Page 1082 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

1014 SECTION | XV Mycotoxins

VetBooks.ir TABLE 71.2 (Continued)

Number of
Animals Dose & Route Duration Toxic Effects Reference
Reported Fumonisin Concentrations From Naturally-Occurring Outbreaks
18 horses 37 122 ppm FB 1 Unknown ELEM confirmed in 14 horses Wilson et al.
(1990)
45 horses 8 126 ppm FB 1 7 35 days All cases had confirmed Ross et al.
leukoencephalomalacia (1991)
6 horses 370 ppm FB 1 & Unknown 4 horses died with ELEM; 2 horses Wilkins et al.
105 ppm FB 2 with neurologic signs apparently (1994)
recovered
100 1 4 29 ppm FB 1 Unknown many donkeys died of neurologic Rosiles et al.
donkeys disease-ELEM confirmed in 3 cases (1998)
7 horses 12.5 ppm FB 1 and 10 days At least 7 horses died with ELEM—at Giannitti et al.
5.3 ppm FB 2 least one other horse with neurologic (2011)
signs recovered with feed was
removed
1
100 horses 6.0 ppm FB 1 and ,30 days 21 horses developed neurologic Jovanovi´ c
2.4 ppm FB 2 signs—15 died within a month et al. (2015)
period

In a large study with varying doses of fumonisin, horses movement (Foreman et al., 2004). These signs progressed
treated with higher doses developed leukoencephalomalacia over 12 48 h to become more readily apparent. Hindlimb
(in 5 8 days), whereas horses that received lower concentra- and trunkal ataxia in particular became more apparent
tions developed primarily hepatic lesions without any evidence with time. A variety of behavioral changes were observed
of neurotoxicity (Foreman et al., 2004). Therefore it can be including depression, hyperesthesia, and intermittent
concluded ELEM results from an acute exposure to feed dementia. All horses had intact menace and pupillary light
containing high concentrations of fumonisin B 1 , while hepato- responses at the time of death.
toxicity occurs with chronic ingestion of lower levels. Cerebrospinal fluid findings from horses with ELEM
Serum biochemical changes associated with fumonisin include elevations in protein concentration, albumin, and
toxicity in horses have been predominantly related to hepato- IgG concentrations and increased albumin quotients
toxicity (increased AST, Wang et al., 1992; increased AST (Foreman et al., 2004). Cerebrospinal fluid red blood cell,
and GGT, Laurentetal.,1989; Kellerman et al., 1990; leukocyte, and glucose concentrations along with creatine
increased GGT and SDH, Schumacher et al., 1995; increased kinase activity are not altered in horses with neurologic dis-
AST, GGT, and ALP, Ross et al., 1993; increased AST, ease. Along with the histopathologic findings, these cere-
GGT, ALP, total bilirubin, and bile acids, Wilson et al., brospinal fluid changes indicate the presence of a vasogenic
1992; and “elevated liver enzymes,” Ross et al., 1994). cerebral edema in horses with leukoencephalomalacia.
The neurologic signs are usually summarized as sud-
den onset of one or more of the following: frenzy, aimless
circling, head pressing, paresis, ataxia, blindness, depres- Fumonisin Toxicity in Cattle
sion, and hyperexcitability (Ross et al., 1991; Wilson
et al., 1992). Other reports have stated that “the disease Adult beef cattle appear relatively resistant to fumonisin.
started with lack of appetite, followed by the disturbance Feeder calves fed a diet containing fumonisin concentrations
of swallowing and chewing indicating the paralysis of up to 148 ppm for 31 days had only mild hepatotoxicity
cephalic and pharyngeal muscles. Paralysis of cephalic (Osweiler et al., 1993). Although it is tempting to speculate
and cervical muscles spread to the muscles of the extremi- that cattle are able to break down the toxin, it has been
ties and trunk. The animals moved with difficulties, totter- shown that fumonisin is poorly metabolized by the rumen.
ing and ataxia developed. Signs of ‘blindness’ developed Instead it is though that cattle have an increased tolerance to
in one animal. At the final stage of disease, the affected fumonisin because of differences in the mechanism of
animals lied down and died. In a comprehensive study, action. In milk-fed calves treated with purified fumonisin
early neurologic signs included mild proprioceptive B 1 , the kidney was the target organ of toxicity (Mathur
abnormalities, including hindlimb ataxia, delayed fore- et al., 2001). However this study also demonstrated that
limb placing reactions, and decreased tongue tone and sphingosine and sphinganine concentrations did not increase