Issues raised by a recent case involving GI Distress and life threatening symptoms attributed to 'edible' mushrooms.
By Bill Bakaitis
In mid-July an experienced mushrooming family had a weekend foray, collected and ate mushrooms which they had identified from authoritative field guides as edible species. Three people, an elderly father and two adults shared a cooked meal of only two mushrooms, following which two of the three experienced severe gastro-intestinal distress. The symptoms were strong enough to send one adult to the emergency room of a local hospital. This person was treated symptomatically and released. A few hours later the elderly father also was stricken with the same symptoms. He did not seek treatment that evening. By the following day he was experiencing profound malaise and lethargy. Three days later he was hospitalized with a platelet count near zero. At counts of 20,000 or less capillary leakages readily occur. In his advanced stage he was in severe danger with bruises across his entire body, bleeding from his brain and other internal organs.
I was contacted by the Responsible Poison Control Center for help in identifying the mushrooms presumed to have caused these symptoms. When Leccinum was mentioned as being one of the mushrooms eaten, Marilyn Shaw of the Rocky Mountain Poison and Drug Center, who has considerable experience in handling Leccinum poisonings, was contacted. A five way, hour and a half, telephone consultation was initiated following which the two mushrooms were 'identified' as probably being a member of the (safe) Boletus edulis complex and a (probably toxic) Leccinum. The medical authorities involved independently developed a plan of treatment for the patient based upon his symptoms. Shortly after the conclusion of the consultation I filed my normal report with the poison control centers and with Michael Beug at the NAMA Toxicology report center. I also issued a "Leccinum Alert" to clubs active in the Northeast. (See http://leslieland.com/blog/wild-mushroom-warning-the-scaber-stalks-leccinum-species-are-no-longer-considered-safe/ for a version of this report which includes a few images)
The case, and report, immediately caught the interest of area mycologists and set in motion a lively and extensive email exchange. Interest centered upon not only the 'edibility/toxicity' of Leccinum, but also upon the possibility that the 'safe' B. edulis might actually be a potentially toxic B. huronensis. Both Bill Yule and Gary Lincoff were able to alert us to this possibility, and these suggestions were seriously considered.
The actual identity of the mushrooms consumed may never be known for certain, and not to be discounted is the possibility that some other factor may have caused the symptoms. The comments which follow, prompted by the details of this case serve to inform those of us who try to identify mushrooms in such cases of the complexities involved.
In short this case raises issues of 1, the reliability of published accounts of edibility of mushroom species, 2, the updating of new information and distribution of this information, 3, difficulties in identification, both in the field and laboratory of mushrooms distinguished by subtle differences, and 4, alterations in the recall of 'eyewitness testimony' particularly where intervening experiences and leading questions meld with powerful emotions let loose by the distress of those involved. 5. Finally, different witnesses can have quite different memories. All of these factors came into play in this case, each being a powerful lens through which one can see the limitations imposed by the other factors. The relevance of these factors transcends this particular case and has broad application.
Consider the following: In this case there were no actual mushrooms to examine; No images to view. Three mushrooms were apparently collected: one was thrown out and the other two were eaten. What was left then for us to 'identify' was the texture of three day old recall of two of the three people involved and the symptoms they presented.
These mushroomers were self identified 'good, experienced', collectors yet over the course of the conference the descriptions of the mushrooms changed several times and several hypotheses of the identity were forwarded. 'Suillus pictus' was a name first given to Poison Control and used when I was contacted. When I spoke with, the attending Physician, he said that 'Leccinum' and 'King Mushroom' were the names he was given by the family. One family member said that even though she had eaten one of the mushrooms before, the 'King Mushroom', it was a new name for her- but she could not remember its previous name. One of the family members apparently relying upon a description from Lincoff's Audubon Guide offered one name and description of the Leccinum. Another member of the family seemed to lean toward another, perhaps from Miller's Mushrooms of North America (edition not mentioned), and had a very different description of the same mushroom. Based entirely upon the symptoms, the chief toxicologist wondered if we might be dealing with a Paxillus-like syndrome. The names and possibilities which reverberated through conference circuit were enough to make anyone's head spin. More to the point, it seems safe to conclude that this discussion probably affected the very recall of the family members participating in this conference call.
Memory and 'eyewitness testimony':
For thirty eight years before retirement I was a college professor in Behavioral Sciences. The processes of Perception and Cognition, reiterated semester by semester, have scribed themselves rather deeply in my understanding of how we view the world. Think of 'eyewitness testimony'. We commonly assume that these first person eyewitness accounts are both reliable and accurate, yet studies show that they are easily altered by offering suggestions as to what the eyewitness actually saw. Subtle differences in active or passive verbs, for example, are enough to completely change the vectors of force involved in a memory of a viewed film clip, a staged or actual crime. Stop signs appear in the mind where none exist in a film clip. Guns, knives, hair, skin color, gender; all can be altered in the mind of the observer of a staged event by suggestions of the questioner, by comments from others, or by material experienced (read or overheard) between the event and the recall. Subjected to 'lie detection' devices, the witnesses show no signs of deceit. They actually believe that what they recalled is what they saw and characteristically express disbelief when shown the original film footage or are otherwise debriefed at the end of the experiment.
From studies with radioactive isotopes and memory traces in the brains of rats, compelling evidence has emerged which shows that when a memory is recalled, the old memory trace is destroyed and a new one rebuilt. With each retelling of a story then, cognitive psychology teaches us that the original perception fades and is replaced with the current understanding. Indeed this is part of the process of therapy as when a person continually recounts a particularly harrowing event in their life and 'processes' it into a safer and more meaningful form. Over time, and with repeated recall, the memory looses its emotional hold, changes form, becomes more malleable and more easily integrated into the person's self concept.
Not all of the processing is done in the conscious mind. Considerable processing occurs during REM sleep as dreams. And since the emotional parts of the memory are partially stored as autonomic bodily functions they have exceptional staying power, are often difficult to process and 'correct', and are often able to mold the memory into an altered form congruent with the emotion. I'll explain this in a moment.
Mushrooms as 'Ambiguous stimuli':
So, how does this all apply to mushroom identification? Well as we all know there are usually complex and subtle distinctions between mushrooms. They have overlapping colors, textures, gill attachments and other structures that usually take a trained eye and considerable experience to differentiate. In short they might be considered 'ambiguous' in form, structure, texture and color.
