⚠ Regional Poison Control β€” China: +86-10-8313-2345  |  Japan: +81-72-727-2499  |  Korea: 1339  |  India: +91-11-2658-8669

About This Guide

This guide covers the most clinically significant toxic mushroom species documented in Asia β€” including the lethal amatoxin-producing Amanita exitialis, Amanita fuliginea, and Amanita subpallidorosea; the myotoxic Russula subnigricans; the hypoglycemic cardiac toxin Trogia venenata; the dermatotoxic Podostroma cornu-damae; and the gastrointestinal toxin producer Chlorophyllum molybdites. Species are found across East, South, and Southeast Asian habitats.

Data-only reference β€” no photographs. Species identification for clinical management must be confirmed by a toxicologist, mycologist, or poison control specialist, not from this text alone.

Quick Reference β€” All Species

SpeciesTierToxin ClassOnsetPrimary Risk
Amanita exitialis / fuliginea / subpallidorosea Tier 1 Amatoxins (heat-stable bicyclic octapeptides) Biphasic: 6–24h GI / 72–96h hepatic Fulminant hepatic necrosis, death
Russula subnigricans Tier 1 Cycloprop-2-ene-carboxylic acid 30 min–3h GI / 4–72h myotoxic Rhabdomyolysis, AKI, cardiac arrhythmia
Trogia venenata Tier 1 Hypoglycin-A-like amino acids 1–5 hours Fatal ventricular arrhythmia, hypoglycemia
Podostroma cornu-damae Tier 1 Macrocyclic trichothecene mycotoxins 1–4h early GI; Days 2–7 systemic collapse Pancytopenia, multi-organ failure, death
Amanita pseudoporphyria Tier 2 Allenic norleucine 1–12h GI; 24–48h renal/hepatic/cardiac Nephrotoxic, hepatotoxic, myocardial injury
Chlorophyllum molybdites Tier 3 Toxic polymeric protein (GI irritant) Under 2 hours Severe GI toxidrome; rarely fatal in healthy adults
△ Section I β€” Triage Algorithm and Bedside Decision Matrix

Patient Presents Post Ingestion

Early onset under 6 hours branches to: isolated GI distress (Tier 3), myotoxic rigidity (Tier 1), and hypoglycemic cardiac arrhythmia (Tier 1).
Late onset over 6 hours branches to: amatoxin syndrome (Tier 1), nephrotoxic and hepatic mixed (Tier 1), and trichothecene pancytopenia (Tier 1).

Bedside Triage Decision Matrix

OnsetToxidromeSpeciesImmediate Actions
Ultra-rapid 1–5 hours Hypoglycemic cardiomyopathic toxidrome Trogia venenata Immediate IV dextrose D50W bolus, dedicated central line glucose infusion, continuous ECG telemetry throughout entire admission even after glucose normalizes, strictly avoid intravenous lipid emulsions.
Early 1–6 hours Myotoxic rhabdomyolysis toxidrome Russula subnigricans High volume fluid resuscitation targeting urine output above 200 mL per hour in adults, pediatric forced diuresis 3.0 to 4.0 mL per kg per hour β€” this is substantially higher than the hepatotoxic fluid protocol and must never be confused with it, urinary alkalinization targeting urine pH above 6.5, early CRRT with high-flux membrane if CK elevates steeply.
Early under 2 hours Acute gastrointestinal distress Chlorophyllum molybdites IV crystalloid fluid resuscitation, IV Ondansetron 4 to 8 mg adults, 0.15 mg per kg per dose maximum 4 mg pediatric, continuous serum electrolyte and renal function tracking.
Delayed 6–24 hours Hepatotoxic amatoxin toxidrome Amanita exitialis, Amanita fuliginea, Amanita subpallidorosea Immediate ICU admission, continuous IV Silibinin Legalon SIL four discrete 6-hour infusions, extended IV NAC three-bag regimen 300 mg per kg over 21 hours then continuous maintenance, multidose activated charcoal 1g per kg every 4 hours via NG tube, cross match for urgent liver transplantation. Pediatric fluid target 1.5 to 2.0 mL per kg per hour euvolemic β€” do not apply the higher rhabdomyolysis target to hepatotoxic patients.
Delayed 8–24 hours Nephrotoxic hepatotoxic cardiac mixed toxidrome Amanita pseudoporphyria Conservative IV fluid resuscitation 1.0 to 1.5 mL per kg per hour pediatric with strict fluid balance every 2 hours, aggressive fluid diuresis adults, continuous evaluation of renal panels creatinine and urea, liver panels ALT/AST/INR, and cardiac panels troponin and ECG every 6 hours, nephrology and cardiology consultation, early CVVH low threshold in pediatric patients.
Delayed 1–4 hours early GI phase then 2–4 days systemic collapse Trichothecene cellular translation inhibition Podostroma cornu-damae Clinicians must not be falsely reassured by apparent early recovery after the initial GI phase, protective reverse isolation, G-CSF 5 mcg per kg per day subcutaneous, empiric broad spectrum antibiotics, blood products as needed, early therapeutic plasma exchange or CHDF. Treating clinician must wear nitrile gloves when handling any patient or animal that may have had dermal contact.
⚠ Section II β€” Tier 1 Species
Amanita exitialis, Amanita fuliginea, Amanita subpallidorosea Tier 1 β€” Lethal
Primary drivers of mass mushroom poisoning fatalities in China
Distribution
Subtropical and temperate East Asia including southern and central China, Japan, Korea, and northeastern India. Tri-species convergence zone in the Nanling and Wuyi mountain ranges. Associated with Fagaceae oaks and beeches and Pinaceae conifers.
Season
May to October
Identification
Amanita exitialis pure white cap. Amanita fuliginea dark grey to brown cap. Amanita subpallidorosea pale pink to white cap. All three share free white gills, a persistent annulus, a saccate volva at the base, and a white spore print.
Toxin
Heat-stable bicyclic octapeptide amatoxins β€” inhibit RNA polymerase II. Survive cooking at any temperature.
⚠ CRITICAL REGIONAL WARNING: Clinicians in the Nanling and Wuyi mountain range convergence zone must treat any pale Amanita as potentially all three species simultaneously.

