Most strains possessed all the genes associated with evasion of the host defense systems (
sspB,
sspA,
coa, and
hla). The product of
hla, namely, alpha hemolysin, is a major virulence factor of
S. aureus in rabbit models of keratitis
21,36 and is associated with corneal damage. Although an alpha toxin deficient strain of
S. aureus can still produce the niCIE contact lens peripheral ulcers in a rabbit model,
37 the gene seems to have been retained by strains causing niCIE and so it may be needed for survival of these strains before them being isolated from niCIE. The product of
sspA, a serine protease (also called
v8 protease), after maturation targets the Fc regions of immunoglobulins leading to partial loss of antigenic determinants, interfering in the interaction between cell surface antigens and immune effector cells mediated by immunoglobulins.
56 This serine protease is also important in biofilm remodelling.
59,60 This serine protease can cause severe pathology in rabbit corneas.
36 All strains had one or more of the protease genes
scpA (encoding the cysteine protease staphopain A),
sspB (encoding the cysteine protease staphopain B), or
sspA (encoding the serine protease
v8). There is a complex interplay between
scpA and
sspB in which the product of
sspA is important in adhesion and internalization of the bacteria into human corneal epithelial cells by activation of
fnbp and assists with evasion by delaying the host immune system, whereas
sspB is involved in the modulation of bacterial invasion.
30 However for collagen binding adhesin (coa), a study used rabbit model, in which contact lenses soaked in
S. aureus strains containing the collagen-binding adhesin (
cna+) or its isogenic mutant lacking the adhesin (
cna−), were placed on the injured cornea and the outcome showed that
cna significantly contributed to bacterial adherence and corneal colonization and produced suppurative inflammation in a rabbit model of soft contact lens–associated bacterial keratitis more often than its collagen binding–negative isogenic mutant, which suggests that collagen-binding adhesin is involved in the pathogenesis of
S. aureus keratitis.
24 The possession of this gene by most strains in the current study suggests that it may be important for virulence in ocular infection and inflammation.