When Psychologists ask subjects to interpret ambiguous stimuli – the classic example is with Rorschach Cards – a certain protocol is used. The first time through the subject is given complete freedom to describe what it is they see. Notes are taken, of course, and only after the free recall is concluded does questioning of the subject occur. At this stage the perceptions might be directed to a particular part of the experience, such as the color or texture. Only in the third part of the protocol is the subject asked to corroborate a specific perception, such as "Do you see a butterfly?" Responses to directed perceptions are important, but carry different weight and significance than those freely given.
This is a technique well suited to interviewing a person -the patient, family member, nurse, or physician - who holds in their hand, or mind, the mushroom we are asked to identify. When dealing with poison control calls, I always ask the family member to describe the mushroom as they see it, only later asking if they can see certain features and structures that I think might be there. In a final phase I may ask them to do a Google Image search for a particular species that I think might be what they have in hand and ask them to make judgments about the similarity of the mushrooms. This is a particularly valuable technique when the images sent to me for viewing get 'hung up' in the internet or are of poor cell-phone quality.
This is also a great technique for any of us to use when trying to identify a new mushroom that we have just collected. Prior to the widespread use of digital cameras we mushroomers would often take notes and draw the mushroom in some detail as a first step in the identification process. Only later would we compare our drawings with published descriptions and images. I still find this to be a valuable process and recommend it to my students.
As applied to the Leccinum/King Mushroom case, I am quite sure that the perceptions offered were shaped by the texts consulted and also to some extent by the multi-pronged ongoing discussion. In the end we 'accepted' the ID's given by the family, and concluded that their descriptions and symptoms were consistent with the many Leccinum cases with which Marilyn had been involved, but the degree of confidence was less that we would have wished.
Classically conditioned memories:
Before I move on to the huronensis/edulis and then Leccinum part of the discussion allow me one more digression, one which revolves around the perceptions of GI distress and the cause attributed to it. As implied above these classically conditioned autonomic nervous system responses are very powerful and convincing.
Many years ago I needed to call Poison Control to report my own case of food poisoning. It was spring and my live-in partner and I had returned from a botanizing trip to part of the old Delaware - to - Hudson Canal system. Shelagh, a writer, artist, fashion and fabric designer wanted to collect Bloodroot and Bedstraw so that she could compare their dye characteristics with that of Cochineal. Being moderately upscale hippies, we also carried Euell Gibbons Stalking the Wild Asparagus book with us, had our own home garden and had just brewed a batch of homemade root-beer. In short, for a late lunch, we had a wonderfully healthy meal of local, organic produce. In fact, the only purchased ingredient was the Tuna that went into the salad.
Shortly after our meal we both developed a light-headed feeling. At first it was slightly intoxicating and rather pleasant. Then came the hallucinations. We both had the sensation of hovering about five feet above the ground. Within a few minutes we began to float across the landscape. Being analytical about it all, I tried to judge the speed, and see if I could control where I was going. By this time Shelagh had her finger down her throat and her head in the toilet. For me the trip speeded up from a sedate thirty-five mile an hour cruise to something more like a wild hundred mile an hour roller coaster ride. That is when I lost my lunch and we decided to call poison control. A consultant appeared within a half hour, interviewed us and collected both the tuna salad and the root beer.
We were convinced it was the root beer; Convinced beyond a shadow of a doubt. The taste of it was in our mouth nose throat lungs. The smell permeated the house. We immediately called the family of a young friend who had been with us when we made the root beer and had taken some with her to her home in the city.
By evening the symptoms had subsided. Although weaker we were pretty much back to normal by the next a day when the results of the analysis done by Poison Control were returned. Surprisingly there was no problem with either the tuna salad or the root beer. No Contamination? We couldn't believe it. The problem must have been in the bottle we finished. If only we had kept some. We called the family in NY but by this time they had thrown out their bottle. Well, we concluded we were lucky and closed the books on that episode in our lives.
Closed it that is until two or three months later when I looked in our garden at the wild asparagus we collected from the canal and transplanted to our home. Instead of the feathery fern of asparagus was a flattened legume-like leaf structure. Whoa! What the heck is going on here? We had eaten some of this 'asparagus' that day of our illness, but thought nothing of it. Neither did the poison control guy. But what was this?
Well, it turned out to be Wild Indigo (Baptisia tinctoria). If you look up the symptoms produced when ingested you will see that we had them all. But the taste of the regurgitated meal convinced us that home-made root beer was the cause of our misery.
I am quite sure that in a non-trivial number of cases this also plays a part in the attribution of mushrooms as the cause of GI distress. It seems to have been a part in this case: one of the family members maintained in no uncertain terms that when remains of the dinner were regurgitated, and up came the mushrooms, there was no doubt that it was the mushroom (singular) that was responsible.
Behavioral Psychologists have a name for the association of GI illness with food previously eaten: they call it 'Backward Classical Conditioning': Backward, because in this case the Conditioned Stimulus (e.g. my root beer or Pavlov's Bell) appears after the Unconditioned Stimulus (my nausea or Pavlov's dog's food). In the normal course of events the bell (CS) precedes the food (UCS) and consequent salivary response (UCR).
Classical conditioning is automatic learning. It is involuntary, non-verbal, usually non-conscious, and involves glandular secretions controlled by smooth muscles spread throughout the autonomic nervous system. Unlike Operant Conditioning (e.g. learning to use the brain and striated muscles to ride a bike) in Classical Conditioning the Central Nervous System and Brain are only minimally involved, if at all. Because of positive feedback loops, some classically conditioned responses such as nausea and panic reactions are self reinforcing and can also be exceptionally difficult to 'forget' – 'extinguish' is the term used.
The association here is thought to form during the experience of tasting and smelling the regurgitated food while also experiencing the distress of nausea. It is learning at its most powerful, something that cancer patients experience when nauseated by their medications. The regurgitated food becomes indelibly linked with the GI distress and even though the patient rationally understands that it was the medication that caused the symptoms, they will, in the future, be sickened by food that was consumed prior to treatment and subsequently regurgitated. A behavioral prevention strategy sometimes utilized is to eat a decoy food prior to treatment – Maple flavored Ice cream for example.
The huronensis hypothesis:
Bill Yule was the first to suggest B. huronensis as the toxic mushroom in this case. He wrote… I'm curious why the investigators seemed to zero in on the Leccinum group rather than the "King" group as the responsible agent? As many of us know people often mistake Boletus huronensis for "The King" (aka B. edulis complex) and B. huronensis is certainly toxic to some people,[especially an elderly person] Just wondering had anyone considered B. huronensis?
Well, No! Not at the time and this brings us to some of the more traditional issues involves with mushroom identification.
