The Experts below are selected from a list of 193425 Experts worldwide ranked by ideXlab platform
Laurent Poirel - One of the best experts on this subject based on the ideXlab platform.
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cross Resistance to human cationic antimicrobial peptides and to polymyxins mediated by the plasmid encoded mcr 1
Clinical Microbiology and Infection, 2017Co-Authors: Jan Dobias, Laurent Poirel, Patrice NordmannAbstract:Abstract Objectives To evaluate whether acquired Resistance to cationic antimicrobial peptide (CAMP) group molecules, being normal components of the human immune system, may select co-Resistance to antibiotic peptides such as polymyxins, considering they share the same mechanism of action. We aimed to evaluate strains producing the recently identified plasmid-encoded polymyxin Resistance determinant MCR-1, which is a phosphoethanolamine transferase that modifies the lipopolysaccharide structure of Gram-negative bacteria. Methods In vitro susceptibility studies were performed using human CAMPs, namely cathelicidin LL-37, α-defensin 5 (HD5), and β-defensin 3 (HDB3), towards MCR-1-producing and colistin-resistant Escherichia coli or Klebsiella pneumoniae . Results Cross-Resistance to CAMPs and colistin mediated by MCR-1 or chromosomal mechanisms was neither observed in E. coli nor in K. pneumoniae . Conclusion Future therapeutic development of human CAMPs is not likely to be impeded by the spread of MCR-1 Plasmid-Mediated Resistance to polymyxins, at least in E. coli .
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moraxella species as potential sources of mcr like polymyxin Resistance determinants
Antimicrobial Agents and Chemotherapy, 2017Co-Authors: Nicolas Kieffer, Laurent Poirel, Patrice NordmannAbstract:Plasmid-Mediated Resistance to polymyxins mediated by the MCR-1/2 determinants has been reported in Enterobacteriaceae worldwide. Using PCR-based and cloning strategies, a series of Moraxella spp. were screened for mcr-like genes. Moraxella spp. that are mainly animal pathogens but may also be human pathogens were identified as potential reservoirs of mcr-like genes.
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unexpected occurrence of plasmid mediated quinolone Resistance determinants in environmental aeromonas spp
Emerging Infectious Diseases, 2008Co-Authors: Vincent Cattoir, Laurent Poirel, Camille Aubert, C J Soussy, Patrice NordmannAbstract:Quinolones are broad-spectrum antibacterial agents used in human and veterinary medicine. Their extensive use has been associated with a rising level of quinolone Resistance (1). The 2 main mechanisms of quinolone Resistance are chromosomally encoded, either a modification of the quinolone targets with changes of DNA gyrase (gyrA) and/or of topoisomerase IV (parC) genes; or a decreased intracellular concentration due to impermeability of the membrane or to overexpression of efflux pump systems (2). Plasmid-Mediated quinolone Resistance was first identified in a Klebsiella pneumoniae clinical isolate from the United States (3). It is mediated by a 218-aa protein, Qnr (lately termed QnrA), which belongs to the pentapeptide repeat family of proteins that protects DNA from quinolone binding to topoisomerases (4,5). QnrA confers Resistance to quinolones such as nalidixic acid and increases MICs of fluoroquinolones up to 32-fold in Escherichia coli (6). In addition, it enhances selection of associated chromosome-encoded quinolone Resistance determinants that confer additional Resistance to fluoroquinolones (7). The QnrA determinants have been reported worldwide in many enterobacterial species, and 6 of them are known so far (QnrA1 to QnrA6) (8). Other Plasmid-Mediated quinolone Resistance determinants, QnrB (QnrB1 to QnrB10) and QnrS (QnrS1 and QnrS2), have been identified in enterobacterial species, sharing 41% and 60% amino acid identity with QnrA, respectively (8–10). The Plasmid-Mediated qnr genes have been identified so far only in Enterobacteriaceae (6,8). Recent findings indicated that those genes originate from environmental gram-negative bacterial species, such as Shewanella algae, the progenitor of the qnrA genes (11), and Vibrio splendidus, the progenitor of qnrS genes (12). We have shown that many Vibrionaceae species may harbor chromosome-encoded qnr-type genes (13). To further evaluate the spread of Plasmid-Mediated Resistance determinants in the environment, we have searched for those genes in water samples drawn from the Seine River in Paris, France. We identified QnrS determinants in Aeromonas species in uncommon genetic environments.
