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An Interesting Case of Mushroom Poisoning

James R. Addison, MD FACP
Assistant Professor Department of Medicine
Assistant Professor Division of Emergency Medicine
Michigan State University College of Human Medicine, Upper Peninsula Campus
Marquette General Hospital
420 West Magnetic Street
Marquette, Michigan 49855, USA
email: james.addison [at]


Poisoning with amatoxin is the most serious potential toxicity that may result from ingestion of wild mushrooms1. Amatoxin is the cause of the majority of reported deaths from mushroom poisoning2. Amatoxins occur in several common genera: AmanitaGalerina and Lepiota. The potential for fatal poisoning with amatoxin is a significant concern in patients that present with delayed onset (6-24 hours post-ingestion) of gastroenteritis (vomiting and diarrhea) symptoms following mushroom ingestion. In the following paper I will discuss a case of apparent mushroom poisoning, initially attributed to amatoxin, that was reported to the NAMA toxicologist during the summer of 2013.

Case Report

On 7-29-2013 a 64-year-old male patient presented to the Emergency Department of a local hospital in the Upper Peninsula of Michigan and stated that he had eaten “poison mushrooms.” He stated that he had eaten the mushrooms on 7-27 and was still sick. He was unable to identify the mushrooms that he had ingested other than that they were white mushrooms with white gills that he had picked in his backyard. He did not bring any specimens of the mushrooms for identification. He stated that he had eaten about “two handfuls” of the mushrooms. He denied consumption of alcohol at the time of this ingestion. He denied application of insecticides, herbicides or other chemicals to his lawn.

Approximately 12 hours after ingestion he awakened from sleep with severe cramping abdominal pain, initially associated with vomiting and subsequent onset of profuse watery diarrhea. He did not note the presence of blood in either the vomitus or the stools. He noted that the vomiting had subsided after 4-5 hours but diarrhea persisted with frequent and innumerable loose watery stools.

After approximately 24 hours of illness the patient began to experience light-headedness and noted severe muscle cramping. Despite the severity of his symptoms he attempted home hydration. By the afternoon of 7-29 he noted that he knew he was in trouble and decided to go to the Emergency Department. This was approximately 36 hours after onset of symptoms and 48 hours after ingestion.

Past Medical History: significant for aortic valvular stenosis (described as moderate), dyslipidemia, hypertension, gout/hyperuricemia and generalized osteoarthritis.

Past Surgical History: Multiple orthopedic surgeries. He had not had surgery for his heart valve problem.

Medications: Hydrochlorthiazide, 12.5mg per day, Celecoxib 200mg per day, Omeprazole 20mg twice per day, Allopurinol 300mg in the AM and 200mg in the PM, Fluoxetine 20mg per day, Rosuvastatin 20mg per day, Amlodipine 10mg per day, Hydrocodone/acetaminophen 10mg/500mg at bedtime, Lisinopril 20mg per day and fish oil supplement.

Medication Allergies: None identified

Social and Personal History: He is a retired fireman. He was a college football player and remains physically active. He smokes an occasional cigar and drinks alcohol moderately. He denies use of recreational drugs. He picks and eats wild mushrooms regularly and had never become ill from a mushroom ingestion in the past. He was able to identify morels and chanterelles (his favorite edibles) from pictures without difficulty.

Physical exam: A male patient noted to be in moderate distress from persistent muscle and abdominal cramps and diarrhea.

Vital Signs: BP=110/70 with patient supine, P=95/minute, Respirations = 18/minute, Temperature=97.5 degrees F, oxygen saturation 95% while breathing room air.

The only abnormal findings on physical exam that were noted in the record were dry mucous membranes and a soft heart murmur without further description. He was not noted to be jaundiced and his mental status and neurologic exam were described as normal.

