scholarly journals Prevalence of moderate penicillin resistant invasive Neisseria meningitidis infection in Scotland, 1994–9

2001 ◽  
Vol 128 (2) ◽  
pp. 149-156 ◽  
Author(s):  
M. H. KYAW ◽  
J. C. BRAMLEY ◽  
S. CLARKE ◽  
P. CHRISTIE ◽  
I. G. JONES ◽  
...  
Keyword(s):  
Antimicrobial Agents ◽  
Health Interventions ◽  
Penicillin Resistance ◽  
Drug Resistant ◽  
Geographic Variations ◽  
Resistance To Penicillin ◽  
Low Incidence ◽  
High Level ◽  
B 52 ◽  
Level Resistance

We examined the serological characteristics of 774 invasive meningococcal isolates collected through an active laboratory-based surveillance system in Scotland from 1994 to 1999. Of these, 72–73% of isolates were tested for susceptibility to several antimicrobial agents. Meningococci with high-level resistance to sulphadiazine had a prevalence of 10% and incidence of 0·22 per 100000 population. High-level resistance to penicillin and other antibiotics was not detected. The prevalence of moderate penicillin resistant meningococci was 8·3%. There was no increase in moderate penicillin resistant meningococcal isolates during the study period, but there were temporal and geographic variations. The estimated incidence of moderate penicillin resistant meningococci was 0·15 per 100000 population. High and low incidence of moderate penicillin resistant meningococci appeared to correlate with the number of doses of penicillin prescribed in some geographic locations. The majority of moderate penicillin resistant isolates belonged to serogroups B (52·2%) and C (39·2%). However, the prevalence of moderate penicillin resistance in serogroup W135 was substantially higher (51·7%) than serogroups B (7·8%) and C (7·6%). Serogroup W135 accounted for a higher proportion of moderate penicillin resistance (8·7%) than disease (1%). There was no predominant penicillin resistant serotype/subtype within any serogroup. Constant surveillance is necessary to monitor the emergence and spread of resistance and to guide appropriate public health interventions in preventing drug resistant meningococci.

scholarly journals Overexpression of the MtrC-MtrD-MtrE Efflux Pump Due to an mtrR Mutation Is Required for Chromosomally Mediated Penicillin Resistance in Neisseria gonorrhoeae

2002 ◽  
Vol 184 (20) ◽  
pp. 5619-5624 ◽  
Author(s):  
Wendy L. Veal ◽  
Robert A. Nicholas ◽  
William M. Shafer
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Base Pair ◽  
Efflux Pump ◽  
Penicillin Resistance ◽  
Single Base ◽  
Base Pair Deletion ◽  
Resistance To Penicillin ◽  
Single Base Pair ◽  
High Level ◽  
Level Resistance

ABSTRACT The importance of the mtrCDE-encoded efflux pump in conferring chromosomally mediated penicillin resistance on certain strains of Neisseria gonorrhoeae was determined by using genetic derivatives of penicillin-sensitive strain FA19 bearing defined mutations (mtrR, penA, and penB) donated by a clinical isolate (FA6140) expressing high-level resistance to penicillin and antimicrobial hydrophobic agents (HAs). When introduced into strain FA19 by transformation, a single base pair deletion in the mtrR promoter sequence from strain FA6140 was sufficient to provide high-level resistance to HAs (e.g., erythromycin and Triton X-100) but only a twofold increase in resistance to penicillin. When subsequent mutations in penA and porIB were introduced from strain FA6140 into strain WV30 (FA19 mtrR) by transformation, resistance to penicillin increased incrementally up to a MIC of 1.0 μg/ml. Insertional inactivation of the gene (mtrD) encoding the membrane transporter component of the Mtr efflux pump in these transformant strains and in strain FA6140 decreased the MIC of penicillin by 16-fold. Genetic analyses revealed that mtrR mutations, such as the single base pair deletion in its promoter, are needed for phenotypic expression of penicillin and tetracycline resistance afforded by the penB mutation. As penB represents amino acid substitutions within the third loop of the outer membrane PorIB protein that modulate entry of penicillin and tetracycline, the results presented herein suggest that PorIB and the MtrC-MtrD-MtrE efflux pump act synergistically to confer resistance to these antibiotics.