All three are frequently and fatally misidentified as Volvariella volvacea (the Paddy Straw Mushroom) which lacks an annulus and has a pink spore print. This confusion is the primary driver of mass poisoning events in rural China.

  • Phase 1 (6–24h): Severe cholera-like GI distress.
  • Phase 2 (24–72h): False recovery phase β€” apparent clinical improvement while hepatic destruction continues silently.
  • Phase 3 (72–96h and beyond): Fulminant hepatic failure with jaundice, coagulopathy, encephalopathy, and multi-organ failure.
⚠ FALSE RECOVERY PHASE: Do NOT discharge during Phase 2. ICU admission and liver transplant consult must be initiated EARLY regardless of apparent clinical recovery.

Initial Resuscitation & Decontamination

  • Aggressive IV fluid resuscitation
  • Multidose activated charcoal 1 g per kg every 4 hours via NG tube to interrupt enterohepatic amatoxin circulation
  • Notify liver transplant unit immediately on admission
  • Liver and kidney panels every 6 hours

IV Silibinin (Legalon SIL)

  • Loading dose: 5 mg per kg
  • Maintenance: 20 to 30 mg per kg per day total β€” four discrete 6-hour infusion blocks rather than continuous drip for optimal receptor blockade
  • CRITICAL β€” Infusion continuity: The four 6-hour infusion blocks must be continuous and uninterrupted with no gap between bags. Any trough between bags allows unbound amatoxins to enter hepatocytes. Bags must be prepared in advance and swapped without interruption β€” do not allow even a brief lapse in infusion while the next bag is prepared.

IV NAC β€” Extended Regimen (Adults)

  • Bag 1: 150 mg per kg over 1 hour
  • Bag 2: 50 mg per kg over 4 hours
  • Bag 3: 100 mg per kg over 16 hours
  • Then repeat Bag 3 at 150 mg per kg every 24 hours continuously until INR drops below 1.5 and transaminases are clearing linearly. Do not stop early.

IV NAC Three-Bag Regimen (Pediatric β€” Weight Based)

  • Bag 1: 150 mg per kg over 60 minutes
  • Bag 2: 50 mg per kg over 4 hours
  • Bag 3: 100 mg per kg over 16 hours
  • Strict euvolemic fluid balance 1.5 to 2.0 mL per kg per hour to prevent cerebral edema
  • Monitor blood glucose every 2 hours
  • Do not apply the higher rhabdomyolysis fluid target to hepatotoxic patients.

