Abstract
Bacterial pathogens as causative agents of infection constitute an alarming concern in the public health sector. In particular, bacteria with resistance to multiple antimicrobial agents can confound chemotherapeutic efficacy towards infectious diseases. Multidrug-resistant bacteria harbor various molecular and cellular mechanisms for antimicrobial resistance. These antimicrobial resistance mechanisms include active antimicrobial efflux, reduced drug entry into cells of pathogens, enzymatic metabolism of antimicrobial agents to inactive products, biofilm formation, altered drug targets, and protection of antimicrobial targets. These microbial systems represent suitable focuses for investigation to establish the means for their circumvention and to reestablish therapeutic effectiveness. This review briefly summarizes the various antimicrobial resistance mechanisms that are harbored within infectious bacteria.
Highlights
Bacteria as microbial pathogens are causative agents of life-threatening infectious diseases [1]
Speaking, the Sav1866 drug efflux pumps consist of two chief transmembrane domains (TMDs) and two nucleotide-binding domains primary active drug efflux systems in bacteria is the adenosine triphosphate (ATP)-binding cassette (ABC) efflux pump family [101,102]
A distinctly acid different mechanism antibacterial actionand is exhibited biotics interact with the phosphoric group of lipid A of and replace calcium magby cationic antimicrobial thanatin that acts on bacteria cell agglutination upon nesium ions associated withpeptide it leading to destabilization of LPS by and leakage of cellular interacting with LPS [181]
Summary
Systems agents are desired [10]. In order to discover novel approaches to address multiple antimiAlong the timeline of antibiotic discovery and introduction, several enzymatic mechacrobial resistances in these microbial pathogens, it is necessary to attain a clear nisms of antibiotic inactivation were discovered. The enzymatic mechanisms antibiotic resistance β-lactamases before penicillin was clinically employed,ofemphasizing that the production include hydrolysis, group transfer, and redox processes [4]. The structurally altered macrolide antibiotic will no longer be able to bind to its preferred target site in the ribosome [38] Another important mechanism of enzymatic degradation is associated with the manganese ion (Mn2+ )-dependent, chromosomally-encoded FosX that uses water to cleave the epoxide ring of fosfomycin. The aminoglycoside modifying enzymes (AME) responsible for resistance to different aminoglycoside antibiotics include N-acetyltransferases (AAC), Oadenyltransferases (ANT), and O-phosphotransferases (APH) These enzymes catalyze the modification of various hydroxyl or the amino groups of the aminoglycosides resulting in their inability to bind to their 30S ribosomal targets [45]. CATs are widely distributed among Gram-positive and -negative bacteria and show little amino acid sequence similarities, with only 25 amino acid residues conserved among all CAT variants [47]
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