Relevant bibliographies by topics / Evernimicin

Academic literature on the topic 'Evernimicin'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Evernimicin"

1

McNicholas, Paul M., David J. Najarian, Paul A. Mann, David Hesk, Roberta S. Hare, Karen J. Shaw, and Todd A. Black. "Evernimicin Binds Exclusively to the 50S Ribosomal Subunit and Inhibits Translation in Cell-Free Systems Derived from both Gram-Positive and Gram-Negative Bacteria." Antimicrobial Agents and Chemotherapy 44, no. 5 (May 1, 2000): 1121–26. http://dx.doi.org/10.1128/aac.44.5.1121-1126.2000.

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ABSTRACT Evernimicin (SCH 27899) is a new antibiotic with activity against a wide spectrum of gram-positive bacteria and activity against some gram-negative bacteria. Previous metabolic labeling studies indicated that evernimicin specifically inhibited protein synthesis inStaphylococcus aureus. Using a susceptibleEscherichia coli strain, we demonstrated that evernimicin also inhibited protein synthesis in E. coli. In cell-free translation assays with extracts from either E. coli orS. aureus, evernimicin had a 50% inhibitory concentration of approximately 125 nM. In contrast, cell-free systems derived from wheat germ and rabbit reticulocytes were inhibited only by very high levels of evernimicin. Evernimicin did not promote transcript misreading. [14C]evernimicin specifically bound to the 50S subunit from E. coli. Nonlinear regression analysis of binding data generated with 70S ribosomes from E. coli andS. aureus and 50S subunits from E. colireturned dissociation constants of 84, 86, and 160 nM, respectively. In binding experiments, performed in the presence of excess quantities of a selection of antibiotics known to bind to the 50S subunit, only the structurally similar drug avilamycin blocked binding of [14C]evernimicin to ribosomes.
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2

Adrian, Peter V., Wenjun Zhao, Todd A. Black, Karen J. Shaw, Roberta S. Hare, and Keith P. Klugman. "Mutations in Ribosomal Protein L16 Conferring Reduced Susceptibility to Evernimicin (SCH27899): Implications for Mechanism of Action." Antimicrobial Agents and Chemotherapy 44, no. 3 (March 1, 2000): 732–38. http://dx.doi.org/10.1128/aac.44.3.732-738.2000.

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ABSTRACT A clinical isolate of Streptococcus pneumoniae (SP#5) that showed decreased susceptibility to evernimicin (MIC, 1.5 μg/ml) was investigated. A 4,255-bp EcoRI fragment cloned from SP#5 was identified by its ability to transform evernimicin-susceptibleS. pneumoniae R6 (MIC, 0.03 μg/ml) such that the evernimicin MIC was 1.5 μg/ml. Nucleotide sequence analysis of this fragment revealed that it contained portions of the S10-spc ribosomal protein operons. The nucleotide sequences of resistant and susceptible isolates were compared, and a point mutation (thymine to guanine) that causes an Ile52-Ser substitution in ribosomal protein L16 was identified. The role of this mutation in decreasing susceptibility to evernimicin was confirmed by direct transformation of the altered L16 gene. The presence of the L16 mutation in the resistant strain suggests that evernimicin is an inhibitor of protein synthesis. This was confirmed by inhibition studies using radiolabeled substrates, which showed that the addition of evernimicin at sub-MIC levels resulted in a rapid decrease in the incorporation of radiolabeled isoleucine in a susceptible isolate (SP#3) but was much less effective against SP#5. The incorporation of isoleucine showed a linear response to the dose level of evernimicin. The incorporation of other classes of labeled substrates was unaffected or much delayed, indicating that these were secondary effects.
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3

McNicholas, Paul M., Paul A. Mann, David J. Najarian, Lynn Miesel, Roberta S. Hare, and Todd A. Black. "Effects of Mutations in Ribosomal Protein L16 on Susceptibility and Accumulation of Evernimicin." Antimicrobial Agents and Chemotherapy 45, no. 1 (January 1, 2001): 79–83. http://dx.doi.org/10.1128/aac.45.1.79-83.2001.