In the first place, huronensis is a rarely encountered/described/identified mushroom. One may therefore assume that it is, in fact, a rare bird, and, as they say in birding and medicine alike, what is rare is rare. Leccinum, by contrast are rather common mushrooms of summer, often approaching 'weed' status'. As such, and by mere chance, Leccinum is far more likely to have been collected and consumed than huronensis.
I also was aware that Leccinum had a reputation for causing illness, but was unaware, at the time, of the toxicity of huronensis. As I say it is a rare mushroom. On 7/19/09 when I did a Google Images search for 'Boletus huronensis' all I got was Michael Jackson, the Apollo Space Ship and Farrah Fawcet! When I did the same for 'B. huronensis' there was only one image for this mushroom in the 8 pages of images retrieved. It is the first image which appeared and happens to be my image from a post I did last year. (see http://leslieland.com/blog/the-mushrooms-of-autumn-porcini/ )
This raises a few other quite interesting issues. When I collected and attempted to identify this mushroom last year 'huronensis' was the conclusion I came to, but I readily acknowledge that my ID could be incorrect. It was collected in Maine, my microscope and chemicals were in NY but it was the best that could be done with mushroom and references in hand. I have no voucher for that collection and Leslie is quite sure that we ate it. I completely disremember. So goes that fickle flick of memory, but if we did eat it, it did not make us sick.
As we all know, some mushrooms are tough to identify and, according to the sources I consulted, even experts with the full array of tools at their disposal mistake B. huronensis for B. impolitus. That is what was reported in the post. Nothing was said about toxicity because the sources consulted at the time either described it as edible or offered no comment. It is listed as edible, for example, in Bessette, Roody and Bessette's recent North American Boletes, as well as Grund and Harrison's Nova Scotian Boletes. Smith and Thiers, who first published this species in 1968 (The Boletes of Michigan), did not comment on its edibility. Such are some of the problems with the static printed texts, which simply cannot keep up with a rapidly changing world.
For updates we often turn to the internet where Michael Quo's Mushroom Expert site is often the first one turned to. He describes huronensis in two places but offers no comment on edibility. (Interestingly the reference on Page nine appears in such a way that if one were to simply Google huronensis, and arrive at the entry without understanding the graphic layout of the page, one might read the description of huronensis incorrectly thinking instead it to be hypoxanthus, - growing under hardwoods- which in fact was a mistake made more than once in the exchange concerning this case. seehttp://www.mushroomexpert.com/boletus_09.html Two mycologists entered the ongoing, online colloquy to remind us that huronensis is associated with Hemlock, not hardwoods. And the family member who was not sickened by the meal reported that the mushrooms were indeed collected under Hemlock… or was it Fir? He wasn't sure.
A more expansive internet search will show that Gary Lincoff, perhaps as early as 2004, had listed huronensis as a mushroom suspected of causing mild to severe GI symptoms.http://www.nemf.org/files/lincoff/beginners/poison.html (This list interestingly does not include Leccinum.) There is a link on this page which takes one to an image of huronensis which closely resembles mine. In private correspondences Gary reports he knows of one case of huronensis toxicity (from NJ) and thinks there may have been another, perhaps a COMA member. Bill Yule knows of the same NJ case and thinks there may have been two more. I could not find any case of either huronensis or its near twin B. impolitus in the NAMA case registry, but there are reports of toxicity attributed to B. edulis, barrowsii and unidentified spp. Also reported were well over 50 cases (3.5%) where toxicity was attributed to species of Leccinum. seehttp://www.namyco.org/images/pdf%20files/Poisonings30year.pdf
(Since this was first written, the 2008 case reports were published and include this:
Laurie Leonard reported on the consumption of just two forkfuls of Boletus huronensis by a couple of individuals who suffered five hours of severe vomiting and then diarrhea. Ernst Both, who conducted the identification, said that he knew of other cases of upset by Boletus huronensis.http://www.namyco.org/images/publications/9_Toxic_2008.pdf)
Marilyn and I were glad to receive the comments and suggestions offered by both Bill and Gary about the toxicity of huronensis. This feedback is vital. For the record, she and I reviewed our notes and from the descriptions offered by the family and were able to rule out huronensis as a possibility. I also have updated the material on my Blog post to include the toxicity warnings. As this is being written, a local professional mycologist has offered to try to recollect the mushrooms with the family.
Here is a final thought on the huronensis hypothesis, one which must also have occurred to many readers of this article. If this mushroom is so easily mistaken for edulis, then even if it is rather rare, it must have been eaten by many casual collectors and either was non-toxic to them or produced symptoms so delicate that they were ignored. A third possibility, suggested by Gary and one with which I whole-heartedly agree is that for many collectors mild GI distress is simply assumed to be part of the price of admission for the practice of Mycophagy and is never reported to poison control. These same observations can also apply to many other mushrooms, including the Leccinum to which we can now turn.
The Leccinum hypothesis:
As a group, Leccinum is easy to identify as to genus, but distinguishing among species is a difficult work in progress. (Smith and Thiers list over 80 species from Michigan, and suggest this is preliminary. The Bessettes' and Roody's key for Eastern Scaber Stipes include 37 species which they think can be separated by field characteristics.) In recent years a number of cases of GI symptoms have been attributed to various members of this group, including L. atrostipitatum, aurantiacum, scabrum/insigne, and (Tylopilus) eximius. In the past these were all considered as good edibles but case by case evidence has accumulated as to the problems encountered by some who consume them. Recall that 3.5% of the poisonings reported to NAMA involve Leccinum.
OK. So why do they cause illness to some and not to others? Well, if one rules out the macho 'price of admission' factor described two paragraphs above, and also discounts factors involving accidental contamination by chemical spraying or bacteriological decay, three remaining hypotheses seem to present themselves. The first involves undercooking. The second two seem to involve different conceptual frameworks for understanding the distribution of fungal toxins, and presumable the genes involved in their production: in short, how the world works. Let's take the easy one first.
UNDERCOOKING: Many mushrooms can cause gastric distress if eaten raw. In 1983 a large group of NAMA Foray participants became ill after eating Leccinum cooked as part of the Mycophagy program. As Gary put it in a private communication... These upsets were "explained away by saying that the cooking was at fault: the stems were cooked only as long as the caps. It was assumed that the people who got sick essentially ate undercooked Leccinum stems." To which he added…"Hmmmm!" On to the more interesting hypotheses:
CRYPTIC SPECIES: Roz Lowen, trained in taxonomy, suggested "Leccinum aurantiacum is a problem because most people believe that it is an edible species. There must be a cryptic species that is toxic." Within this context, and stripped of the technical complexities, a 'cryptic species' is a separate species that hides undetected among a larger population. It so closely resembles the dominant species that detection is difficult, if not impossible.