King's College Criteria for Liver Transplant Assessment

Single criterion (sufficient alone): pH below 7.3 after adequate resuscitation, regardless of encephalopathy grade.

OR any three of the following five criteria simultaneously:

  • INR above 3.5
  • Serum bilirubin above 300 micromol per L
  • Age under 10 or above 40
  • Jaundice to encephalopathy interval greater than 7 days
  • Confirmed toxic mushroom ingestion

Non-Acetaminophen Mushroom-Induced Liver Failure β€” Transplant Listing Checklist:

  1. Confirm pH below 7.3 after fluid resuscitation is complete (single-criterion threshold). If present, list immediately.
  2. If pH criterion not met, assess for simultaneous presence of three or more multi-factor criteria above and list if threshold met.
  3. Document confirmed or strongly suspected toxic mushroom ingestion as aetiology β€” this satisfies the fifth multi-factor criterion.
  4. Re-assess every 6 hours β€” criteria can be met at any point during deterioration, not only on admission.
  5. Contact regional transplant unit at first sign of encephalopathy regardless of whether full criteria are met β€” early notification significantly shortens organ allocation time.

Meixner Test for Amatoxin Detection

  1. Place a drop of mushroom juice or crushed tissue on uncoated newsprint paper.
  2. Allow to dry completely.
  3. Apply one drop of concentrated hydrochloric acid.
  4. Apply gentle heat from below β€” a lighter or warm surface β€” for 30 seconds.
  5. A positive blue-green color change indicates amatoxin presence. Heat activation is required for reliable results.

A negative result does not rule out amatoxin poisoning β€” treat clinically if history is consistent.

β›” CRITICAL SAFETY WARNING: A negative result cannot exclude amatoxin poisoning. Clinical triage must be biomarker driven. The Meixner test is a supplementary tool only β€” it must never be used to discharge a patient or rule out treatment.

Silibinin (Legalon SIL) Regional Stock Status

  • Reliably available: Singapore (major tertiary hospitals); Bangkok, Thailand (two hospitals only β€” Siriraj Hospital and Ramathibodi Hospital)
  • Sporadic or uncertain availability: Vietnam, Philippines, Indonesia, Malaysia β€” confirm with pharmacy before assuming supply
  • Zero documented stock: Myanmar, Cambodia, Laos β€” assume unavailable; initiate fallback immediately

Penicillin G Fallback Protocol (all settings where Silibinin cannot be sourced within 2 hours)

  • Dose: 1,000,000 units per kg per day
  • Administration: Divided into six doses every 4 hours by continuous IV infusion
  • Indication: Any confirmed or suspected amatoxin ingestion when IV Silibinin is unavailable or cannot be procured within 2 hours of presentation
  • Penicillin G competes with amatoxin at the OATP1B1/1B3 hepatocyte transporter. It is not equivalent to Silibinin but provides meaningful hepatocyte protection in resource-limited settings.
  • Continue until Silibinin is secured, or for the full amatoxin treatment course if Silibinin remains unavailable.

Standardized Pre-Transfer Checklist for District Hospitals

  1. Silver coin detoxifying myth screening: Ask patient or family whether silver coins, silver objects, silverware, or any silver-containing material was used to test the mushroom before eating. Document the answer. This myth is widespread in rural Asia β€” if silver was used, the patient may have delayed seeking care believing the mushroom was safe. Document and communicate to receiving unit.
  2. Dual large-bore IV access mandate: Two large-bore peripheral IV lines (minimum 18G) must be established before transport. Central line preferred if available. Do not transport with a single line β€” access may fail en route.
  3. Gastric aspirate spore microscopy: In rural settings without ELISA capability, collect a gastric aspirate sample in a sealed tube for spore microscopy at the receiving institution. Label with patient name, time of collection, and approximate time of ingestion. This low-cost intervention can confirm ingested species when the mushroom itself is unavailable.
  4. Specimen preservation in tropical heat: If biological specimens (gastric aspirate, mushroom fragments, or urine) must be transported over long distances in tropical heat without refrigeration, pack in desiccant silica gel within a sealed container. Silica gel slows bacterial overgrowth and preserves morphological and toxicological integrity for 8 to 12 hours in ambient tropical temperatures. Label specimen clearly as potentially toxic biological material.
  5. Contact receiving ICU before departure and provide: species suspected, time of ingestion, current urine output, current conscious state, and any antidote given.
  6. Bring any remaining mushroom sample, photograph, or packaging from the source product if available.

