Fumonisins in horses and why they are life-threatening

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Health problems, performance issues, and loss of use can be a significant effect of mycotoxins in horses, writes Radka Borutova MVD, PhD, of NutriAd International in Belgium.

Fumonisins are mycotoxins produced by Fusarium verticillioides, F. proliferatum, and other Fusarium species. Animal and human health problems related to these mycotoxins are almost exclusively associated with the consumption of contaminated maize or products made from maize (Marasas, 2001).

Soils and pasture are other imortant areas where horse owners can make a difference.

Horses are not typically classified as agricultural animals and are used mainly for athletic work, competition and/or breeding. Many horses are afforded ‘companion animal’ status, including ponies, donkeys and those that have been retired from racing, for example. Due to their status in human society, horses have a longer lifespan than agricultural animals, some living to be 30 years old or more and their exposure to toxins can be long term as a result.

Horses used for competitions, such as racing, dressage, polo, long distance riding and show jumping are high value animals and economic losses from poor performance, health problems and even loss of use due to mycotoxins can be significant.

Fumonisin levels guided by the FDA

Consumption of moldy maize has long been recognized as a cause of equine leukoencephalomalacia (ELEM) (Kellerman et al., 1990). Fumonisins B1 (FB1) have been shown to be cardiotoxic and cause pulmonary edema in pigs, a syndrome termed porcine pulmonary edema or PPE (Haschek et al., 2001). Cattle and poultry are considerably less sensitive to fumonisins than horses, pigs, rabbits, or laboratory rodents (Bolger et al., 2001).

The USFDA Center for Food Safety and Nutrition has issued guidance levels for fumonisins in maize and maize by-products used in animal feeds (Center for Food Safety and Nutrition, 2001). The levels vary by species, reflecting their relative sensitivities to fumonisins:

FDA guidance levels for total fumonisins (FB1 +FB2 +FB3) in animal feed.
FDA guidance levels for total fumonisins (FB1 +FB2 +FB3) in animal feed. Adopted from Center for Food Safety and Nutrition (2001).

Fumonisins in horses

Fumonisins induce spontaneous disease in horses and pigs, with horses being more susceptible. The spontaneous diseases, ELEM and PPE, refer to critical species-specific target organs; the brain in horses and the lung in pigs. The level of fumonisin contamination required to induce ELEM, which is unique to Equidae, is quite low, and as a result fumonisin toxicosis in horses occurs periodically. In addition to the life-threatening effects of fumonisins, the effects on the immune system should not be underestimated. Adverse effects on immune function can increase susceptibility to opportunistic microorganisms or result in more severe infections, including those related to food safety and zoonotic diseases. In addition, immune suppression can interfere with vaccination responses and can predispose to cancer induction. The effects of long term, low level exposures on the immune system are especially important.

Why are they so dangerous?

Fumonisins inhibit production of ceramide synthase, an enzyme of critical importance in sphingolipid biosynthesis, increasing the concentration of sphingoid bases (sphinganine [Sa] and sphingosine [So]) and depleting complex sphingolipids. Accumulation of sphinganine and consequently sphingosine in tissues seems to be the primary mode of action of fumonisins toxicity. Blood serum and urine concentrations of sphingoid bases (Sa/So) could be used as a sensitive biomarker for fumonisins exposure.

Horses are the most sensitive species to fumonisin toxicity with disease occurring worldwide. The target organs in the horse are heart, central nervous system and liver. The disease syndrome was named leukoencephalomalacia due to the type (malacia = softening [due to necrosis]) and distribution (leuko = white matter) of the most prominent lesion in the brain. Equids are the only species in which fumonisins induce this lesion.

This is the brain from a horse with mycotoxic leukoencephalomalacia. Note the swelling, softening, and hemorrhage of the subcortical white matter at *. A good lesion diagnosis would be leukoencephalomalacia with multiple hemorrhages. Note how a row of hemorrhage delineates the gray and white matter.
The brain from a horse with mycotoxic leukoencephalomalacia. Note the swelling, softening, and hemorrhage of the subcortical white matter at *.  © University of Georgia

Onset of disease can occur as early as 7 days after exposure to contaminated feed, but usually after 14–21 days; occasionally onset may be delayed to 90 days or more. Outbreaks that affect several horses on the same farm are common. In 1901 through 1902, over 2000 horses died in the USA as a result of ELEM and in 1934 through 1935 over 5000 horses died in the state of Illinois alone. Large numbers of outbreaks were reported in the USA during the 1980s, especially following the heavy contamination of the 1989 maize crop (Ross et al., 1991). Additional outbreaks of ELEM were reported in the mid-1990s from the USA and Hungary (Bela and Endre, 1996). Outbreaks continue to occur each year in the USA. The rare surviving animals will usually have permanent neurological disease.

