Toxic Fungi of Western North America
Clinical picture, presumed toxin and treatment
The clinical presentation begins with gastrointestinal symptoms (especially nausea and vomiting) usually beginning 2-12 hours after ingestion, although in one atypical case GI symptoms began very early at 20-30 minutes. (116,117) These symptoms usually go on to include kidney failure (or rarely liver failure) within a few days (usually 2-6 days). The atypical findings may represent mixed collections. The initial urine output is dilute and the flow normal or even increased despite abnormal kidney tests. Patients later display the usual oliguria (reduced flow) of acute kidney failure. Almost all of these patients had been searching for autumn specimens of “matsutake”.
The first two reported cases (1976,1982) had only nausea, abdominal discomfort, anxiety and malaise. Neither one had renal failure. The Toxicology Committee of the Oregon Mycological Society reviewed a more severe case near The Dalles. After a delay of 8 hours, the man had nausea and repeated vomiting before both renal and liver failure ensued. The liver failure was reversible, but he required intermittent kidney dialysis. In 1988, another poisoning occurred, but this time near Vancouver, British Columbia. After a local physician examined him, and found nothing the patient went back to Vancouver after having vomited for three days. He had renal failure, but did not require dialysis. (116)
Another patient, a Laotian immigrant, began vomiting after a 10½ hour delay. (116) On hospital admission, he had a slightly elevated temperature and a very alkaline urine (pH 9). Starting the next day, he became oliguric with the urine output dropping increasingly. He then went into overt renal failure without any evidence of liver toxicity. He was intermittently dialyzed and finally discharged. The patient’s relatives gathered a bag of mushrooms from the original collection site, which included Amanita smithiana. The very alkaline urine reported is very unusual unless excessive amounts of bicarbonate were given intravenously to combat acidosis. The pH of the urine in other possible cases of Amanita smithiana poisoning should be reported.
In 1998, four more patients were reported from the Northwest with Amanita smithiana poisoning. All of these recovered after hemodialysis with return to normal kidney function. One of these cases is notable because the patient was seen in the ER and diagnosed as irritant GI poisoning; the patient later returned to the same facility and was admitted with kidney failure (this time with the proper diagnosis). (117)
The exact toxins have not yet been fully identified, but are not similar to the renal toxins in some species of Cortinarius. Including Europe, a total of nine cases is known. One compound isolated from Amanita smithiana, allenic norleucine (an amino sugar), was toxic in animal cells. (17e),(118) The amino acid, pentynoic acid, may also play a role. These compounds were first found in Europe's Amanita proxima poisonings. Amanita smithiana's potential toxins require much more study.
One California case in the early 1960's was puzzling at the time and may have been a case of Amanita smithiana poisoning. (119) The University of California ascribed the case to Amanita phalloides without mushroom identification. It may have been Amanita smithiana toxicity, although the symptoms were more severe than in any case noted by Tulloss and Lindgren. (116) Two hours after a meal, this lady had three episodes of urinary urgency and slightly watery eyes followed by vomiting. She was seen at a local hospital for "muscarine poisoning" and treated with atropine, but put out only 3 1/3 ounces of urine over the next three days. She was then transferred to the University of California. There was no evidence of any liver injury and she survived after intermittent peritoneal dialysis (cleansing solution flushed in and out of the abdomen using the gut wall membranes instead of the artificial membranes of a kidney dialysis machine). Just before discharge, a kidney biopsy was done which showed marked diffuse interstitial fibrosis (microscopic scarring between cells) and regenerating kidney tubules without inflammation.