mouth) can occur, making it resemble anticholinergic toxidrome.
Intentional ingestion: Sometimes consumed recreationally for hallucinogenic effects. Patient history may be unreliable.
Duration typically 4–8 hours, occasionally up to 24 hours.
Intentional ingestion: Sometimes consumed recreationally for hallucinogenic effects. Patient history may be unreliable.
Duration typically 4–8 hours, occasionally up to 24 hours.
Treatment Direction
Primarily supportive. Activated charcoal if early and patient is alert. Benzodiazepines for agitation or seizures. Atropine is NOT indicated (and may worsen CNS symptoms). Physostigmine has been used but is not standard. Airway protection for CNS depression. Monitor for respiratory depression in children.
False Morel
Gyromitra esculenta
Severity 3 — Life-Threatening
Delayed onset 6–12 hr ⚠
🔍 Field Identification Details
Toxin Type
Gyromitrin — a volatile hydrazine compound that hydrolyzes to monomethylhydrazine (MMH). MMH inhibits pyridoxal phosphate (vitamin B6), disrupting GABA synthesis and producing a toxidrome resembling hydrazine poisoning / INH toxicity.
Onset Time
6–12 hours (range 2–24 hr). Delayed onset signals hepatotoxic potential.
Severity Rating
3 / 4 — Life-Threatening
Can be fatal. Fatality rate lower than amatoxins but significant. Raw consumption far more dangerous than cooked.
Can be fatal. Fatality rate lower than amatoxins but significant. Raw consumption far more dangerous than cooked.
Symptoms by Organ System
Gastrointestinal (primary)
- Nausea, vomiting, diarrhea, abdominal pain
- Bloating, cramping (6–12 hr onset)
Neurological
- Headache, dizziness, weakness
- Seizures (refractory, B6-responsive)
- Confusion, agitation
Hepatic / Hematological
- Hemolysis — hemolytic anemia, jaundice, hemoglobinuria
- Hepatotoxicity — transaminase elevation
- Methemoglobinemia (MMH mechanism)
Renal
- Renal failure secondary to hemolysis and hepatic failure
Clinical Notes
Morel look-alike: Gyromitra is commonly confused with true morels (Morchella spp.) — one of the most dangerous ID errors in North American foraging. Gyromitra has brain/saddle-shaped cap vs. morel's honeycomb cap. Confusion is most common in spring.
Volatile toxin: Gyromitrin is partially volatilized by cooking and by drying, which is why some foraging traditions consider it "safe when parboiled." Not reliably detoxified — treat as toxic regardless of preparation method. Inhalation of steam from cooking can also cause symptoms in bystanders.
B6-responsive seizures: Pyridoxine (vitamin B6) is a critical component of treatment.
Volatile toxin: Gyromitrin is partially volatilized by cooking and by drying, which is why some foraging traditions consider it "safe when parboiled." Not reliably detoxified — treat as toxic regardless of preparation method. Inhalation of steam from cooking can also cause symptoms in bystanders.
B6-responsive seizures: Pyridoxine (vitamin B6) is a critical component of treatment.
Treatment Direction
Activated charcoal if early. IV fluids. Pyridoxine (vitamin B6) 25 mg/kg IV for seizures — this is the specific antidote mechanism (replaces B6 depleted by MMH). Benzodiazepines for refractory seizures. Monitor CBC for hemolysis, methemoglobin level. Methylene blue for significant methemoglobinemia. Monitor LFTs and renal function.
Jack-o-Lantern
Omphalotus olivascens (Pacific Coast Jack-o’-Lantern)
Severity 2 — Serious
Fast onset: 30 min–2 hr
🔍 Field Identification Details
Toxin Type
Illudin S (and illudin M) — sesquiterpene cytotoxins that cause intense GI irritation. No systemic organ toxicity in typical doses.
Onset Time
30 minutes to 2 hours. Fast onset, self-limiting GI illness.
Severity Rating
2 / 4 — Serious
Not typically life-threatening in adults. Profuse vomiting and diarrhea; dehydration risk, especially in children and elderly.
Not typically life-threatening in adults. Profuse vomiting and diarrhea; dehydration risk, especially in children and elderly.
Symptoms by Organ System
Gastrointestinal (primary)
- Profuse, forceful vomiting (hallmark)
- Severe watery diarrhea
- Intense abdominal cramping
- Nausea, diaphoresis during acute phase
Systemic (secondary)
- Dehydration, electrolyte imbalance
- Weakness, pallor during acute GI phase
- Resolution typically within 6–12 hours
Clinical Notes
Pacific Coast chanterelle look-alike: Most commonly confused with golden chanterelles (Cantharellus californicus, C. cibarius) — among the most popular foraged edibles in California and the PNW. Key differences: Jack-o’-Lanterns (O. olivascens) grow in dense clusters at the base of oaks or eucalyptus; chanterelles grow singly from soil. Jack-o’-Lanterns glow faint blue-green in the dark (bioluminescent).
Reassuring prognosis: Unlike amatoxin poisonings, Jack-o-lantern illness is purely GI and self-limiting. No hepatic or renal involvement. Resolution within 12–24 hours typical.
Early-onset GI illness (<2 hr) after mushroom ingestion helps distinguish from amatoxins (6+ hr onset).
Reassuring prognosis: Unlike amatoxin poisonings, Jack-o-lantern illness is purely GI and self-limiting. No hepatic or renal involvement. Resolution within 12–24 hours typical.
Early-onset GI illness (<2 hr) after mushroom ingestion helps distinguish from amatoxins (6+ hr onset).
Treatment Direction
Supportive care. IV fluids and antiemetics for dehydration and symptom control. No specific antidote needed. No activated charcoal indication given self-limiting course. Admit for IV hydration if severe dehydration. Monitor for electrolyte disturbances. Reassure regarding good prognosis.
Little Brown Mushrooms (LBMs)
Inocybe spp. and Clitocybe spp. (various)
Severity 3 — Life-Threatening
Fast onset: 15 min–2 hr
🔍 Field Identification Details
Toxin Type
Muscarine — a parasympathomimetic alkaloid that acts as a muscarinic acetylcholine receptor agonist, producing a cholinergic toxidrome (SLUDGE/DUMBELS).
Onset Time
15 minutes to 2 hours. Rapid cholinergic presentation.
Severity Rating
3 / 4 — Life-Threatening
Life-threatening in large doses or in vulnerable patients (cardiac, pulmonary). Bronchospasm and bradycardia are the most dangerous features.
Life-threatening in large doses or in vulnerable patients (cardiac, pulmonary). Bronchospasm and bradycardia are the most dangerous features.
