抄録
Bifidobacteria (Lac-B; a Bifidobacterium preparation for oral use) were orally administered in serial doses to germ-free mice (ICR, IQI) with Escherichia coli O157: H7 NK2 intestinal infections. The effects of the oral administration of bifidobacteria on E. coli O157: H7 cell counts in the feces of the infected mice and on the in vivo production of verotoxins were then investigated. Bifidobacteria and norfloxacin (NFLX) were administered in serial doses according to three different schedules. The localization of bifidobacteria in the intestine was markedly disturbed when the serial administrations of bifidobacteria and NFLX were initiated on the same day. However, no disturbance in bacterial colonization was found when the administration of bifidobacteria was initiated prior to the administration of NFLX. No mice died when bifidobacteria (2.6 ∼ 107 CFU/kg ∼ 2/day) were given orally to 4 mice infected with E. coli O157: H7 for 18 days, beginning 5 days before the start of the NFLX administration regime (3 mg/kg x 2/day for 6 days). However, when the oral administration of bifidobacteria and NFLX was initiated on the same day, 3 of the 4 infected mice died. The same results were obtained in a group of mice that did not receive bifidobacteria. When mice infected with E. coli O 157: H7 were given oral doses of NFLX for 6 days, the production of verotoxins in the intestine was markedly enhanced, and large amounts of toxins were excreted in the feces of the mice and then several of the mice died. However, the NFLX-induced production of toxins in the infected mice was inhibited when bifidobacteria were administered in serial doses prior to the administration of NFLX. No toxins were found in the feces of the mice who received this treatment regime. In the present study, serial doses of bifidobacteria, a major component of the normal intestinal flora in infants, effectively demonstrated the inhibitory effects of bifidobacteria on the in vivo production of verotoxins by E. coli 0157: H7 in germ-free mice, providing protection against the fatal action of verotoxins.
