Fusariotoxicosis

The disease is caused by toxins produced by fungi belong­ing to the genus Fusarium, which infect cereals in the summer and autumn while crops are in the field. These toxins can be produced at relatively cool temperatures and can reach high levels during storage, where conditions for fungal growth and mycotoxin formation are favourable.

Fusariotoxins of great socio-economic importance include zearalenone, trichothecenes and the fumonisins.

Zearalenone is produced by Fusarium graminearum or Fusarium culmorum. Effects of intoxication by Zearalenone include precocious development of mammae and other oestrogenic effects in young gilts and prepucial enlarge­ment in young boars. Zearalenone is thought to bind to oestrogen receptors, thus leading to hormonal changes. Swine are significantly affected, together with cattle and poultry and laboratory rodents. Effects of zearalenone fed to sows during gestation can include weak piglets and reduced litter size. Levels of 0.5 to 1.0 μg∕g of dietary zearalenone have been associated with the latter effects, whereas hyperoestrogenism has been associated with dietary levels of 1.5 to 5 μg∕g(⁴).

Trichothecene comprises more than 50 different toxins, with deoxynivalenol (DON) being the commonest one followed by T-2 toxin. DON, also known as vomitoxin, is produced principally by Fusarium graminearum⁽⁴⁾; this toxin is immunosuppressive and may cause inflammation and tubular damage in the animal kidney. Swine are the species most frequently affected. Levels above 1 μg∕g are considered potentially harmful to these animals. Con­versely, birds seem to be less sensitive to intoxication by DON.

T-2 toxin is produced by Fusarium sporotrichioid.es. The major effect of T-2 toxin is the inhibition of protein syn­thesis, followed by a secondary destruction of DNA and RNA synthesis. This results in an impaired function of the actively dividing cells such as those lining the gastrointes­tinal tract, skin, lymphoid and erythroid cells and can lead to decreased levels of antibodies and cytokines⁽⁴⁾. The clini­cal signs of disease include weight loss, bloody diarrhoea, dermal necrosis or beak and mouth lesions, haemorrhage and decreased production of milk and eggs. Yellow caseous plaques, occurring at the margin of the beak, mucosa of the hard palate, and angle of the mouth and tongue, rep­resent typical oral lesions in poultry. These lesions can occur at dietary levels of 4 mg/kg after 1 week, 0.4 mg/kg after 7 weeks.

Fumonisins are a group of mycotoxins produced prima­rily by Fusarium Verticillioides and Fusarium proliferatum. Horses are most frequently affected and develop liquefac- tive necrosis of the white matter in the cerebrum (leucoen- cephalomalacia). Lung oedema in swine can also occur. Other manifestations such as liver disease, and tumours of the liver and kidney, have been reported experimentally using rodents. Experimentally, poultry and cattle have shown a much lower sensitivity to the toxic action of fumonisins when compared with horses and pigs⁽⁶⁾. Regardless of the effects on animals, the fumonisins are often responsible for liver toxicity, and their major mode of action is by interference with the metabolism of sphingolipids.

Diagnosis of fusoriotoxicosis is challenging because clinical signs are not specific. The observation of appropri­ate gross and microscopic lesions, and the detection of toxins in grains, forages or the ingesta of affected animals can help in formulating a diagnosis. The samples of choice for diagnosis should be frozen, as toxins are produced under cold temperatures. However, the diagnostic tests required to detect these toxins are complex and available only in a few specialized diagnostic laboratories.