Symptoms by Organ System
Cholinergic (SLUDGE) — Full Toxidrome
- Salivation — hypersalivation, drooling
- Lacrimation — excessive tearing
- Urination — urinary incontinence
- Defecation, GI distress — diarrhea, cramping
- Emesis — nausea, vomiting
Cardiovascular
- Bradycardia, hypotension
- Possible cardiac arrest (severe)
Respiratory
- Bronchospasm, bronchorrhea
- Respiratory distress — most dangerous feature
Ophthalmological
- Miosis (pinpoint pupils)
Clinical Notes
Classic cholinergic toxidrome. SLUDGE/DUMBELS mnemonic applies. Presentation can mimic organophosphate poisoning — ask about pesticide exposure as differential. Miosis + bradycardia + bronchospasm + hypersalivation = muscarine until proven otherwise.
Note on A. muscaria: Despite its name, Amanita muscaria contains very little muscarine. Its primary toxidrome is isoxazole (neurological), not cholinergic. Muscarine toxidrome = Inocybe / Clitocybe species in practice.
Many LBM species: Inocybe and Clitocybe comprise hundreds of species, most nondescript brown or gray mushrooms. Definitive species ID is rarely possible. Treat the toxidrome, not the species.
Note on A. muscaria: Despite its name, Amanita muscaria contains very little muscarine. Its primary toxidrome is isoxazole (neurological), not cholinergic. Muscarine toxidrome = Inocybe / Clitocybe species in practice.
Many LBM species: Inocybe and Clitocybe comprise hundreds of species, most nondescript brown or gray mushrooms. Definitive species ID is rarely possible. Treat the toxidrome, not the species.
Treatment Direction
Atropine is the antidote — competitive antagonist at muscarinic receptors. Dose: 1–2 mg IV (adult) every 5–10 minutes until bronchorrhea dries; may require large cumulative doses. Titrate to secretions, not heart rate. Bronchospasm is priority — early intubation if airway threatened. Activated charcoal if alert and airway protected. Do NOT use pralidoxime (2-PAM) — not effective for muscarine (only for organophosphate). Monitor cardiac rhythm continuously.
⚠ Tier 1 — Life-Threatening
Tier 1 — Life-Threatening (Full Profiles)
All species in this tier can cause death or permanent organ failure. Amatoxin species — Death Cap (A. phalloides), Destroying Angel (A. ocreata), Deadly Galerina (G. marginata), Western Destroying Angel (A. elliptoides), and Deadly Dapperling (L. brunneoincarnata) — feature critical delayed onset of 6–24 hours followed by an apparent-recovery phase that must NOT result in discharge. The Deadly Webcap and Sorrel Webcap (orellanine nephrotoxin) have an extreme 2–3 week delay before renal symptoms appear. Detailed quick-reference profiles for Death Cap, Destroying Angel, Deadly Galerina, and Deadly Webcap appear in the top section above; expanded profiles for additional Tier 1 species follow.
⚠ Tier 2 — Serious Toxicity
Tier 2 — Serious but Not Typically Fatal
The species below cause significant medical harm including neurological toxidromes, severe gastrointestinal injury, hemolysis, or multi-organ stress. Fatalities occur but are uncommon compared to Tier 1 amatoxin and orellanine species. All require clinical evaluation; some require hospitalization and organ-function monitoring. Always contact Poison Control (1-800-222-1222) for any suspected ingestion.
Jack-o’-Lantern Mushroom
Omphalotus olivascens (Pacific Coast Jack-o’-Lantern)
Tier 2 — Serious
Severity 2 — Serious
Onset 30 min–2 hr (fast)
🔍 Field Identification Details
Toxin Type
Illudin S and illudin M — sesquiterpene compounds that inhibit DNA repair and RNA synthesis. Concentrated in both fresh and cooked mushroom tissue.
Key Identification Features
- Cap orange to orange-brown with olive tones (distinguishes it from the more purely orange eastern O. illudens); 5–15 cm
- Grows in large clusters at the base of dead or dying hardwood trees — oaks and eucalyptus are primary hosts in California
- Gills are true gills, crowded, running down the stem (decurrent) — not forked like chanterelles
- Stem often off-center; cap may be 5–20 cm across
- Gills glow faintly green in total darkness (bioluminescence) — diagnostic if observable
Onset & Duration
30 minutes to 2 hours after ingestion. GI illness resolves in most cases within 6–12 hours. Rarely progresses to systemic illness. Severity correlates with quantity consumed.
Symptoms
Gastrointestinal (primary)
- Severe nausea, vomiting — often projectile
- Profuse watery diarrhea, abdominal cramping
- Symptoms may be severe enough to cause dehydration
Systemic (rare, large ingestion)
- Transient mild LFT elevation reported in some cases
- Headache, muscle weakness, diaphoresis
First Responder Guidance
IV fluid replacement for dehydration. Activated charcoal if alert and within 1–2 hours of ingestion. Anti-emetics for symptom control. Monitor for dehydration and electrolyte imbalance. Most cases managed with supportive care; hospital admission seldom required unless dehydration is severe. No specific antidote.
Clinical Notes
Most common confusion: Patients frequently mistake the Pacific Coast Jack-o’-Lantern (O. olivascens) for edible golden chanterelles (Cantharellus californicus, C. cibarius). Both are orange and grow near oaks, but chanterelles have forked ridges (not true gills), grow singly from soil, and lack the clustered base-of-tree growth habit. The Pacific Coast chanterelle (C. californicus) is one of the most sought-after edible fungi in California — this confusion is extremely common in foraging communities. Ask specifically about cluster growth from wood or buried roots.
Cooking does not neutralize toxins. Illudins are heat-stable. Thorough cooking of large quantities still causes illness.
Cooking does not neutralize toxins. Illudins are heat-stable. Thorough cooking of large quantities still causes illness.
☏ Poison Control: 1-800-222-1222 — call for case management guidance
Panther Cap
Amanita pantherina
Tier 2 — Serious
Severity 3 — Life-Threatening
Onset 30 min–2 hr (fast)
🔍 Field Identification Details
Toxin Type
Ibotenic acid and muscimol — isoxazole compounds acting on GABA-A and NMDA receptors. Higher concentrations than A. muscaria, making it more dangerous per gram. No amatoxins.
