Toxic mushrooms

Abstract

Poisonous mushrooms contain toxins that are as diverse as the mushrooms themselves. Clinical syndromes often involve multiple organ systems, and progression of clinical signs is often directly related to the quantity eaten. Diagnostic detection of the toxins is rarely an option; rather, diagnosis is based on a history of possible exposure and identification of mushroom species in the stomach contents and environment. Treatments are usually based on clinical signs, as most mushroom toxins are without an antidote. There are exceptions, however, and prompt identification of mushroom species involved is vital whenever possible. Collection of the toxicologic minimum database and gastrointestinal decontamination are important in all cases where mushroom ingestion is suspected.

Amanita muscaria toxicosis in two dogs

“…11 Muscarinic cholinergic receptors capable of binding muscarine are found in highest concentrations in the cardiac muscle and nodes, smooth muscle, and glands. 9 Both dogs reported here displayed variably severe degrees of cholinergic signs, such as ptyalism, miosis, vomiting, diarrhea, and second degree atrioventricular block. Cholinergic crises are rarely reported in adult humans with pantherina-muscaria poisoning which results from recreational or ritualistic consumption of fly agaric.…”

“…[6][7][8][9][10][11][12] The concentrations of muscarine found in A. muscaria, although variable, are generally considered insufficient to cause the pantherina-muscaria syndrome, and explain the paucity of cholinergic clinical signs demonstrated by humans with A. muscaria toxicosis. 9,13 The quaternary ammonium group present on muscarine prohibits entrance into the CNS, and thus muscarine functions as a competitive muscarinic receptor agonist in the peripheral nervous system, and is not subject to acetylcholinesterasemediated degradation. 11 Muscarinic cholinergic receptors capable of binding muscarine are found in highest concentrations in the cardiac muscle and nodes, smooth muscle, and glands.…”

“…Both ibotenic acid and muscimol, although zwitterionic structures, are capable of crossing the blood-brain barrier by active transport, which explains their ability to produce CNS dysfunction. 9 Ibotenic acid and muscimol are alkaloids that biochemically function in vivo as agonists of the neurotransmitters Glu and GABA, respectively. [10][11][12] The amino acid Glu and its conformational analogs, which include ibotenic acid, mediate most of the excitatory synaptic neurotransmission in the mammalian brain through 2 distinct classes of Glu receptors, ligand-gated ionotropic receptors (iGlu) and G protein-coupled metaboreceptors (mGlu).…”

“…Previous veterinary reports of mushroom poisoning are likely rare because of the difficulty associated with establishing a definitive diagnosis. 9 An empirical diagnosis is usually made based on historical evidence of mushroom exposure and ingestion in combination with concurrent clinical signs. Visualization of ingested mushrooms obtained from vomitus or gastric lavage fluid further supports the diagnosis, but definitive taxonomic identification of mushroom samples obtained in this manner can be very difficult, and may require mycological expertise that is not readily available.…”

“…However, the psychoactive properties of A. muscaria have been recognized for centuries, and voluntary ingestion of fly agaric for both ritualistic and recreational purposes result in most human intoxications requiring medical treatment. [7][8][9] Presumptive cases of A. pantherina poisoning have been reported to cause muscle tremors, somnolence, delirium, and convulsions in cats and dogs, 3,5 but to the authors' knowledge, descriptions of disease resulting from ingestion of A. muscaria have not appeared previously in the veterinary literature. The purpose of this case series is to describe the clinical signs, history, and pathophysiologic basis of disease in 2 dogs with A. muscaria poisoning.…”