Lab values at presentation with abnormal values in red:

  • Electrolytes: Sodium=137, potassium=5.3, chloride=102, dissolved CO2=11 (low)
  • Anion gap=24 (elevated)—an indication of elevated acid load/acidosis
  • BUN=59 (high), creatinine=5.7 (high)—tests of kidney function
  • ALT=59—liver enzyme
  • AST=60 (upper limit of normal is 59)—liver enzyme
  • Alkaline phosphatase=96
  • Lipase=77—pancreatic enzyme
  • INR=1.1, prothrombin time=1.1—test of liver function and coagulation
  • WBC=13,400 (high) with normal differential, Hb=17.3 (high), platelets=352,000
  • Creatine kinase (CK)=1383 (high) and myoglobin=3293 (high)—muscle enzymes
  • Blood ketones: negative
  • Glucose=128 (slightly high)
  • Urine screen for drugs of abuse negative for all substances except opiates (a prescribed medication)
  • Measured serum osmolality=302, calculated serum osmolality=302
  • Salicylates: negative
  • Lactic acid=1.0
  • Arterial blood gas analysis: pO2=73, pCO2=29, pH=7.19—a measure of respiratory competence
  • Urinalysis: yellow in color with specific gravity of 1.014, Protein 1+, occult blood 2+; 2 white cells and 2 red cells noted on microscopic exam

Hospital Course

While in the Emergency Department the patient was rehydrated with normal saline intravenously and was subsequently admitted for observation. He received no specific intervention (silibinin, penicillin, activated charcoal) directed toward the potential of amatoxin intoxication while in the ED or while an inpatient.

Following admission, hydration was continued and his medications were stopped. His abnormal kidney function slowly improved and he was discharged from the hospital after 3 days. At the time of discharge (7-31) he felt well with the exception of mild residual muscle pain. His kidney function was nearly normal.

Table 1: progression of lab results

Date BUN Creatinine AST ALT INR
7-29 59 5.7 60 59 1.1
7-30 57 3.59
7-31 40 1.6 1.1
8-7 28 1.37
8-12 30 1.34 22 39
8-19 29 1.34 23 29


I recently retired from my clinical practice in Emergency Medicine and my name had erroneously been removed from the list of consultants available to evaluate mushroom-related cases. Thus, I was not initially informed of this case and learned of it “through the grapevine” 2 weeks after the encounter. The regional poison control center had been consulted at the time of patient presentation and suggested vigilance regarding the possibility of amatoxin ingestion due to the time course of the patient’s illness. Amatoxin toxicity typically has a delay in onset of 6-24 hours after ingestion with onset of gastroenteritis which may last for 24-48 hours. Following resolution of the gastrointestinal symptoms there is a quiescent asymptomatic period during which liver toxicity may be progressing3. In this case the delay in onset of symptoms from the time of ingestion was certainly suggestive of the possibility of amatoxin poisoning.

In the above reported case the initial contact with the NAMA toxicologist included a photograph of Amanita virosa and a report from a family member that the patient had “severe liver failure” at the time of the initial presentation to the Emergency Department.

The invariable feature of amatoxin poisoning is hepatic (liver) toxicity. This is a result of inactivation of DNA dependent RNA polymerase in the hepatocytes (liver cells) after the toxin crosses the cell membrane2. This results in immediate cessation of protein synthesis. Entry into the cell is facilitated by a specific transport protein. Once the toxin enters the cell, the toxicity is irreversible and ultimately results in apoptosis or cell death2. Outcomes are markedly improved in patients who are treated aggressively with medications that inhibit the entry of the toxin into the intracellular space (intravenous silibinin), gut decontamination and supportive care with hydration and maintenance of adequate circulation2. During the initial treatment period it is important to monitor liver function carefully, and if there is evidence of persistent or worsening liver toxicity, the patient should be evaluated for liver transplantation.

As I evaluated this case it became apparent that there was no evidence of hepatic toxicity at any time during the course of this patient’s illness as evidenced by normal lab tests of liver function (AST, ALT, Alk phos and INR). This made it very unlikely that this represented an amatoxin ingestion. Thus, there must have been some other toxicity if this was indeed related to ingestion of a toxic mushroom.