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emergence of plasmid mediated Resistance to quinolones in enterobacteriaceae
Journal of Antimicrobial Chemotherapy, 2005Co-Authors: Patrice Nordmann, Laurent PoirelAbstract:: Although quinolone Resistance results mostly from chromosomal mutations in Enterobacteriaceae, it may also be mediated by plasmid-encoded Qnr determinants. Qnr proteins protect DNA from quinolone binding and compromise the efficacy of quinolones such as nalidixic acid. Qnr proteins (QnrA-like, QnrB and QnrS) have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid inhibited expanded-spectrum beta-lactamases and Plasmid-Mediated cephalosporinases. The qnrA genes are embedded in complex sul1-type integrons. A very recent identification of the origin of QnrA determinants in the water-borne species Shewanella algae underlines the role of the environment as a reservoir for this emerging threat. It may help to determine the location of in vivo transfer of qnrA genes. Further analysis of the role (if any) of quinolones for enhancing this gene transfer may be conducted. This could prevent the spread, if still possible, of this novel antibiotic Resistance mechanism.
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emergence of plasmid mediated Resistance to quinolones in enterobacteriaceae
Journal of Antimicrobial Chemotherapy, 2005Co-Authors: Patrice Nordmann, Laurent PoirelAbstract:Although quinolone Resistance results mostly from chromosomal mutations in Enterobacteriaceae, it may also be mediated by plasmid-encoded Qnr determinants. Qnr proteins protect DNA from quinolone binding and compromise the efficacy of quinolones such as nalidixic acid. Qnr proteins (QnrA-like, QnrB and QnrS) have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid inhibited expanded-spectrum beta-lactamases and Plasmid-Mediated cephalosporinases. The qnrA genes are embedded in complex sul1-type integrons. A very recent identification of the origin of QnrA determinants in the water-borne species Shewanella algae underlines the role of the environment as a reservoir for this emerging threat. It may help to determine the location of in vivo transfer of qnrA genes. Further analysis of the role (if any) of quinolones for enhancing this gene transfer may be conducted. This could prevent the spread, if still possible, of this novel antibiotic Resistance mechanism.
Patrice Nordmann - One of the best experts on this subject based on the ideXlab platform.
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cross Resistance to human cationic antimicrobial peptides and to polymyxins mediated by the plasmid encoded mcr 1
Clinical Microbiology and Infection, 2017Co-Authors: Jan Dobias, Laurent Poirel, Patrice NordmannAbstract:Abstract Objectives To evaluate whether acquired Resistance to cationic antimicrobial peptide (CAMP) group molecules, being normal components of the human immune system, may select co-Resistance to antibiotic peptides such as polymyxins, considering they share the same mechanism of action. We aimed to evaluate strains producing the recently identified plasmid-encoded polymyxin Resistance determinant MCR-1, which is a phosphoethanolamine transferase that modifies the lipopolysaccharide structure of Gram-negative bacteria. Methods In vitro susceptibility studies were performed using human CAMPs, namely cathelicidin LL-37, α-defensin 5 (HD5), and β-defensin 3 (HDB3), towards MCR-1-producing and colistin-resistant Escherichia coli or Klebsiella pneumoniae . Results Cross-Resistance to CAMPs and colistin mediated by MCR-1 or chromosomal mechanisms was neither observed in E. coli nor in K. pneumoniae . Conclusion Future therapeutic development of human CAMPs is not likely to be impeded by the spread of MCR-1 Plasmid-Mediated Resistance to polymyxins, at least in E. coli .
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moraxella species as potential sources of mcr like polymyxin Resistance determinants
Antimicrobial Agents and Chemotherapy, 2017Co-Authors: Nicolas Kieffer, Laurent Poirel, Patrice NordmannAbstract:Plasmid-Mediated Resistance to polymyxins mediated by the MCR-1/2 determinants has been reported in Enterobacteriaceae worldwide. Using PCR-based and cloning strategies, a series of Moraxella spp. were screened for mcr-like genes. Moraxella spp. that are mainly animal pathogens but may also be human pathogens were identified as potential reservoirs of mcr-like genes.