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ABSTRACT Chemical mutagenesis of Staphylococcus aureus RN450 generated two strains that displayed a stable reduction (30- to 60-fold) in susceptibility to evernimicin. Cell-free translation reactions demonstrated that the resistance determinant was located in the ribosomal fraction. Compared to ribosomes isolated from a wild-type strain, ribosomes from the mutant strains displayed an 8- to 10-fold reduction in affinity for [14C]evernimicin. In contrast, the mutants displayed no alteration in either binding affinity or in vitro susceptibility to erythromycin. Exponential cultures of the mutant strains accumulated significantly less [14C]evernimicin than the wild-type strain, suggesting that accumulation is dependent on the high affinity that evernimicin displays for its binding site. Sequencing rplP (encodes ribosomal protein L16) in the mutant strains revealed a single base change in each strain, which resulted in a substitution of either cysteine or histidine for arginine at residue 51. Introduction of a multicopy plasmid carrying wild-type rplP into the mutant strains restored sensitivity to evernimicin, confirming that the alterations in rplP were responsible for the change in susceptibility. Overexpression of the mutant alleles in S. aureus RN450 had no effect on susceptibility to evernimicin, demonstrating that susceptibility is dominant over resistance.
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4

Souli, Maria, Claudie Thauvin-Eliopoulos, and George M. Eliopoulos. "In Vivo Activities of Evernimicin (SCH 27899) against Vancomycin-Susceptible and Vancomycin-Resistant Enterococci in Experimental Endocarditis." Antimicrobial Agents and Chemotherapy 44, no. 10 (October 1, 2000): 2733–39. http://dx.doi.org/10.1128/aac.44.10.2733-2739.2000.

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ABSTRACT To assess the potential efficacy of evernimicin (SCH 27899) against serious enterococcal infections, we used a rat model of aortic valve endocarditis established with either a vancomycin-susceptibleEnterococcus faecalis or a vancomycin-resistantEnterococcus faecium strain. Animals infected with either one of the test strains were assigned to receive no treatment (controls) or 5-day therapy with one of the following regimens: evernimicin 60-mg/kg of body weight intravenous (i.v.) bolus once daily, 60-mg/kg i.v. bolus twice daily (b.i.d.), 60 mg/kg/day i.v. by continuous infusion, or 120 mg/kg/day i.v. by continuous infusion. These regimens were compared with vancomycin at 150 mg/kg/day. In animals infected with E. faecalis, evernimicin at 120 mg/kg/day by continuous infusion significantly reduced bacterial counts in vegetations (final density, 5.75 ± 3.38 log10CFU/g) compared with controls (8.51 ± 1.11 log10CFU/g). In animals infected with 0.5 ml of an 8 × 107-CFU/ml inoculum of the vancomycin-resistant E. faecium, both 60-mg/kg bolus once a day and b.i.d. dose regimens of evernimicin were very effective (viable counts, 3.45 ± 1.44 and 3.81 ± 1.98 log10 CFU/g, respectively). Vancomycin was unexpectedly active against infections induced with that inoculum. In animals infected with a 109-CFU/ml inoculum of the vancomycin-resistant E. faecium, the evernimicin 60-mg/kg i.v. bolus b.i.d. reduced viable counts in vegetations compared with controls (6.27 ± 1.63 versus 8.34 ± 0.91 log10 CFU/g; P < 0.05), whereas vancomycin was ineffective. Although resistant colonies could be selected in vitro, we were not able to identify evernimicin-resistant clones from cardiac vegetations. An unexplained observation from these experiments was the great variability in final bacterial densities within cardiac vegetations from animals in each of the evernimicin treatment groups.
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5

Boucher, Helen W., Claudie Thauvin-Eliopoulos, David Loebenberg, and George M. Eliopoulos. "In Vivo Activity of Evernimicin (SCH 27899) against Methicillin-Resistant Staphylococcus aureus in Experimental Infective Endocarditis." Antimicrobial Agents and Chemotherapy 45, no. 1 (January 1, 2001): 208–11. http://dx.doi.org/10.1128/aac.45.1.208-211.2001.

