Page 1079 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Fumonisins Chapter | 71 1011

VetBooks.ir with $ 20 ppm of fumonisin in the feed were at signifi- suspensions and filtrates were inoculated into laboratory
animals, however no infectious etiology could be identi-
cantly greater risk for pneumonia as compared to farms
fied. Graham then placed 8 horses into a field containing
with low fumonisin concentrations (Bane et al., 1992). As
the concentration of fumonisin in the feed increased, the cornstalks in Rantoul, Illinois. Two of these animals died,
risk of respiratory disease continued to increase. Later it 23 and 26 days after being placed in the field (Graham,
was shown that exposure to fumonisins depressed pulmo- 1936). These outbreaks were similar to those reported in
nary intravascular macrophage function, and pigs exposed 1893 and 1914, which had occurred following a summer
to this toxin had decreased pulmonary clearance of drought (Graham, 1936). Neurologic deaths with similar
blood borne particulates and bacteria when compared to lesions were also reported in Iowa during the winter of
control animals (Smith et al., 1996c). In a more recent 1914 and in the spring of 1935 (Schwarte et al., 1937).
study, exposure to fumonisin exacerbated respiratory Histologic examination of the brain revealed no evidence
disease in a Pasteurella multocida challenge model of infectious agents. This “syndrome” was then subse-
quently reproduced by feeding moldy corn and corn fod-
(Halloy et al., 2005). Pigs that were fed 0.5 mg of FB 1
per kg of body weight/day for 7 days had delayed growth, der to five horses (Schwarte et al., 1937). A similar
increased coughing and more severe lung lesions that disease syndrome was identified and confirmed by feed-
control pigs. In another study, pigs fed FB 1 at 20 ppm and ing trials in Egypt (Badiali et al., 1968; Wilson and
exposed to Mycoplasma hyopneumoniae had more severe Maronpot, 1971) and in South Africa (Marasas et al.,
lung lesions as assessed by CT and histopathology as 1976). At necropsy, these studies were able to consis-
compared to pigs exposed to Mycoplasma but diets with- tently demonstrate swelling of the cerebral hemispheres
out FB 1 (Po ´sa et al., 2013). Therefore at levels well below and flattening of the overlying gyri. On coronal sections,
those needed to cause hepatic lesions or pulmonary there were cavities of varying sizes with liquefactive
edema, fumonisins are likely to reduce growth rates and necrosis of subcortical white matter in one or both cere-
increase disease in pigs. bral hemispheres (Fig. 71.5). There was also scattered
multifocal hemorrhages in the surrounding white matter
(Marasas et al., 1976; Haliburton et al., 1979). Based on
Fumonisin Toxicosis in Horses-Historical
these findings, Marasas et al. (1976) coined the term
Several outbreaks of a neurologic disease in horses “ELEM” as a distinct clinical and morphologic syndrome
occurred in the United States in the early 1900s with in horses associated with the feeding of corn.
thousands of deaths reported in several states. The earliest F. verticillioides was later isolated from corn collected
citation of neurologic deaths associated with the feeding from field outbreaks in Egypt, and leukoencephalomalacia
of contaminated corn was from Maryland (MacCallum was subsequently reproduced in donkeys fed corn inocu-
and Buckley, 1902). The condition was commonly lated with the fungus (Wilson and Maronpot, 1971). In
referred to as “cerebrospinal meningitis” and presented South Africa however, samples of corn inoculated with
with fairly characteristic signs. The duration of disease F. verticillioides produced liver damage and icterus in
varied from a few hours to a week, and the brains from several horses and donkeys, but not brain lesions
affected horses had “softened” areas in the cerebrum
involving only the white matter. Additional outbreaks
were subsequently reported from Kansas, Iowa,
Mississippi, and North Carolina. A similar disease,
described as “epizootic cerebritis” had been encountered
in 1891, however it is not known whether this was associ-
ated with corn (Butler, 1902). When feed from an out-
break of “leucoencephalitis” in Kansas was fed to a horse,
it died after developing neurologic signs (Butler, 1902).
At necropsy, the left cerebral hemisphere was “soft to the
touch, and when cut through, the white matter was broken
down extensively, nearly the entire hemisphere being
involved.” Several attempts were made to identify an
infectious agent in the brain of affected horses and all
were negative (MacCallum and Buckley, 1902). The
authors concluded that a toxic etiology was likely.
In Central Illinois, more than 5,000 horses died during
FIGURE 71.5 A cross section of a cerebral hemisphere from a horse
the winter of 1934 35 from a syndrome referred to demonstrating liquefactive necrosis of the white matter typical of equine
as “cornstalk disease” (Graham, 1935). Brain tissue leukoencephalomalacia.