The most important mycotoxins produced by the mold Fusarium. They can be classified as 12,13-epoxytrichothecenes and macrocyclic resorcyclates (naturally occurring derivatives of b-resorcyclic acid). The production of trichothecenes is shared by the species of Trichothecium, Myrothecium, Trichoderma, and Cephulosporium. There are three types of trichothecenes. (1) monoepoxytrichothecenes (8-deoxymonoepoxytrichothecenes (structure I), including diacetoxy- scirpenol and T-2 toxin; (8-ketomonoepoxytrichothecenes (structure II), including trichothecin and fusarenone; (2) diepoxytrichothecenes (structure III), including crotocin and crotocol; (3) macrocyclic trichothecenes (macrocyclic diesters [structure IV], including the roroidins; and (4) macrocyclic triesters (structure V), including the verrucarins). Most trichothecenes are phytotoxic and zootoxic. The in vitro toxic effects of the trichothecenes include skin necrosis, inflammatory effects, massive hemorrhages, and effects on heart and respiration rates. Furthermore, many of the trichothecenes have been shown to be inhibitors of protein synthesis; the most toxic types inhibiting at the initiation step (e.g., T-2 toxin, diacetoxyscirpenol, many of the verrucarins), the least toxic types at the elongation-termination process (e.g., crotocin, trichothecin, trichodermin). The actual toxicities of some of the trichothecenes were probably demonstrated in the field by both animal and human mycotoxicoses. An example of the latter is alimentary toxic aleukia, a toxic syndrome caused by Fusarium spp. This disease was traced to the consumption of grain that was allowed to overwinter in the fields. The grains became invaded by cryophilic molds from which several fungal genera and species were identified. In order to produce toxins, the most important requirement of these molds appeared to be the presence of alternate freezing and thawing cycles. The clinical course of alimentary toxic aleukia occurs in four stages. In the first stage (3-9 days) there is a burning sensation in the mouth and tongue and in the gastrointestinal tract, headache, dizziness, weakness, fatigue. In the latent second stage (2-8 weeks) there is progressive leukopenia, granulopenia, lymphocytosis, anemia, bacterial infections, disturbances in the central and autonomic nervous system, such as weak¬ ness, headache, palpitation, asthmatic attacks, icterus, hypotension, dilation of the pupils, soft and labile pulse, diarrhea, or constipation. In the third stage there are petechial hemorrhages in the skin, mucous membranes in the mouth, tongue, gastrointestinal tract and nasal area, necrosis in parts of the buccal cavity, enlargement and edema of the cervical lymph nodes, lesions in the esophagus and epiglottis, and edema in the larynx. In the fourth stage (>2 months), if death does not intervene, the patient may recover.