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. Author manuscript; available in PMC: 2016 Oct 18.
Published in final edited form as: Annu Rev Pathol. 2016 Feb 25;11:343–364. doi: 10.1146/annurev-pathol-012615-044351

Table 1.

Secreted virulence factors and their possible contributions to abscess formation and pathology

Secreted virulence factors involved in survival in the bloodstream
Name Gene Proposed functiona Virulence defect associated with loss of geneb
Adenosine synthase adsA Synthesis of immune suppressors Ado, dAdo Decreased survival in blood
Nuclease nuc Degradation of NETs Decreased survival in blood
Clumping factor A clfA Agglutination Increased phagocytic uptake
Coagulases coa
vwb
Agglutination Increased phagocytic uptake
Protein A (SpA) spa Binding of the Fcγ domain of Igs Increased opsonization and phagocytosis of bacteria
Leukocidins hlgAB
hlgCB
lukAB
Lysis of leukocytes Unknown
Unknown
Decreased survival in blood
Fibronectin-binding repeat protein A, B fnBPA
fnBPB
Recognition of fibronectin-FnBR complexes by α5β1 integrin; fibrinogen binding Unknown
Staphylococcal complement inhibitor (SCIN), SCIN-B, SCIN-C scin
scinB
scinC
Blockage of C3 convertases Unknown
Extracellular complement–binding protein ecb Blockage of C3 convertases Unknown
Aureolysin aur Degradation of antimicrobial peptides Unknown
Secreted virulence factors required to breach the bloodstream
α-Hemolysin hla Disruption of epithelial or endothelial surfaces Reduced bacterial loads in organs
Serine Aspartic Repeat protein C, D sdrC
sdrD
Members of the MSCRAMM, ligands unknown Reduced bacterial loads in organs
Secreted factors required for bacterial replication and persistence in abscesses
Iron surface determinant A, B, C isdA
isdB
isdC
Heme iron scavenging Reduced bacterial loads
Coagulases coa
vwb
Coagulation, agglutination Reduced bacterial loads and numbers of abscesses
Protein A (SpA) spa B cell superantigen activity that prevents humoral immune response Reduced bacterial loads and numbers of abscesses in organs
Lipoprotein diacyl-glyceride transferase lgt Lipidation of lipoproteins Hypervirulence, abscesses devoid of immune cells due to loss of TLR2 ligands
Extracellular adherence protein eap Blockade of neutrophil adherence to endothelia Reduced bacterial loads in organs
Extracellular fibrinogen–binding protein efb Blockade of C3 convertase; fibrinogen binding Reduced bacterial loads in organs
Phenol soluble modulins α3 psmα3 Generation of inflammatory signals for the recruitment of immune cells Increased bacterial loads in organs
Staphylococcal superantigen-like 5, 10 ssl5
ssl10
Impediment of neutrophil chemotaxis Unknown
Chemotaxis inhibitory protein chips Impediment of neutrophil chemotaxis Unknown
Formyl peptide receptor-like inhibitory proteins flipr
flipr-like
Impediment of neutrophil chemotaxis Unknown
a

The proposed function is derived from in vitro biochemical experimentation.

b

Virulence defect was tested as survival of bacteria in whole blood or enumeration of bacterial loads in animal organ tissues following infection.