🐾 Veterinary β€” Dogs

Highly toxic and fatal. Onset 6 to 12 hours.

Clinical signs: Delayed bloody diarrhea, progressive weakness, jaundice, hypoglycemia, falling BUN as hepatic synthetic function collapses, and terminal hepatic coma.

Treatment: Immediate GI decontamination if within 2 hours of ingestion, aggressive IV fluid diuresis, multidose activated charcoal, IV NAC, fentanyl CRI for analgesia β€” avoid NSAIDs due to nephrotoxic synergy. High mortality without early intervention.

🐾 Veterinary β€” Cats

Highly toxic and fatal. Onset 6 to 12 hours.

Clinical signs: Sudden severe dehydration, vomiting, extreme lethargy, yellowed mucous membranes, hypoglycemia, and falling BUN.

Treatment: Intensive IV fluid therapy, liver protectants SAMe and NAC, buprenorphine or methadone for analgesia β€” avoid NSAIDs, thermal support. Guarded prognosis.

Russula subnigricans Tier 1 β€” Lethal
Myotoxic rhabdomyolysis β€” southern and eastern Asia
Distribution
Southern and eastern China, Japan, Taiwan, and Korea. Found in broad-leaved and mixed forests as an ectomycorrhizal partner.
Season
June to September
Identification
Smoky grey to grey-brown cap with distant white gills and brittle flesh. Key distinguishing feature: flesh bruises reddish-orange and stays red. Russula nigricans turns red briefly then shifts to jet-black β€” that single color shift is the critical field distinction.
Toxin
Cycloprop-2-ene-carboxylic acid β€” causes rapid rhabdomyolysis with massive myoglobin release driving acute kidney injury and fatal cardiac arrhythmias.

Russula nigricans which turns black not reddish-orange on bruising and is considered edible in some regions of Asia.

  • GI distress 30 minutes to 3 hours
  • Severe myalgia and progressive muscle rigidity 4 to 12 hours
  • Tea-colored urine indicating myoglobinuria
  • Acute kidney injury and cardiac failure 12 to 72 hours

Fluid Resuscitation & Urinary Alkalinization

  • Rapid IV fluid resuscitation 200 to 300 mL per hour in adults targeting urine output above 200 mL per hour
  • Urinary alkalinization with sodium bicarbonate targeting urine pH above 6.5
  • Continuous CK monitoring every 4 hours
  • Continuous cardiac monitoring throughout admission

CRRT Protocol

  • CRRT with high-flux membrane if CK rises above 50,000 U per L or renal function deteriorates
  • Blood flow 150 to 200 mL per min, dialysate flow 1.5 to 2.0 L per hour
  • Regional citrate anticoagulation preferred β€” monitor for citrate accumulation syndrome
  • Extracorporeal clearance becomes ineffective after 24 to 36 hours of toxin exposure β€” initiate early

Pediatric Rhabdomyolysis Protocol

  • Forced diuresis target 3.0 to 4.0 mL per kg per hour specifically for rhabdomyolysis to prevent myoglobin crystallization in pediatric proximal tubules
  • This is substantially higher than the hepatotoxic fluid protocol and must never be confused with it.
  • Sodium bicarbonate 1 to 2 mEq per kg per hour for urinary alkalinization
  • Continuous CK and cardiac monitoring

🐾 Veterinary β€” Dogs

Onset 1 to 3 hours. Rapid vomiting, muscle tremors, progressive weakness, dark tea-colored urine.

Treatment: Aggressive IV fluid diuresis, urinary alkalinization, continuous CK monitoring, supportive cardiac care, fentanyl CRI for myalgia β€” avoid NSAIDs due to nephrotoxic synergy.

🐾 Veterinary β€” Cats

Vomiting, muscle rigidity, pigmented urine, weakness.

Treatment: IV fluids, urinary alkalinization, supportive cardiac care, buprenorphine or methadone for analgesia β€” avoid NSAIDs.

