%0 Journal Article %T Barriers to coliphage infection of commensal intestinal flora of laboratory mice %A Laura M Kasman %J Virology Journal %D 2005 %I BioMed Central %R 10.1186/1743-422x-2-34 %X Contrary to expectations, coliphage were not evident in the GI tracts of laboratory mice, although they were occasionally detected in feces. Commensal flora showed extreme variability within groups of mice despite identical handling and diet. Less than 20% of 48 mice tested carried E. coli in their gut, and of 22 commensal E. coli strains isolated and tested, 59% were completely resistant to infection by lambda, M13, P1, T4, T7, and PhiX174 coliphage. Lysogeny could not be demonstrated in the commensal strains as mitomycin C failed to induce detectable phage. Pre-existing immunity to phages was not evident as sera and fecal washes did not contain significant antibody titers to six laboratory phage types.Lack of sufficient susceptible host bacteria seems to be the most likely barrier to establishment of new coliphage infections in the mouse gut.Coliphage have traditionally been isolated from sewage, where they arrived, presumably, after passing through the GI tracts of animals inhabited by commensal coliform bacteria. However, information on the interaction of natural coliphage with the commensal flora of the GI tract in situ is sparse. The results of ingestion of defined high titer bacteriophage preparations by laboratory animals or by humans have been described in many previous studies (reviewed in [1]). Although there is evidence in some reports of coliphage replication in the gut, the phage infections are consistently transient, becoming undetectable in 3¨C10 days [2-4]. Notable exceptions are cases of gnotobiotic mice inoculated with defined phage-host systems, in which phage and host populations in feces were detectable for up to 98 days [4]. However, in animals with complex, established gastrointestinal microflora, observations concur that exogenous phage do not establish sustained productive infections of the commensal bacteria. The nature of this apparent barrier to persistent bacteriophage infection of the normal GI tract is of practical interest since as pa %U http://www.virologyj.com/content/2/1/34