Key Identification Features
- Cap brown to grayish-brown, 5–12 cm; scattered white warts from universal veil remnants
- White free gills; membranous ring on upper stem
- Stem base with bulb and collar-like volva rim (not a true cup like Death Cap)
- Flesh white throughout — does NOT flush pink or red when cut (unlike edible Blusher)
- Associated with conifers and mixed woods throughout the Pacific Coast; among the most common toxic mushroom calls to Pacific Northwest poison centers
Onset & Duration
30 minutes to 2 hours. Peak neurological effects at 1–3 hours. Duration typically 6–8 hours but can persist up to 24 hours in severe cases. No delayed organ toxicity phase (no amatoxins).
Symptoms
Neurological (primary — isoxazole toxidrome)
- Confusion, disorientation, delirium, hallucinations
- Ataxia, muscle twitching, myoclonic jerks
- Sedation alternating with agitation; coma in severe cases
- Hyperthermia, tachycardia, mydriasis (dilated pupils)
Gastrointestinal
- Nausea, vomiting (may be absent — toxidrome can present without prominent GI)
First Responder Guidance
Supportive care; airway protection is priority. Benzodiazepines for agitation or seizures. Do NOT use physostigmine. Activated charcoal if alert and airway protected. Monitor temperature, BP, and cardiac rhythm. Most patients recover within 12–24 hours with supportive management. Admit for observation in any symptomatic case. Consult toxicology.
Clinical Notes
More toxic than A. muscaria: The Panther Cap typically contains higher ibotenic acid concentrations than Fly Agaric and is responsible for more serious poisonings. Do not treat as equivalent to Fly Agaric based on name alone — clinical severity may exceed expectations.
Confusion with edible Blusher (A. rubescens): The most common misidentification. Key differential: Blusher flesh reddens (blushes) when cut or bruised; Panther Cap flesh remains white. Also confused with other brown-capped Amanita species in the field.
Confusion with edible Blusher (A. rubescens): The most common misidentification. Key differential: Blusher flesh reddens (blushes) when cut or bruised; Panther Cap flesh remains white. Also confused with other brown-capped Amanita species in the field.
☏ Poison Control: 1-800-222-1222 — call immediately; admit all symptomatic patients
Fly Agaric
Amanita muscaria
Tier 2 — Serious
Severity 3 — Life-Threatening
Onset 30 min–2 hr (fast)
🔍 Field Identification Details
Toxin Type
Ibotenic acid (converts to muscimol post-ingestion) — psychoactive isoxazole compounds acting as NMDA agonist and GABA-A agonist. Despite the name, very low muscarine content — toxidrome is isoxazole (neurological), NOT cholinergic.
Key Identification Features
- Iconic red cap (5–20 cm) with white warts (may wash off in rain)
- White free gills, skirt-like ring on upper stem, bulbous base
- Found near birch, pine, spruce; mycorrhizal
- Cap color varies — orange and yellow varieties exist (var. formosa, var. guessowii)
- Young button stage emerges from white egg — easily mistaken for other Amanita species
Onset & Duration
30 minutes to 2 hours. Peak at 1–3 hours; typically resolves in 6–12 hours. Variable with individual metabolism and quantity consumed. No hepatotoxic delayed phase.
Symptoms
Neurological (primary)
- Sedation, drowsiness, hypnotic sleep — then excitation
- Visual hallucinations, confusion, disorientation
- Ataxia, myoclonus, muscle twitching
- Mydriasis (dilated pupils — key differential from muscarine)
Gastrointestinal
- Nausea, vomiting (variable severity)
First Responder Guidance
Supportive care; protect airway. Benzodiazepines for agitation or seizure. Do NOT give atropine — toxidrome is isoxazole, not cholinergic; atropine will worsen tachycardia and hyperthermia. Activated charcoal if alert. Observation for 6+ hours. Fatalities are rare but have occurred in children and with very large ingestions.
Clinical Notes
Critical differential: Do NOT confuse the isoxazole toxidrome (mydriasis, sedation, ataxia) with the muscarine toxidrome (miosis, bradycardia, bronchospasm, salivation). Atropine is the antidote for muscarine (Inocybe/Clitocybe) but contraindicated here. Confirm pupils: mydriasis = isoxazole; miosis = muscarine.
Intentional ingestion: A. muscaria is sometimes intentionally consumed for psychoactive effects. Presentation may be delayed reporting and patient may minimize symptoms. Obtain full ingestion history.
Intentional ingestion: A. muscaria is sometimes intentionally consumed for psychoactive effects. Presentation may be delayed reporting and patient may minimize symptoms. Obtain full ingestion history.
False Morel
Gyromitra esculenta
Tier 2 — Serious
Severity 3 — Life-Threatening
Onset 6–12 hr (delayed)
🔍 Field Identification Details
Toxin Type
Gyromitrin — a volatile hydrazine precursor that hydrolyzes to monomethylhydrazine (MMH), a rocket fuel component. Inhibits pyridoxine-dependent enzymes (including GABA synthesis). Toxin partially volatilizes with parboiling but not reliably eliminated.
Key Identification Features
- Cap irregularly convoluted, brain- or saddle-shaped — NOT pitted and honeycomb-like (true morel)
- Reddish-brown to dark brown cap; whitish stout stem
- Interior chambered/folded when cut (true morel is hollow from cap tip to stem base)
- Fruits in spring, often near sandy pine forests
- Distinctive chemical odor sometimes noted
Onset & Duration
6–12 hours post-ingestion. GI phase 6–12 hr, hepatic phase days 1–3. Duration of hepatotoxicity variable; full recovery in mild cases within 1–2 weeks. Severe cases may result in hepatic failure.
Symptoms
Gastrointestinal (6–12 hr)
- Nausea, vomiting, cramping, watery diarrhea
- Bloating, abdominal pain
Hepatic / Hematologic (12–72 hr)
- Hemolytic anemia — jaundice, pallor, hemoglobinuria (dark urine)
- Elevated LFTs; potential hepatic failure in severe cases
- Methemoglobinemia in severe poisoning
Neurological
- Headache, dizziness; seizures in severe poisoning
First Responder Guidance
IV fluids, electrolyte monitoring. Serial CBC, LFTs, methemoglobin level. Pyridoxine (vitamin B6) IV for seizures (MMH depletes pyridoxal phosphate — same mechanism as isoniazid toxicity). Methylene blue for symptomatic methemoglobinemia (>20–25% or symptomatic). Activated charcoal if early. Monitor for renal failure. Hepatology consultation for any liver involvement.
Clinical Notes
Partial cooking danger: Gyromitrin partially volatilizes with parboiling and discarding the water — but this is unreliable. European tradition of consuming parboiled G. esculenta has caused deaths. Advise patients that no home preparation makes this mushroom safe.