Implied by this mental construct is a world composed of discrete, discontinuous material objects, call them species, each with their own distinct chemical and genetic compositions. This is the major way we tend to think about the world, and we are all familiar with the classic taxonomic literature, in both field guides and monographs which rest upon this framework. If we can only determine the subtle distinctions involved, we will have segregated out two different species. The cryptic will become obvious and, in this case, future illness can be avoided.
FLUID PROCESSES: Marilyn Shaw, experienced in toxicology, offers this hypothesis: "… many if not all Leccinum contain a toxin, that only under certain conditions rises to a level to cause GI symptoms even when cooked". In this view, toxins are spread throughout [at least segments of] the fungal community. The implied conceptual framework is a world of continuous [energy] processes, not discrete [physical] objects. Although not the major way western science conceptualizes the world, it is nonetheless one which has been highly developed by ecologists, field and systems theorists, and theoretical physicists. (See for example Fritjof Kapra's The Web of Life, a summary of which can be found herehttp://www.amazon.com/Web-Life-Scientific-Understanding-Systems/dp/0385476760)
In this view the genes can be thought of as energy processes which move around on the chromosome, from chromosome to chromosome within the genome, and from genome to genome throughout a larger biological community, their effects varying as a function of neighboring energy processes – neighboring genes for those of us who are materialists. This is a world of Jumping Genes, RNA retroviruses and DNA transposons; the Farandolae of Madeleine L'Engle, perhaps. It is a world where Amatoxin producing genes move around from Amanita to Amanita, from Amanita to Galerina, to Conocybe, perhaps to all fungi. Although I don't recall the specific source, my memory holds bits of a discussion where it was maintained that Amatoxins, and presumably the gene responsible, could be found in all, or nearly all fungi, including the common, commercially grown Agaricus. Being found in such minute concentrations, they were not considered to constitute a health threat.
Not inconsequential, these fluid units account for large portions of the genome of various species: about half of the total Maize (corn) genome, for example. In some species individual units are thought to migrate about once a month or so to once a year or so. Under stress this rate of transmission increases. A new transposon can apparently force its way through the genome of an entire genetic population in fifty years or so. (See http://en.wikipedia.org/wiki/Transposon for a quick overview)
This is apparently only one of several mechanisms that allow for the rapid modification of organisms. From this point of view the genome of fungi can be thought of as dynamic, evolution on the go, so to speak, and the toxicity of certain 'species' might be expected to change and to vary over time and place.
As Jonathan Weiner puts it in The Beak of the Finch, “The [genetic] borders between species are as fluid and adaptable, as sensitive to changes in pressure, as the heaving waves in a high sea.” (p171) And from the US Forest Service General and Technical manual 710 concerning morels, we find that "morels … cannot be understood as unique or distinct dikaryotic individuals that always produce genetically identical mushrooms. Rather, they should be considered populations of nuclei or genes. For instance, Aegerter (1995) quoted geneticist Dr. Carol Carter that no two morels she has analyzed are identical, even if they are growing in a cluster" …and connected at the base by a common mycelium. http://www.fs.fed.us/pnw/publications/gtr710/pnw_gtr710c.pdf (p. 49).
CONCLUSIONS: Well, this is certainly a lot of cud to chew, a great deal to consider, hold in mind and attempt to apply. The reader, I think, is entitled to know how I evaluate the arguments presented.
Concerning the last philosophical piece; although I have trained in traditional taxonomy and respect the methods of our mentors and the monographs and field guides that we use, I am more and more inclined to think the world to be more fluid and dynamic than is conventionally assumed. I think, for example, that it is entirely possible for rapid adaptation in species to occur, and it would not surprise me to learn that the 'edibility' of a 'species' could also undergo changes over the course of a human lifetime or less.
Concerning the psychological aspects; I believe that we tend to see a world we want, need, and expect to see. An extended piece on Perception and Cognition in Mycology appears here:http://web.mac.com/diannasmith1/FUNGIPHOTOS/BILL_BAKAITIS_Articles/Entries/2009/7/29_PSYCHOLOGICAL_FACTORS_INFLUENCING_THE_IDENTIFICATION_OF_MUSHROOMSBy_Bill_Bakaitis.html
Concerning the ID and toxicity of the mushrooms in this case; it seems likely that one of the two mushrooms consumed probably caused the GI symptoms, and if so, it was probably the Leccinum rather than the King Mushroom. Although there was some disagreement among the family members, the person with the most convincing recall was able to describe a 'violet' staining reaction to the flesh of the Leccinum. Although this could have been prompted by one of the field guides, under direct questioning she also reported that it darkened upon cooking, a fact that is not in the sources she referred to. Also described was the white reticulation of the stem of the King Bolete, and its non-staining flesh, observations which would seem to rule out the huronensis hypothesis.
Today, as I was concluding this piece, I received word that the elder family member has died, ten days after consuming the mushrooms, and a week after the email exchange which prompted this article. The question will be asked, "Did he die from eating the Leccinum?"
Medical authorities will need to evaluate the pieces of his medical history and his health condition prior to the meal in which the mushrooms were consumed, but it is quite likely that the rather severe Gastro-intestinal symptoms experienced by both he and the other family member were sufficient in his case to trigger the cascade of events which led to his death. In short, the mushrooms probably did contribute to his failing condition. They might be described as a proximate, though not ultimate cause.
COMMENTS OF READERS:
Comment from Bill Yule
I just read your article and I admit both the story and your analysis were fascinating. You're writing is excellent too by the way. I was interested in the "undercooking" hypothesis especially. I accept that the more likely culprit in this case was Leccinum and I was interested in whether the family was asked about how and how long they cooked the mushrooms. The stories that I've heard of GI distress from B. huronensis may have been cases where the mushrooms were under-cooked. Gerry Miller, the Amazonian-Mushroom-Shaman Eco-tour leader from East Haddam CT has eaten huronensis for years without problem but I remember his caution to NOT under-cook it. B. huronensis is an extremely dense, hefty mushroom and probably requires a long time to cook through to avoid problems (but I wouldn't eat it or recommend it). From my own experience the worse case of GI poisoning I've had was the result of under-cooking another extremely dense mushroom, Boletus auripes. So the idea, considering the comments about under-cooked Leccinums, rang true that it (under-cooking) may be a possible factor in the poisonings.
What an unfortunate tragedy for the family.
I'm happy to have contributed to the discussion if only to suggest an alternative hypothesis.
