The failure of trichothecene mycotoxins and whole cultures of Fusarium tricinctum to cause experimental haemorrhagic syndromes in calves and pigs

Abstract

Piglets and calves were dosed orally with pure diacetoxyscirpenol (DAS) and T-2 toxin, crude extracts of Fusarium tricinctum containing T-2 toxin, and whole cultures of F tricinctum containing T-2 toxin at a constant daily rate of 0.1 mg toxin per kg body-weight (piglets) or 0.2 mg toxin per kg body-weight (calves). The treatment continued for periods of seven to 78 days but it failed to induce clinical haemorrhagic syndromes. Increasing the dose of F tricinctum culture five-fold for eight days following 78 days at the lower dose was equally ineffective. The lack of an effect by daily intakes of toxin that could have been ingested with naturally contaminated feedstuffs suggests that DAS, T-2 toxin and other metabolites of F tricinctum probably have little or no part to play in the aetiology of feed associated haemorrhagic disease.

Progress in Molecular and Subcellular Biology

“…Huff et al (1981) reported that large doses of deoxynivalenol administered to day old chicks via oral intubation caused extensive ecchymotic hemorrhaging throughout the body along with other symptoms consistent with the description of hemorrhagic anemia snydrome in chickens caused by moldy feed (Forgacs and Carll 1962). Other workers, however, have reported that oral administration of large doses (0.1-0.6 mg/kg) of purified T-2 toxin or diacetoxyscirpenol to cows, calves or pigs failed to induce any evidence of hemorrhagic syndrome (Matthews et al 1977(Matthews et al , 1979Weaver et al 1980). This failure to obtain hemorrhaging probably does not eliminate the trichothecenes from the etiology of the hemorrhagic syndrome but rather indicates that the syndrome is of a far more complicated nature than having a single cause.…”

“…Other workers, however, have reported that oral administration of large doses (0.1-0.6 mg/kg) of purified T-2 toxin or diacetoxyscirpenol to cows, calves or pigs failed to induce any evidence of hemorrhagic syndrome (Matthews et al 1977(Matthews et al , 1979Weaver et al 1980). The slight increase in prothrombin and partial thromboplastin times observed in T-2 toxin treated animals (Patterson et al 1979), probably arise through partial inhibition of liver protein synthesis, and may also make the animals more prone to hemorrphage. The extravization of plasma proteins and red cells from capillaries observed following fusarenon-X treatment of rats indicates the potential for hemorrhage, but other dietary factors almost certainly are involved.…”

“…As with many of the natural outbreaks of mycotoxicosis where trichothecenes have been implicated as a causative agent, moldy corn toxicosis usually occurs following cold and damp harvest seasons when the corn has not had time to dry sufficiently before harvest. However, oral administration of either the toxins or a crude fungal extract containing the toxins failed to produce hemorrhagic lesions (Patterson et al 1979). It is the hemorrhaging that gives this disease its characteristic feature (hemorrhagic syndrome), and massive blood loss through the intestine and into the abdominal cavity is often the cause of death.…”

“…Symptoms of the toxicosis in pigs and cattle are diarrhea, reduced milk production in dairy cattle, and oftentimes hemorrhagic lesions in the liver, stomach, heart, lungs, bladder, kidney and intestine. More recent reports indicate that while trichothecenes and T-2 toxin in particular may be present in moldy feed responsible for hemorrhagic syndrome (Petrie et al 1977), these compounds alone can not be the causative agent (Patterson et al 1979;Weaver et al 1978d;Weaver et al 1980;Weaver et al 1981). Hsu et al (1972) were the first to identify a trichothecene, T-2 toxin, in extracts of moldy corn which caused hemorrhagic syndrome and death in a herd of dairy cattle.…”

“…The effects of several trichothecenes on hematological parameters have been studied in mice ), guinea-pigs (DeNicola et al 1978), rabbits (RUsch and Stahelin 1965Gentry andCooper 1981), cats (Sato et al 1975;Lutsky et al 1978), dogs (RUsch and, chickens Richard et al 1978;Pearson 1978;Chi et al 1981;Chi et al 1977b;Doerr et al 1981), pigs (RUsch andWeaver et al 1978bWeaver et al , 1978dWeaver et al , 1981Patterson et al 1979), calves (Patterson et al 1979;Mann et al 1982), monkeys (RUsch andJagadeesan et al 1982) and man (Goodwin et al 1978).…”