The primary problem in this case is kidney failure as evidenced by the presence of elevated BUN and creatinine levels. This sometimes results from amatoxin ingestion as a late complication of multi-organ failure, but has not been reported as a primary feature of amatoxin intoxication in the absence of hepatic injury4. Without some evidence of liver involvement it is very unlikely that the patient had ingested an amatoxin containing species.

There are several species of mushrooms that do cause kidney injury as their primary toxicity (Cortinarius species and Amanita smithiana), but the onset of this problem is generally significantly delayed from the time of ingestion (weeks) so these are not likely to be responsible for this patient’s illness4.

The question then becomes: what did happen and why did the patient develop kidney failure? After some study and discussion with colleagues Dr. Michael Beug and Dr. Todd Mitchell it was felt that the problems that this patient developed were multifactorial and that the mushrooms that he ate were not the direct cause of his kidney failure. It was felt very unlikely that this represented an amatoxin ingestion. It is unclear why he developed gastroenteritis.

Could the patient have developed gastroenteritis due to a cause other than a mushroom ingestion? As viral causes of gastroenteritis are prevalent throughout the year, that could certainly be a possibility. As the problem occurred proximate to the time of a mushroom ingestion, a mushroom related gastroenteritis could certainly be a possibility. As his follow-up labs did not address tests of liver function until 8-12-2013 there is a slight chance that abnormal liver function tests were missed. I feel that this is unlikely as the patient was never jaundiced and INR remained stable, indicating active protein synthesis throughout the course of his illness.

Could the patient have ingested a non-mushroom toxin? At the time of presentation the patient had an elevated anion gap metabolic acidosis. This may result from ingestion of a number of toxins, including salicylates and ethylene glycol, which may be associated with kidney failure. An extensive search for such toxins in the emergency department was non-productive. The acidosis appears to have been multifactorial and resolved with re-hydration and normalization of kidney function.

This patient is taking numerous medications, some of which are capable of causing impaired kidney function, especially in the presence of dehydration. These medications are reviewed below.

Lisinopril is a medication used to treat hypertension. This medication inhibits an enzyme (angiotensin converting enzyme/ACE) and may cause decreased kidney perfusion and kidney failure in the presence of dehydration5.

Celecoxib, a cyclo-oxygenase II inhibitor used to treat inflammation (NSAID), may also cause decreased renal perfusion and kidney failure due to its effect on prostaglandin synthesis6. The risk of kidney injury is especially high when Celecoxib is taken in high doses in combination with diuretics (i.e., hydrochlorthiazide) and ACE inhibitors5. Dehydration also increases the risk of kidney injury.

Rosuvastatin is one of the statin drugs that are used to treat high blood lipid levels. Statins are known to cause rhabdomyolysis (breakdown of muscle tissue)9. As the muscle cells are injured they release enzymes (creatine kinase) and pigments (myoglobin). Myoglobin is toxic to the kidneys when present in high levels and also when elevated at fairly low levels for prolonged periods of time7. This patient did have evidence of rhabdomyolysis as evidenced by elevations of creatine kinase and myoglobin.

Omeprazole, a proton pump inhibitor antacid, may cause interstitial nephritis and kidney failure8). This is generally a more chronic process, but may, in combination with all of the other medications the patient was taking, have contributed to his kidney failure.


I think there are several points in this case that are opportunities for education for the physicians that cared for this patient as well as for the patient and his family. Although it is gratifying to ascertain that the patient did not have amatoxin poisoning, during the initial period of care his liver function was not monitored and a significant serious toxicity may have been missed. Fortunately this was not the case. I think this emphasizes the need for accurate diagnosis, but also the need for added vigilance in the presence of a risky ingestion. It is unclear why the admitting physicians did not grasp the serious nature of this problem after initial consultation with a poison center had advised caution regarding the possibility of amatoxin.

