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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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Historically, eating grain products, particularly rye, contaminated with the fungus "Claviceps purpurea" was the cause of ergotism.
The toxic ergoline derivatives are found in ergot-based drugs (such as methylergometrine, ergotamine or, previously, ergotoxine). The deleterious side-effects occur either under high dose or when moderate doses interact with potentiators such as erythromycin.
The alkaloids can pass through lactation from mother to child, causing ergotism in infants.
Dark-purple or black grain kernels, known as ergot bodies, can be identifiable in the heads of cereal or grass just before harvest. In most plants the ergot bodies are larger than normal grain kernels, but can be smaller if the grain is a type of wheat. A larger separation between the bodies and the grain kernels show the removal of ergot bodies during grain cleaning.
Mushrooms may be rendered poisonous by insecticides or herbicides sprayed on lawns or reserves. At least one author recommends never picking them in non-natural landscapes for this reason.
Also, mushrooms are sometimes contaminated by concentrating pollutants, such as heavy metals or radioactive material (see Chernobyl disaster effects).
Rotten mushrooms may cause food poisoning. Mushrooms that are mushy, bad-smelling, or moldy (even of a choice edible species) may be toxic due to bacterial decay or mold.
Many mushrooms are high in fiber. Excessive consumption of mushrooms may lead to indigestion, which may be diagnosed as mushroom "poisoning".
New species of fungi are continuing to be discovered, with an estimated number of 800 new species registered annually. This, added to the fact that many investigations have recently reclassified some species of mushrooms from edible to poisonous has made older classifications insufficient at describing what now is known about the different species of fungi that are harmful to humans. Thus, contrary to what older registers state, it is now thought that of the approximately 100,000 known fungi species found worldwide, about 100 of them are poisonous to humans. However, by far the majority of mushroom poisonings are not fatal, and the majority of fatal poisonings are attributable to the "Amanita phalloides" mushroom.
A majority of these cases are due to mistaken identity. This is a common occurrence with "A. phalloides" in particular, due to its resemblance to the Asian paddy-straw mushroom, "Volvariella volvacea". Both are light-colored and covered with a universal veil when young.
"Amanita"s can be mistaken for other species, as well, in particular when immature. On at least one occasion they have been mistaken for "Coprinus comatus". In this case, the victim had some limited experience in identifying mushrooms, but did not take the time to correctly identify these particular mushrooms until after he began to experience symptoms of mushroom poisoning.
The author of "Mushrooms Demystified", David Arora cautions puffball-hunters to beware of "Amanita" "eggs", which are "Amanita"s still entirely encased in their universal veil. "Amanita"s at this stage are difficult to distinguish from puffballs. Foragers are encouraged to always cut the fruiting bodies of suspected puffballs in half, as this will reveal the outline of a developing "Amanita" should it be present within the structure.
A majority of mushroom poisonings in general are the result of small children, especially toddlers in the "grazing" stage, ingesting mushrooms found in the lawn. While this can happen with any mushroom, "Chlorophyllum molybdites" is often implicated due to its preference for growing in lawns. "C. molybdites" causes severe gastrointestinal upset but is not considered deadly poisonous.
A few poisonings are the result of misidentification while attempting to collect hallucinogenic mushrooms for recreational use. In 1981, one fatality and two hospitalizations occurred following consumption of "Galerina autumnalis", mistaken for a "Psilocybe" species. "Galerina" and "Psilocybe" species are both small, brown, and sticky, and can be found growing together. However, "Galerina" contains amatoxins, the same poison found in the deadly "Amanita" species. Another case reports kidney failure following ingestion of "Cortinarius orellanus", a mushroom containing orellanine.
It is natural that accidental ingestion of hallucinogenic species also occurs, but is rarely harmful when ingested in small quantities. Cases of serious toxicity have been reported in small children. "Amanita pantherina", while containing the same hallucinogens as "Amanita muscaria" (e.g., ibotenic acid and muscimol), has been more commonly associated with severe gastrointestinal upset than its better-known counterpart.
Although usually not fatal, "Omphalotus" spp., "Jack-o-lantern mushrooms," are another cause of sometimes significant toxicity. They are sometimes mistaken for chanterelles. Both are bright-orange and fruit at the same time of year, although "Omphalotus" grows on wood and has true gills rather than the veins of a "Cantharellus". They contain toxins known as illudins, which causes gastrointestinal symptoms.
Bioluminescent species are generally inedible and often mildly toxic.
"Clitocybe dealbata", which is occasionally mistaken for an oyster mushroom or other edible species contains muscarine.
