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Endotoxin, Antibiotics, and Inflammation in Gram-Negative Infections
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Penicillin-binding proteins (PBPs) are the primary biochemical targets of β-lactam antibiotics in bacteria. These PBPs catalyze terminal stages in the assembly of the peptidoglycan network of the bacterial cell wall (47). Whereas the older penicillins (penicillin G) aspecifically bind to all of these PBPs, the newer β-lactams often specifically bind to only one or two of the PBPs. Treatment of Enterobacteriaceae with (β-lactam antibiotics that have a high selective affinity for PBP 1a and especially 1b causes rapid and extensive killing of the bacteria, with degradation of cell wall material and cellular lysis. Antibiotics with selective affinity for PBP 2 cause conversion of the bacilli to round-shaped cells (also called spheroplasts). Inhibitors of PBP 3 cause selective inhibition of bacterial septation, which leads to the formation of long filaments, but initially only limited bactericidal activity and lysis takes place (47).
Bacteriology of Ophthalmic Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
Arumugam Priya, Shunmugiah Karutha Pandian
S. pneumoniae and S. pyogenes have been reported to show resistant against a wide range of antibiotics including penicillin, cephalosporin, macrolide, and lincosamide. The alteration of penicillin-binding protein (PBP) confers resistance to penicillin. The efficiency of other antibiotics such as beta-lactam, cephalosporin, and carbapenem are also reliant on PBP. Hence, the activity of these antibiotics is reduced in penicillin resistant Streptococcus spp. (Baquero et al., 1991; Doern et al., 1996). Most of the clinical isolates are now being found resistance to treatment with single or combination of antibiotics, an indication of multidrug resistance.
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.
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].