The patient also had evidence of significant rhabdomyolysis and his muscle enzymes and myoglobin were not re-evaluated at any time during the course of his illness. In general, for myoglobin to induce renal failure, levels would be expected to be higher than those found at the time of admission. However, persistent low-grade muscle injury, especially when associated with statin medications, has been reported to be a cause of renal failure7. Indeed, the labs were not repeated prior to resumption of his statin, thus leaving open the possibility of chronic injury and recurrent renal failure.

The purpose of reporting this case is not to disparage anyone involved in the case. It does emphasize the importance of accurate diagnosis of potential toxic ingestions to facilitate initiation of appropriate treatment and monitoring. Had this patient truly eaten an amatoxin containing species, the opportunity to intervene early was missed. This may have resulted in serious long-term consequences or even death.

For those of us that forage for edibles, it emphasizes the necessity of certain identification of species prior to ingestion of any mushroom. I did do a follow up home visit with this patient and he has promised to follow “Addison’s rule”: he will not eat any mushroom that he cannot identify to species.

Last I would like to emphasize the importance of accurate reporting of toxic mushroom ingestions. It is gratifying to know that the family of this patient made the effort to report it to NAMA, but unfortunate that the information that was communicated was misleading (recall the family member’s report of severe liver failure and photo of Amanita virosa). Had no one carefully reviewed the features of this case with accurate information it would have been reported in the NAMA annual toxicology report as an amatoxin ingestion with a favorable outcome.


  1. Beug, M. 2012 NAMA Toxicology Committee Report North American Mushrooms. McIlvainea 19: 25-38.
  2. Mengs, Ulrich, Ralf-Torsten Pohl and Todd Mitchell. 2012. Legalon™ SIL: The Antidote of Choice in Patients with Acute Hepatotoxicity from Amatoxin Poisoning. Current Pharmaceutical Biotechnology, 2012, 13: 1964-1970.
  3. Koppel, C. Clinical symptomatology and management of mushroom poisoning. Toxicon 1993, 12: 1513-1540.
  4. Diaz, James H. MD, DrPH, FCCM. 2005. Syndromic diagnosis and management of confirmed mushroom poisonings. Critical Care Medicine 2005, 33, No.2: 427-436.
  5. Lapi, Francesco; Laurent Asoulay; Hui Yin; Sharon J. Nessim; Samy Suissa. 2013. Concurrent use of diuretics, angiotensin converting enzyme inhibitors, and angiotensin blockers with non-steroidal anti-inflammatory drugs and risk of acute kidney injury: nested case control study. British Medical Journal 2013, 346e8525: 1-11.
  6. Risser, Amanda, MD MPH; Deirdre Donovan, MD; John Heintzman, MD; and Tanya Page, MD. NSAID prescribing precautions. American Family Physician 2009 Dec 15;80(12): 1371-1378.
  7. Dormuth, Colin R; Brenda R Hemmelgarn; J Michael Paterson, Matthew T James; Gary F Teare; Colette B Raymond; Jean-Phillipe Lafrance; Adrian Levy; Amit X Garg, Pierre Ernst. Use of high potency statins and rates of admission for acute kidney injury: multicenter observational analysis of administrative databases. British Medical Journal 2013; 346:f880: 1-10
  8. Klepser, Donald; Dean S Collier, Gary L Cochran. Proton pump inhibitors and acute kidney injury: a nested case-control study. 2013 BMC Nephrology 14:150 1-7.
  9. Sakamoto, Kazuho and Junko Kimura. Mechanism of statin-induced rhabdomyolysis. Journal of Pharmacological Science 2013; 123, 289-294.

Citation: James R. Addison, MD FACP (2014) An Interesting Case of Mushroom Poisoning, McIlvainea 23 (19-20):

Editor: Michael W. Beug
Publisher: North American Mycological Association
Published: May 1, 2014
Copyright: © 2014 James R. Addison, MD FACP

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