Topic
Penicillin
About: Penicillin is a research topic. Over the lifetime, 17916 publications have been published within this topic receiving 368480 citations. The topic is also known as: penicillin antibiotic & PCN.
Papers published on a yearly basis
Papers
More filters
TL;DR: The kinetic study shows that penicillin tolerance is not rare among group B streptococci isolated in the authors' hospital, and two strains with intermediate susceptibility to Penicillin and eight strains to ampicillin are found.
Abstract: The aim of this study was to determine the susceptibility patterns of 100 group B streptococcal strains isolated in our hospital and to ascertain tolerance to penicillin by determining quantitative killing curves. We found two strains with intermediate susceptibility to penicillin and eight strains to ampicillin. Seventeen isolates were tolerant to penicillin, with bacterial counts decreasing 2 to 3 log during the first 8 h but still above 10(2) CFU/ml after 24 h. The kinetic study shows that penicillin tolerance is not rare among group B streptococci isolated in our hospital.
90 citations
TL;DR: In this paper, a single chamber microbial fuel cell (MFC) with an air-cathode was successfully demonstrated using glucose-penicillin mixtures or penicillin as fuel.
90 citations
TL;DR: A total of 193 bacterial strains were tested for their susceptibilities to 14 antimicrobial agents and metronidazole was active against more than 90% of the anaerobic bacteria and Capnocytophaga but was inactive against most other microaerophilic and facultative strains.
Abstract: A total of 193 bacterial strains were tested for their susceptibilities to 14 antimicrobial agents. Penicillin G was active at 2 U/ml against 98% of the oral isolates. Other antibiotics with good activity were cefoperazone, moxalactam, Sch 29,482, and clindamycin. Metronidazole was active against more than 90% of the anaerobic bacteria and Capnocytophaga but was inactive against most other microaerophilic and facultative strains.
90 citations
TL;DR: It is demonstrated that capsular polysaccharides negatively influence the lytic process and contribute to antibiotic tolerance in clinical isolates of pneumococci.
Abstract: Penicillin and vancomycin induce a lytic response in Streptococcus pneumoniae that requires the N-acetylmuramyl-l-alanine amidase LytA. We show that clinical isolates of pneumococci of capsular serotypes 1, 4, 6B, and 23F were generally less lytic to penicillin than pneumococci of serotypes 14 and 3. In addition, most 9V isolates were less lytic to vancomycin, compared with isolates of other serotypes. Parent-mutant pairs expressing and not expressing capsular serotypes 2, 4, and 9V were compared for antibiotic-induced lysis. The nonencapsulated variants were considerably more lytic after beta-lactam and/or vancomycin treatment, and antibiotic tolerance was seen only in the context of capsule expression. Conversion from a nonlytic to a lytic phenotype, after loss of capsule expression, required an intact lytA autolysin gene. Exogenous addition of purified LytA gave a lower lytic response in capsulated strains, compared with that in nonencapsulated mutants. Spontaneous autolysis in stationary phase also was negatively affected by capsule expression in an autolysin-dependent manner. Long-term starvation in the stationary phase of the vancomycin- and penicillin-tolerant isolate I95 yielded nonencapsulated mutants that had lost antibiotic tolerance and were lytic to penicillin and vancomycin. The 9V capsular locus of I95 and one of these stationary phase-selected mutants were completely sequenced. The only difference found was a 1-bp frameshift deletion in the cps9vE gene of the lytic mutant, encoding a uridine diphosphate-glucosyl-1-phosphate transferase. Two additional independently isolated lytic mutants of I95 from the stationary phase also contained mutations in the same region of cps9vE, which identified it as a mutational hot spot. This report demonstrates that capsular polysaccharides negatively influence the lytic process and contribute to antibiotic tolerance in clinical isolates of pneumococci.
90 citations
TL;DR: Multiple explanations have been offered by investigators to explain penicillin treatment failures in GAS tonsillopharyngitis, but the evidence base to support the proposed explanations is generally weak by current standards.
Abstract: Objective Review the evidence for various explanations for microbiologic treatment failure following use of penicillin in group A streptococcal (GAS) tonsillopharyngitis. Data Source Systematic review of the literature based on Medline and EMBASE searches, and review of reference lists of included studies. Results The explanations for penicillin treatment failure in GAS tonsillopharyngitis include 1) carrier state, 2) lack of compliance, 3) recurrent exposure, 4) in vivo copathogenicity of β-lactamase–producing normal pharyngeal flora, 5) in vivo bacterial coaggregation, 6) poor antibiotic penetration to tonsillopharyngeal tissue, 7) in vivo eradication of normal protective flora, 8) early initiation of antibiotic therapy resulting in suppression of an adequate host immune response, 9) intracellular localization of GAS, 10) GAS tolerance to penicillin, 11) contaminated toothbrushes or orthodontic appliances, and 12) transmission from the family pet. There is very little type I or II evidence to support any of the above-cited explanations for treatment failure in GAS tonsillopharyngitis; available studies are mostly observational (in patients) or laboratory-based without clinical confirmation. Conclusion Multiple explanations have been offered by investigators to explain penicillin treatment failures in GAS tonsillopharyngitis, but the evidence base to support the proposed explanations is generally weak by current standards. Further research is needed to better understand the mechanism(s) of penicillin treatment failure in GAS tonsillopharyngitis.
90 citations