Two syndromes have been described, the neurotoxic (which is termed ELEM) and hepatotoxic forms. These forms may appear independently or concurrently. In the field, high-dose exposure is thought to increase the likelihood of the hepatotoxic form, with the more frequently encountered lower doses favoring the neurotoxic form. The clinical course of ELEM is generally short with an acute onset of signs followed by death within hours or days. Decreased feed intake, depression, ataxia, blindness, and hysteria are reported. Anorexia occurs due to glossopharyngeal paralysis, and paralysis of the lips and tongue, with loss of ability to grasp and chew food. Incoordination, circling, ataxia, head pressing, marked stupor, and hyperesthesia (excessive physical sensitivity, especially of the skin) are common, as are hyperexcitability, profuse sweating, mania, and convulsions.

Death may also occur without clinical signs being observed. In classical ELEM, there is liquefactive necrosis of the white matter, primarily in the cerebrum. The hepatotoxic syndrome occurs much less frequently than the neurotoxic form. This syndrome usually takes 5 to 10 days from time of onset of clinical signs to death. Icterus is usually prominent, sometimes with edema of the head and submandibular space. Elevated serum bilirubin concentration and liver enzyme activities are typically present. Neurologic signs may be present terminally. The liver is often small and firm.

Effective mycotoxin management

The best practical way to control fumonisins levels is to use rapid test kit systems for the analysis of mycotoxins in raw ingredients which are not yet in silos. Different rapid test kit systems are validated for different mycotoxins and commodities which offer a very quick and effective way of raw material screening before they enter the feed mill. Once the levels are known, every feed mill or farm can estimate the quality of its raw ingredients in terms of mycotoxin contamination and can effectively and more precisely (dosage adjustment) apply feed additives during feed production.

Another strategy of mycotoxin risk management is to test for the presence of mycotoxins in finished feeds. This is an advantage as every raw ingredient can bring its own mycotoxins into the finished feed. Some important raw ingredients whose inclusion is not high (5-10%) and which can still cause significant contamination of finished feed can be inadvertently overlooked if not tested.

As already mentioned, blood serum and urine concentrations of sphingoid bases (Sa/So) can be used as a sensitive biomarker for fumonisins exposure. In case of elevated concentrations of Sa/So in blood serum or urine of horses the contaminated feed has to be removed immediately and replaced by clean feed. Application of specific feed additives which are able to help negate the negative effects of fumonisins in horses are highly recommended.

 

References

  1. Bela, F., Endre, B., 1996. Occurrence of equine leukoencephalomalacia (ELEM) caused by fumonisin B1 mycotoxin in Hungary. Magyar Allatorvosok Lapja 8, 484–487.
  2. Center for Food Safety and Nutrition, US Food and Drug Administration, 2001. Background Paper in Support of Fumonisin Levels in Animal Feed: Executive Summary of this Scientific Document (November 9, 2001). http://www.cfsan.fda.gov/∼dms/fumonbg4.html.
  3. Haschek, W.M., Gumprecht, L.A., Smith, G., Tumbleson, M.E., Constable, P.D., 2001. Fumonisin toxicosis in swine: an overview of porcine pulmonary edema and current perspectives. Environ. Health Persp. 109 (Suppl. 2), 251–257.
  4. Kellerman, T.S., Marasas,W.F., Thiel, P.G., Gelderblom,W.C., Cawood, M., Coetzer, J.A., 1990. Leukoencephalomalacia in two horses induced by oral dosing of fumonisin B1. Onderstepoort J. Vet. Res. 57, 269–275.
  5. Marasas, W.F.O., 2001. Discovery and occurrence of the fumonisins: a historical perspective. Environ. Health Persp. 109 (Suppl. 2), 239–243.
  6. Ross, P.F., Rice, L.G., Reagor, J.C., Osweiler, G.D., Wilson, T.M., Nelson, H.A., Owens, D.L., Plattner, R.D., Harlin, K.A., Richard, J.L., Colvin, B.M., Banton, M.I., 1991. Fumonisin B1 concentrations in feeds from 45 confirmed equine leukoencephalomalacia cases. J. Vet. Diagn. Invest. 3, 238–241.

Table details:
b Percent of formulated ration composed of maize or maize byproduct.
c Maize screenings not to be included in rations for Equidae.
d Other species not listed in table.
e Includes beef cattle, sheep, goats and other ruminants.
f Animals ≥3 months of age.
g Includes chickens, turkeys, ducklings and other poultry species.

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This article has been written by a contributor to Horsetalk.co.nz.

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