Inhalation risk during cooking: Gyromitrin vapors released during cooking can cause toxic symptoms in people who inhale steam while preparing the mushroom — a rare but documented exposure route.
Inhalation risk during cooking: Gyromitrin vapors released during cooking can cause toxic symptoms in people who inhale steam while preparing the mushroom — a rare but documented exposure route.
Deadly Webcap
Cortinarius rubellus
Tier 1 — Life-Threatening
Severity 4 — Potentially Fatal
2–3 weeks (extreme delay)
🔍 Field Identification Details
Toxin Type
Orellanine — a bipyridyl compound that generates free radicals and causes selective tubular damage. Thermostable (not destroyed by cooking). Eliminated slowly via kidneys, damaging tubules during excretion.
Key Identification Features
- Cap tawny to reddish-brown, conical to umbonate, 3–8 cm
- Gills rusty brown at maturity; rust-brown spore print
- Stem fibrous, brown with cortina (cobweb veil) remnant — no true ring
- Associated with spruce and pine; often in boreal or mixed conifer forests
- No distinctive odor or taste — highly dangerous LBM (little brown mushroom)
Onset & Duration
2–3 weeks (extreme delayed onset) — patients are typically asymptomatic for 2–21 days after ingestion. By the time renal symptoms appear, the ingestion event may not be connected. Chronic renal failure and need for dialysis or transplant may result.
Symptoms
Early (days 1–14 — often absent or mild)
- Possible nausea, metallic taste, headache, fatigue
- Most patients have NO early symptoms
Nephrotoxic phase (weeks 2–4)
- Polyuria, polydipsia progressing to oliguria
- Nausea, vomiting, flank pain
- Rising creatinine and BUN — acute tubular necrosis
- End-stage renal failure in severe cases
First Responder Guidance
Serial renal function labs (BUN, creatinine, electrolytes, urinalysis) over 3 weeks after suspected exposure. No antidote. Supportive renal care; early nephrology consultation. Dialysis for renal failure. Orellanine is detectable by HPLC urine testing at some reference labs — may confirm exposure but not widely available clinically. Liver function generally preserved.
Clinical Notes
The delayed onset is diagnostically critical. Patients presenting with unexplained renal failure should be asked about wild mushroom consumption in the preceding 3 weeks. Most emergency presentations occur at 2–3 weeks post-ingestion; the acute ingestion is often forgotten or not mentioned.
Lookalike risk: Resembles numerous edible species including chanterelles (young specimens) and various brown-capped woodland mushrooms. The rusty brown spore print and fibrous cortina remnant on the stem are the most reliable field clues, but definitive ID requires expertise.
Lookalike risk: Resembles numerous edible species including chanterelles (young specimens) and various brown-capped woodland mushrooms. The rusty brown spore print and fibrous cortina remnant on the stem are the most reliable field clues, but definitive ID requires expertise.
☏ Poison Control: 1-800-222-1222 — call for any suspected Cortinarius exposure even weeks after ingestion
Deadly Dapperling
Lepiota brunneoincarnata
Tier 1 — Life-Threatening
Severity 4 — Potentially Fatal
Onset 6–24 hr (delayed)
Toxin Type
Amatoxins (α-amanitin) — same toxin class as Death Cap and Destroying Angel. Per-gram amatoxin content is comparable to Amanita phalloides; a single cap can be lethal.
Key Identification Features
- Small cap (2–7 cm), pinkish-brown to brownish with concentric scaly zones; center darker
- White free gills; slight ring on stem; no volva (distinguishes from Amanita)
- Flesh white, faintly pinkish; mild smell or slightly unpleasant
- Found in lawns, gardens, parks, roadsides, wood-chip mulch beds — suburban and urban settings
- Fruits in fall and winter in California; can be mistaken for edible parasol mushrooms
Onset & Duration
GI phase: 6–24 hours. Hepatic and renal failure phase: 24–96 hours. Biphasic progression identical to A. phalloides including the deceptive honeymoon period.
Symptoms
Gastrointestinal (6–24 hr)
- Severe nausea, vomiting, watery diarrhea, dehydration
Hepatic / Renal (24–96 hr)
- Rising AST/ALT, jaundice, coagulopathy
- Hepatic encephalopathy; fulminant liver failure
- Acute tubular necrosis, renal failure
First Responder Guidance
Treat identically to Death Cap amatoxin poisoning. Activated charcoal if within 1–2 hours. Aggressive IV fluid resuscitation. Serial LFTs every 6–12 hours. Hepatology and nephrology consultation. Silibinin consideration via Poison Control. Transplant surgery evaluation for fulminant hepatic failure. Do NOT discharge on clinical improvement alone — the honeymoon period is deceptive.
Clinical Notes
Suburban garden hazard — Pacific Coast clinical significance: Lepiota brunneoincarnata is a major concern in California because it appears in maintained suburban and urban green spaces — lawns, parks, gardens, and wood-chip mulch beds — where it may be collected by foragers or accidentally consumed by children. Unlike the Death Cap which favors oak woodland, this species grows where people expect only benign garden fungi.
No volva — differs from Amanita: The Deadly Dapperling lacks the volva cup at the stem base seen in Death Cap and Destroying Angel. It may be confused with edible Parasol mushrooms (Macrolepiota procera) and the Shaggy Parasol (Chlorophyllum rhacodes). Key differential: Deadly Dapperling is much smaller (cap 2–7 cm vs. 15–30 cm for edible parasols).
No volva — differs from Amanita: The Deadly Dapperling lacks the volva cup at the stem base seen in Death Cap and Destroying Angel. It may be confused with edible Parasol mushrooms (Macrolepiota procera) and the Shaggy Parasol (Chlorophyllum rhacodes). Key differential: Deadly Dapperling is much smaller (cap 2–7 cm vs. 15–30 cm for edible parasols).
☏ Poison Control: 1-800-222-1222 — call immediately; admit all suspected amatoxin ingestions
Western Destroying Angel
Amanita elliptoides
Tier 1 — Life-Threatening
Severity 4 — Potentially Fatal
Onset 6–24 hr (delayed)
Toxin Type
Amatoxins (α-amanitin, β-amanitin, phallotoxins) — identical mechanism to Death Cap. Inhibits RNA polymerase II causing cessation of cellular protein synthesis; irreversible hepatocellular and renal tubular necrosis.
