**1. Introduction**

*Staphylococcus aureus* is a mammalian commensal [1] that colonizes mucosal membranes of its hosts around the world. The virulent *S. aureus* strains promote infections by producing potent protein toxins, colonizing factors and cell surface proteins that inactivate antibodies [2]. Contrastingly, genetic diversity in the *S. aureus* causes the variation in disease severity of the clinical strains [3]. This genetic diversity among *S. aureus* population around the world suggests the variation in spatial distribution. The development of different techniques such as multi-locus sequence typing (MLST) [4], Pulsed-field gel electrophoresis (PFGE) [5], and core genome phylogenetic reconstruction [6] have facilitated analysis of the genetic diversity in *S. aureus* population*.* MLST is commonly used to understand the *S. aureus* lineages [7]. It relies on the allelic profiles of housekeeping genes present throughout the core genome [8]. Previous studies showed that *S. aureus* population structure is composed of limited clonal complexes (CCs) that further comprises of new sequence types (STs) [9]. ST precisely defines a strain with a unique allelic

profile that have descended from the same recent common ancestor. Such ST types indicate the evolution based on point mutations. Additionally, recombination also appears to have played a relatively minor role in shaping *S. aureus* population [10]. Such techniques and studies are well suited to undermine the global epidemiology and genetic diversity of *S. aureus* population [11].

*S. aureus* infections can be recurred and costs for a long-term treatment along with productivity losses [12]. This recurrence is the result of biofilm formation and persistence inside body. Similarly, *S. aureus* biofilms also poses a major problem in the device-related infections (DRIs) [13]. Biofilms provides a shelter to *S. aureus* that resist antibiotics and other cellular immunity defenses [14]. *S. aureus* biofilms are more potent as it can be formed on the fomites, pipelines in the food industry and on the skin [15]. In this way, biofilms can also act as source of spread for long term without being observed. Recent findings have shown that staphylococcal biofilm mechanisms are adaptable to the environmental changes and help the pathogen in adherence to the surfaces at any cost [12]. Genetic diversity could be one of the influencers among the biofilm production ability of this pathogen [16]. A deep understanding of mechanisms for such variation in biofilm production is yet to be discovered.

Here we will review how diversity has affected the *Staphylococcus aureus* population structure and its biofilm mechanisms.
