Evaluation of the Low Dose Level of a Heat-Killed and Dried Cell Preparation of Enterococcus faecalis to Prevent Porcine Edema Disease Using Experimental Infection Model with Enterotoxcemic Escherichia coli in Weaning Pigs

Abstract

ABSTRACT. Porcine edema disease (ED) is caused by Shiga toxin 2e-producing Escherichia coli (STEC). ED has become frequent in pig farms, and the use of antimicrobials has resulted in the development of antimicrobial-resistant STEC. Accordingly, the use of materials other than antimicrobials is requested for the prevention of ED. Oral administration of a heat-killed and dried cell preparation of Enterococcus faecalis strain EC-12 (EC-12) to weaning pigs was previously demonstrated to decrease animal mortality in a STEC-contaminated farm at 0.05% (w/w) dose level. In this study, pigs experimentally infected with STEC were used as a model for ED to evaluate the low dose level of EC-12 to prevent ED. Fifteen 21-day-old pigs were divided into 5 groups: STEC challenge with the basal diet, STEC challenge with EC-12 supplemented at 0.005, 0.01, or 0.05% (w/w) to the basal diet, and no STEC challenge with the basal diet. The challenge was carried out when the animals were 25, 26, and 27 days old using STEC contained in capsules resistant against gastric digestion. All pigs were euthanized at 32 days of age. The daily weight gain, feed conversion ratio, and palpebral edema were improved by supplementation with 0.05% EC-12, but not by the low dose levels. Accordingly, 0.05% level of supplementation was needed for EC-12 to improve clinical symptoms in weaning piglets infected by STEC. KEY WORDS: Enterococcus faecalis strain EC-12, enterotoxcemic Escherichia coli, experimental infection, porcine edema disease.

Alpha-Linked Galactooligosaccharide Suppresses Small Intestinal Eosinophil Infiltration and Improves Growth Performance in Weaning Pigs

“…The composition of the small intestinal and cecal microbiota was examined using Temperature Gradient Gel Electrophoresis (TGGE) analysis as described previously [15], with slight modifications. Briefly, bacterial genomic DNA was extracted from the digesta using the method of Godon et al [2].…”

“…Histological studies: The histological studies were similar to those described elsewhere [15]. Briefly, the formalinfixed intestinal tissues were further cut into cross sections with approximate lengths of 10 mm.…”

“…However, GOS administration had no effect on the organic acid level or microbial composition in the small and large intestinal digesta. A healthy pig shows significant eosinophil infiltration in the lamina propria of the small intestine despite the absence of parasite infection [15]. In a previous study, it was also reported that eosinophils are observed predominantly in the small intestines of germ-free pigs [9].…”

Improved porcine model for Shiga toxin‐producing Escherichia coli infection by deprivation of colostrum feeding in newborn piglets

“…The STEC infection procedure was the same as that previously described (Tsukahara et al 2005). The excretion of STEC was measured in the feces on days 0, 3 and 11 after infection by quantitative real-time PCR for the stx2e gene as previously described (Tsukahara et al 2007). After 4 days of acclimatization, the piglets (25 days old) belonging to the designated infection groups were orogastrically inoculated using an enteric-coated capsule (Sunsho, Tokyo, Japan) filled with 10 11 colony-forming units (cfu) of STEC for 3 consecutive days.…”

Preventive Effects of Heat-Killed Enterococcus faecalis Strain EC-12 on Mouse Intestinal Tumor Development

“…Its cell walls are reported to induce B-cell activation along with stimulation of IgA secretion in the intestine [12], which could remove pathogens from the intestine [13]. To date, several functions of EC-12 have been reported [14,15,16]. However, the preventive effects of heat-killed EC-12 on intestinal carcinogenesis have not yet been elucidated.…”