Evaluation of the components of a commercial probiotic in gnotobiotic mice experimentally challenged with Salmonella enterica subsp enterica ser. Typhimurium

Vitacanis(R), a probiotic preparation containing a Lactobacillus acidophilus, an Enterococcus faecium and a Saccharomyces cerevisiae, has been developed for the prevention of intestinal disorders in dogs and cats. In the present study, these microorganisms were tested jointly or singly during experimental infection of gnotobiotic mice with Salmonella Typhimurium. Four experimental groups consisting of animals given probiotics jointly or singly and a control group consisting of germfree mice were used. The groups were treated with one or three of the microorganisms (experimental) or PBS (control) 10 days before intragastric challenge with a suspension containing about 10(2) cells of the bacterial pathogen. A higher survival (P < 0.05) was observed in gnotobiotic mice given E. faecium (82%). All the animals in the other groups died after the challenge but the survival time was longer (P < 0.05) for groups given all three of the microorganisms (7.4 +/- 2.4 days) or given only L. acidophilus (7.2 +/- 2.9 days) than for the control mice (4.4 +/- 1.1 days) and the mice that received S. cerevisiae (4.9 +/- 1.6 days) mice. The survival data agreed with the histopathological findings which showed more severe liver and intestinal lesions in control mice and in mice given Saccharomyces. In vitro antagonistic assays showed inhibition growth of E. faecium and S. Typhimurium around the colonies of L. acidophilus and for S. Typhimurium around the colonies of E, faecium. However in vivo, S. Typhimurium became similarly established in the digestive tract of gnotobiotic mice at levels ranging from 10(8) to 10(10) CFU/g of feces and remained at these high levels until the animals died or were sacrificed. Among the three probiotic components of the commercial product Vitacanis(R), E. faecium was the only one that provided protection against challenge with S. Typhimurium. Protection was not due to the reduction of the intestinal populations of the pathogenic bacteria. (C) 2001 Elsevier Science B.V. All rights reserved.