The use of antimicrobials in broilers is considered to be a cause of the appearance of vancomycin-resistant enterococci (VRE). Once VRE penetration occurs, whatever its origin, it is difficult to expel the enterococci from the intestine because of their multiple resistance, whether natural or acquired. In this study, we evaluated the prevention of VRE colonization by the dietary supplementation of a cell-wall preparation of Enterococcus faecalis strain EC-12 (EC-12) in newly hatched broilers that were challenged by experimental infection with VRE. The chicks were fed a basal diet supplemented with 0.05% (wt/wt) EC-12 powder for 15 d. The control group and that administered Lactobacillus sp. were fed the basal diet. The VRE challenge was administered orally when the chicks were 2 d old (d 0). Dietary EC-12 reduced VRE colonization in the intestine from d 3 to 14. Total IgA in the cecal digesta and total IgG in the serum were higher on d 14 in the EC-12 treatment group. However, VRE-specific and EC-12-specific antibodies were not affected in serum. Hence, it appeared that dietary EC-12 stimulated the gut immune system and reinforced the immune reaction against the VRE challenge to accelerate its defecation from the chick intestine.

In our previous study, a cell wall preparation of Enterococcus faecalis strain EC‐12 (EC‐12) prevented the colonization of vancomycin‐resistant enterococci (VRE) in newly hatched broiler chicks. Relatively early prevention against VRE colonization by EC‐12 administration may be related to the enhanced innate immune system. In this study we examined the effect of EC‐12 on the kinetics of immunoglobulin A (IgA) concentration in the cecal digesta of chicks from 1 day to 14 days old to evaluate humoral immunity. We also examined the effect of EC‐12 on β‐defensin mRNA expression and lysozyme production. The IgA concentration in the cecal digesta showed a decline in chicks from 2 to 8 days old and then a recovery up to when they were 14 days old. The concentration tended to be higher in EC‐12‐administered chicks than in control chicks at 14 days old. EC‐12 administration did not stimulate the lysozyme activities in the alimentary tract. However, β‐defensin mRNA expression in the tongue and the bursa of Fabricius was higher in chicks administered EC‐12 than in the control chicks at 5 days old. These results indicate that β‐defensin may be one of the major defense mechanisms inhibiting VRE colonization in young chicks.

In this study, vancomycin‐resistant enterococci (VRE) from humans and vancomycin‐resistant gram‐positive cocci (VRPC) from pigs were examined for their ability to transmit in the chick intestine (Experiment 1). A model study on the spread speed of VRPC was also estimated from chick to chick under semi‐production conditions with different administration routes (not inoculated, oral administration to a chick, sprayed on the floor) (Experiment 2). Furthermore, the disappearance of VRPC from their litter with composting processes was examined (Experiment 3). Each of six chicks was inoculated with VRPC or VRE at 1 day old in Experiment 1. All the chicks had VRPC or VRE in their glandular stomach at 22 days of age. In Experiment 2, 6 floor pens covered with sawdust were prepared and 20 chicks were allotted to each pen. The chicks were inoculated with VRPC at 1 day of age. The VRPC were detected in each group in cloacal swabs at 2 days of age (detection rate; 20–80%). And they were also detected in the not‐inoculated group. The VRPC detection rate gradually decreased, and detection was rare (0–10%) in the packing chicks (50 days old). VRPC were detected in the litter of each pen in Experiment 2. A composting process was effectively used to eliminate VRPC by the 6th week (Experiment 3).

Forty vancomycin-resistant enterococci (VRE) were isolated from feces of pigs in one pig farm. Two strains were further elucidated and these were biochemically identified as Enterococcus faecium possessing the vanB gene. These isolates showed high resistance to vancomycin and nine other antibiotics. This is the first report of VRE contamination in pigs in Japan.