COMMENT from Gary Lincoff
Very good article............and I’m sure by now you’ve seen the Andrus Voitk piece in NAMA’s McIlvainea........I’m reluctant to jump on the Leccinum Warning Bandwagon because there are so many people in so many cultures around the world who consume Leccinums in great quantities. I don’t doubt there are people getting sick from eating Leccinum. In the current issue of the NYMS newsletter, a woman from Italy notes that she was surprised to discover that Boletus edulis is high on the list of mushrooms in Italy reported to cause “poisonings.” I’m sure the “real” Boletus edulis causes lots of GI upsets – old mushrooms, decaying mushrooms, bug infested mushrooms, overeating, overdrinking, undercooking, etc. - and voila! our beloved porcini makes the poster cut for the Mushroom Hall of Shame. What this all means is anybody’s guess, but I’m not willing to impugn the Leccinum scabrum complex just yet. Leccinum aurantiacum/insigne...atrostipitatum might contain compounds of interest. This might be a useful dichotomy to pursue.
and from another of Gary's Comments to Dianna,
I didn’t see mention in Bill’s article of the Boletus huronensis/Boletus edulis mistake & poisoning chillingly described in Andrus Voitk’s article “The rewards of indiscriminate mycophagia” in NAMA’s Mcilvanea on-line. I think it adds something important to the King bolete/Leccinum poisoning dilemma. The difference between all the Leccinum “poisonings” that I know about and the Boletus huronensis poisonings is one of degree – the huronensis is far and away the most powerful gastro-intestinal irritant I know about among all the boletes in our area – including B. sensibilis and all the red-pored boletes. I’m not putting my money on huronensis as the cause of the poisoning in the case Bill’s describes. I’m just thinking that it is a much more likely cause of so much distress. Whatever 3.5% of all reported poisonings referable to Leccinums means I don’t really know. It might just mean diarrhea or a simple up-chuck. From what Andrus Voitk describes, Boletus huronensis is no simple “evacuation.” I don’t think the case is nearly closed yet. Where is Sherlock Holmes when we need him?
These are two very interesting comments. When you first suggested that I check the NAMA report of B. huronensis, all I found was the mention of the two forks full eaten by the father and son in Maine. Not too disturbing, I thought, but Voitk's description is very graphic, and for others who may also have missed it, I am putting the link here: http://www.namyco.org/images/publications/6_Andrus.pdf
There are several issues raised by his account of mixed ingestion of Coprinus atramentarius and (what he presumed to be) B. huronensis, followed by alcohol. It does present the possibility of drug/food interaction, especially in light of the quality and suddenness of the initial symptoms following the small amount of alcohol. "Some 5–10 minutes after alcohol intake, the patient may experience the effects of a severe hangover for a period of 30 minutes up to several hours. Symptoms include flushing of the skin, accelerated heart rate, shortness of breath, nausea, vomiting, throbbing headache, visual disturbance, mental confusion, postural fainting, and circulatory collapse." fromhttp://en.wikipedia.org/wiki/Disulfiram
In this case this primary Coprine/alcohol/acetaldehyde reaction may also have interacted with a presumed GI reaction from the other mushroom, the timing of the latter coincidental with the consumption of alcohol. It does not take much alcohol to trigger the Coprine reaction. A sip or two seems sufficient. The profound dizziness, vertigo, and tachycardia described by Viotk are all consistent with the Antabuse/Coprine reactions with which I am familiar.
In the 1960's I was a New York City Social Worker specializing in Heroin Addiction, and helped administer the original Nyswander/Dole Methadone Maintenance program at Rockefeller Institute. In cases where alcohol was also involved we often used Antabuse in conjunction with Methadone. I was struck by the respect these addicts had for the effects of Antabuse. They feared the acetaldehyde reaction much, much more than even cold turkey withdrawal from either Heroin or Methadone, and if they planned to drink –say at an upcoming wedding or graduation- they would invariably stop taking Antabuse two weeks prior to the drink. The acetaldehyde reaction was sudden, sure and severe - potentially lethal – but totally the opposite of an opiate death which many addicts seemed to approach with eager anticipation.
The inclusion of Voitk's later ingestion of atramentarius + alcohol to test his reaction to Coprine alone is admirable, though not, I think, conclusive. My first inclination would be to question the variability of Coprine within different collections of atramentarius, as well as the amount eaten by Voitk in this instance. I don't understand his comment that the alcohol intoxication worked even better because of the Coprine.
I would also remind us all of the process by which memories of emotional events undergo seamless transition over time. What we truly think we remember is a highly edited dramatic reconstruction of the immediate experience. This is clearly as true of Voitk's story as it is of the attempt of Marilyn and me to identify the mushrooms which existed only in the memories of the family members who ate them.
The experience of the daughter eating raw 'huronensis' however does seem to align well with Bill Yule's previous comment that huronensis is a very dense Bolete and needs to be well cooked to be safe. And then there is Gerry Miller's experience of eating well-cooked huronensis for years, without incident.
Michael Beug indicates in his Editor's Notes that the experiences of the Father and Son who both ate two forks full of huronensis (Maine 2008) were "remarkably similar to those experienced by Andrus Voitk". I wonder if Dr. Lauri Leonard agrees. Do we know if this is the same experience of the NJ case? And does it fit the few others that Gary Lincoff, Bill Yule, and Ernst Both know of? If so, these bits and pieces could begin to fit together into a more coherent whole even given the constraints of mediated memories.
At the least we have what I suspect may be variability in both the mushrooms and eaters of the mushrooms. Here are two similar cases where I am sure of the ID of the mushroom.
A few years ago I cooked up one very fresh, firm and tasty Armillaria caligata, only one because it often has a very strong flavor and I didn't want to overburden our guests. It was sliced thin lengthwise, was well fried till crisp in butter, and served w/o any other treatment. All five of us had one thin slice, with drinks, as an appetizer. Everyone wanted more it was so good. The next day one of the guests called me, she said she was dizzy and wondered if the mushroom was responsible. I checked with everyone else and they were all fine. Days later I learned that she was really dizzy: so dizzy that she had crawled to the phone, was weak, unable to eat, could not stand, and remained so for the duration of the day! So, what was that all about? Even though she said she had previously had other, milder, dizzy spells, and we judged coincidence as being key to understanding this event, I haven't had caligata since!
And I recall a case in which I was able to identify with certainty the B. subvelutipes outside of the Gifford House at the Cary Arboretum in Millbrook, N.Y. which had been sampled raw by a visitor. He had tasted a mere pinch, "about thumbnail size" he later told me, and swallowed it. Within hours he was hospitalized for at least a day, perhaps three, I disremember. He was quite sick, bedridden, for three days, with powerful GI symptoms accompanied by dizziness, nausea and a cluster of what probably was a fear syndrome. I was able to observe, photograph in situ, and collect these mushrooms. They weresubvelutipes. In thirty years I have not had another case involving this reaction to this mushroom.