Trogia venenata Tier 1 β€” Lethal
Yunnan Sudden Unexplained Death Syndrome β€” southwestern China
Distribution
High altitude forested areas 1,500 to 3,000 meters in Yunnan, Guizhou, and Sichuan provinces of southwestern China. Saprotrophic on decaying wood. Responsible for Yunnan Sudden Unexplained Death Syndrome documented across multiple cluster poisoning events.
Season
June to September
Identification
Small white delicate fan-shaped or oyster-like fruiting body growing in clusters on decaying wood. White spore print.
Toxin
Native toxic amino acids including 2R-amino-4S-hydroxy-5-hexynoic acid and L-pipecolic acid act identically to hypoglycin A found in ackee fruit. They irreversibly inhibit acyl-CoA dehydrogenases completely blocking mitochondrial fatty acid beta-oxidation.

Frequently and fatally confused with edible Pleurotus species (oyster mushrooms) which grow in similar configurations on wood and have a nearly identical appearance.

⚠ CRITICAL MECHANISM: Because the human myocardium relies on fatty acid beta-oxidation for approximately 70 percent of its ATP production, this toxin induces sudden metabolic starvation of the heart muscle precipitating fatal ventricular arrhythmias. This mechanism is completely independent of systemic blood glucose levels β€” cardiac arrest can occur even when finger-stick glucose reads as entirely normal.
  • Rapid onset 1 to 5 hours
  • Extreme weakness and dizziness
  • Severe hypoglycemia below 2 mmol per L
  • Neurological collapse, generalized seizures
  • Sudden cardiac arrest

Glucose & Cardiac Protocol

  • Immediate IV dextrose D50W bolus
  • Followed by continuous central line glucose infusion D10 or D20 to maintain normoglycemia
  • Mandatory continuous ECG telemetry throughout the entire admission even after glucose normalizes because the cardiac mechanism is completely independent of blood glucose
  • Strictly avoid intravenous lipid emulsions which will worsen the beta-oxidation blockade.

Pediatric Glucose Protocol

  • IV dextrose 0.5 to 1.0 g per kg D25W bolus
  • Continuous glucose infusion at 6 to 8 mg per kg per minute via central access titrated to maintain blood glucose above 4 mmol per L
  • Continuous cardiac monitoring mandatory throughout admission
  • Strictly avoid propofol and all lipid-based sedatives due to beta-oxidation blockade.

🐾 Veterinary β€” Dogs

Onset 1 to 3 hours. Severe seizures, sudden weakness, hypoglycemia, cardiac collapse.

Treatment: Immediate IV dextrose bolus, continuous glucose infusion, cardiac monitoring. Avoid propofol and lipid-based sedatives.

🐾 Veterinary β€” Cats

Similar presentation to dogs.

Treatment: Immediate dextrose supplementation, continuous glucose monitoring, cardiac support. Avoid propofol and lipid-based sedatives.

Podostroma cornu-damae Tier 1 β€” Lethal
Toxic on skin contact alone β€” Japan, Korea, eastern Russia, parts of China
Distribution
Japan, South Korea, eastern Russia, and parts of China. Found in deciduous forests as a saprotrophic species.
Season
July to October
Identification
Distinctive upright bright red to orange finger-like or coral-shaped fruiting body with white interior flesh. Does not resemble a typical mushroom cap and stem structure.
Toxin
Macrocyclic trichothecene mycotoxins β€” specifically satratoxin H, roridin E, and verrucarin J β€” inhibit the 60S ribosomal subunit halting protein synthesis throughout all rapidly dividing cells.
⚠ SAFETY CRITICAL: This species is toxic on skin contact alone β€” handling without nitrile gloves is sufficient to cause systemic toxicity. Treating clinician must wear nitrile gloves when examining any patient or animal with suspected dermal exposure.

Young Ganoderma lucidum and red Cordyceps species but neither has the distinctive vertical finger-like structure with white interior flesh.

  • Early GI symptoms including nausea and vomiting onset 1 to 4 hours following ingestion or dermal contact
  • Then a delayed multi-system collapse over days 2 to 7 including severe skin and mucosal membrane peeling, total body hair loss alopecia, pancytopenia, bone marrow suppression, and multi-organ failure
  • Clinicians must not be falsely reassured by apparent early recovery after the initial GI phase.

Decontamination & Systemic Management

  • Immediate full dermal decontamination with high volume running water for 15 to 20 minutes β€” avoid scrubbing to prevent further toxin penetration
  • Protective reverse isolation
  • G-CSF 5 mcg per kg per day subcutaneous to stimulate neutrophil recovery
  • Empiric broad spectrum antibiotics for immunocompromised coverage
  • Blood products as needed for pancytopenia
  • Early therapeutic plasma exchange or continuous hemodiafiltration (CHDF)

Pediatric Protocol

  • G-CSF 5 mcg per kg per day weight based β€” same as adult dosing
  • Strict infection control given severity of bone marrow suppression
  • Blood product transfusion thresholds should be set lower than adult thresholds given pediatric cardiovascular reserve limitations

🐾 Veterinary β€” Dogs

High mortality, severe progressive GI distress, systemic toxicity, bone marrow suppression. Treating veterinarian must wear nitrile gloves.