Key Identification Features
- Pure white throughout — cap, gills, stem, ring, and volva cup; no color variation
- Cap 5–12 cm; smooth, dry, convex to flat; often pure white without warts
- Prominent white cup-shaped volva at base (partially buried — dig to reveal)
- Skirt-like ring on upper stem; free white gills
- Found under Douglas fir, hemlock, and mixed conifers in the Pacific Northwest
Onset & Duration
GI phase: 6–24 hours. Hepatic phase: 24–96 hours. Biphasic pattern with honeymoon period identical to Death Cap and Destroying Angel (A. ocreata).
Symptoms
Gastrointestinal (6–24 hr)
- Severe nausea, vomiting, profuse watery diarrhea
- Severe dehydration, electrolyte disturbance
Hepatic / Renal (24–96 hr)
- Fulminant hepatic failure with rising AST/ALT, coagulopathy, encephalopathy
- Acute tubular necrosis, renal failure
First Responder Guidance
Identical management to Death Cap. Activated charcoal if early. Aggressive IV fluids. Serial LFTs every 6–12 hours. Hepatology consult. Silibinin (silymarin IV) consideration via Poison Control. Liver transplant evaluation for severe cases. Admit all patients regardless of clinical improvement at 24–48 hours.
Clinical Notes
PNW conifer associate: Unlike A. ocreata (which fruits under oaks in California and Oregon spring), A. elliptoides is associated with conifer forests — Douglas fir, western hemlock, Sitka spruce — and fruits in fall throughout Oregon and Washington. Pure white appearance in a conifer forest is an immediate danger sign.
Confusion with edible white mushrooms: May be mistaken for edible white Amanita species (e.g., A. lanei), button mushrooms, or puffballs in the button stage. The most dangerous error: foragers finding white egg-stage Amanitas near conifers and assuming they are edible. Always advise: any pure white mushroom with a cup at the base found under conifers in the PNW must be assumed lethal until proven otherwise by an expert.
Confusion with edible white mushrooms: May be mistaken for edible white Amanita species (e.g., A. lanei), button mushrooms, or puffballs in the button stage. The most dangerous error: foragers finding white egg-stage Amanitas near conifers and assuming they are edible. Always advise: any pure white mushroom with a cup at the base found under conifers in the PNW must be assumed lethal until proven otherwise by an expert.
☏ Poison Control: 1-800-222-1222 — call immediately; treat as amatoxin poisoning
Sorrel Webcap
Cortinarius orellanus
Tier 2 — Serious
Severity 4 — Potentially Fatal
2–3 weeks (extreme delay)
Toxin Type
Orellanine — a bipyridine N-oxide toxin that generates free radicals and causes selective damage to renal proximal tubular cells. Mechanism is delayed and cumulative; irreversible nephropathy leads to chronic kidney disease or renal failure requiring dialysis/transplantation. Also found in the closely related Deadly Webcap (C. rubellus).
Key Identification Features
- Cap 3–8 cm, brick-red to rusty orange-brown; surface dry, often with fibrous or slightly scaly texture; margin wavy
- Gills widely spaced, rust-brown, becoming rusty from spores; cortina (cobweb-like veil) remnants on stem when young
- Stem orange-brown, fibrous, often with cortina remnant zone
- Found under mixed woodland — oak and conifer — in Pacific Coast states
- No distinctive odor; lack of distinctive features makes it dangerous
Onset & Duration
2–3 weeks (range: 3 days to 3 weeks). This extreme delay is the defining clinical feature. By the time renal symptoms appear, the window for decontamination is long past. Renal failure may progress to end-stage over weeks to months.
Symptoms
Early (days 1–3)
- Mild nausea, anorexia, headache — often dismissed
- Thirst, excessive urination (early tubular damage)
Delayed Renal Phase (weeks 2–3)
- Rising creatinine and BUN; oliguria progressing to anuria
- Flank or lumbar pain; nausea, fatigue
- Progressive interstitial nephritis, renal failure
- Up to 15% of untreated cases require long-term dialysis
First Responder Guidance
No antidote. Supportive care: IV fluids, renal function monitoring (creatinine, BUN, eGFR), strict fluid balance. Nephrology consultation immediately on suspected exposure — do not wait for symptom onset. Serial creatinine monitoring for 3 weeks following any suspected Cortinarius ingestion. Hemodialysis for renal failure. Renal transplant evaluation for end-stage disease. Activated charcoal only if very recent ingestion.
Clinical Notes
Identical delayed nephrotoxic syndrome to Deadly Webcap (C. rubellus): Both C. orellanus and C. rubellus produce orellanine; clinical management is identical. Any patient presenting with unexplained progressive renal failure should be asked about wild mushroom ingestion in the preceding 2–4 weeks. The mushroom is often no longer recalled as relevant by the time symptoms appear.
Pacific Coast relevance: Multiple Cortinarius species containing orellanine are documented in Pacific Coast forests. Identification of the exact species is often impossible in the field — treat any Cortinarius ingestion associated with delayed GI symptoms and/or progressive renal function decline as orellanine poisoning pending Poison Control and nephrology consultation.
Pacific Coast relevance: Multiple Cortinarius species containing orellanine are documented in Pacific Coast forests. Identification of the exact species is often impossible in the field — treat any Cortinarius ingestion associated with delayed GI symptoms and/or progressive renal function decline as orellanine poisoning pending Poison Control and nephrology consultation.
☏ Poison Control: 1-800-222-1222 — call for any suspected Cortinarius exposure even weeks after ingestion
Pigskin Poison Puffball
Scleroderma citrinum
Tier 2 — Serious
Severity 3 — Life-Threatening
Onset 30 min–2 hr (fast)
🔍 Field Identification Details
Toxin Type
Sclerodermin and related compounds including alkaloids not fully characterized. Primary toxicity is gastrointestinal and cardiovascular. Some sources report atropine-like alkaloids in trace amounts; pharmacology not fully characterized.
Key Identification Features
- Round to irregular puffball, 3–12 cm across; yellowish-brown, thick tough outer skin
- Surface covered in flat warts or scales with cracked pattern (resembles pigskin)
- Interior dark purple to black at maturity (NOT white like edible puffballs)
- No stem; attached to ground by root-like mycelial cords
- Found on sandy or gravelly soil near hardwoods, disturbed ground, roadsides
Onset & Duration
30 minutes to 2 hours post-ingestion. GI symptoms typically resolve in 6–12 hours. Cardiovascular effects (when they occur) can persist longer. Severity depends heavily on quantity consumed.