Toxicities can also occur with collection of morels. Even true morels, if eaten raw, will cause gastrointestinal upset. Typically, morels are thoroughly cooked before eating. "Verpa bohemica", although referred to as "thimble morels" or "early morels" by some, have caused toxic effects in some individuals. "Gyromitra" spp., "false morels", are deadly poisonous if eaten raw. They contain a toxin called gyromitrin, which can cause neurotoxicity, gastrointestinal toxicity, and destruction of the blood cells. The Finns consume "Gyromitra esculenta" after parboiling, but this may not render the mushroom entirely safe, resulting in its being called the "fugu of the Finnish cuisine".
A more unusual toxin is coprine, a disulfiram-like compound that is harmless unless ingested within a few days of ingesting alcohol. It inhibits aldehyde dehydrogenase, an enzyme required for breaking down alcohol. Thus, the symptoms of toxicity are similar to being hung over—flushing, headache, nausea, palpitations, and, in severe cases, trouble breathing. "Coprinus" species, including "Coprinopsis atramentaria", contain coprine. "Coprinus comatus" does not, but it is best to avoid mixing alcohol with other members of this genus.
Recently, poisonings have also been associated with "Amanita smithiana". These poisonings may be due to orellanine, but the onset of symptoms occurs in 4 to 11 hours, which is much quicker than the 3 to 20 days normally associated with orellanine.
"Paxillus involutus" is also inedible when raw, but is eaten in Europe after pickling or parboiling. However, after the death of the German mycologist Dr Julius Schäffer, it was discovered that the mushroom contains a toxin that can stimulate the immune system to attack its own red blood cells. This reaction is rare, but can occur even after safely eating the mushroom for many years. Similarly, "Tricholoma equestre" was widely considered edible and good, until it was connected with rare cases of rhabdomyolysis.
In the fall of 2004, thirteen deaths were associated with consumption of "Pleurocybella porrigens" or "angel's wings". In general, these mushrooms are considered edible. All the victims died of an acute brain disorder, and all had pre-existing kidney disease. The exact cause of the toxicity was not known at this time and the deaths cannot be definitively attributed to mushroom consumption.
However, mushroom poisoning is not always due to mistaken identity. For example, the highly toxic ergot "Claviceps purpurea", which grows on rye, is sometimes ground up with rye, unnoticed, and later consumed. This can cause devastating, even fatal effects, which is called ergotism.
Cases of idiosyncratic or unusual reactions to fungi can also occur. Some are probably due to allergy, others to some other kind of sensitivity. It is not uncommon for an individual person to experience gastrointestinal upset associated with one particular mushroom species or genus.
Dancing mania (also known as dancing plague, choreomania, St John's Dance and, historically, St. Vitus's Dance) was a social phenomenon that occurred primarily in mainland Europe between the 14th and 17th centuries. It involved groups of people dancing erratically, sometimes thousands at a time. The mania affected men, women, and children who danced until they collapsed from exhaustion. One of the first major outbreaks was in Aachen, in the Holy Roman Empire, in 1374, and it quickly spread throughout Europe; one particularly notable outbreak occurred in Strasbourg in 1518, also in the Holy Roman Empire.
Affecting thousands of people across several centuries, dancing mania was not an isolated event, and was well documented in contemporary reports. It was nevertheless poorly understood, and remedies were based on guesswork. Generally, musicians accompanied dancers, to help ward off the mania, but this tactic sometimes backfired by encouraging more to join in. There is no consensus among modern-day scholars as to the cause of dancing mania.
The several theories proposed range from religious cults being behind the processions to people dancing to relieve themselves of stress and put the poverty of the period out of their minds. It is, however, thought to have been a mass psychogenic illness in which the occurrence of similar physical symptoms, with no known physical cause, affect a large or small group of people as a form of social influence.
In Italy, a similar phenomenon was tarantism, in which the victims were said to have been poisoned by a tarantula or scorpion. Its earliest known outbreak was in the 13th century, and the only antidote known was to dance to particular music to separate the venom from the blood. It occurred only in the summer months. As with dancing mania, people would suddenly begin to dance, sometimes affected by a perceived bite or sting and were joined by others, who believed the venom from their own old bites was reactivated by the heat or the music. Dancers would perform a tarantella, accompanied by music which would eventually "cure" the victim, at least temporarily.
Some participated in further activities, such as tying themselves up with vines and whipping each other, pretending to sword fight, drinking large amounts of wine, and jumping into the sea. Some died if there was no music to accompany their dancing. Sufferers typically had symptoms resembling those of dancing mania, such as headaches, trembling, twitching and visions.
