The Cell Wall, Cell Membrane and Virulence Factors of Staphylococcus aureus and Their Role in Antibiotic Resistance

Microorganisms. 2023 Jan 19;11(2):259. doi: 10.3390/microorganisms11020259.

Abstract

Antibiotic resistant strains of bacteria are a serious threat to human health. With increasing antibiotic resistance in common human pathogens, fewer antibiotics remain effective against infectious diseases. Staphylococcus aureus is a pathogenic bacterium of particular concern to human health as it has developed resistance to many of the currently used antibiotics leaving very few remaining as effective treatment. Alternatives to conventional antibiotics are needed for treating resistant bacterial infections. A deeper understanding of the cellular characteristics of resistant bacteria beyond well characterized resistance mechanisms can allow for increased ability to properly treat them and to potentially identify targetable changes. This review looks at antibiotic resistance in S aureus in relation to its cellular components, the cell wall, cell membrane and virulence factors. Methicillin resistant S aureus bacteria are resistant to most antibiotics and some strains have even developed resistance to the last resort antibiotics vancomycin and daptomycin. Modifications in cell wall peptidoglycan and teichoic acids are noted in antibiotic resistant bacteria. Alterations in cell membrane lipids affect susceptibility to antibiotics through surface charge, permeability, fluidity, and stability of the bacterial membrane. Virulence factors such as adhesins, toxins and immunomodulators serve versatile pathogenic functions in S aureus. New antimicrobial strategies can target cell membrane lipids and virulence factors including anti-virulence treatment as an adjuvant to traditional antibiotic therapy.

Keywords: MRSA; Staphylococcus aureus; antibiotic resistance; cell membrane lipids; cell wall; infectious diseases; virulence factors.

Publication types

  • Review

Grants and funding

This research received no external funding.