S. epidermidis present in the patient's periocular flora plays a significant role in causing POE [
1,
2]. This has been proven by a few studies using pulse field gel electrophoresis (PFGE) technique [
2‐
4]. Application of advanced genotyping tools for typing of bacteria can give useful information regarding species distribution in periocular surfaces as well as help in understanding transmission dynamics and sources of infection, besides being useful in determining strain diversity with precision [
4,
7]. FAFLP typing in the present investigation established vitreous isolates of
S. epidermidis strains were indistinguishable from the strains isolated from the patient's conjunctival swabs in all the 3 cases. These findings underscore the significant role of periocular flora in causation of POE. In this study, we examined the two important virulence factors of
S epidermidis namely the biofilm production and multidrug resistance (MDR) of the strains associated with POE [
8]. Biofilm- formation (BF) is one of the factors associated with increased virulence wherein
icaAB genes were detected significantly more in infecting strains rather than in commensals [
8]. MDR strains are known to cause greater intraocular inflammation than the susceptible strains in animal models [
10] implying that these strains are more virulent. MR
S epidermidis (MRSE) causing POE is difficult to treat. In recent years, the susceptibility of
S. epidermidis has changed dramatically wherein nearly half of the strains are MDR. In particular, MR is frequent among
S. epidermidis strains on a global scale [
10] and the findings were similar in this study. In the present study, all the strains were MR, seven out of eight strains were positive for BF which is striking and substantiates earlier findings [
8,
10]. Presence of local/systemic risk factors and prophylactic antibiotic may enhance the role of MDR Coagulase negative Staphylococci in causing POE. One of our patients (no. 3) was diabetic for past 10 years, which is a possible risk factor. Information about prior antibiotic usage in our patients was not available. i
caAB gene was detected in seven strains in this study indicating biofilm positivity. Strain 1030b appear to be ancestral with the absence of
icaAB. 1030b generated four polymorphic bands (171, 191, 223, 235 bp) in FAFLP that were lacking in other three strains obtained from the same patient (figure
2) and this was the only
icaAB negative strain. This finding suggests that biofilm-producing clones of resistant
S. epidermidis were clonally evolving with changes occurring in their genomes. These clones appear to have genetic alteration that possibly indicates enhanced ability to cause POE. Strain 1030b from the lid of patient 3 is most likely nonpathogenic and ancient while other three strains from the same patient might have evolved from 1030b into more virulent types.
Predictive insilico AFLP methods with
EcoRI+0 and
MseI+A selectivity used on sequenced genomes of two
S. epidermidis strains that are in the public domain and their extrapolation and comparison with our data showed interesting results. 1030b strain showed differential amplification of four genomic regions whereas 1030a, 1030c, 1030d lacked amplification of these regions which might be due to the mutation {insertion and deletion (Indels)} in
EcoRI and
MseI restriction site sequences. These corresponding polymorphisms are mapped to ORFs such as SE0884, SE0177, SE2068, SE0841 in ATCC 12228 and SE0775, SE2397, SE 2081, SE1995 in RP62a strain. Modification in at least two of the above ORFs namely SE0775 (fbe gene) and SE2081 putatively coding for fibronectin/fibrinogen binding protein and an adhesion protein respectively, seems to have definite role in increasing virulence. One recent study has showed that Fbe is a major factor involved in adherence of
S. epidermidis to fibrinogen [
11]. Antibodies against Fbe could block adherence of the bacteria to fibrinogen-coated surfaces. SE2081 is putative adhesion lipoprotein that may also have role in adhesion. Mutations in these two ORFs in the genomes of 1030a, 1030c, and 1030d might have enhanced their virulence favoring their survival under stressed condition.