Blood-brain barrier invasion by group B Streptococcus depends upon proper cell-surface anchoring of lipoteichoic acid
J. Clin. Invest. Kelly S. Doran, et al. 115:2499 doi:10.1172/JCI23829 [Go to this article.]

Figure 3
In vivo analysis of the ΔiagA mutant using a mouse model. Deletion of iagA does not effect GBS survival in mouse blood (A) or sensitivity to antimicrobial peptide CRAMP (B) but does render GBS less pathogenic in vivo. Groups of 10 mice were inoculated i.v. with WT or ΔiagA GBS strains. (C) Kaplan-Meier survival plot. (D) Bacterial counts (CFU) in mouse blood, brain, and spleen at time of death of WT (circles) and ΔiagA (squares); filled symbols represent mice that died before the experiemental endpoint. Histopathology of H&E- (E–H) or Gram-stained (F) brain tissues of individual mice (identified by arrows in D). (E and G) Samples from mice infected with WT GBS show meningeal thickening and cellular infiltration (open arrows) and bacterial microabscess formation (filled arrow). (F) Gram stain of mouse infected with WT GBS. (H) A sample from the mouse infected with the iagA mutant shows normal brain histopathology.