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Infections
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
Macrolides, lincosamides, ketolides, and streptogramins share overlapping binding sites on ribosomes, and have similar antimicrobial activities, as well as similar mechanisms of resistance [4]. The macrolides are a family of large cyclic molecules, all containing a macrocyclic lactone ring. The macrolide class of antibiotic agents includes compounds with 14-membered (erythromycin, clarithromycin) (Figure 17), 15-membered (azithromycin), and 16-membered (rokitamycin, spiramycin and josamycin) ring structures. Streptogramin antibiotics, such as pristinamycim or dalfopristin-quinupristin, contain two active components, type A and type B, which synergistically inhibit peptide elongation. Streptogramin B agents include quinupristin (Figure 18) and pristinamycin IA. Streptogramin A agents include dalfopristin and pristinamycim II A.
Quinupristin–Dalfopristin
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
The mechanisms of resistance in staphylococci and Enterococcus faecium to quinupristin–dalfopristin are summarized in Table 77.2. Two genes, vat(D) and vat(E), confer resistance to group A streptogramins, and another two (vgb and erm) confer resistance to group B streptogramins. These genes have been found in Enterococcus species. Quinupristin–dalfopristin resistance, which was caused by a combination of erm and vat genes, was first found among S. aureus clinical isolates in China (Yu et al., 2014). Resistance to streptogramins is mediated by three possible mechanisms: drug inactivation by enzymes, efflux or active transport of the antibiotic out of the cell, and plasmid-coded conformational alterations in ribosomal target binding site (Nadler et al., 1999). The third is the most common expression of bacterial resistance to streptogramins. Constitutive or induced expression of macrolide–lincosamide–streptogramin B resistance occurs in some staphylococcal species (Eliopoulos et al., 1998; Luh et al., 2000). Drug inactivation can occur in some staphylococcal and enterococcal species by production of a quinupristin- inactivating hydrolase or a dalfopristin-inactivating acetyltransferase. Some species of coagulase-negative staphylococci and E. faecium become resistant by active efflux of dalfopristin (Cocito et al., 1997; Johnson and Livermore, 1999). Emerging resistance during the treatment of infections caused by vancomycin-resistant E. faecium has generally been to both components of the formulation (Linden et al., 1997). The antibiotic susceptibility of glycopeptide-resistant enterococci was investigated in a Tertiary Greek Hospital. Seventy consecutive glycopeptide-resistant enterococci were tested. Sixty-two isolates were identified as E. faecium (88.6%), and 8 (11.4%) as E. faecalis. All strains were susceptible to linezolid and daptomycin, whereas 17.1% (12/70) and 11.4% (8/70) were resistant to quinupristin–dalfopristin and tigecycline, respectively. All E. faecalis isolates were resistant to quinupristin–dalfopristin, and 4 of 62 (6.5%) E. faecium isolates were resistant to quinupristin–dalfopristin (Sambatakou et al., 1998).
Distribution and antibiotic-resistance of different Staphylococcus species identified by matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) isolated from the oral cavity
Published in Journal of Oral Microbiology, 2021
Katarzyna Garbacz, Maria Wierzbowska, Ewa Kwapisz, Maja Kosecka-Strojek, Marek Bronk, Morteza Saki, Jacek Międzobrodzki
The antimicrobial susceptibility was performed by the disk diffusion method according to the European Committee on Antimicrobial Susceptibility Testing (EUCAST) [9]. Fifteen antimicrobial agents on Mueller-Hinton agar plates (Becton Dickinson, Franklin Lakes, NJ, USA) were tested: oxacillin, cefoxitin, gentamicin, erythromycin, clindamycin, tetracycline, chloramphenicol, ciprofloxacin, trimethoprim/sulfamethoxazole, fusidic acid, linezolid, rifampicin, tigecycline and vancomycin (Bio-Rad, Marnes la Coquette, France) and penicillin G (Oxoid, Basingstoke, England). The phenotype of resistance to macrolide-lincosamide-streptogramin B was tested and interpreted according to the EUCAST. Vancomycin susceptibility was determined with E-test method (bioMerieux, Marcy-l’Etoile, France). Multidrug resistance (MDR) was defined as a resistance to three or more classes of antibiotics.
Antimicrobial resistance in Clostridium difficile ribotype 017
Published in Expert Review of Anti-infective Therapy, 2020
Korakrit Imwattana, Daniel R. Knight, Brian Kullin, Deirdre A. Collins, Papanin Putsathit, Pattarachai Kiratisin, Thomas V. Riley
Clindamycin belongs to the macrolide-lincosamide-streptogramin B (MLSB) group of antimicrobial agents. These agents target the bacterial 50S ribosome and inhibit bacterial protein synthesis. The MLSB resistance phenotype is common in C. difficile; 65.9% – 90.9% of C. difficile strains in Asia and 49.6% – 56.6% in Europe are resistant to clindamycin [29,30,48–51]. Resistance is principally conferred by a 23S rRNA methyltransferase encoded by the ermB (erythromycin ribosomal methylase B) gene [30]. Methylation of the 23S rRNA of the bacterial 50S ribosomal subunit reduces the binding affinity of MLSB class antimicrobials. This ermB gene is carried on Tn6194, Tn6215, Tn6218 and Tn5398 [36], the latter having two copies [37]. In C. difficile strain M68, the ermB gene is found on Tn6194 – a 28k bp Tn, which is the most common ermB-containing element found in European clinical isolates of C. difficile [52]. The ermB gene is capable of horizontal transfer and C. difficile can acquire ermB from different sources, making it possible for C. difficile in different regions of the world to independently acquire an MLSB resistance phenotype. Besides the ermB gene, a recent study reported a novel ermG gene in 11 C. difficile RT 017 isolates. This gene also confers an MLSB resistance phenotype and is located on a mobile genetic element capable of interspecies horizontal gene transfer [53].
Streptogramins for the treatment of infections caused by Gram-positive pathogens
Published in Expert Review of Anti-infective Therapy, 2021
Sophie Reissier, Vincent Cattoir
Other mechanisms affecting the activity of type B streptogramins are enzymatic modification (hydrolysis) and ribosome protection. Lyases and lactonases, enzymes encoded by vgb genes, could inactivate streptogramins B Table 3 [20,21,48,50,51]. They cause a cleavage of the ester linkage leading to a linearization of the molecule. A Low-level of resistance to streptogramins B, mediated by ribosomal protection through acquisition of msr-like genes, is described in staphylococci, streptococci, or enterococci [57].