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

^aThe proposed function is derived from in vitro biochemical experimentation.

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