Discussion

Deoxynivalenol is a prevalent Type B-trichothecene produced by Fusarium fungi that commonly contaminates cereal grains used in swine diets. Swine are recognized as one of the most sensitive livestock species to DON exposure, with reduced voluntary feed intake and subsequent growth depression consistently identified as the primary clinical manifestations at practical dietary concentration (Pestka 2010). The study objective was to characterize the quantitative dose-response relationship between increasing dietary DON concentrations (0.2 to 5.1 mg/kg) on nursery pig growth performance, with particular emphasis on determining whether responses follow a linear or non-linear threshold-based pattern within a commercially relevant exposure range. Unlike multiple previous studies that evaluated only one or two DON concentrations (Frobose et al. 2015a; Wilson et al. 2022), the seven-point titration design used here allowed for more precise characterization of the dose-response relationship across commercially relevant exposure levels with DON sourced from naturally contaminated corn. Current DON guidance values for swine diets are approximately 0.9 mg/kg in complete feed in Europe, whereas in the United States, FDA guidance limits contaminated grains to 5 mg/kg DON at a maximum of 20% of the diet, corresponding to approximately 1 mg/kg in finished feed (FDA 2010; EFSA COMTAM 2017). However, the FDA does not report the literature that is used to determine their guidance level whereas the EFSA summarized all of the data that went into their decision. Surveys of cereal grains and finished feeds frequently report DON contamination within or above this 0.9–5.0 mg/kg DON range, suggesting that nursery pigs may routinely encounter concentrations capable of impairing performance under commercial production conditions (Streit et al. 2013).

To our knowledge, few published studies have applied segmented regression to identify potential breakpoints where dietary DON concentration alters nursery pig performance (Dersjant-Li et al. 2003). Linear models provided the best overall fit for the relationship between DON mg/d intake and ADG. The absence of identifiable breakpoints in the segmented regression analysis and lack of significant quadratic responses further support the interpretation that performance responses to DON are proportional across the evaluated concentration range (0.2–5.1 mg/kg). Young et al. (1983) similarly reported linear reductions in ADFI and ADG in 7.1 kg pigs fed diets containing 0.14, 1.34, 2.55, and 5.12 mg/kg DON for 21 d. In this study, ADG declined 7.4% per mg/kg and ADFI declined 8.0% per mg/kg increase in dietary DON when expressed relative to performance at 0.2 mg/kg. These proportional reductions exceed previously reported summary estimates of approximately 4.6% for ADG and 6.7% for ADFI per mg/kg DON in nursery pigs (Etienne and Wache 2008). This comparison suggests that growth performance responses to DON may be more pronounced in young, lightweight pigs used in controlled titration studies, while meta-analytical estimates represent composite responses across pigs of varying body weights and physiological stages, potentially diluting age- or size-dependent sensitivity.

A meta-analysis by Andretta et al. (2012) reported that dietary DON exposure is strongly correlated to reduced ADFI and ADG, while increasing feed efficiency (_R_2 = 0.87, 0.57, and 0.43, respectively) in studies combining nursery and grower pigs. Data from the present study are consistent with these observations, where DON concentration accounted for 58%, 48%, and 39% of the variation in overall ADFI, ADG, and BW, respectively, indicating that reduced feed intake was the primary driver of impaired growth. Only 64% of the studies included in Andretta et al. (2012) were conducted in nursery pigs; the remaining 36% performed in grow-finish pigs, which may partially inflate the reported feed efficiency relationship. This may reflect differences in effective DON exposure relative to body weight, as younger pigs receive a greater dose per unit of body weight compared to heavier pigs when consuming diets with similar DON concentrations, potentially resulting in a more pronounced response. Additionally, data compiled from eight studies showed an 8.45% decrease in weight gain per mg/kg DON (_R_2 = 0.66) (Dersjant-Li et al. 2003).

Across the 24-d period, cumulative BW remained linearly suppressed, demonstrating that early intake depression exerts persistent effects on overall performance. These findings align with the well-established anorectic effect of DON, in which reduced voluntary feed intake has been consistently identified as the principal mechanism underlying growth suppression in pigs (Dänicke et al. 2004; Frobose et al. 2015a; Wellington et al. 2020). While DON can impair intestinal integrity and immune function (Ghareeb et al. 2015), these gastrointestinal disruptions did not result in consistent changes in feed efficiency in the present study (_R_2 = 0.01), indicating that reduced voluntary feed intake, rather than impaired nutrient utilization, was the primary factor limiting growth performance within this exposure range.

In conclusion, increasing dietary DON concentration from 0.2 to 5.1 mg/kg resulted in clear, linear, and dose-dependent suppression of nursery pig growth performance. Reductions in ADG and ADFI were linear across the evaluated range, with no evidence of a biologically meaningful breakpoint within the DON dose range tested. However, one could speculate that at higher dietary DON concentrations above 5.1 mg/kg, a biological breakpoint could be plausible. When expressed relative to the lowest dietary concentration (0.2 mg/kg), ADG and ADFI declined by 7.4% and 8.0% per mg/kg DON, respectively. Ultimately, translating to slower time to market, increased days on feed, and higher production costs per pig. Growth suppression was driven primarily by progressive reductions in voluntary feed intake, as feed efficiency was not associated with DON concentration. Collectively, the linear exposure response relationship defined in this study provides a quantitative framework for interpreting DON associated performance losses and establishes a foundation for subsequent mechanistic investigations aimed at determining the biological pathways driving DON induced anorexia and growth suppression. These findings provide context for interpreting DON contamination risk relative to FDA guidance, demonstrating that growth suppression can occur at or below recommended limits and highlighting the importance of minimizing dietary exposure in nursery pig diets. The hypothesis that voluntary feed intake and growth performance would be reduced in a quadratic or segmented manner was rejected, as responses followed a linear pattern across the evaluated DON concentrations.