Symptoms
Gastrointestinal (primary)
- Severe nausea, vomiting, diarrhea, abdominal pain
Cardiovascular (moderate to large ingestion)
- Bradycardia, hypotension
- Dizziness, syncope
Neurological
- Headache, weakness, diaphoresis
- Coma and cardiovascular collapse reported with large ingestions
First Responder Guidance
Supportive care; IV fluids. Monitor cardiac rhythm and blood pressure — bradycardia may require atropine. Activated charcoal if early. Admit for cardiac monitoring if bradycardia or hypotension present. Contact Poison Control for case-specific guidance — toxicology of this species is incompletely characterized.
Clinical Notes
Critical differential from edible puffballs: Always advise foragers to cut puffballs in half before consuming. Edible puffballs (Calvatia, Lycoperdon, Calbovista) are uniformly white inside when fresh. Any purple, gray, black, or yellow coloration, or any internal structure, indicates the specimen is NOT a safe edible puffball.
Note: Scleroderma species also serve as a parasitic host for the edible Parasitic Bolete (Pseudoboletus parasiticus) — a forager finding an unusual bolete attached to a puffball should suspect Scleroderma.
Note: Scleroderma species also serve as a parasitic host for the edible Parasitic Bolete (Pseudoboletus parasiticus) — a forager finding an unusual bolete attached to a puffball should suspect Scleroderma.
⚠ Tier 3 — Caution Advised
Tier 3 — Problematic, Rarely Fatal
The species below cause significant gastrointestinal distress, allergic reactions, metabolic interactions, or illness that typically resolves without lasting harm. Fatalities are extremely rare or limited to exceptional circumstances (very large ingestion, underlying conditions, specific drug interactions). Supportive care is usually sufficient. Contact Poison Control (1-800-222-1222) for any suspected ingestion.
Inky Cap (Common Ink Cap)
Coprinopsis atramentaria
Tier 3 — Problematic
Severity 2 — Serious
Onset 15–30 min (with alcohol)
🔍 Field Identification Details
Toxin Type
Coprine — a cyclopropyl-glutamine analogue that inhibits acetaldehyde dehydrogenase (ALDH). Reaction occurs ONLY when combined with alcohol. Safe when consumed without any alcohol. The mushroom itself causes no illness in the absence of alcohol.
Key Identification Features
- Gray to grayish-brown oval or bell-shaped caps, 3–7 cm across, often ribbed at margin
- Grows in dense clusters from buried wood or near stumps and disturbed soil
- Caps liquefy (autodigest) from margin inward as they age — characteristic black ink drip
- No ring on stem; stem white, fragile
- Very common in lawns, gardens, parks across the Pacific Coast
Onset & Duration
15–30 minutes after consuming alcohol (up to 72 hours after eating the mushroom). Symptoms last 1–4 hours and resolve when alcohol is metabolized. Can be triggered by alcohol consumed 1–3 days after ingestion of the mushroom. Re-exposure to alcohol re-triggers symptoms until coprine clears the system.
Symptoms
Disulfiram-like reaction (with alcohol only)
- Facial flushing, warmth, erythema — especially face, neck, upper chest
- Tachycardia, palpitations, headache
- Nausea, vomiting, diaphoresis
- Hypotension in severe reactions; chest pain (rare)
Without alcohol
- None — mushroom consumed without alcohol causes no symptoms
First Responder Guidance
Remove alcohol source. IV fluids for hypotension. Antihistamines for flushing. Cardiac monitoring if palpitations or chest pain. Advise patient: do not consume any alcohol for at least 72 hours. No specific antidote; reaction is self-limiting once alcohol is metabolized. Provide written discharge instructions about the alcohol interaction and duration of restriction.
Clinical Notes
Critical alcohol interaction — up to 72 hours: Coprine sensitization persists for 1–3 days after consuming the mushroom. A patient who ate the mushroom at dinner and feels fine may still develop a severe reaction the following evening with social drinking. Explicit discharge instructions about this delayed interaction window are essential.
Disulfiram analogy: The mechanism is nearly identical to disulfiram (Antabuse) — acetaldehyde accumulation from blocked ALDH. Ask about prescribed disulfiram in the history, as this may compound the reaction. The mushroom is safe and edible in the absence of alcohol.
Disulfiram analogy: The mechanism is nearly identical to disulfiram (Antabuse) — acetaldehyde accumulation from blocked ALDH. Ask about prescribed disulfiram in the history, as this may compound the reaction. The mushroom is safe and edible in the absence of alcohol.
Sulfur Tuft
Hypholoma fasciculare
Tier 3 — Problematic
Severity 2 — Serious
Onset 30 min–3 hr (fast)
🔍 Field Identification Details
Toxin Type
Fasciculol E and fasciculol F (triterpene compounds) plus other poorly characterized toxins. Primarily causes GI irritation. High-dose animal studies show hepatotoxicity and potential neurotoxicity, though systemic effects in humans are rare and typically mild.
Key Identification Features
- Grows in large, dense clusters on dead wood (never from soil directly)
- Cap sulfur-yellow with orange-brown center, 2–8 cm
- Gills sulfur-yellow when young, aging to greenish then dark purple-brown
- Intensely bitter taste — most accidental poisonings involve raw or barely cooked mushrooms
- No ring on stem; dark spore print (distinguishes from similar edible species)
Onset & Duration
30 minutes to 3 hours post-ingestion. Symptoms typically self-limiting, resolving in 12–24 hours. Persistent symptoms beyond 24 hours warrant evaluation for deeper toxicity.
Symptoms
Gastrointestinal (primary)
- Nausea, vomiting, diarrhea, abdominal cramping
- Symptoms can be severe with large ingestion
Neurological (rare, large ingestion)
- Weakness, visual disturbance, ataxia reported in literature
- Rare case reports of more severe outcomes
First Responder Guidance
Supportive care — IV fluids for dehydration, anti-emetics. Activated charcoal if early and symptomatic. Monitor LFTs if symptoms are severe or prolonged. Most cases resolve with supportive care. Contact Poison Control for case guidance if neurological symptoms present.
Clinical Notes
Common confusion: Sulfur Tuft is frequently confused with edible Honey Mushroom (Armillaria mellea). Both grow in clusters on wood in fall. Key differentials: Honey Mushroom has a ring on the stem, lighter brown caps, and white spores; Sulfur Tuft has no ring, yellow-green gills aging dark, and dark purple-brown spores. The intensely bitter taste of Sulfur Tuft is also distinctive — but bitter taste requires raw tasting and some patients eat without noticing.
The Sickener
Russula emetica
Tier 3 — Problematic
Severity 2 — Serious
Onset 30 min–2 hr (fast)
🔍 Field Identification Details
Toxin Type
Sesquiterpene compounds and phenolic acids — primary emetic and GI irritant action. Toxins partially degraded by thorough cooking; raw ingestion causes more severe symptoms than cooked ingestion. Exact toxic compound profile not fully characterized.
