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The ability of Bifidobacterium bifidum from a commercial bifidus milk to antagonize Salmonella enteritidis subsp. typhimurium in vivo, and to reduce the pathological consequences for the host, was determined using conventional and gnotobiotic mice. Conventional animals received daily, by gavage, 0.1 ml bifidus milk containing about 10(9) cfu B. bifidum and germ-free animals received a single 0.1 ml dose. The conventional and gnotobiotic groups were challenged orally with 10(2) cfu of the pathogenic bacteria 5 and/or 10 d after the beginning of treatment. Control groups were treated with milk. Bifidus milk protected both animal models against the challenge with the pathogenic bacteria, as demonstrated by survival and histopathological data. However, to obtain the protective effect in gnotobiotic animals, the treatment had to be initiated 10 d before the challenge. In experimental and control gnotobiotic mice, Salm. enteritidis subsp. typhimurium became similarly established at levels ranging from 10(8) to 10(9) viable cells g-1 of faeces and remained at these high levels until the animals died or were sacrificed. It was concluded that the protection against Salm. enteritidis subsp. typhimurium observed in conventional and gnotobiotic mice treated with bifidus milk was not due to the reduction of the intestinal populations of the pathogenic bacteria.

Saccharomyces boulardii was shown to be capable of inhibiting multiplication of enteropathogenic bacteria in vitro and is currently used for its anti-diarrhoea properties. We studied the capacity of this yeast to antagonize Salmonella typhimurium and Shigella flexneri in the intestinal tract of conventional or gnotobiotic NMRI mice. Conventional animals were given daily 10 mg doses of S. boulardii, whereas germ-free animals were given a single 10 mg dose. Both groups were challenged orally 5 d later with the pathogenic bacteria (10(8) or 10(2) viable cells, respectively). Control groups were treated with saline instead of S. boulardii. Mortality and/or histopathological data showed a protective effect against the pathogenic bacteria in yeast-treated mice. Saccharomyces boulardii colonized the digestive tract of gnotobiotic mice and the number of viable cells ranged around 10(10) g-1 of faeces. In experimental and control gnotobiotic animals, Salm. typhimurium and Sh. flexneri became rapidly established at a level of about 10(10) viable cells g-1 of faeces and remained at high levels until the animals died or were sacrificed. The protection against Salm. typhimurium and Sh. flexneri obtained in conventional and/or gnotobiotic mice previously associated with S. boulardii is not due to the reduction of the bacterial populations in the intestines.

Bacterial invasiveness and immunological responses were studied in germfree (GF) and conventional (CV) mice infected with Salmonella typhimurium. Bacterial counts of homogenates prepared from liver and spleen showed that the colony forming units (CFU) increased rapidly in GF mice and reached lethal proportions (10(9) cell per organ) by day 6. In CV mice, these counts increased to about 10(4.5) log cell per organ by day 6 and then declined slowly. An increase in serotype-specific IgM and IgG levels was noted in CV mice with a maximum by day 2. Very low values of these IgM and IgG were observed in GF mice during the course of infection. Delayed type hypersensitivity (DTH) response as measured by footpad swelling was higher in CV animals. Higher hypersensitivity to LPS during infection in GF animals resulted in death of all the animals tested for DTH after day 2. The data obtained suggest that during a rapid invasive bacterial infection, the slow development of immune response of GF mice may result in death of these animals.

The present study investigates the lethality of intragastric Salmonella typhimurium infection of germfree (GF) and conventional (CV, not germfree) mice. The introduction of only 10 viable S. typhimurium into the gastrointestinal tract of GF mice resulted in death of all animals within 8 days of inoculation. In contrast, the 50% lethal dose for CV mice was 4.7 x 10(3) viable organisms. The results demonstrate that resident microbes protect mice from the pathogenic effect of S. typhimurium infection.