The in vitro antimicrobial activity of imipenem against recent clinical isolates of Pseudomonas spp. (94 strains) and penicillin-resistant Staphylococcus spp. (50 Staph. aureus and 50 coagulase-negative Staphylococcus) was assessed using the Mueller-Hinton agar dilution method. Results were compared with those simultaneously obtained for amikacin, netilmicin, tobramycin, norfloxacin, piperacillin, ceftazidime, ceftriaxone and azthreonam against Pseudomonas spp., and for rifampicin, clindamycin, netilmicin and cefoxitin, besides penicillin and methacillin, against Staphylococcus spp. About 50 and 90% of 84 Pseudomonas aeruginosa isolates were inhibited by concentrations of imipenem equal to or less than 2 and 8 mg/l respectively. The in vitro activity of imipenem was comparable to that of ceftazidime and norfloxacin, but superior to that of the aminoglycosides and all the other antibiotics tested, in terms of potency by weight. Among other Pseudomonas spp. only P. malthophilia (2 strains) proved resistant to imipenem. Rifampicin was the most active antibiotic by weight against Staph. aureus but imipenem was more active than clindamycin and, especially, netilmicin and cefoxitin. Imipenem was highly active also against coagulase-negative staphylococci, with some differences related to the high incidence of methicillin-resistant strains. MICs of imipenem in Mueller-Hinton broth correlated with those obtained in agar, unlike the aminoglycosides. There were no significant inoculum effects on MICs of imipenem and MBCs were within one twofold dilution of MICs in over 75% of assays.
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J Glob Antimicrob Resist
January 2025
Department of Medicine, Division of Clinical Infectious Diseases, Showa University School of Medicine, Tokyo, Japan.
Objectives: In Pseudomonas aeruginosa isolates, emerging meropenem resistance beyond imipenem resistance has become a problem. In this study, we aimed to investigate the relationship between the in vivo acquisition of antimicrobial resistance in fluoroquinolone- and carbapenem-resistant P. aeruginosa clinical isolates, the underlying molecular mechanisms, and exposure to antimicrobial agents.
View Article and Find Full Text PDFBMC Complement Med Ther
January 2025
Department of Faculty of Health Sciences, American University of Madaba, Madaba, Jordan.
Pseudomonas aeruginosa is an opportunistic pathogen belonging to the γ-proteobacteria family, known to cause pneumonia linked with ventilator use and nosocomial infections. With the increasing prevalence of antibiotic-resistant bacteria, there is a pressing need to identify alternatives to conventional antibiotics. Plant-derived substances (PDSs) offer potential not only as antibacterial agents but also as modulators of antibiotic resistance.
View Article and Find Full Text PDFJ Pediatric Infect Dis Soc
January 2025
IHMA, Schaumburg, IL, USA.
Objectives: To evaluate the in vitro susceptibility of recent Gram-negative pathogens collected from pediatric patients to imipenem/relebactam (IMI/REL) and comparator agents.
Methods: From 2018 to 2022, 254 hospitals in 62 countries collected Enterobacterales or P. aeruginosa isolates from patients <18 years old as part of the SMART global surveillance program.
Plants (Basel)
December 2024
Unidad Médica de Alta Especialidad, Centro Médico Ignacio García Téllez, Instituto Mexicano del Seguro Social, Mérida 97150, Yucatán, Mexico.
(1) Background: Carbapenem-resistant (CBRAB) and (CBRPA) are critical and high-priority pathogens that require new therapeutic developments. Medicinal plants are valuable pharmaceutical resources. This study explored the anti-infective properties of Mayan plants, , and .
View Article and Find Full Text PDFAntibiotics (Basel)
December 2024
Dipartimento di Scienze Biotecnologiche di Base, Cliniche Intensivologiche e Perioperatorie, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
Metallo-β-lactamases (MBLs) in and other Gram-negative organisms pose significant public health threats due to their association with multidrug resistance (MDR). Although aztreonam (AZT) can target MBL-producing organisms, its efficacy is compromised in organisms expressing additional β-lactamases that inactivate it. Combining AZT with the β-lactamase inhibitor avibactam (AVI) may restore its activity against MBL-producing isolates.
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