Mycotoxin contamination of poultry feeds is a worldwide problem, as this can increase the incidence of disease and reduce production efficiency (Murugesan et al., 2015). In general, the contamination of livestock feed with mycotoxins has a profound effect on animal welfare and productivity (Gallo et al., 2015, Magnin et al., 2016). Furthermore, contrary to pathogens exposure, there are no clear clinical signs of mycotoxin intoxication, as mycotoxins are normally present at low levels. However, they are able to damage epithelial tissue, increase intestinal permeability, and therefore may result in a weakened immune system (Döll et al., 2009; Murugesan et al., 2015; Ghareeb et al., 2015; Awad et al., 2019).
Mechanisms how mycotoxins influence prokaryotes also began to emerge as an important area of future research perspectives (Payros et al., 2017; Hassan et al., 2019). Recently presented evidence indicates that DON can negatively affect the gut microbiota of either humans or animals (Robert et al., 2017; Lucke et al., 2018). This, in turn, has led to a greater interest in understanding bacterial responses toward DON. Applying an experimental model for necrotic enteritis Antonissen et al. (2014) found that broiler chickens fed a diet contaminated with 5 mg DON/kg feed were more prone to develop necrotic enteritis compared to chickens fed with the control diet. Previously it was also shown that the co-exposure of broiler chickens to DON and C. jejuni supported the C. jejuni colonization in the gut at certain time points post infection, revealing that DON might provide a favorable condition for Campylobacter growth (Ruhnau et al., 2020).
The high prevalence of Campylobacter jejuni in broilers combined with the fear to spread multi-drug resistance genes underlines its high importance from a socio-economic perspective. In consequence, many studies attempted to combat the burden of this bacterium in poultry in order to decrease the risk of human infection (Buckley et al., 2010; El-Shibiny et al., 2009; Arsi et al., 2015; Kumar et al., 2016). It has been shown that the use of competitive exclusion to control Campylobacter results in a contradictory outcome and until today there is no commercial product available with good efficacy (Willis and Reid, 2008; Santini et al., 2010; Ghareeb et al., 2012). Similarly, for DON, it was reported that mycotoxin deactivators were capable to transform DON into the non-toxic metabolite DOM-1 due to enzymatic biotransformation, thus decreasing the DON burden in the chicken. However, direct effects of purified DOM-1 on gut barrier and performance have never been assessed in chickens. Furthermore, no data are available about the interaction of DON or the non-toxic metabolite DOM-1 in context of an C. jejuni infection in broiler chickens, altogether the subject of the actual study.
Overall, the actual study demonstrated that the dietary inclusion of a non-toxic metabolite of DON, DOM-1, does not lead to negative effects in broiler chickens. Concurrently, DOM-1 -supplemented birds had a better performance compared to all other groups, as shown by the higher body weight and body weight gain, as well as an improved feed conversion ratio. On the contrary, the BW and feed intake were negatively affected by DON at 5.0 mg/kg. The impaired growth performance results may be related to changes in gut physiology caused by the mycotoxin. Negative effects on nutrient digestibility and BW could be explained by suppressed villus length and a decrease in the nutrient absorption surface area in the jejunum (Awad et al., 2011). Similarly, a linear decrease in feed intake and weight gain with increasing dietary proportions of DON-contaminated wheat in the diet of male broilers reared for 5 weeks was reported (Dänicke et al. 2003). Currently, the guidance level for DON in the European Union in complete feed for poultry is set at 5 mg DON/kg feed (EC 2006). However, the toxic effects of DON in poultry depend not only on the dose but also on the length of exposure to DON as well as other factors whereby the interactions with other dietary components that are affecting intestinal health may play a role (Ghareeb et al. 2015). Moreover, the inconsistency of the performance does not only rely on DON as such, but also on the genetic growth potential and feed efficiency traits of birds. Consequently, it is important to reevaluate threshold levels for DON in chicken feed which are reflected in the currently applicable guidance values (EC2006).
In this context, the results of the actual study also indicated that DON increased the intestinal paracellular permeability as reported in previous studies (Awad et al., 2019, Ruhnau et al., 2020). Similarly, effects of C. jejuni on the gut physiology of chickens have also been reported (Awad et al., 2020). It was shown that these bacteria have a negative impact on the nutrient absorption indicating that a lower slaughter weight might probably be due to the reduction in the feed efficiency (Awad et al., 2015). Furthermore, the occurrence of a leaky gut syndrome caused by C. jejuni is known to enhance bacterial translocation from the gut to internal organs (Awad et al., 2016). The study also revealed that the co-exposure to DON and C. jejuni potentiates a significant increase in paracellular permeability. Interestingly, the intestinal permeability was not negatively influenced by the feeding of DOM-1 and led to comparable intestinal permeability as in the control group.
Effects of purified DOM-1 on the intestine have never been tested. However nutritional strategies including bacteria/enzyme transforming DON to deepoxy-DON have reduced the occurrence and extent of intestinal lesions resulting in the same zootechnical performance as the control animals (Awad et al., 2004; Li et al., 2011; Grenier et al., 2013). Recently, an increase in the colonization and translocation of C. jejuni and E. coli could be demonstrated in birds fed with DON, again confirmed in the actual study (Ruhnau et al., 2020). By contrast, feeding of DOM-1 reduced the colonization of all measured parts of the intestine with C. jejuni in a range of 1.5-3.0 log during the first two weeks post infection compared to the DON + C. jejuni treatment. Furthermore, it can also be hypothesized that DOM-1 may create a different intestinal milieu to which C. jejuni could adapt after a certain time period. However, these findings warrant additional studies to explain how DON and DOM-1 could affect (directly or indirectly) a prokaryote such as Campylobacter in chickens