Treatment: Immediate dermal decontamination, aggressive supportive care, G-CSF if available. Near 100 percent fatal without immediate decontamination.

🐾 Veterinary β€” Cats

Similar presentation to dogs with near 100 percent mortality without immediate decontamination. Treating veterinarian must wear nitrile gloves.

Treatment: Immediate decontamination, intensive supportive care. Guarded to poor prognosis.

△ Section III β€” Tier 2 Species
Amanita pseudoporphyria Tier 2 β€” Severe
Triple threat nephrotoxic hepatotoxic cardiac toxidrome β€” Japan, Korea, China, Thailand
Distribution
Japan, Korea, China, and Thailand. Mid-summer to autumn. Found in mixed forests associated with both deciduous and coniferous trees.
Identification
White to pale grey cap with grey wart patches, bulbous base with a rimmed volva, white gills, white spore print.
Lookalike
Amanita princeps which is considered edible in parts of Asia and has a similar pale appearance and large volva but typically has a yellowish tint.
Toxin
Allenic norleucine β€” 2-amino-4,5-hexadienoic acid β€” causes severe oxidative stress concentrating within the renal parenchyma. East Asian CDC cohort data confirms concurrent direct hepatotoxicity and acute myocardial injury.
⚠ TRIPLE THREAT: This toxin affects renal, hepatic, and cardiac systems simultaneously. Clinicians must never assume non-renal organ systems are spared.
  • Mild GI distress 1 to 12 hours
  • Severe bilateral flank pain and acute renal failure with oliguria or anuria 24 to 48 hours
  • Concurrent liver enzyme elevation and INR rise
  • Myocardial injury markers including troponin elevation and ECG changes

Multi-Organ Monitoring Protocol

  • Euvolemic targeted resuscitation with central venous pressure monitoring titrated hourly β€” do NOT apply aggressive fluid diuresis to adult patients with this toxidrome
  • Mandatory continuous monitoring of renal panels (creatinine and urea), liver panels (ALT, AST, INR), and cardiac panels (troponin and ECG) every 6 hours
  • Urgent nephrology consultation for early intermittent hemodialysis or CVVH
  • Cardiology consultation for myocardial injury monitoring
  • Supportive liver care
β›” FATAL RISK β€” PULMONARY EDEMA: A patient with toxin-induced myocardial injury and oliguric renal failure who receives aggressive fluid loading will rapidly develop fatal acute pulmonary edema. Adult fluid management must be euvolemic and CVP-guided, never aggressive diuresis.

Pediatric Fluid Protocol

  • Conservative weight-based IV fluid resuscitation at 1.0 to 1.5 mL per kg per hour with strict fluid balance monitoring every 2 hours
  • Do not exceed this restrictive target β€” volume overload in a pediatric patient with nephrotoxic acute kidney injury will rapidly precipitate acute pulmonary edema and cerebral swelling
  • Maintain exceptionally low threshold for early CVVH given the child's highly limited renal reserve

🐾 Veterinary β€” Dogs

Expand diagnostic screening immediately to include baseline and serial urinalysis tracking for renal casts and acute proteinuria, serum creatinine, BUN, liver transaminases, cardiac troponin, and continuous ECG telemetry.

Treatment: Cautious IV fluid diuresis strictly titrated to actual hourly urine output β€” avoid aggressive fluid loading or traditional flushing targets as oliguric or anuric renal failure will trigger life-threatening volume overload. Guarded prognosis.

🐾 Veterinary β€” Cats

Immediate urinalysis, comprehensive renal and hepatic biochemistry panels, cardiac troponin, and ECG tracking.

Treatment: Conservative IV fluid therapy titrated with extreme caution via syringe pump to match strict insensible losses if urine output drops. Prognosis guarded to poor if acute kidney injury or myocardial changes manifest.

