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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: The mechanism of killing of Escherichia coli by a novel beta-lactam antibiotic, an amidino penicillin, has been investigated and mutants resistant to the amidino Penicillin were isolated and several were studied in detail.
Abstract: The mechanism of killing of Escherichia coli by a novel beta-lactam antibiotic, an amidino penicillin, has been investigated. This compound converts E. coli to relatively stable spherical forms at low concentration. However, the amidino penicillin caused no alteration in any of those parameters of peptidoglycan synthesis which can be studied. Above 10 mug of the antibiotic per ml the cells began to lyse, and a second mode of killing appeared. Mutants resistant to the amidino penicillin were isolated and several were studied in detail. Three mutant phenotypes were distinguished: (i) spherical shape and hypersensitive to lysis by either amidino penicillin or ampicillin; (ii) spherical shape and normally sensitive to lysis; (iii) rod shape, converted to viable spheres by amidino penicillin and normally sensitive to lysis.

109 citations

Journal ArticleDOI
TL;DR: All the experimental evidence is consistent with the clinical observation that right-sided endocarditis is a more benign and responsive infection than left-sided disease and combination therapy with -lactam and aminoglycoside antibiotics synergistically and rapidly kill S. aureus.
Abstract: Right-sided endocarditis caused by Staphylococcus aureus is a frequent complication of injection drug use. Fortunately, the prognosis for this infection when treated with the standard regimen of 4 to 6 weeks of parenteral antistaphylococcal antibiotics is favorable. Nevertheless, in many cases, once drug users feel better, they leave the hospital against medical advice before completing the full course of antibiotic therapy. This problem has stimulated interest in shortening the duration of antibiotic to a penicillinase-resistant penicillin. Data from in vitro synergy studies and animal models of endocarditis suggest that S. aureus can be eradicated more quickly by combination therapy than by monotherapy. Reports of three prospective, nonrandomized clinical trials have been published that support the use of a 2-week course of a penicillinase-resistant penicillin and an aminoglycoside antibiotic to treat uncomplicated, exclusively right-sided endocarditis caused by methicillin-susceptible S. aureus in injection drug users.

109 citations

Journal ArticleDOI
TL;DR: The important chemotherapeutic agents, Prontosil and pentenylpenicillin (Penicillin F) and the very different pathways leading to their development and to that of the successor antibacterials (sulfa drugs, further penicillins, semi-synthetic penicills), including the role played by patents are discussed.
Abstract: The important chemotherapeutic agents, Prontosil and pentenylpenicillin (penicillin F), were investigated initially by two men, Domagk and Fleming, who had been influenced by the horrendous wound infections of World War I. The very different pathways leading to their development and to that of the successor antibacterials (sulfa drugs, further penicillins, semi-synthetic penicillins), including the role played by patents, are discussed.

109 citations

Journal ArticleDOI
TL;DR: This review describes how PBP alterations are involved in the intrinsic resistance of both gram-positive and gramnegative bacteria and the clinical relevance of such mechanisms of resistance.
Abstract: Beta-lactam drugs must bind to specific targets located in the cytoplasmic membrane of bacteria to exert their inhibitory effect. These target proteins can be identified by their ability to covalently bind isotope-labeled penicillin and are termed penicillin-binding proteins (PBPs). The enzymatic functions of higher-molecular-weight PBPs are essential in cell wall peptidoglycan synthesis. Betalactams exert their initial bacteriostatic effect through inhibition of these high-molecular-weight PBPs as substrate analogs of the acyl-D-alanyl-D-alanine component of peptidoglycan (16, 39, 44). Resistance to beta-lactam antimicrobial agents can be acquired by alterations in the targets of these drugs, resulting in a decrease in amount or loss of affinity for beta-lactams of a crucial PBP(s). This mechanism of intrinsic resistance has been involved in the emergence of resistant strains of Pseudomonas aeruginosa during therapy (18), and it is likely responsible for methicillin-resistant Staphylococcus aureus, an emerging problem in hospitals (20, 26, 32). In a community outbreak involving non-beta-lactamase penicillinresistant Neisseria gonorrhoeae isolates, resistance was also partly attributed to this mechanism (11). This review describes how PBP alterations are involved in the intrinsic resistance of both gram-positive and gramnegative bacteria and the clinical relevance of such mechanisms of resistance.

109 citations

Journal ArticleDOI
TL;DR: It is suggested that the hepatitis found in these 17 cases of early syphilis was produced by treponemes.

108 citations


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