Data from strains USA300 LAC and ST88 JSNZ. The experimental set-up is the same as in Fig. 2: mice received by oral gavage either 100 μl containing 108 CFU ml−1 of wild-type S. aureus strain USA300 LAC or ST88 JSNZ plus another 100 μl of 108 CFU ml−1 of the corresponding isogenic agr mutant (n = 5 per group; competitive experiment shown in a, b); or 200 μl containing 108 CFU ml−1 wild-type, isogenic agr mutant or Agr (RNAIII)-complemented agr mutant (n = 5 per group, non-competitive experiment shown in c). CFU in the faeces were determined two, four and six days after infection. At the end of the experiment (day seven), CFU in the small and large intestines were determined. a, b, Competitive experiment. Total obtained CFU are shown as dot plots; also shown are mean ± s.d. Bars show the percentage of wild-type among total determined CFU, of which 100 were analysed for tetracycline resistance that is present only in the agr mutant. No agr mutants were detected in any experiment; thus, all bars show 100%. Given that 100 isolates were tested, the competitive index wild-type/agr mutant in all cases is ≥100. c, Non-competitive experiment with genetically complemented strains. Wild-type and isogenic agr mutant strains all harboured the pKXΔ16 control plasmid; Agr-complemented strains harboured pKXΔRNAIII and thus constitutively expressed RNAIII, which is the intracellular effector of Agr. During the experiment, mice received 200 μg ml−1 kanamycin in their drinking water to maintain plasmids. Statistical analysis was performed using Poisson regression versus values obtained with the agr mutant strains. *P < 0.0001. Data are mean ± s.d. Note that no bacteria were found in the faeces or intestines of any mouse receiving S. aureus Δagr with vector control. The corresponding zero values are plotted on the x axis of the logarithmic scale.