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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.


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Journal ArticleDOI
TL;DR: One hundred and fifty samples of raw calf/lamb meat samples (mince and chunks) and chicken parts (giblets, carcass) were analysed for the presence of Staphylococcus aureus as discussed by the authors.

97 citations

Journal ArticleDOI
TL;DR: The results indicate that a few coagulase gene types of S. aureus are responsible for the majority of bovine clinical mastitis cases in one province of Central Anatolia region, Turkey.

97 citations

Journal ArticleDOI
TL;DR: Analysis of metabolic trajectory data indicated that, as the mice recovered from infection, their urinary metabolic profile became similar to that of the preinfected state, underline the potential of metabolomics as a tool for diagnosis, health monitoring, and drug development, and show its usefulness for understanding microbial-host interactions.
Abstract: Pneumonia is an infection of the lower respiratory tract caused by microbial pathogens. Two such pathogens, Streptococcus pneumoniae and Staphylococcus aureus, are the most common causes of community-acquired and hospital-acquired pneumonia respectively. Each expresses strains highly resistant to penicillin and other antibiotics, and a significant number of people succumb to infection by these pathogens every year. Urinary metabolite changes in a C57Bl/6 mouse model with lung infection from either S. pneumoniae or S. aureus were characterized using multivariate targeted profiling data obtained from 1H NMR spectra. Marked changes in the urinary metabolite profile occurred within 24 h after infection with either pathogen. Specifically, significant decreases in TCA cycle intermediates, coupled with increases in fucose, creatine, and taurine were observed in the urine of S. pneumoniae-treated mice. Infection with S. aureus resulted in the decrease of a number of urinary metabolites including 1-methylnicotinam...

97 citations

Journal ArticleDOI
TL;DR: The proposed PKPD model successfully described and predicted the pronounced inoculum effect of ceftazidime in vitro and integrated data from eight literature studies to support translation from time-kill experiments to in vitro infection models.
Abstract: Pseudomonas aeruginosa is an opportunistic, gram-negative pathogen responsible for high morbidity and mortality (19). P. aeruginosa has multiple mechanisms of resistance to antibiotics, including efflux pumps, the enzymatic degradation of antibiotics by, e.g., beta-lactamases, and target structure alteration (19, 25, 45). Due to its remarkable ability to resist killing by antibiotics (45), many P. aeruginosa isolates from nosocomial infections are multidrug resistant. The proportion of ceftazidime-resistant P. aeruginosa isolates from intensive care units increased from approximately 14% in 1997 to 24% in 2003 in the United States (23). Infections with a high bacterial density at the initiation of antibiotic therapy may present a therapeutic problem, including a higher risk for the emergence of resistance due to the larger number of bacteria present and the higher probability of having at least one resistant bacterial cell within a large initial inoculum (CFUo) (32). The probability of the emergence of resistance may be substantially increased at high CFUo, as the amplification of resistant subpopulations has been demonstrated to occur secondarily to low-intensity antimicrobial exposure (60). The inoculum effect was first described by Kirby (34) in vitro for penicillin activity against staphylococci. Subsequently, many studies assessed the effect of CFUo on the MIC (6, 16). Mouton et al. (47, 48) derived the relationship between MIC and CFUo if the growth rate and maximal killing rate constant are independent of the CFUo. This effect of the CFUo on the MIC needs to be distinguished from the inoculum effect in our time-kill study, since we assessed the effect of the CFUo on the rate of bacterial killing. Importantly, high CFUo are associated with increased mortality and attenuate antibiotic effects in animal infection models (6, 20, 57). Potential mechanistic explanations for the inoculum effect of beta-lactams include the breakdown of beta-lactams by beta-lactamases, cell-to-cell communication, and the differential expression of penicillin-binding proteins (PBPs) at a high bacterial density (14, 57). In P. aeruginosa, cell-to-cell communication is known to be mediated by the release of freely diffusible signal molecules such as two N-acylhomoserine lactones and the Pseudomonas quinolone signal molecule (2-heptyl-3-hydroxy-4-quinolone) (29, 54). High concentrations of the N-butyryl-l-homoserine lactone signal molecule induce the expression of MexAB-OprM in P. aeruginosa (40, 53), for which ceftazidime is a substrate (5, 19, 41), and the mexAB-oprM operon has its highest expression during the mid-stationary-growth phase (40). These signal molecules are known to affect the expression of several hundred genes in P. aeruginosa (54). Mathematical models that can describe a slower bacterial killing rate at high CFUo have not been published. A pharmacokinetic/pharmacodynamic (PKPD) model that can describe the inoculum effect of P. aeruginosa may support the optimization of dosage regimens and generate hypotheses on how to minimize the emergence of resistance for new and established antibiotics. The objectives of the current study were to (i) study the effect of CFUo on the rate and extent of the killing of P. aeruginosa PAO1 by ceftazidime in vitro, (ii) develop a mechanism-based, mathematical model that can accommodate a range of CFUo, and (iii) qualify this model by integrating literature results for in vitro PD models with P. aeruginosa PAO1 and P. aeruginosa ATCC 27853 for ceftazidime monotherapy. (This work was presented in part at the 2008 Annual Meeting of the Population Approach Group in Australia & New Zealand, Dunedin, New Zealand, and at the 2007 Annual Meeting of the American Association of Pharmaceutical Scientists, San Diego, CA.)

97 citations

Journal ArticleDOI
TL;DR: The analysis suggests that there is a very small risk of post-dental endocarditis in MVP which is outweighed by a greater risk of fatal reactions to parenteral penicillin, and oral peniillin prophylaxis appears to spare life only in older adults with MVP and at an extremely high cost.

97 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023459
2022907
2021249
2020269
2019221
2018192