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ABSTRACT Currently, there exist few satisfactory alternatives to vancomycin for therapy of serious methicillin-resistant Staphylococcus aureus (MRSA) infections. We employed a rat model of aortic valve endocarditis to assess the potential efficacy of evernimicin (SCH 27899) compared with vancomycin against infection with a strain susceptible to both agents (MICs of 0.25 and 0.50 μg/ml, respectively). Infected animals were assigned to one of three groups: controls (no treatment), evernimicin at 60 mg/kg of body weight by intravenous (i.v.) infusion once daily, or vancomycin at 150 mg/kg of body weight per day by continuous i.v. infusion. Therapy was administered for 5.5 days. At the start of therapy, colony counts in vegetations were 6.63 ± 0.44 log10 CFU/g. In both treatment groups, bacterial density within vegetations was significantly reduced in comparison with control animals that had not been treated. Final colony counts were as follows (mean ± standard deviation): controls, 10.12 ± 1.51 log10 CFU/g of vegetation; evernimicin, 7.22 ± 2.91 log10 CFU/g of vegetation; vancomycin, 5.65 ± 1.76 log10 CFU/g of vegetation. The difference between the evernimicin and vancomycin groups was not significant. These results confirmed the bacteriostatic activity of evernimicin in vivo in an experimental model of severe MRSA infection.
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6

Pavia, Charles S., Gary P. Wormser, John Nowakowski, and Anthony Cacciapuoti. "Efficacy of an Evernimicin (SCH27899) In Vitro and in an Animal Model of Lyme Disease." Antimicrobial Agents and Chemotherapy 45, no. 3 (March 1, 2001): 936–37. http://dx.doi.org/10.1128/aac.45.3.936-937.2001.

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ABSTRACT The MICs of evernimicin at which 90% of Borrelia burgdorferi patient isolates were inhibited ranged from 0.1 to 0.5 μg/ml. Evernimicin was as effective as ceftriaxone againstB. burgdorferi in a murine model of experimental Lyme disease. As assessed by culturing the urinary bladders of infected C3H mice, no live Borrelia isolates were recoverable following antibiotic treatment.
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7

Aarestrup, Frank Møller, and Paul M. McNicholas. "Incidence of High-Level Evernimicin Resistance in Enterococcus faecium among Food Animals and Humans." Antimicrobial Agents and Chemotherapy 46, no. 9 (September 2002): 3088–90. http://dx.doi.org/10.1128/aac.46.9.3088-3090.2002.

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ABSTRACT Six high-level evernimicin-resistant Enterococcus faecium isolates were identified among 304 avilamycin-resistant E. faecium isolates from animals and 404 stool samples from humans with diarrhea. All four animal isolates, and one of the human isolates, were able to transfer resistance to a susceptible E. faecium strain. The resulting transconjugants all tested positive for the presence of emtA, a gene encoding a methyltransferase previously linked with high-level evernimicin resistance. The four transconjugants derived from animal isolates all carried the same plasmid, while a differently sized plasmid was found in the isolate from humans. This study demonstrated a low incidence of high-level evernimicin resistance mediated by the emtA gene in different E. faecium isolates of animal and human origin.
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8

Zbaida, Shmuel, Joan Brieland, Philip Krieter, David Loebenberg, Gopal Krishna, Debra Horne, Xiaowen Lu, et al. "In Vitro Uptake of SCH 27899 (Evernimicin) by Rat Alveolar Macrophages." Antimicrobial Agents and Chemotherapy 45, no. 3 (March 1, 2001): 959–61. http://dx.doi.org/10.1128/aac.45.3.959-961.2001.