△ Section IV β€” Tier 3 Species
Chlorophyllum molybdites Tier 3 β€” GI Toxin
Most common cause of mushroom poisoning in tropical Asia β€” widespread
Distribution
Widespread across tropical and subtropical Asia including India, southern China, Thailand, Vietnam, Philippines, and Indonesia. Common in lawns, parks, and disturbed grassland areas.
Season
Year round in tropical regions; summer to autumn in temperate zones.
Identification
Large white to pale grey convex cap becoming flat with age. Gills start white and turn distinctly green at spore maturity. Green spore print is the definitive distinguishing feature. Thick white stem with a prominent double ring. Cap can reach 30 cm across.
Toxin
Severe GI irritation caused by a toxic polymeric protein.

Most dangerous confusion is with Macrolepiota procera (the Parasol Mushroom) which is edible and has a similar large white appearance and prominent ring. Critical difference is the green spore print on Chlorophyllum molybdites versus white on Macrolepiota procera. Also confused with young Amanita species before the cap flattens.

  • Onset under 2 hours
  • Violent projectile vomiting, profuse watery to bloody diarrhea, severe abdominal cramping, rapid dehydration
  • Self-limiting in most healthy adults but can cause serious electrolyte and renal complications in children, elderly patients, and immunocompromised patients

Supportive Care

  • IV crystalloid fluid resuscitation
  • IV Ondansetron 4 to 8 mg for nausea control
  • Continuous electrolyte monitoring including sodium, potassium, and chloride
  • Renal function tracking
  • Hospital admission recommended for all pediatric patients and all vulnerable adults

Pediatric Protocol

  • IV fluid resuscitation 20 mL per kg bolus then titrated to clinical response
  • IV Ondansetron 0.15 mg per kg per dose maximum 4 mg per dose
  • Continuous electrolyte replacement
  • Close monitoring for hypokalemia and metabolic alkalosis from prolonged vomiting

🐾 Veterinary β€” Dogs

Onset under 2 hours. Rapid explosive vomiting, bloody diarrhea, weakness, severe dehydration.

Treatment: IV fluid resuscitation, Maropitant or Ondansetron antiemetics, electrolyte replacement, supportive care.

🐾 Veterinary β€” Cats

Vomiting, diarrhea, lethargy, dehydration.

Treatment: IV fluids, antiemetics, electrolyte support, supportive care.

☎ Section V β€” Regional Poison Control Contacts
IMPORTANT NOTE: Phone numbers for regional poison control centers change periodically. Verify these numbers are currently active before relying on them in a clinical emergency.

Asia Regional Poison Control Centers

China β€” Beijing Poison Control Center
24 hours
+86-10-8313-2345
Japan β€” Poison Information Center Osaka
24 hours
+81-72-727-2499
South Korea β€” National Emergency Poison Line (domestic)
24 hours
1339
South Korea β€” National Emergency Poison Line (international)
24 hours
+82-43-719-7777
India β€” National Poisons Information Centre, AIIMS New Delhi
24 hours
+91-11-2658-8669
+91-11-2659-3677
⚙ Section VI β€” Clinical Case Intake Protocol

Demographics

Patient age, weight, and number of people exposed from the same meal or foraging event.

Location

Province and specific habitat type where the mushroom was collected including forest type, elevation, and substrate.

Timeline

Precise ingestion time and precise onset time of first symptoms.

Preparation Method

Raw or cooked, whether cooking appeared to alter the mushroom appearance, whether other species were collected at the same time.

Sample Preservation

Preserve any remaining raw physical mushroom material refrigerated in a paper bag β€” never plastic which accelerates cellular decomposition and mold growth.

Gastric Aspirate Protocol for Cooked Specimens

In critical scenarios where the ingested mushrooms were entirely cooked or consumed leaving no raw material behind, collect a gastric aspirate sample via nasogastric tube within the first 6 hours post-ingestion. While cooking completely destroys macro-morphological identification features, heat-stable bicyclic octapeptide amatoxins easily survive cooking temperatures. Submit the gastric aspirate for ELISA or immunoassay analysis to definitively confirm amatoxin exposure even when zero physical mushroom tissue remains available.

Clinical Disclaimer: This guide is intended as a quick reference for healthcare professionals and does not replace clinical judgment, specialist consultation, or local protocols. All treatment decisions should be made in consultation with a toxicologist and/or poison control center. Species identification from text alone is insufficient β€” always consult a qualified mycologist or poison control specialist. This guide is provided for educational purposes only.