Key Identification Features
- Bright scarlet to cherry-red cap, 3–9 cm; shiny surface; cuticle peels easily
- White gills and stem; gills brittle, snapping cleanly (characteristic of all Russula)
- Distinctly acrid, peppery taste on tongue — diagnostic when raw tasting is safe
- White spore print; no ring on stem; no volva at base
- Grows in Sphagnum bogs or conifer forests; mycorrhizal with conifers
Onset & Duration
30 minutes to 2 hours post-ingestion. Symptoms typically resolve within 6–12 hours with supportive care. No delayed toxicity phase; no organ damage expected in typical cases.
Symptoms
Gastrointestinal (primary)
- Severe nausea, vomiting (emesis often prominent and forceful — hence common name)
- Diarrhea, abdominal cramping
- Dehydration with large ingestion
First Responder Guidance
Supportive care — oral or IV hydration, anti-emetics. Activated charcoal if early (though vomiting often clears much of the ingestion naturally). Symptoms are self-limiting; hospitalization rarely needed unless dehydration is severe or patient is elderly or pediatric. Monitor electrolytes if vomiting is prolonged.
Clinical Notes
Confusion risk with edible red Russula species: Several Russula species with red caps are edible (e.g. R. xerampelina — shrimp Russula). The acrid peppery taste in R. emetica is the primary field differential. However, taste testing is unreliable in an emergency presentation — treat any red Russula as potentially toxic unless definitive identification is confirmed by an expert. Spore print color alone is insufficient to distinguish species within the red-capped Russula group.
Angel Wings
Pleurocybella porrigens
Tier 3 — Problematic
Severity 2 — Serious
Onset variable (suspected neurotoxin)
🔍 Field Identification Details
Toxin Type
Toxin(s) not fully characterized. Associated with a cluster of deaths in Japan (2004) involving neurological failure. Suspected amino acid analog toxins affecting glutamate receptors. Historically considered edible; reclassified as toxic following fatalities. Risk may be higher in patients with chronic kidney disease.
Key Identification Features
- Small, pure white fan- or spatula-shaped fruiting bodies, 1–8 cm across
- Grows in dense overlapping clusters on decaying conifer logs (hemlock, fir, spruce) — rarely on hardwood
- No stem; attached directly to wood; gills white, radiating from attachment point
- Thin-fleshed; fragile; white throughout; no distinctive odor
- Very common in Pacific Northwest fall/winter; also found in CA and OR mountains
Onset & Duration
Onset variable — reported from hours to several days. In the 2004 Japan cluster, neurological decline followed multiple-day consumption. Duration and reversibility unclear; fatalities in renally compromised patients.
Symptoms
Neurological (primary, based on 2004 Japan cases)
- Progressive neurological deterioration — confusion, decreased consciousness
- Seizures; coma
- Motor dysfunction, tremor
Renal
- Acute renal failure (especially in patients with pre-existing kidney disease)
Gastrointestinal
- Nausea, vomiting (may be absent)
First Responder Guidance
Supportive care; airway protection. Benzodiazepines for seizures. Renal function monitoring. Contact Poison Control for guidance — this is an emerging toxidrome with limited antidote options. No confirmed antidote. Admission warranted for any symptomatic case. Risk is particularly high in patients with chronic kidney disease.
Clinical Notes
Previously considered edible — reclassification in progress: Angel Wings (Pleurocybella porrigens) was historically eaten in some regions. Following 17 deaths in Japan in 2004 — all in patients with chronic kidney disease — it has been reclassified as toxic. The risk appears amplified in renal-impaired patients. Clinicians should be aware this species may still appear in older foraging guides as "safe."
Pacific Northwest significance: This species is abundant on Pacific Northwest conifer logs from September through January. Confusion with edible oyster mushroom (Pleurotus ostreatus and P. pulmonarius) occurs — oyster mushrooms are far larger (10–25 cm), grow on hardwoods or dead hardwood stumps, and have a distinct mealy odor. Angel Wings are always on conifers and much smaller.
Pacific Northwest significance: This species is abundant on Pacific Northwest conifer logs from September through January. Confusion with edible oyster mushroom (Pleurotus ostreatus and P. pulmonarius) occurs — oyster mushrooms are far larger (10–25 cm), grow on hardwoods or dead hardwood stumps, and have a distinct mealy odor. Angel Wings are always on conifers and much smaller.
Poison Pie
Hebeloma crustuliniforme
Tier 3 — Problematic
Severity 2 — Serious
Onset 30 min–2 hr (fast)
Toxin Type
Hebeloma toxins — exact compounds not fully characterized; include muscarinic and GI irritant compounds. Some species in the genus also contain trace cyanic acid precursors. Primarily GI toxicity; no known hepato- or nephrotoxic delayed phase.
Key Identification Features
- Cap pale buff to tan-brown, 4–10 cm; convex becoming flatter; smooth, slightly greasy when moist; margin often wavy
- Gills pale buff, becoming brown as spores mature; with distinctive water droplets (beads) on gill edges in fresh specimens
- Distinctive radish-like odor — strong and persistent; key field character
- White stem, fibrous; no ring; base slightly clubbed
- Mycorrhizal — found in woodland, parks, gardens with trees throughout Pacific Coast
Onset & Duration
30 minutes to 2 hours. GI illness typically resolves within 12–24 hours with supportive care. No delayed organ failure expected. Severity increases with quantity consumed.
Symptoms
Gastrointestinal (primary)
- Nausea, vomiting, abdominal cramping, diarrhea
- May be severe with large ingestion — dehydration risk
Neurological (mild, occasional)
- Headache, dizziness
First Responder Guidance
Supportive care — IV fluids, anti-emetics, electrolyte monitoring. Activated charcoal if within 1–2 hours. Most cases managed as outpatient. Hospital admission for dehydration or in pediatric cases. Contact Poison Control to document and for guidance on monitoring duration.
Clinical Notes
Common and widespread on the Pacific Coast: Hebeloma crustuliniforme and closely related species are very common in Pacific Coast parks, suburban gardens, and forests — fruiting wherever trees are present. The strong radish odor is the most reliable field character; no edible species shares this smell. However, misidentification is frequent among foragers.
No delayed toxicity: Unlike Death Cap and Galerina, there is no hepatic or renal failure phase. Rapid onset (<2 hr) and absence of delayed organ injury helps distinguish from amatoxin species. However, any suspected mushroom ingestion with GI onset should prompt baseline LFTs to exclude co-ingestion of amatoxin species.
