Equine leukoencephalomalacia (ELEM) due to fumonisins B1 and B2 in Argentina

Abstract

The animals were on a pasture of native grasses and supplemented ad libitum with corn kernels and wheat bran. Three horses were observed having acute neurologic signs including blindness, four leg ataxia, hyperexcitability, aimless walking and circling, followed by death in two of them. Four other horses were found dead overnight without a history of neurologic signs. The morbidity, mortality and lethality rates were 11.6%, 10% and 85.7%, respectively. Grossly, the brain showed focal areas of hemorrhage, brown-yellow discoloration and softening of the sub-cortical white matter. The microscopic brain lesions consisted of extensive areas of malacia within the white matter of the cerebral hemispheres, brainstem and cerebellum, characterized by rarefaction of the white matter with cavitations filled with proteinaceous edema, multifocal hemorrhages and mild infiltration by neutrophils, and rare eosinophils. Swollen glial cells with abundant eosinophilic cytoplasm, distinct cell borders, intracytoplasmic deeply eosinophilic globules and eccentric, hyperchromatic, occasionally pyknotic nucleus were present throughout the areas of rarefaction hemorrhage, edema and necrosis. The feed supplements contained 12,490μg/kg of fumonisin B1 and 5,251μg/ kg of fumonisin B2. This is the first reported outbreak of ELEM associated with consumption of feed supplements containing high concentrations of fumonisins in Argentina.

Mycotoxicoses of ruminants and horses

“…2,12,27,63,64,67 The clinical manifestation period is 2-72 hr, but most affected animals die within 6-24 hr. Occasionally, the clinical course may last up to 13 days.…”

Prevalence of fumonisin-producing Fusarium species in Brazilian corn grains

“…Fumonisins are involved in the inhibition of sphingolipids with serious consequences to the cell structure of eukaryotic organisms (Marasas et al, 2004;Wang et al, 1991). The ingestion of fumonisin-contaminated corn can lead to serious diseases in animals, such as horse leukoencephalomalacia (Giannitti et al, 2011;Marasas et al, 1988), pulmonary edema in swine (Harrison et al, 1990), and hepatotoxicity in rats (Gelderblom et al, 1996). Fumonisins are also directly related to human esophageal cancer and defects in neural tube formation in fetuses (Doi and Uetsuka, 2011;V€ olkel et al, 2011;Jackson and Jablonski, 2004;Ueno, 2000).…”

Hepatoencephalopathy syndrome due to Cassia occidentalis (Leguminosae, Caesalpinioideae) seed ingestion in horses

“…In the present study, C. occidentalis poisoning was confirmed after the identification of clinical and post mortem findings associated with the presence of the seeds within the horses' ration and by exclusion after anamnesis and epidemiological analysis of the other causes of encephalopathy, e.g. rabies, aflatoxins, fumonisins [31] and other plants toxicoses [32–34].…”

“…[32] and Crotalaria retusa [33] poisoning in horses is caused by pyrrolizidine alkaloids. Outbreaks of neurological disease and sudden death in horses may also be caused by ingestion of one or more type of fumonisin mycotoxins [31]. Neither fumonisins nor aflatoxins were detected in the mares' feedstuff by HPLC and no white matter malacia was detected [31].…”