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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.
Antimicrobial Therapy
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Ursula Altmeyer, Penelope Redding, Nitish Khanna
Usually, penicillin disrupts cell wall synthesis by attaching to a part of the peptidoglycan component known as the penicillin binding protein (PBP) and prevents cross linking of the components into a normal cell wall structure.
Lessons learned from the SARS-CoV-2 pandemic; from nucleic acid nanomedicines, to clinical trials, herd immunity, and the vaccination divide
Published in Expert Opinion on Drug Delivery, 2023
Hiba Hussain, Aishwarya Ganesh, Lara Milane, Mansoor Amiji
An additional tool that could aid in the optimization of vaccine design is immunoinformatics [45,46]. Immunoinformatic approaches to vaccine design have been deployed successfully to develop a multi-epitope vaccine for treating multidrug resistant Enterococcus faecium (a common nosocomial infection) and a vaccine for treating Acinetobacter baumannii (a pathogen with a high mortality rate) [45,46]. For these approaches, the amino acid sequence of a bacterial target protein (penicillin binding protein 5) was obtained from the UniProt database [45,46]. Different software was then used to predict the B cell, cytotoxic T lymphocyte, and helper T lymphocyte epitopes and to predict the antigenicity and toxicity [45,46]. The predicted episodes were joined with linkers and the multi-epitope vaccine was optimized in immune simulations until a 172 amino acid multi-peptide vaccine was generated and predicted to have superior immune activation [45,46]. Exploiting immunoinformatics in SARS-CoV-2 vaccine design could aid in the development of more effective vaccines.
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].
Comparative in vitro effectiveness of ceftolozane/tazobactam against pediatric gram-negative drug-resistant isolates
Published in Journal of Chemotherapy, 2021
Neena Kanwar, Dithi Banerjee, Christopher J. Harrison, Jason G. Newland, Xuan Qin, Danielle M. Zerr, Theoklis Zaoutis, Rangaraj Selvarangan
Rates of global antibiotic resistance have increased drastically in recent decades with the emergence of more strains resistant to multiple antibiotic classes, e.g. Escherichia coli (E. coli) sequence type 131.1,2 In the United States, the Centers for Disease Control and Prevention (CDC) estimated that two million illnesses and 23,000 deaths annually are attributed to antibiotic-resistant bacteria.3 Compared with prior CDC estimates, recent estimates in 2019 indicate sevenfold higher death incidence, with approximately 153,000 deaths attributed annually to antibiotic-resistant bacteria.4 Bacteria that are non-susceptible to at least one agent among three or more antimicrobial categories, including trimethoprim/sulfamethoxazole, cephalosporins, and quinolones, are known as multidrug-resistant (MDR) bacteria.5 MDR Gram-negative rods (GNRs) often produce extended-spectrum beta-lactamases (ESBLs) or AmpC enzymes, which render organisms resistant to most beta-lactams, including cephalosporins, unless combined with a beta-lactamase inhibitor.6,7 Other resistance mechanisms include porin mutations, efflux pumps, and altered antibiotic targets such as penicillin-binding proteins.8