Staphylococcal Infections (Host and Pathogenic Factors)

Dear Colleagues,

Although 30% of the healthy human population is colonized with various Staphylococcus spp., some staphylococcal strains, referred to as opportunistic pathogens, can cause minor to life-threatening diseases. The pathogenicity of these bacteria depends on their virulence factors and the robustness of the regulatory networks expressing these virulence factors. Virulence factors of pathogenic Staphylococcus spp. consist of numerous toxins, enterotoxins (some of which act as superantigens), enzymes, and proteins (cytoplasmic, extracellular, and surface) that are regulated by two-component (TC) and quorum-sensing (QS) regulatory networks. For example, based on their homology with quorum-sensing molecules/components, one Staphylococcus aureus species can alter the toxin/surface protein production of another S. aureus species either synergistically or antagonistically. To invade this niche, some other Staphylococcus species, such as Staphylococcus simulans, produce a potent endopeptidase called lysostaphin, which can lyse and eradicate the pathogenic S. aureus. Some other Staphylococcus species produce autolysins and cationic peptides to win the intra- and inter-species competition. The outcome of this microbial invasion depends not only on pathogenic factors but also on the host’s internal and external defense mechanisms, including a healthy skin microbiome. A healthy skin microbiome population consisting of Staphylococcus epidermidis can prevent colonization by other major pathogens. As normal host microflora, these commensals establish a complex relationship with the host as well as the surrounding microbial communities. This Special Issue of Microorganisms is focused on studies and recent advancements in our understanding of staphylococcal virulence mechanisms that enable Staphylococcus spp. either to successfully establish themselves as a colonizer or to overcome the host’s defense system to cause infection.

Dr. Rajan P. Adhikari
Guest Editor

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