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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: Med Res Rev. 2010 Jan;30(1):1–22. doi: 10.1002/med.20160

Table 1.

Virulence determinants of CA-MRSA evaluated in animal infection models using isogenic deletion mutants

Protein Gene(s) Model/animal Bacterial strain Result Conclusion Remarks Ref.
α-toxin hla Pneumonia, mice (C57BL/6J) LAC (USA300) Strong reduction of mortality in hla mutant α-toxin is a crucial virulence determinant in mouse pneumonia. No effect for lukSF (PVL) deletion in same strain and model 87
α-toxin hla Pneumonia, mice (C57BL/6J) LAC (USA300), MW2 (USA400) Protection from pneumonia by anti-Hla antibodies α-toxin is a crucial virulence determinant in mouse pneumonia. No protection achieved using anti-PVL antisera 94
PSMα psmα1, psmα2, psmα3, psmα4 Abscess, mice (SKH1-hrBR) bacteremia, mice (CD1 Swiss) LAC (USA300): abscess MW2 (USA400): bacteremia Strong reduction in mortality and abscess formation α-PSMs are crucial virulence determinants in mouse skin infection and sepsis. Results directly comparable to δ-toxin, PSMα 51
δ-toxin hld Abscess, mice (SKH1-hrBR) bacteremia, mice (CD1 Swiss) LAC (USA300): abscess MW2 (USA400): bacteremia Small (insignificant) reduction in mortality and abscess formation δ-toxin is not a significant virulence determinants in mouse skin infection and sepsis. Results directly comparable to PSMα, PSMβ 51
PSMα psmα1, psmα2 Abscess, mice (SKH1-hrBR) bacteremia, mice (CD1 Swiss) LAC (USA300): abscess MW2 (USA400): bacteremia No reduction in mortality and abscess formation α-PSMs do not impact mouse skin infections and sepsis. Results directly comparable to PSMα, δ-toxin 51
ACME 37 kb ACME fragment containing arc and opp loci Bacteremia, rabbits SF8300 (USA300) Significantly more wild-type than ACME mutant bacteria at end of experiment ACME is a significant contributor to rabbit sepsis. Highly discriminative competition model 96
PVL lukS, lukF Abscess, mice (SKH1-hrBR) bacteremia, mice (CD1 Swiss) LAC (USA300), MW2 (USA400) No significant differences PVL is not a virulence determinant in mouse sepsis or skin infections. 86
PVL lukS, lukF Pneumonia, mice (C57BL/6J) LAC (USA300) No reduction of mortality in lukSF mutant PVL is not a virulence determinant in mouse pneumonia. Strong effect for hla deletion in same strain and model 87
PVL lukS, lukF Pneumonia, mice (C57BL/6J) LAC (USA300), MW2 (USA400) No protection from pneumonia by anti-PVL antibodies PVL is not a virulence determinant in mouse pneumonia. Protection achieved using anti-Hla antisera in same model 87
PVL lukS, lukF Pneumonia, mice (BALB/cJ, BALB/cAnNHsd), skin infection, mice (BALB/cJ, BALB/cAnNHsd) LAC (USA300) No significant effect of PVL PVL is not a virulence determinant in mouse pneumonia or skin infection. 88
PVL lukS, lukF Bacteremia, rabbits SF8300, LAC (USA300), MW2 (USA400) Transiently significantly more wild-type than lukSF mutant bacteria, but not at end of experiment PVL has a modest, transient effect on the progress of rabbit bacteremia. Highly discriminative competition model 85
PVL lukS, lukF Necrotizing pneumonia, rats LAC (USA300) No significant effect of PVL PVL is not a virulence determinant in rat pneumonia. No significant effect of PVL on expression of host inflammatory genes 89
PVL lukS, lukF Necrotizing pneumonia and skin infection, mice (BALB/c) LAC (USA300) PVL impacts necrotizing pneumonia and skin infection in mice. PVL is a virulence determinant in mouse pneumonia and skin infection. Only study showing a prolonged effect of PVL in experimental disease. 90
Anti-PVL antibodies protect from infection.