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. 2010 Jan 4;107(2):888–893. doi: 10.1073/pnas.0911811107

Fig. 1.

Fig. 1.

Inactivation of mtsR significantly decreases GAS necrotizing fasciitis capacity in mice. (A) Mice were inoculated intramuscularly in the hindlimb with wild-type strain MGAS315 or naturally occurring mtsR mutant strain MGAS9887 (actual dose: MGAS315 1.04 × 106 cfu; MGAS9887 1.02 × 106 cfu). Survival is shown with P value for Kaplan–Meier analysis. (B) Kaplan–Meier survival curves for mice inoculated intramuscularly with wild-type ΔmtsR isogenic mutant or complemented mutant strains (actual dose: MGAS315 1.10 × 106 cfu; MGAS315ΔmtsR 1.12 × 106 cfu; MGAS315ΔmtsRcomp 1.10 × 106 cfu). Gross (C–H) and microscopic (I–N) histopathology (original magnification 4×) of mouse hindlimb lesions at 60 h postinfection. PBS-treated animals had normal hindlimb appearance (C and I). Animals given wild-type strain MGAS315 had extensive myonecrosis (D and J), whereas lesions from animals inoculated with isogenic mtsR mutant strain MGAS315ΔmtsR were confined to the inoculation site (E and K). The boxed area and arrows denote a circumscribed, walled-off lesion. Gene complementation restored the wild-type tissue pathology phenotype (F and L). Lesions from mice inoculated with naturally occurring mtsR mutant strain MGAS9887 have features identical to those in MGAS315ΔmtsR (G and M), and providing a wild-type copy of mtsR to create strain MGAS9887comp restored the wild-type tissue pathology phenotype (H and N). Micrographs show tissue taken from the inoculation site.