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unexpected occurrence of plasmid mediated quinolone Resistance determinants in environmental aeromonas spp
Emerging Infectious Diseases, 2008Co-Authors: Vincent Cattoir, Laurent Poirel, Camille Aubert, C J Soussy, Patrice NordmannAbstract:Quinolones are broad-spectrum antibacterial agents used in human and veterinary medicine. Their extensive use has been associated with a rising level of quinolone Resistance (1). The 2 main mechanisms of quinolone Resistance are chromosomally encoded, either a modification of the quinolone targets with changes of DNA gyrase (gyrA) and/or of topoisomerase IV (parC) genes; or a decreased intracellular concentration due to impermeability of the membrane or to overexpression of efflux pump systems (2). Plasmid-Mediated quinolone Resistance was first identified in a Klebsiella pneumoniae clinical isolate from the United States (3). It is mediated by a 218-aa protein, Qnr (lately termed QnrA), which belongs to the pentapeptide repeat family of proteins that protects DNA from quinolone binding to topoisomerases (4,5). QnrA confers Resistance to quinolones such as nalidixic acid and increases MICs of fluoroquinolones up to 32-fold in Escherichia coli (6). In addition, it enhances selection of associated chromosome-encoded quinolone Resistance determinants that confer additional Resistance to fluoroquinolones (7). The QnrA determinants have been reported worldwide in many enterobacterial species, and 6 of them are known so far (QnrA1 to QnrA6) (8). Other Plasmid-Mediated quinolone Resistance determinants, QnrB (QnrB1 to QnrB10) and QnrS (QnrS1 and QnrS2), have been identified in enterobacterial species, sharing 41% and 60% amino acid identity with QnrA, respectively (8–10). The Plasmid-Mediated qnr genes have been identified so far only in Enterobacteriaceae (6,8). Recent findings indicated that those genes originate from environmental gram-negative bacterial species, such as Shewanella algae, the progenitor of the qnrA genes (11), and Vibrio splendidus, the progenitor of qnrS genes (12). We have shown that many Vibrionaceae species may harbor chromosome-encoded qnr-type genes (13). To further evaluate the spread of Plasmid-Mediated Resistance determinants in the environment, we have searched for those genes in water samples drawn from the Seine River in Paris, France. We identified QnrS determinants in Aeromonas species in uncommon genetic environments.
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emergence of plasmid mediated Resistance to quinolones in enterobacteriaceae
Journal of Antimicrobial Chemotherapy, 2005Co-Authors: Patrice Nordmann, Laurent PoirelAbstract:: Although quinolone Resistance results mostly from chromosomal mutations in Enterobacteriaceae, it may also be mediated by plasmid-encoded Qnr determinants. Qnr proteins protect DNA from quinolone binding and compromise the efficacy of quinolones such as nalidixic acid. Qnr proteins (QnrA-like, QnrB and QnrS) have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid inhibited expanded-spectrum beta-lactamases and Plasmid-Mediated cephalosporinases. The qnrA genes are embedded in complex sul1-type integrons. A very recent identification of the origin of QnrA determinants in the water-borne species Shewanella algae underlines the role of the environment as a reservoir for this emerging threat. It may help to determine the location of in vivo transfer of qnrA genes. Further analysis of the role (if any) of quinolones for enhancing this gene transfer may be conducted. This could prevent the spread, if still possible, of this novel antibiotic Resistance mechanism.
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emergence of plasmid mediated Resistance to quinolones in enterobacteriaceae
Journal of Antimicrobial Chemotherapy, 2005Co-Authors: Patrice Nordmann, Laurent PoirelAbstract:Although quinolone Resistance results mostly from chromosomal mutations in Enterobacteriaceae, it may also be mediated by plasmid-encoded Qnr determinants. Qnr proteins protect DNA from quinolone binding and compromise the efficacy of quinolones such as nalidixic acid. Qnr proteins (QnrA-like, QnrB and QnrS) have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid inhibited expanded-spectrum beta-lactamases and Plasmid-Mediated cephalosporinases. The qnrA genes are embedded in complex sul1-type integrons. A very recent identification of the origin of QnrA determinants in the water-borne species Shewanella algae underlines the role of the environment as a reservoir for this emerging threat. It may help to determine the location of in vivo transfer of qnrA genes. Further analysis of the role (if any) of quinolones for enhancing this gene transfer may be conducted. This could prevent the spread, if still possible, of this novel antibiotic Resistance mechanism.
Lindsay M Grayson - One of the best experts on this subject based on the ideXlab platform.