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ABSTRACT The in vitro uptake of [14C]evernimicin ([14C]SCH 27899) by primary cultures of rat alveolar macrophages and hepatocytes was determined. Both cell populations exhibited linear rates of uptake. However, the initial rate of drug uptake by alveolar macrophages was about threefold higher than that by hepatocytes. These findings demonstrate that [14C]evernimicin is taken up by rat alveolar macrophages, supporting the likelihood that the drug is able to reach sites of infection.
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9

Champney, W. Scott, and Craig L. Tober. "Evernimicin (SCH27899) Inhibits both Translation and 50S Ribosomal Subunit Formation in Staphylococcus aureusCells." Antimicrobial Agents and Chemotherapy 44, no. 6 (June 1, 2000): 1413–17. http://dx.doi.org/10.1128/aac.44.6.1413-1417.2000.

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ABSTRACT The effects of the everninomicin antibiotic evernimicin (SCH27899) on growing Staphylococcus aureus cells were investigated. Cellular growth rates and viable cell numbers decreased with increasing antibiotic concentrations. The rate of protein synthesis, measured as35S-amino acid incorporation, declined in parallel with the growth rate. Significantly, the formation of the 50S ribosomal subunit was inhibited in a dose-dependent fashion as well. 30S ribosomal subunit synthesis was not affected over the same concentration range. Evernimicin did not stimulate the breakdown of mature ribosomal subunits. Pulse-chase labeling experiments revealed a reduced rate of 50S subunit formation in drug-treated cells. Two erythromycin-resistant strains of S. aureus that carried the ermC gene were as sensitive as wild-type cells to antibiotic inhibition. In addition, two methicillin-resistant S. aureus organisms, one sensitive to erythromycin and one resistant to the macrolide, showed similar sensitivities to evernimicin. These results suggest a use for this novel antimicrobial agent against antibiotic-resistant bacterial infections.
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10

Adrian, Peter V., Cara Mendrick, David Loebenberg, Paul McNicholas, Karen J. Shaw, Keith P. Klugman, Roberta S. Hare, and Todd A. Black. "Evernimicin (SCH27899) Inhibits a Novel Ribosome Target Site: Analysis of 23S Ribosomal DNA Mutants." Antimicrobial Agents and Chemotherapy 44, no. 11 (November 1, 2000): 3101–6. http://dx.doi.org/10.1128/aac.44.11.3101-3106.2000.

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ABSTRACT Spontaneous mutants of susceptible clinical and laboratory isolates of Streptococcus pneumoniae exhibiting reduced susceptibility to evernimicin (SCH27899; MIC, 0.5 to 4.0 mg/liter) were selected on plates containing evernimicin. Four isolates that did not harbor mutations in rplP (which encodes ribosomal protein L16) were further analyzed. Whole chromosomal DNA or PCR products of the 23S ribosomal DNA (rDNA) operons from these mutants could be used to transform the susceptible S. pneumoniae strain R6 to resistance at frequencies of 10−5 and 10−4, respectively, rates 10- to 100-fold lower than that for a single-allele chromosomal marker. The transformants appeared slowly (48 to 72 h) on selective medium, and primary transformants passaged on nonselective medium produced single colonies that displayed heterogeneous susceptibilities to evernimicin. A single passage on selective medium of colonies derived from a single primary transformant homogenized the resistance phenotype. Sequence analysis of the 23S rDNA and rRNA from the resistant mutants revealed single, unique mutations in each isolate at the equivalent Escherichia coli positions 2469 (A → C), 2480 (C → T), 2535 (G → A), and 2536 (G → C). The mutations map within two different stems of the peptidyltransferase region of domain V. Because multiple copies of rDNA are present in the chromosome, gene conversion between mutant and wild-type 23S rDNA alleles may be necessary for stable resistance. Additionally, none of the characterized mutants showed cross-resistance to any of a spectrum of protein synthesis inhibitors, suggesting that the target site of evernimicin may be unique.
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