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

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.

Mechanism Insights of Antibacterial Surfaces Coated with Dead Probiotics

“…For UV-killed LGG, more nutrients and antibacterial substances are still maintained in cells until the loss of membrane physiological functions . Compared with nutrients, more antibacterial substances would be released because of the selective permeability of the membrane . Thus, an optimal ratio of antibacterial and nutritive lysate release exists to comprehensively affect the motion and viability of PAO1, which leads to the decrease of active motion and R v on the UV-killed LGG surface.…”

Nucleoside‐Based Drug Target with General Antimicrobial Screening and Specific Computational Studies against SARS‐CoV‐2 Main Protease

“…This difference in susceptibility is partly attributed to the outer membrane of gram‐negative bacteria, which forms a formidable barrier due to its lipopolysaccharide layer, limiting the diffusion of thymidine analogs [149] . In contrast, gram‐positive bacteria possess a relatively thick, hydrophilic, and porous cell wall structure, which renders them more permeable to these analogs [150] …”

“…[149] In contrast, gram-positive bacteria possess a relatively thick, hydrophilic, and porous cell wall structure, which renders them more permeable to these analogs. [150] In the context of antimicrobial research, it is crucial to consider the role of aliphatic alcohols. These compounds, characterized by their low lipid solubility, can exert a lethal effect on bacteria.…”

“…This understanding of the underlying mechanisms provides valuable insights for the development of antimicrobial agents and highlights the importance of tailoring compounds to target specific microbial structures and processes. The successive introduction of these functional groups resulted in a gradual increase in the hydro- (141)(142)(143)(144)(145)(146)(147)(148)(149)(150)(151)(152)(153). [197] phobicity of the tested compounds.…”

“…This information provides valuable insights into the structural dynamics and stability of these complexes, which is essential for understanding their potential as antiviral agents. [195,196] According to Maowa et al, [197] thirteen uridine derivatives with varying amounts of aromatic and aliphatic chains (141)(142)(143)(144)(145)(146)(147)(148)(149)(150)(151)(152)(153) were synthesized and investigated (Figure 15). Mulliken population analysis and natural bond orbital methods were used to calculate the partial charges of atoms involved in the drug-protein interactions.…”