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dumb and dumber the potential waste of a useful antistaphylococcal agent emerging fusidic acid Resistance in staphylococcus aureus
Clinical Infectious Diseases, 2006Co-Authors: Benjamin P Howden, Lindsay M GraysonAbstract:Fusidic acid has activity against a range of pathogens but has mainly been used to treat staphylococcal infections. Fusidic acid monotherapy, especially topical preparations, has been strongly associated with the emergence of fusidic acid Resistance among both methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible S. aureus. Key Resistance determinants include mutations in the fusA gene, which encodes elongation factor G, and Plasmid-Mediated Resistance (i.e., acquisition of Resistance gene fusB). Clonal outbreaks of fusidic acid-resistant S. aureus have been noted throughout the United Kingdom and Europe, such that the efficacy of fusidic acid is threatened. Fusidic acid in combination with other agents, such as rifampicin, has proven effective for difficult-to-treat MRSA infections and provides a convenient oral alternative to oxazolidinones. Ensuring that systemic fusidic acid is always used in combination and that the use of topical fusidic acid is either abolished or restricted will be vital if we are to prevent the loss of this potentially useful agent.
Joanne R Dillon - One of the best experts on this subject based on the ideXlab platform.
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behavioral and socioeconomic risk factors associated with probable Resistance to ceftriaxone and Resistance to penicillin and tetracycline in neisseria gonorrhoeae in shanghai
PLOS ONE, 2014Co-Authors: Joanne R Dillon, Molly A Trecker, Cheryl L Waldner, Ann M Jolly, Mingmin LiaoAbstract:Globally, incidence of Neisseria gonorrhoeae infection is once again the highest of the bacterial sexually transmitted infections. The bacterium can produce serious complications in those infected, and emerging Resistance to third generation cephalosporins could usher in an era of potentially untreatable gonorrhea. This research aimed to identify risk factors for antibiotic resistant gonorrhea infection among clients at a Shanghai sexually transmitted infection clinic over two time periods, 2004-2005 and 2008-2011. Demographic and risk factor behavior data, and biological samples for antimicrobial Resistance analysis, were collected. Statistical models were built to identify risk factors associated with probable Resistance to ceftriaxone and Resistance to penicillin and tetracycline. High levels of ciprofloxacin Resistance (98%) in our sample precluded examining its risk factors; all isolates were susceptible to spectinomycin. Overall (P<0.001), chromosomal (P<0.001), and Plasmid-Mediated (P = 0.01) penicillin Resistance decreased from the first to second period of the study. For tetracycline, chromosomal Resistance decreased (P = 0.01) and Plasmid-Mediated Resistance increased (P<0.001) between the first and second periods of study. In multi-level multivariable regression models, male gender (P = 0.03) and older age (P = 0.01) were associated with increased minimum inhibitory concentrations to ceftriaxone. Male gender (P = 0.03) and alcohol use (P = 0.02) were associated with increased odds of overall tetracycline Resistance. Male gender was associated with increased odds of chromosomally-mediated tetracycline Resistance (P = 0.04), and alcohol use was associated with increased odds of Plasmid-Mediated tetracycline Resistance (P = 0.02). Additionally, individuals in middle-salary categories were found to have lower odds of Plasmid-Mediated Resistance to tetracycline compared with those in the lowest salary category (P≤0.02). This study is one of the first to use multilevel analysis to consider the association between risk factors for gonorrhea infections and mechanisms of Resistance to individual antibiotics. Such information is urgently needed to combat the growing threat of untreatable gonorrhea.
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reduced susceptibility to azithromycin and high percentages of penicillin and tetracycline Resistance in neisseria gonorrhoeae isolates from manaus brazil 1998
Sexually Transmitted Diseases, 2001Co-Authors: Joanne R Dillon, Jeanplacide A Rubabaza, Adele Schwartz Benzaken, Jose Carlos Gomes Sardinha, Maria Goretti Campos Bandeira, Edivar Dos Santos Fernando FilhoAbstract:Background The identification of Neisseria gonorrhoeae isolates resistant to antimicrobial agents currently recommended for the treatment of gonococcal infections continues to escalate globally. Thus, in some areas, Resistance to fluoroquinolone drugs is commonplace; several reports document Resistance to third-generation cephalosporins, and the sporadic isolation of spectinomycin-resistant isolates continues unabated. Gonococcal Resistance to azithromycin, an antibiotic used for the primary treatment of gonococcal infections in some Latin American countries, also has been described. Because the prevalence of resistant isolates is insufficiently documented in many areas of Latin America, the efficacy of locally recommended therapies for gonococcal infections is often unknown. Goal To determine the antimicrobial susceptibility and strain types of N gonorrhoeae isolates collected in Manaus, Brazil. These data will establish antimicrobial susceptibility baseline data for the region as a reference point for future surveillance. Study Design Consecutive N gonorrhoeae isolates from urethral and endocervical specimens were collected and examined for identity, antimicrobial susceptibility, and strain type (plasmid content, tet M type, auxotype, and serovar). Results Most of the isolates (65/81; 85.2%) were resistant to tetracycline, penicillin, or both, with the majority (n = 62) carrying Plasmid-Mediated Resistance to tetracycline (tetracycline-resistant N gonorrhoeae [TRNG]). All of the TRNG contained the Dutch-type tet M plasmid, and 18 were A/S class NR/IA-02. Penicillinase-producing N gonorrhoeae comprised 8.2% (7/81) of the isolates. Of these seven isolates, four also were TRNG, and two carried chromosomal Resistance to tetracycline. The isolates were susceptible to ciprofloxacin, spectinomycin, and ceftriaxone. However, 23 isolates were characterized by reduced susceptibility to azithromycin (MIC, 0.25–0.5 μg/ml), and one isolate had reduced susceptibility to ciprofloxacin (MIC, 0.25 μg/ml). Conclusions This study supports the continued use of third-generation cephalosporins, spectinomycin, and fluoroquinolone drugs for the primary treatment of gonococcal infections in Manaus. The occurrence of isolates with reduced susceptibility to azithromycin and ciprofloxacin underscores the importance of ongoing antimicrobial susceptibility monitoring to support decisions regarding appropriate drugs for the treatment of gonococcal infections.
