Fungi: Trichothecenes - Food Poisoning

Trichothecenes

These mycotoxins are produced by Fusarium roseum, F. monili-forme, F. nivale, and F. oxysporum. Other fungal genera thatproduce similar toxins include Myrothecium, Trichoderma, Cephalosporium, Verticimonosporium, and Stachybotrys. Over 100 trichothecenes have been identified. The most frequent natural contaminants are deoxynivalenol, diacetoxyscirpenol, HT-toxin, nivalenol, and T-2 toxin.

Contamination of corn, sorghum, barley, or wheat with these toxins, is not uncommon leading to outbreaks of poisoning characterised by abdominal pain, throat irritation, vomiting, diarrhoea, vertigo, and headache. Trichothecene toxins are multi-toxins affecting many systems. Acute toxicity resembles the damage done by radiation, nitrogen mustard, or mitomycin C. Primary damage is to the GI tract, and lymphoid and haematopoietic systems.

Chronic toxicity has not been reported in humans. But inhalation exposure to Stachybotrys chartarum and Aspergillusversicolor, in moisture affected office buildings, was associatedwith the development of cough, dyspnoea, wheezing, and chest tightness among employees. The mouldy vinyl wall covering was found to contain the trichothecene toxin, deoxynivalenol; however it is unclear if it really was the culprit. Similarly, exposure to Stachybotrys atra and a Trichoderma species, has been associated with the development of pulmonary haemor-rhage and haemosiderosis in infants. Contributing risk factors included tobacco smoke, and living in water-damaged homes which may enhance fungal growth. However, following investi-gations by the CDC, USA, it was decided that the evidence was not strong enough to prove an association between Stachybotrysatra found in water-damaged homes and the development ofpulmonary haemosiderosis among infants.

·      Alimentary toxic aleukia, first identified in Siberia, has been associated, in humans, with the consumption of grain contaminated with T-2 toxin. The aleukia usually occurs in four stages:

·              Hyperaemia of the mucosa, accompanied by weakness, fever, nausea, and vomiting. In more severe cases, acute oesophagitis, gastritis, and gastroenteritis may occur. Seizures and circulatory failure may occur in rare instances.

·              The second stage is characterised by the development of leukopenia, granulopenia, and progressive lympho-cytosis.

·              In the third stage, severe haemorrhagic diathesis, and necrotic pharyngitis and laryngitis can occur, resulting in death in some instances, by total oclusion of the larynx. Severe bone marrow suppression may also occur.

·              The fourth stage is characterised by recovery, though exposed individuals are susceptible to secondary infec-tions.

Visual disturbances and salivation have been reported in acute poisoning, as have conjunctivitis, rhinitis, pharyngitis, and epistaxis. Angina, tachycardia, and hypotension may occur. Conditions resembling septic shock, and poor perfusion of the GI system and other organs have also been reported.

Treatment involves administration of activated charcoal, which may be beneficial in decontamination of GI tract, and supportive measures for haemopoietic problems, GI damage, and skin damage.

Although prohibited by the 1972 Biological & Toxic Weapon Convention and the 1925 Geneva Protocol, these toxins were used both in Southeast Asia and Afghanistan.