No delayed toxicity: Unlike Death Cap and Galerina, there is no hepatic or renal failure phase. Rapid onset (<2 hr) and absence of delayed organ injury helps distinguish from amatoxin species. However, any suspected mushroom ingestion with GI onset should prompt baseline LFTs to exclude co-ingestion of amatoxin species.
Magic Mushrooms (Psilocybin Species)
Psilocybe spp. (P. semilanceata, P. cyanescens, P. azurescens and others)
Tier 3 — Problematic
Severity 2 — Serious
Onset 15–60 min (fast)
Toxin Type
Psilocybin and psilocin — prodrug/active serotonergic hallucinogens. Psilocybin is dephosphorylated to psilocin, a 5-HT2A agonist.
Onset Time
15–60 minutes post-ingestion. Peak at 1–2 hours; duration 4–8 hours.
Key Field Features
Small brown mushrooms (1–4 cm cap). P. semilanceata (Liberty Cap): conical cap with nipple-like apex, grows in grassy fields and pastures — very common in Oregon and Washington. P. cyanescens (Wavy Cap): wavy cap margin, very potent; common in PNW wood-chip mulch. P. azurescens: coastal OR/WA dune grasses, very high psilocybin content. Blue staining on bruising or tissue damage — key field marker for all Psilocybe species. Dark purple-brown spore print. Very common in PNW lawns, grassy fields, wood chips, and coastal areas.
Clinical Symptoms
Visual hallucinations, synesthesia, perceptual distortions; euphoria or panic ("bad trip"); confusion, tachycardia, mild hypertension, mydriasis. Hyperthermia (rare, high-dose). Pediatric presentations: confusion, agitation, ataxia — may not exhibit typical hallucinogenic symptoms. Serotonin syndrome risk with concurrent serotonergic medications.
First Responder Guidance
Calm, low-stimulation environment; reassurance. Benzodiazepines (lorazepam 1–2 mg IV/IM) for severe anxiety, agitation, or delirium. Monitor temperature — cool agitated patients. Avoid antipsychotics first-line; consider olanzapine PO/IM if benzodiazepines insufficient. Cyproheptadine if serotonin syndrome features present. Most adults resolve within 6–8 hours without pharmacotherapy beyond reassurance.
Clinical Notes
Galerina marginata confusion: Psilocybe cyanescens and related species share habitat (wood chips, mulch) and appearance with the deadly Galerina marginata. Blue bruising distinguishes Psilocybe; Galerina does NOT bruise blue. Any unclear small brown mushroom from mulch where CNS symptoms develop: order liver function tests at 24 and 48 hours even if presentation appears consistent with psilocybin — failure to do so has resulted in missed amatoxin poisoning.
False Parasol (Green-Spored Parasol)
Chlorophyllum molybdites
Tier 3 — Problematic
Severity 2 — Serious
Onset 1–3 hr (fast)
Toxin Type
Molybdophyllysin (zinc metalloprotease) and other heat-stable GI toxins. NOT amatoxin. No organ failure toxidrome.
Onset Time
1–3 hours post-ingestion. Rapid onset helps distinguish from amatoxin species (>6 hr onset). Self-limiting in most cases within 6–12 hours.
Key Field Features
Large (10–30 cm) white mushroom with brownish fibrous scales and prominent double ring. Gills initially white, turning green at spore maturity. Green spore print — diagnostic (no edible species has a green spore print). Grows in lawns, parks, and suburbs across California and the Pacific Coast after summer and fall rains. Among the most common toxic mushroom calls to Pacific Coast poison centers.
Clinical Symptoms
Explosive nausea, vomiting, profuse watery to bloody diarrhea, severe abdominal cramping. Dehydration and electrolyte imbalance in severe cases. Hypotension from volume depletion. Liver and kidney NOT typically affected. Symptoms generally self-limited to 6–12 hours.
First Responder Guidance
Supportive: IV hydration, antiemetics, electrolyte replacement. No antidote. Monitor for dehydration. The rapid onset (<3 hr) is diagnostically useful — amatoxin poisoning (Death Cap, Galerina) has minimum 6-hour onset. Order LFTs if any uncertainty about species or timing.
Clinical Notes
Most dangerously confused with the edible Shaggy Parasol (Chlorophyllum rhacodes) and edible Parasol Mushroom (Macrolepiota procera) — all are large white scaly-capped lawn/field fungi. The green spore print is the definitive differentiator; edible species have white spore prints. Advise all foragers to always take a spore print before eating any large parasol-shaped mushroom.
Lead Poisoner
Entoloma sinuatum
Tier 3 — Problematic
Severity 2 — Serious
Onset 30 min–4 hr (fast)
Toxin Type
GI toxins — exact chemistry not fully characterized. Heat-stable compounds causing severe gastrointestinal irritation. No amatoxins, no orellanine — organ failure is rare.
Onset Time
30 minutes to 4 hours post-ingestion. GI symptoms can be violent and sudden. Most cases resolve within 12–24 hours with supportive care.
Key Field Features
Cap 5–20 cm, pale yellowish-gray to grayish-white, broadly convex with umbo. Gills initially white or pale, turning distinctly pink with age (from pink spore deposit). Stem white, stout. Pleasant mealy or floury odor. Pink spore print — diagnostic. Grows in mixed hardwood and oak woodland across the Pacific Coast — California, Oregon, and Washington — summer and fall.
Clinical Symptoms
Sudden explosive onset of nausea, vomiting, severe abdominal cramps, profuse watery to bloody diarrhea. Severe dehydration in prolonged cases. Liver function generally NOT affected. Rare fatalities from dehydration in elderly or children.
First Responder Guidance
Supportive: IV hydration, antiemetics, electrolyte replacement. No antidote. Symptoms typically resolve within 12–24 hours. Consider GI decontamination if early ingestion with no contraindication.
Clinical Notes
A significant cause of mushroom poisoning across the Pacific Coast. Dangerously confused with edible St. George's Mushroom (Calocybe gambosa), Tricholoma species, and other pale-capped woodland fungi. The pink gills at maturity (from pink spores) are the key differentiator — edible look-alikes have white gills. The mealy odor is shared by edible Calocybe. Always examine gill color carefully: pink gills = danger.
Clinical Disclaimer: This guide is an educational reference and does not replace clinical judgment, direct Poison Control guidance, or toxicology consultation. Species identification based on patient history is unreliable — treat suspected ingestions based on the clinical toxidrome and timeline, not assumed species. Always contact Poison Control (1-800-222-1222) for case-specific management guidance.