I agree with you about Leccinum. I am sure that some collections probably cause GI distress, though I have never experienced it. I collected and ate them regularly for decades, but since living with Leslie (some 20 years now) I have accepted her veto of this mushroom for our table, not because of the toxicity, but because, compared to other mushrooms, they leave much to be desired in the flavor department. In thirty years of poison control work, I had never had a referral which involved Leccinum related symptoms until this summer.
In the case of the elderly gentleman who died following the meal of the 'King Mushroom' and 'Leccinum', which initiated this exchange, I suspect that a delicate balance of preexisting age related conditions could easily have been triggered off by GI distress. At least one toxicologist involved also suggested that a degenerative process may have already been in play, only to be noticed after the mushroom incident. In this interpretation the mushrooms could be seen as minimally if not completely unrelated to the severity of the medical condition which led to his death..
A local mycologist familiar with the details of this case has offered to attempt to recollect the mushrooms involved, but the family has so far not responded.
Leccinum/Huronensis reply by Sandy Sheine
Boletus huronensis is on the Rogerson Foray species list for 2008. It was not listed on the 2007 list but we have found it several times at the COMA forays, from1999 onward. All the collections came from a trail in Day Pond State Park I have never been up there myself because the trail is long and steep, but I think that there is a hemlock forest up there. Mike Pack is coming to the COMA Foray this year, as far as I know, and he has found it up there. I believe that Steve Rock and others have gone up there as well. When we first saw it at the COMA foray nobody knew what it was, including Sam and Gary but it was later identified. At the COMA Foray this year we can send people up there to look for it. I think that two COMA members took the first one home with them, ate it and became ill.
Some people cannot eat some "edible" mushrooms and become ill from them. I and quite a few other people cannot consume well cooked Laetiporus sulphureus without becoming ill. I also cannot consume more than a taste of alcohol without becoming ill. A friend of mine and COMA member worked for Dr. Dole, a researcher in addictive substances at Rockefeller University. She told me that people who cannot consume alcohol without becoming ill have a genetic deficiency of alcohol dehydrogenase. Perhaps this same deficiency or a similar one causes a negative reaction with some mushrooms.
I think that Bill Yule is correct in saying that many people become ill from some mushrooms because they undercook them. If you look at mushroom recipes, you will see that the recipe calls for cooking the mushrooms for two or three minutes, certainly an insufficient amount of time for many mushrooms with some toxicity.
Bill Bakaitis’ reply:
Wow Sandy, just think, if Y'all can find enough huronensis up at Day Pond, you could set up a randomized, double-blinded, split-plot design at Mycophagy this year!!!
Just kidding, of course, but the joke does point up one major problem of moving beyond case histories to a more rigorous experimental approach to sorting all of this out. I have expanded upon this problem at greater length in the conclusion of the Morel/Arsenic piece which appears elsewhere on this site.
Since this is the second time the disulfuram/disulfuram (Antabuse) reaction [both spellings are used by the medical community] has appeared I think it merits additional treatment here. The following brief citations are from http://en.wikipedia.org/wiki/Disulfiram, additional sites are easily Googled.
"Under normal metabolism, alcohol is broken down in the liver by the enzyme alcohol dehydrogenase to acetaldehyde, which is then converted by the enzyme acetaldehyde dehydrogenase to the harmless acetic acid. Disulfiram blocks this reaction at the intermediate stage by blocking the enzyme acetaldehyde dehydrogenase."
"Coprine (N5-1-hydroxycyclopropyl-L-glutamine) which metabolises to 1-aminocyclopropanol, a closely-related chemical having the same metabolic effects, occurs naturally in the otherwise edible mushroom, the common ink cap (Coprinopsis atramentaria). Similar reactions have been recorded withClitocybe clavipes and Boletus luridus, although the agent in those species is unknown."
When I was working with substance abuse programs in NYC and later in my teaching career, it was the accepted position of AA and similar groups that addiction was, in fact, a consequence of the type of liver enzyme malfunction that your friend has described. There was considerable controversy about this among the Phoenix House clientele and professional staff which I also served, and also in subsequent literature.
Since retiring, I have not followed the current thinking about this issue, but will point out that much of the efficacy of the AA approach is to 'surrender' to the overpowering effects that alcohol has upon the individual, and the liver enzyme deficiency hypothesis fits snugly into this mythology. The equally effective Phoenix House approach depends upon an opposite mythology.
I use the term mythology here not in a derogatory sense, but to emphasize the power of our mental framework, particularly as it relates to 'placebo effects' and endorphin release mechanisms. About 70% of the pain-killing effect of morphine, for example, is thought to be a placebo effect.
Certain enzymatic factors have been demonstrated to play a part in food sensitivities and they are also thought to vary as to genetic (ethnic) background, environmental exposure, and maturational factors. Lactose intolerance is a prime example (and is easily Googled). Asian males in particular (and perhaps Northern Europeans) are thought to have a variant of the liver enzyme that you describe. Your hypothesis that similar mechanisms may play a part in mushroom induced illness is certainly one worth considering.
A final comment: I think we have to thank Bill Roody and the Bessette's for includinghuronensis in their splendid North American Boletes. That is certainly how I was able to 'identify ' huronensis in the single collection of which I have made. Like you all, I will certainly be on the look-out for it this fall, and I am again led to wonder about all of us who must have eaten it in the past and given it little thought. I also wonder about old "Iron Guts" himself, Charles McIlvaine who got many of us started on this enterprise. He could eat anything, it seems, and pronounced it all delicious. I have met modern day mycologists [names deliberately omitted] who apparently have an equally strong constitution, particularly when pickled!
On huronensis: Elinoar Shavit's comment
Wonderful articles on Dianna’s page, very informative and important.
The first definite poisoning by B. huronensis in the Northeast took place at the NEMF foray some 10 years ago or more, in Connecticut. I used to bring to the COMA foray each year a huge specimen of B. huronensis that grows in a park in Connecticut. Allen Bessette was fascinated by it and I brought a sample to that NEMF foray for him from the same CT park. At the time it was an unfamiliar mushroom to most mycologists and certainly to collectors, but it is not uncommon now and this year I have collected in a number of places in Mass and in CT B. huronensis.