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discriminatory power of typing schemes based on simpson s index of diversity for neisseria gonorrhoeae
Journal of Clinical Microbiology, 1993Co-Authors: Joanne R Dillon, Maksudar Rahman, Kwokhim YeungAbstract:Simpson9s index of diversity was used to produce a single numerical value to compare the abilities of single or combined typing schemes to discriminate between unrelated isolates. This calculation was used to compare the discriminating power of auxotype and serovar determination and plasmid content analysis, either singly or in combination, for Neisseria gonorrhoeae isolates having different antimicrobial susceptibilities (i.e., antibiotic-susceptible isolates and those that produce penicillinase, carry Plasmid-Mediated Resistance to tetracycline, have chromosomally mediated penicillin Resistance, or both produce penicillinase and carry Plasmid-Mediated Resistance to tetracycline). Plasmid content analysis and auxotype determination produced the lowest level of discrimination, while a combination of auxotype and serovar typing schemes generally provided higher levels of discrimination. Addition of plasmid content analysis to auxotype and serovar typing provided additional discrimination only with penicillinase-producing isolates. For isolates that carried Plasmid-Mediated Resistance to tetracycline, isolates that were tetracycline resistant, isolates that both produced penicillinase and carried Plasmid-Mediated Resistance to tetracycline, or isolates that had chromosomally mediated penicillin Resistance, none of the typing methods produced high discriminatory indices, indicating that these isolates are probably derived from relatively few clones.
C. M. Parry - One of the best experts on this subject based on the ideXlab platform.
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Epidemiology, clinical presentation, laboratory diagnosis, antimicrobial Resistance, and antimicrobial management of invasive Salmonella infections
Clinical Microbiology Reviews, 2015Co-Authors: John A. Crump, Melita A Gordon, Maria Sjölund-karlsson, C. M. ParryAbstract:Salmonella enterica infections are common causes of bloodstream infection in low-resource areas, where they may be difficult to distinguish from other febrile illnesses and may be associated with a high case fatality ratio. Microbiologic culture of blood or bone marrow remains the mainstay of laboratory diagnosis. Antimicrobial Resistance has emerged in Salmonella enterica, initially to the traditional first-line drugs chloramphenicol, ampicillin, and trimethoprim-sulfamethoxazole. Decreased fluoroquinolone susceptibility and then fluoroquinolone Resistance have developed in association with chromosomal mutations in the quinolone Resistance-determining region of genes encoding DNA gyrase and topoisomerase IV and also by Plasmid-Mediated Resistance mechanisms. Resistance to extended-spectrum cephalosporins has occurred more often in nontyphoidal than in typhoidal Salmonella strains. Azithromycin is effective for the management of uncomplicated typhoid fever and may serve as an alternative oral drug in areas where fluoroquinolone Resistance is common. In 2013, CLSI lowered the ciprofloxacin susceptibility breakpoints to account for accumulating clinical, microbiologic, and pharmacokinetic-pharmacodynamic data suggesting that revision was needed for contemporary invasive Salmonella infections. Newly established CLSI guidelines for azithromycin and Salmonella enterica serovar Typhi were published in CLSI document M100 in 2015.