Staphylococcus epidermidis is the major human skin normal flora, however the causative agent of more than 30% of nosocomial bacteremia with high morbidity and healthcare cost [1,2]. Skin is an adverse environment, where the commensal S. epidermidis must cope with extreme, diverse and fluctuating environmental conditions [3,4]. A sudden rapid change in the landscape occurs upon accidental invasion through an IV-device; the main transmission route for S. epidermidis bacteremia. Bacteria inserted into the main blood stream face with a rapid changing environment, immune system and antibiotics selective pressure [5], [6], [7]. S. epidermidis is capable of invasion and has the ability of swift adaptation to the new niche through a rapid metabolic change [8].

Use of virulence and antibiotic resistance markers is a strategy to investigate the microbial invasiveness and pathogenicity. The markers like intercellular adhesin involved in polysaccharide-dependent biofilm formation e.g., icaADBC operon, an insertion sequence IS256 regulating virulence and biofilm formation, the methicillin resistance gene mecA encoding a modified penicillin binding protein (PBP2a), the arginine catabolic mobile element (ACME), which is a genomic island involved in pathogenicity by mucosal colonization, the microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) genes as bhp encoding a biofilm associated protein (bap) homologue involved in protein-dependent biofilm formation [9] and SdrF encoding a cell wall-associated protein facilitating binding to host proteins and S. epidermidis surface protein I (sesI) involved in biofilm formation [10], and the fdh encoding a putative formate dehydrogenase oxidizing formate to CO2 [8] were reported as clinically significant and having discriminatory potential of invasiveness and commensalism. However, other studies contradicted these findings. Studies have discouraged the discriminatory potential of pathogenicity and commensalism of such markers. Conlan group reported that 73% of commensal isolates were lacking fdh as a commensal marker [11]. Detection of MSCRAMMs, mecA, IS256, IS257 and icaADBC operon were reported as nonsignificant and not useful for discrimination between highly invasive and commensal isolates of S. epidermidis [12]. Moreover, formate dehydrogenase has been considered as an essential factor in biofilm formation and a significant contributor to the pathogenicity of Staphylococcus aureus, which is highly contrasting to its commensal identity in S. epidermidis [13,14].

Despite its frequent isolation particularly in pediatric bacteremia, the distinguishing features of S. epidermidis are quite challenging in clinical bacteriology. Besides, regional and high clonal variations in multi locus sequence typing (MLST) and pulse field gel electrophoresis (PFGE) typing of S. epidermidis have been detected in isolates of a specific origin e.g., nosocomial isolates, indicating their lower sensitivities in differentiating clinical and commensal isolates [15], [16], [17], [18]. Hence, the current study aimed to check the differential markers of pathogenicity and commensalism through PCR typing of isolates based on the presence of selected virulence factors in S. epidermidis of pediatric origin at KP, Pakistan.