While studying the oral bacterial biota of mice, we observed an unidentified streptococcus (TG) that eventually became the dominant species of the oral cavities of all other mice in our animal facility. We found that the strain is indigenous to Jackson Laboratory mice but is absent in animals from Charles River Laboratories. TG was also transmitted from artificially contaminated BALB/c mice to the oral cavities of 4 other mouse strains. Streptococcus sp. TG stimulated the secretory and systemic immune systems of artificially contaminated Charles River BALB/c mice but did not provoke clinical symptoms. The increase in antibody level to TG did not prevent its colonization and persistence in these mice. In mice from Jackson Laboratory, the secretory and systemic immune response to TG was significantly lower. In vitro, Streptococcus sp. TG inhibited murine oral lactobacilli and staphylococci, probably due to the production of hydrogen peroxide.

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The acquisition of the human oral bacterial flora follows a relatively well known sequence of succession that can be influenced by various host factors. These factors have not been studied in the mouse. In the present work, we followed the bacterial colonization of the oral cavity of mice from birth, and tested our mouse model for its suitability in studying the influence of weaning and puberty on the indigenous oral bacterial flora. We observed that the first colonizers were staphylococci, followed by lactobacilli. The proportions of these two predominant bacteria fluctuated for a period of 30-50 days, but evolved towards the proportions previously observed among the indigenous bacterial species of 6-8 week-old BALB/c male mice (predominantly Lactobacillus murinus and Staphylococcus aureus). The weaning period significantly altered the equilibrium among the oral bacterial flora. This equilibrium was not significantly modified during puberty.

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