New aspects of the impact of fumonisin on pig health

Brand new results from the BIOMIN Mycotoxin Survey 2014 (January – September) confirm that fumonisins are globally most common in corn. 

Out of 512 corn samples 82% contained up to 130 246 ppb (corn sampled in Malaysia) of fumonisins. The average fumonisin contamination of positive corn samples was 2 280 ppb. Similar to other fusariotoxins, occurrence of fumonisins is ubiquitous and not limited to a specific climate (compare figure 1). In the biggest corn producing countries such as Brazil, Argentina and USA, the contamination of corn with fumonisins was up to 100% with an average contamination of 3 297 ppb and a maximum contamination of 44 752 ppb (Brazil). 

Figure 1: Percentage of corn contaminated with fumonisins (fumonisin B1 + fumonisin B2) worldwide and in selected areas (analyzed between January and September 2014).

Fumonisins exert their main toxic effects by blocking ceramide synthase in the sphingolipid metabolism leading to accumulation of free sphinganine and to a lesser extent sphingosine. As a consequence, the production of complex sphingolipids - necessary components of nerves, muscles and also membranes is interrupted. Pigs are – besides horses and rabbits - the species most affected by the detrimental effects of fumonisins. The reason for different sensitivities between species lies in the different absorption of fumonisins in the gastrointestinal tract and furthermore different metabolization.

In pigs, intoxication with high doses of fumonisins lead to porcine pulmonary edema which results from the capacity of fumonisins to decrease cardiac contractility and increase mean pulmonary artery pressure. Low contaminations of fumonisins predispose pigs to lung pneumonitis. Toxic hepatosis can occur in the presence of porcine pulmonary edema but also without any visible effect on the lung.

Do fumonisins also impact the integrity of the gastrointestinal tract of pigs?

The guidance value for fumonisin B1 + fumonisin B2 for complete feed for pigs in the European Union is 5 000 ppb – which might seem high, compared to the maximum tolerated value of aflatoxin B1 which is 20 ppb.

This is partially due to the low absorption of 3 - 6% fumonisins in the gastrointestinal tract. On the other hand, this low absorption of fumonisins leaves the gut itself exposed to a substantial part of the original contamination.

It was found that the barrier function of porcine intestinal epithelial cells is reduced by fumonisins in the feed and that fumonisins also exert a cytotoxic effect on these cells. The destruction of the natural barrier, the intestinal epithelium, leads to a facilitated uptake of chemical products, mycotoxins and also pathogens.

Already low dosages of fumonisins increase intestinal colonization Escherichia coli 400- to 700- times. In 75% of fumonisin B1 treated pigs, E. coli were translocated to the mesenteric lymph nodes and disseminated in the lungs, and in some pigs even to liver and spleen.

When growing pigs were chronically exposed to fumonisins the cellular immune response after Salmonella typhimurium inoculation was compromised and their microbiota profile of the gastrointestinal tract was modified rapidly compared to the group of pigs without fumonisin in the diet. This change in balance of the intestinal flora can have several adverse effects on the health of the pig.

Additionally fumonisins in the diet reduce the height of the intestinal villi and lead to villi fusion in the small intestine thus compromising the nutrient uptake.

Picture 1: Effect of fumonisin exposure on intestinal histology.
Left side: Healthy jejunum.
Right side: Jejunum of a fumonisin treated piglet where fusion of villi was observed.
Source: A.P. Bracarense, Universidade Estadual de Londrina, Brazil.

Contamination with fumonisins does not only cause severe damage to lungs and livers of affected pigs but also compromises the integrity of the gastrointestinal tract of animals. The induced intestinal damage may lead to higher incidences of pathogens, act as a predisposing factor to infectious diseases and compromises the nutrient uptake.

For further information contact the contributor:


Verena STARKL MSc 
Product Manager

BIOMIN Holding GmbH 
Erber Campus 1
3131 Getzersdorf, Austria

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