**5. Mushroom toxicity**

Since prehistoric times humans have heavily consumed mushrooms for nutritional and therapeutic use. Mushroom toxicity has also been known since man started the consumption of mushrooms, and has been the cause of death of many historical figures, including the Roman Emperor Claudius [3, 77]. Currently, several mushrooms are cultivated commercially, but foraging for mushrooms has gained popularity as a form of recreational activity in the community. Mushroom poisonings increasingly are common due to a lack of knowledge by foragers to identify and distinguish a poisonous mushroom species from edible species, and in some cases, problems occur as intentional ingestions [9, 31, 86]. Mushroom poisonings may an indication from a benign symptom of generalized gastrointestinal upset to very devastating outcomes that include liver failure, kidney failure, and neurologic disorders. Up to 14 described syndromes are documented, which manifest depending on the mushroom species, toxins, and quantity ingested [11, 94]. The mushroom poisoning symptoms are related to the toxin ingested, which include amatoxin, psilocybin, muscarine, coprine, allenic norleucine, gyromitrin, etc. [3, 7, 89]. Within the several mushroom species, there are about 100 species that are toxic in nature. Annual ingestion is recorded at a level of about 6000 ingestions yearly alone in the United States, and out of these, over 50% of the exposures are pediatric in nature, recorded in children under 6 years of age [88]. Most poisonings exhibit symptoms mainly of gastrointestinal upset, which is a common feature across several toxidromes, and this is most likely to occur with ingestions of small quantities of toxic mushrooms. Severe mushroom poisonings that take place, are primarily a consequence of misidentification by adults foraging for wild mushrooms who consume them as food [3, 14]. A summary table of Mushroom toxicity effects, symptoms, and examples of Mushrooms having the toxin has been illustrated in **Table 4**.

### **5.1 Pathophysiology of mushroom poisoning**

The clinical presentation differs depending on the species of mushroom and toxin ingested. For **Acute gastroenteritis**: Most often secondary to one of a variety of "backyard mushrooms" such as *Chlorophyllum molybdites*. In most cases are developing symptoms of nausea, vomiting, gastrointestinal upset like abdominal cramping and possibly diarrhea associated with ingestion accounting for most of the reported poisonings [31, 90]. The symptoms of poisoning are manifested usually or typically within 1–3 hours of ingestion [3].


#### **Table 4.**

*Of mushroom toxicity effects, symptoms, and examples of mushrooms having the toxin [12, 86, 95].*

**Hallucinations**: The main cause is produced by the bioactive compounds from psilocybin and psilocin from the mushroom species such as *Psilocybe*, *Conocybe*, *Gymnopilus*, and *Panaeolus*. These chemically bioactive compounds act as agonists or partial agonists at 5-hydroxytryptamine (5-HT) subtype receptors [19, 40]. These species of mushrooms are cultivated for recreational purposes as substances of abuse, although they can grow naturally in warm, moist climates. The mushroom can be ingested as fresh mushroom caps or dried mushrooms preparations and can cause altered sensorium and euphoria occurring 30 minutes to 2 hours after ingestion that can last for about 4–12 hours, depending on the quantity ingested [24].

**Cholinergic toxicity**: This is caused by muscarine-containing mushroom in the genera *Clitocybe* and *Inocybe*. *Amanita muscari* contains small amounts of muscarine, but the concentrations are generally low to cause a cholinergic effect. Cholinergic effects, however, of diaphoresis, salivation, lacrimation, bronchospasm, abdominal cramping, bronchorrhea, and bradycardia generally may occur within 30 minutes of ingestion, and the duration is dose-dependent and usually short-lived as compared to other pesticide-related cholinergic poisoning [95].

**Disulfiram-like reaction**: Caused by coprine-containing species such as *Coprinus atramentarius*, known as inky cap mushrooms. The toxin's bioactive metabolites can result in the inhibition of aldehyde dehydrogenase causing headache, nausea,

*Medicinal Mushroom of Potential Pharmaceutical Toxic Importance: Contribution… DOI: http://dx.doi.org/10.5772/intechopen.103845*

vomiting, flushing, tachycardia, and in rare cases hypotension. The adverse effect is very obvious and only occurs in cases where alcohol is ingested a few hours to days after the consumption of coprine-containing mushrooms. Co-ingestion of alcohol and the toxin can lead to reduced toxic effects due to slower metabolism of coprine to its toxic secondary metabolites [8, 15].

## **5.2 Mushroom liver toxicity**

Toxicity from different species can be caused by amatoxin observed in species like *Galerina*, *Lepiota* and particularly *Amanita* [41]. The toxins can disrupt RNA polymerase II, resulting in cellular level protein deficiency. The toxicity consists of three distinct phases. Gastrointestinal effects can be observed typically 6–12 hours after ingestion, followed by a quiescent phase of 24–36 hours after ingestion with a symptomatic improvement [8, 14, 69]. During the quiescent phase, there may be clinical signs of hepatotoxicity. After 48 hours of ingestion, hepatic damage increases, leading to liver failure and other related clinical complications. Lethal occurrence recorded in mushroom toxicity may occur within a week in severe cases or require liver transplantation.
