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Infections
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Beta-lactams inhibit cell wall synthesis by binding to enzymes known as ‘penicillin binding proteins’ (PBPs). These proteins are carboxypeptidases and transpeptidases responsible for the final stages of cross-linking the bacterial cell wall structure [8,9].
Antibiotics
Published in Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod, The Primary FRCA Structured Oral Examination Study Guide 2, 2017
Kate McCombe, Lara Wijayasiri, Paul Hatton, David Bogod
Inappropriate use of antibiotics and poor prescribing play a vital role in propagating antibiotic resistance. There are several mechanisms by which bacteria develop resistance to penicillins: Drug inactivation – bacterial production of β-lactamase leads to hydrolysis of the β-lactam ring.Alteration of penicillin binding proteins – this prevents the antibiotics from binding onto the bacterial cell wall.Alteration of bacterial cell wall permeability – this prevents antibiotics from penetrating the cell wall.
The Aims of Operative Surgery
Published in Hutan Ashrafian, Surgical Philosophy, 2015
The most common form of biological deception in surgery includes antibiotics such as those of the large β-lactam antibiotic family. Examples include the famous penicillin derivatives, cephalosporins, monobactams and carbapenems. These antibiotics all contain β-lactam segments, which are structural analogues to the D-alanyl-D-ala amino acid residues of the precursor NAM/NAG-peptide subunits of the peptidoglycan layer of the bacterial cell wall. When they are exposed to bacteria, antibiotics irreversibly bind to penicillin-binding proteins (PBPs) in competition with the reversible D-alanyl-D-alanine residues. As the PBPs regulate the final transpeptidation step in the synthesis of the pepti-doglycan layer of the bacterial cell wall, further transpeptidation is limited and bacterial cell wall synthesis is disrupted and exposed. Consequently bacterial structural integrity and subsequent division is halted so that the bacteria cannot survive. As a result, β-lactam antibiotics are considered bactericidal and have saved millions of patient lives through bio-deception.
Acute bacterial skin and skin structure infections in pediatric patients: potential role of dalbavancin
Published in Expert Review of Anti-infective Therapy, 2023
Lorenzo Volpicelli, Mario Venditti, Alessandra Oliva
Ceftaroline is a new parenteral beta-lactam agent, a fifth-generation cephalosporin with activity against Gram-positive pathogens including MRSA. Being provided with a greater binding affinity to penicillin-binding proteins in comparison to other beta-lactams, it exhibits a very rapid bactericidal effect. Ceftaroline has no activity on Enterococci and Pseudomonas spp and exerts only moderate activity on other Gram-negatives [45], although these agents are rarely implicated in pediatric SSTI. Multiple daily administrations are required but, noteworthyly, the standard doses were found to achieve similar probability of target attainment against S. aureus and S. pneumoniae with infusion duration of 5 or 60 minutes [45]. A meta-analysis of three randomized controlled trials found ceftaroline to have a clinical cure rate similar to comparators with no significant differences for the risk of treating emergent adverse events in children affected by acute bacterial infection [46].
Bioprospecting of aqueous phase from pyrolysis of plant waste residues to disrupt MRSA biofilms
Published in Biofouling, 2023
Srividhya Krishnan, Subramaniyasharma Sivaraman, Sowndarya Jothipandiyan, Ponnusami Venkatachalam, Saravanan Ramiah Shanmugam, Nithyanand Paramasivam
Moreover, S. aureus has acquired drug resistance against a wide class of antibiotics, and Methicillin Resistant Staphylococcus aureus (MRSA) are wide spread (Kouyos et al. 2013). Currently, vancomycin, telavancin, ceftaroline, daptomycin are some of the commonly prescribed classes of antibiotics used for the treatment of bacterial infections by binding to the penicillin binding protein sites (Verma et al. 2021). It was reported that almost 40% of the S. aureus isolates from hospital environments were recently identified as MRSA (Shiadeh et al. 2022). In the U.S., the Centre for Disease Control and Prevention (CDC) has estimated that close to 80,000 infections and 11,000 deaths are caused by MRSA every year (Grigg et al. 2018). More than 100,000 deaths were reported in 2019 due to MRSA infections (Shiadeh et al. 2022). Several possible mechanisms on the acquirement of antibiotic resistance by MRSA have been proposed in the literature. One such mechanism involves the modification in the penicillin binding protein sites (PBP2a) present in the cell membrane of the bacteria thereby preventing antibiotic binding (Yuan et al. 2011). There are several small molecule inhibitors that have been developed to treat the MRSA infection, among which, quaternary ammonium salts with oxadiazoles moiety were found to be effective against MRSA variants. Quaternary ammonium salts damage the membrane potential and affects the cytoplasmic components (Verma et al. 2021).
Impact of chronic medications in the perioperative period: mechanisms of action and adverse drug effects (Part I)
Published in Postgraduate Medicine, 2021
Ofelia Loani Elvir-Lazo, Paul F White, Hillenn Cruz Eng, Firuz Yumul, Raissa Chua, Roya Yumul
Aminoglycosides inhibit bacterial protein synthesis by binding to the 16S rRNA component of the 30S ribosome subunit [56]. Beta-lactams (e.g. penicillins, cephalosporins, and carbapenems) and glycopeptides (e.g. vancomycin) interfere with specific steps in bacterial cell wall biosynthesis, resulting in cell lysis. Beta-lactams block the cross-linking of peptidoglycan units by inhibiting the peptide bond formation reaction catalyzed by penicillin-binding proteins (PBP). Vancomycin achieves the same inhibition by blocking the transglucosylase and PBP activity [56]. Fluoroquinolones inhibit DNA synthesis by targeting the enzyme DNA gyrase, which is a topoisomerase, which prevents bacteria from replicating its DNA. Cyclic lipopeptides (daptomycin) also inhibit cell wall synthesis by altering the structural integrity of bacteria by inserting themselves into the cell membrane and inducing membrane depolarization [57]. Nitroimidazoles (metronidazole) inhibits protein synthesis by forming cytotoxic nitro-radical anions that result in DNA strand breakage [58].