At the foray, just after Allan Bessette introduced the mushroom to the crowd and talked about it, Ursula Pole asked him if the mushroom was edible, and Allan suggested that she try it. She and Carlene Skefington took the mushroom to their room and Ursula Pohl cooked it. She sautéed it long enough. Ursula Pohl is a well trained and experienced cook who is in charge of many NAMA mycophagy sessions and knows to properly cook a mushroom. She ate a very small amount of the mushroom. She became violently ill, and I am not sure but may have been taken to the hospital. You may want to contact her and compare her symptoms with the ones these poor people in your article experienced. This mushroom has been found in many places in the Northeast this summer, perhaps due to the a-typical weather. I was asked a number of times to identify this mushroom since the beginning of July in Connecticut and Massachusetts. Last year, for the Connecticut NEMF foray, I brought 2 young specimens to show people at the foray that they need to know their Boletus edulis well enough to avoid look-alikes like B. huronensis. Most obviously difference is this bolete’s exceptional heft, not so much the bluing phenomenon because in certain weathers it is slow and not so obvious. The blue mark turns brown rather fast in dry weather. One person even told me: “Oh, it’s only my dirty finger, mushroomers have a brown thumb, not a green one”. We took the time to explain about this mushroom around the display tables, since Bill Yule was too busy running the foray... I think one young specimen can be seen in the photo of Sam and Ed photo (on the NEMF page).
What a season,
Your detailed description of the staining reaction seems quite important so I have highlighted it in your email.
I did call Ursula Pohl (the New Jersey case) who agreed to have her experience recounted here. She remembers the night. She said she ate perhaps a spoonful of well-cooked huronensis late in the evening, before bed, and after a glass of wine. Responsibly she refused to allow others to try it as she was in charge of Mycophagy and needed to test it on herself. Two hours later she awoke with a bout of vomiting which lasted off and on for the next two or three hours. There was some diarrhea at the end. At times she felt cold and shivered, and others recall that she reported that her muscles ached. She does not recall dizziness or vertigo, and she did not go to the hospital. She also knows that some people can eat this mushroom with no ill effect, but feels that there is something in it which disagrees with her. She emphasized the tiny amount she ate which apparently caused these symptoms. She also said the mushroom smelled good to her but was not that tasty. And there was something about the odor in the vomit which was quite strong.
I am sending her link to this developing story and she may wish to comment further.
Bill Bakaitis and Marilyn Shaw reply to Bill Yule's question about the cooking of the mushrooms in this case, and to Leccinum toxicity in general:
Since I (Bill B.) am currently in Maine and the handwritten notes I took on this case are in NY, I wanted to check with Marilyn Shaw to have the most accurate description of the cooking process of both of these mushrooms that we were able to obtain from the family.
That done, I can report that we both recall that both mushrooms were well cooked: Marilyn, who was conducting the interview at this point, recalls that the family member who seemed most aware of what had happened said that they were sautéed for ten minutes. I remember that the phrase "cooked in oil for some time" was used, and that one mushroom (presumably the Leccinum) "stained violet" before cooking and "turned black when cooked". Marilyn asked about the color changes of the King Mushroom and was told that when sliced prior to cooking, it did not stain. These details were obtained by direct questioning rather than spontaneous recall of the person being interviewed. If my hand-written notes reveal anything other than this I will add those observations later.
Marilyn concludes, "I have a little more faith than you in the recollection of the [person being interviewed] ..who…seemed quite clear. With my experience over a period of years with so many Leccinum cases, I have no doubt that it was the culprit."
Marilyn Shaw's other comments follow:
Since the comments following your article indicate that many folks are unconvinced that Leccinum can be a problem, you might want to append Michael Kuo's comment on "Steelheader" web page about his experience. [added below] You could also add that many years ago, Vera Evenson, curator of the Sam Mitchel Herbarium of Fungi, Denver Botanic Gardens, Denver, herself had an unfortunate experience with Leccinum. She took her then young son and some of his friends on a camping trip. She found Leccinum, cooked it, and served it to the boys. All became quite sick during the night. Not fun especially on a camping trip. I might mention that at the time she was an assistant to Dr. D.H. "Sam" Mitchel, MD, early student of Dr. Alexander Smith's at his summer "Bug Camp", and founder of CMS. He also co-authored Toxic and Hallucinogenic Mushroom Poisoning with Gary Lincoff.
Another case, the first one I was ever aware of, involved the president of CMS, her husband (both MDs) and a couple of friends. They picked Leccinum from a spot on their own property where they had collected them before, cooked and ate them. This resulted in rather severe GI symptoms. At that time (probably 20 years ago) I, too, doubted the culprit, but within a month, I had received another report involving a group from the Univ. of Colo. Health Sciences Center, who had a similar experience.
Since then there has been a steady stream of reports of illnesses from what seem to be a variety of Leccinum species. There are never any surviving specimens, so we don't have the luxury of being able to make a species identification. Dr. Joe Ammirati has also reported Leccinum illnesses from his area in the Pacific Northwest. These are reports from knowledgeable people, experts in the field of mycology. I, too, have eaten Leccinum many years ago without ill effect, but I never thought they were worth bothering with.
My advice has been, "If you want to eat them yourself, fine, but please don't recommend them or feed them to others." As Michael Kuo (mushroomexpert.com) says from his personal experience, "I can tell you that the poisoning is not at all how you want to spend one or two days of your life!"
[Here is the Michael Kuo, "Steelheader" (11-5-05) quote that Marilyn referred to and provided. It was retrieved from http://leslieland.com/blog/2009/07/wild-mushroom-warning-the-scaber-stalks-leccinum-species-may-no-longer-be-considered-safe/ where a discussion of the Leccinum issue has been underway. Readers of this article may wish to review the other comments posted there.]
"Avoid Orange-Capped Leccinum Species
Leccinum includes some very good edibles, but the record is becoming more and more clear: some people are adversely affected by some of the orange-capped species. Marilyn Shaw has documented this in Colorado (see Bessette, 2000, 374), and some field guides will mention the possibility. I know from personal experience; I am one of the "some people" adversely affected--and I can tell you that the poisoning is not at all how you want to spend one or two days of your life!
There are many Leccinum mushrooms with orange caps. But since Leccinum species are notoriously difficult to separate, even for experts, you should avoid any orange-capped species. If you are not sure you can distinguish Leccinum species from other boletes, you should change this rule and not eat any boletes with orange or orangeish caps."
Laurie Leonard chitin question
Enjoyed your long discussion of Leccinum etc.
Do you know anything about the digestion of chitin and how do we actually digest mushrooms and their chitin. I note that until recently humans apparently were not thought to have any chitinases but recently some were identified. I wonder, does cooking break down chitin, etc etc.
