Effects of zinc oxide and Enterococcus faecium SF68 dietary supplementation on the performance, intestinal microbiota and immune status of weaned piglets

The objective of this study was to determine the effects of zinc oxide (ZnO) and the probiotic Enterococcus faecium SF68 (Cylactin) dietary supplementation on the performance, intestinal microbiota and immune parameters of the weaned piglet reared under commercial conditions. The diets were devoid of antibiotic growth promoters (AGP). Two hundred and eight crossbred piglets were allocated to a 2 x 2 factorial experiment involving two levels of zinc oxide supplementation (0 or 3100 mg ZnO/kg feed), and two levels of E. faecium SF68 supplementation (0 or 1.4 x 10(9)CFU/kg feed (Cylactin ME10)). The diets were offered ad libitum for 20 days post-weaning. Piglet performance was assessed by calculating average daily gain (ADG), average daily feed intake (ADFI) and feed conversion ratio (FCR) on a pen basis. In addition, components of the distal ileal digesta, tissue-associated and mesenteric lymph node (MLN) bacterial populations were enumerated and serum immunoglobulin G (IgG) and intestinal immunoglobulin A (IgA) concentrations were determined on days 6 and 20 post-weaning. Regression analysis was used to determine the relationship between the bacterial populations at the different sites. Supplementation of the post-weaning diet with either ZnO or E. faecium SF68 did not affect piglet performance. E. faecium SF68 did not affect gastrointestinal bacterial populations but did tend to reduce serum IgG (P<0.1) on day 20. Zinc oxide reduced anaerobic (P<0.05) and tended to decrease lactic acid (P<0.1) bacterial translocation to the MLN, and tended to increase intestinal IgA concentration (P<0.1) on day 20. Generally, luminal bacterial populations were found to be poor predictors of tissue-associated or MLN populations. ZnO and E. faecium SF68 dietary supplementation were ineffective under these trial conditions. Further investigations into the possible immunomodulator role of dietary ZnO are warranted.     

The food contaminant fumonisin B1 reduces the maturation of porcine CD11R1+ intestinal antigen presenting cells and antigen-specific immune responses, leading to a prolonged intestinal ETEC infection

Consumption of food or feed contaminated with fumonisin B₁ (FB₁), a mycotoxin produced by Fusarium verticillioides, can lead to disease in humans and animals. The present study was conducted to examine the effect of FB₁ intake on the intestinal immune system. Piglets were used as a target and as a model species for humans since their gastro-intestinal tract is very similar. The animals were orally exposed to a low dose of FB₁ (1 mg/kg body weight FB₁) for 10 days which did not result in clinical signs. However, when compared to non-exposed animals, FB₁-exposed animals showed a longer shedding of F4⁺ enterotoxigenic Escherichia coli (ETEC) following infection and a lower induction of the antigen-specific immune response following oral immunization. Further analyses to elucidate the mechanisms behind these observations revealed a reduced intestinal expression of IL-12p40, an impaired function of intestinal antigen presenting cells (APC), with decreased upregulation of Major Histocompatibility Complex Class II molecule (MHC-II) and reduced T cell stimulatory capacity upon stimulation. Taken together, these results indicate an FB₁-mediated reduction of in vivo APC maturation.