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.
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