Of interest, there have been some articles that have linked asthma to chitanase levels. And there was an article in 2007 that finally identified chitinase in 20 of 25 Italians....whether or not the level was significant to digest insects and mushrooms I do not know, so will just have to keep my eye out for literature about it. . Perhaps cooking breaks it down a bit and so we can eat them and thus the admonition not to eat mushrooms unless cooked. It probably also is a matter of degree; I ate some fried grasshoppers in Mexico without trouble....real crispy.
Nope, I know nothing about this, except the general mycological understanding that fungal cell walls are made of chitin, the same stuff in lobster shells. The reason for this apparently is that fungi digest their food (such as cellulose and lignin) outside of their bodies by enzymatic degradation. They would be in real trouble if these enzymes also destroyed the cell membrane which separates them from the world..
About your allergy observation: Perhaps in humans this chitin digestion process is somehow related to shrimp allergies? The usual understanding, I think, has to do with levels of contamination in shellfish, but this question adds a quite different dimension to an understanding of the problem.
Gary Lincoff writes:
I enjoyed your [Leccinum of the Northeast] talk the other night.
From your talk about the poisoning last year I got, for the first time, just how few mushrooms (just 2) were actually eaten by 3 people. Even a destroying angel or death cap requires a minimum amount of mushroom eaten to produce a deadly effect. This is a bizarre aspect of this poisoning. Boletus huronensis causes its severe reaction from just a small piece of mushroom eaten. Andrus Voitk describes this in graphic detail in his account in McIlvainea (on the NAMA website). Ursula Pohl’s reaction to this mushroom was about the same – extraordinarily violent vomiting from a small cooked piece of Boletus huronenesis. That Andrus thought he had Boletus edulis, that he mentions someone driving by who also thought he had Boletus edulis, suggests that this little known mushroom is a very real look-alike out there. Now, given the “tonnage” of orange capped Leccinum gathered in the northeast – from at least as far south as Maryland to at least Cape Cod – and this mostly gathered by Russians or eastern Europeans who (as I heard at NEMF last year) come by busloads and comb the woods for just this mushroom........given this.....I think calling the poisoning (and subsequent death) a Leccinum poisoning is possibly misplaced. I’m going to try to get someone who speaks Russian to interview some of the collectors this year to see if they’ve heard of anyone getting sick from Leccinum. Whatever the accounts in the Rocky Mountains or the Pacific Northwest, with this amount of Leccinum gathering in the east, it’s not as likely that a Leccinum contributed to the death as, perhaps, a Boletus huronensis. I’ll let you know what I find out, if anything comes of this.
Bill Bakaitis replies:
Thanks for your thoughts Gary.
As I noted in the original posting, the details of this case were very murky: There were no mushrooms to see. The story changed depending upon who was reporting and who was questioning. There were lots of 'leading' questions asked, etc.
True that three people ate two mushrooms, but it was not at all clear if they were shared equally, etc. or even if it was mushrooms which caused the initial GI illness. As far as I know no other food item was implicated, suggested, or investigated. Mushrooms were attributed as 'the cause' only after bits of one (mushroom singular if I recall correctly) appeared in the vomitus of the daughter. In short, hardly a definitive case, or one even approaching the clarity needed for attribution of cause from a logical, medical or scientific perspective.
It seems likely that the fellow who died suffered a cascade of effects which followed from the GI symptoms, but this too is a hypothesis. One of the doctors suggested to me that his symptoms could have been underway independently of and prior to the ingestion of any mushroom.
Concerning the amount ingested, here is an alternative hypothesis which also utilizes your statistical probability speculation: That the reaction was caused by a developed sensitivity.
When one develop such a sensitivity to foreign protein even a small amount can cause a severe reaction, be it from huronensis, aurantiacum, peanuts, wheat or milk. Bee keepers, for example, who have successfully worked with bees for decades can suddenly develop a sensitivity to a single sting that can kill.
As you know many sensitivities appear only after one's system has been primed by a prior exposure to the substance. This being the case, one could also make the argument that given the plentitude of orange capped Leccinum, and the rarity of huronensis, there is a much greater statistical chance of a developed sensitivity to L. aurantiacum than B. huronensis.
Developed sensitivity aside, the hypothesis you suggest is that huronensis, in and of itself, is powerfully toxic. I suspect one would want to qualify this statement into "some huronensis are powerfully toxic to some individuals".
Of course, these GI symptoms could have been caused by another substance (not from the mushrooms) that is in and of itself toxic. This would be another hypothesis.
I remain agnostic as to the cause of these GI episodes. But in the future I doubt that Leslie or I will eat either of the mushrooms which are thought to be involved.
Last night during the discussion, Leslie was quite emphatic that we ate the huronensis which I identified and photographed. And today as we discussed this in light of your email I think she has convinced me of the possibility that we did eat the huronensis. The photo of the sliced specimen shows the base 'field-dressed' in a manner consistent with our culinary habits. It is likely that I too took this in the field to be an edulis, only later deciding to look deeper, and we had previously eaten a few other 'new' Boletes identified from the Bessette text, finding one of them B. gertrudii to be simply the best mushroom either of us had ever tasted.
So, although I can't say for certain if we ate it or not, neither of us had any symptoms, and we are both rather sensitive to foods. (Lately, for example, I seem to have developed a sensitivity to wheat and can tell within 10-20 minutes if I have eaten even a small bit hidden in an otherwise wheat-free product as my gut just blows up with cramps and gas. Of interest in light of the similar reactions of both the Father/Daughter in the Voitk case, my own daughter has had wheat sensitivity for most of her life. Somehow mine developed only recently).
I am glad you have taken an interest in disproving the 'toxic orange capped Leccinum' hypothesis. This would be of real value to collectors here in the northeast.
Here are a few thoughts on the matter:
Since NAMA has accumulated a data-base on toxic mushroom reactions stretching back over several decades I wonder if that data could be mined to extract sufficient information to clarify this issue.
I doubt if there is data sufficiently precise to perform the robust Scheffe a posteriori analysis of variance.(where interval or ratio scale measures would be needed) But there may be ways to extract non-parametric measures sufficient to test your hypothesis. For example a 'sick – non sick', 'Colorado – non Colorado' comparison (of nominal or perhaps ordinal value) might allow a 2X2 chi square calculation. A competent epidemiologist could probably find other ways to determine if the information already collected could shed light on the issue you raise.
I suspect a double blind test of eastern orange-capped Leccinum this summer might also by attempted, but shudder to think of the controls needed.
Finally, the Eastern Europeans that I meet in the woods both here in NY and in Maine seem to be particularly fond of Boletus bicolor, and do not distinguish between those which stain blue and those which do not. One old-timer in Maine eats everything and seems to either nor regret or not notice untoward effects. Digest that if you can!