As with dancing mania, participants apparently did not like the color black, and women were reported to be most affected. Unlike dancing mania, tarantism was confined to Italy and southern Europe. It was common until the 17th century, but ended suddenly, with only very small outbreaks in Italy until as late as 1959.
A study of the phenomenon in 1959 by religious history professor Ernesto de Martino revealed that most cases of tarantism were probably unrelated to spider bites. Many participants admitted that they had not been bitten, but believed they were infected by someone who had been, or that they had simply touched a spider. The result was mass panic, with a "cure" that allowed people to behave in ways that were, normally, prohibited at the time. Despite their differences, tarantism and dancing mania are often considered synonymous.
Varicella zoster virus (VZV) has a high level of infectivity and has a worldwide prevalence. Shingles is a re-activation of latent VZV infection: zoster can only occur in someone who has previously had chickenpox (varicella).
Shingles has no relationship to season and does not occur in epidemics. There is, however, a strong relationship with increasing age. The incidence rate of shingles ranges from 1.2 to 3.4 per 1,000 person‐years among younger healthy individuals, increasing to 3.9–11.8 per 1,000 person‐years among those older than 65 years, and incidence rates worldwide are similar.
This relationship with age has been demonstrated in many countries, and is attributed to the fact that cellular immunity declines as people grow older.
Another important risk factor is immunosuppression. Other risk factors include psychological stress. According to a study in North Carolina, "black subjects were significantly less likely to develop zoster than were white subjects." It is unclear whether the risk is different by gender. Other potential risk factors include mechanical trauma and exposure to immunotoxins.
There is no strong evidence for a genetic link or a link to family history. A 2008 study showed that people with close relatives who had had shingles were twice as likely to develop it themselves, but a 2010 study found no such link.
Adults with latent VZV infection who are exposed intermittently to children with chickenpox receive an immune boost. This periodic boost to the immune system helps to prevent shingles in older adults. When routine chickenpox vaccination was introduced in the United States, there was concern that, because older adults would no longer receive this natural periodic boost, there would be an increase in the incidence of shingles.
Multiple studies and surveillance data, at least when viewed superficially, demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995. However, upon closer inspection, the two studies that showed no increase in shingles incidence were conducted among populations where varicella vaccination was not as yet widespread in the community. A later study by Patel "et al." concluded that since the introduction of the chickenpox vaccine, hospitalization costs for complications of shingles increased by more than $700 million annually for those over age 60. Another study by Yih "et al". reported that as varicella vaccine coverage in children increased, the incidence of varicella decreased, and the occurrence of shingles among adults increased by 90%. The results of a further study by Yawn "et al". showed a 28% increase in shingles incidence from 1996 to 2001. It is likely that incidence rate will change in the future, due to the aging of the population, changes in therapy for malignant and autoimmune diseases, and changes in chickenpox vaccination rates; a wide adoption of zoster vaccination could dramatically reduce the incidence rate.
In one study, it was estimated that 26% of those who contract shingles eventually present complications. Postherpetic neuralgia arises in approximately 20% of people with shingles. A study of 1994 California data found hospitalization rates of 2.1 per 100,000 person-years, rising to 9.3 per 100,000 person-years for ages 60 and up. An earlier Connecticut study found a higher hospitalization rate; the difference may be due to the prevalence of HIV in the earlier study, or to the introduction of antivirals in California before 1994.
The rash and pain usually subside within three to five weeks, but about one in five people develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some people, shingles can reactivate presenting as "zoster sine herpete": pain radiating along the path of a single spinal nerve (a "dermatomal distribution"), but without an accompanying rash. This condition may involve complications that affect several levels of the nervous system and cause many cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Other serious effects that may occur in some cases include partial facial paralysis (usually temporary), ear damage, or encephalitis. During pregnancy, first infections with VZV, causing chickenpox, may lead to infection of the fetus and complications in the newborn, but chronic infection or reactivation in shingles are not associated with fetal infection.
There is a slightly increased risk of developing cancer after a shingles infection. However, the mechanism is unclear and mortality from cancer did not appear to increase as a direct result of the presence of the virus. Instead, the increased risk may result from the immune suppression that allows the reactivation of the virus.
Although shingles typically resolves within 3–5 weeks, certain complications may arise:
- Secondary bacterial infection
- Motor involvement, including weakness especially in "motor herpes zoster"
- Eye involvement: trigeminal nerve involvement (as seen in herpes ophthalmicus) should be treated early and aggressively as it may lead to blindness. Involvement of the tip of the nose in the zoster rash is a strong predictor of herpes ophthalmicus.
- Postherpetic neuralgia, a condition of chronic pain following shingles