Gonococcal resistance: evolving from penicillin, tetracycline to the quinolones in South Africa – implications for treatment guidelines

2007 ◽  
Vol 18 (10) ◽  
pp. 697-699 ◽  
Author(s):  
Mari De Jongh ◽  
Yusuf Dangor ◽  
Anvir Adam ◽  
Anwar A Hoosen
Keyword(s):  
South Africa ◽  
Antimicrobial Agents ◽  
Treatment Guidelines ◽  
Tetracycline Resistance ◽  
Sexually Transmitted ◽  
Antimicrobial Susceptibility Profile ◽  
Resistance To Penicillin ◽  
Agar Dilution ◽  
High Level ◽  
First Time

Resistant Neisseria gonorrhoeae has been evolving. This study assessed the antimicrobial susceptibility profile of isolates in the Pretoria region, South Africa. Isolates of N. gonorrhoeae from men with urethritis were tested for susceptibility to eight antimicrobial agents by disc diffusion, Etest and agar dilution methods. Chromosomal resistance to penicillin was found in 16% of isolates, 16% showed plasmid-mediated resistance and decreased susceptibility was seen in 73% of isolates. For the first time, there is evidence of high-level tetracycline resistance (36%). Ciprofloxacin resistance emerged at 7%. All isolates remained susceptible to ceftriaxone. In view of these findings of the emergence of quinolone-resistant N. gonorrhoeae, national treatment guidelines for syndromic management of sexually transmitted infections need to be urgently reviewed. The injectable preparation, ceftriaxone has to be considered as a first-line agent for the management of gonococcal infections. Overall, the gonococcal isolates in the Pretoria region remain susceptible to ceftriaxone, cefoxitin, cefpodoxime and spectinomycin.

scholarly journals Susceptibility trends of zoliflodacin against multidrug-resistant Neisseria gonorrhoeae clinical isolates in Nanjing, China (2014-2018)

2020 ◽  
Author(s):  
Wenjing Le ◽  
Xiaohong Su ◽  
Xiangdi Lou ◽  
Xuechun Li ◽  
Xiangdong Gong ◽  
...  
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Dna Sequencing ◽  
Multidrug Resistant ◽  
Quinolone Resistance ◽  
Clinical Isolates ◽  
Drug Resistant ◽  
Extended Spectrum ◽  
High Level ◽  
Level Resistance

ABSTRACTPreviously, we reported potent activity of a novel spiropyrimidinetrione, zoliflodacin, against N. gonorrhoeae isolates from symptomatic men in Nanjing, China, collected in 2013. Here, we investigated trends of susceptibilities of zoliflodacin in 986 gonococcal isolates collected from men between 2014 and 2018. N. gonorrhoeae isolates were tested for susceptibility to zoliflodacin and seven other antibiotics. Mutations in gyrA, gyrB, parC and parE genes were determined by PCR and DNA sequencing. The MIC of zoliflodacin for N. gonorrhoeae ranged from ≤0.002 to 0.25 mg/L; the overall MIC50s and MIC90s were 0.06 mg/L and 0.125mg/L in 2018, increasing two-fold from 2014. However, the percent of isolates with lower zoliflodacin MICs declined in each year sequentially while the percent with higher MICs increased yearly (P≤0.00001). All isolates were susceptible to spectinomycin but resistant to ciprofloxacin (MIC ≥1 μg/ml); 21.2% (209/986) were resistant to azithromycin (≥1 μg/ml), 43.4% (428/986) were penicillinase-producing (PPNG), 26.9% (265/986) tetracycline-resistant (TRNG) and 19.4% (191/986) were multi-drug resistant (MDR) isolates. Among 143 isolates with higher zoliflodacin MICs (0.125-0.25 mg/L), all had quinolone resistance associated double or triple mutations in gyrA; 139/143 (97.2%) also had mutations in parC. There were no D429N/A and/or K450T mutations in GyrB identified in the 143 isolates with higher zoliflodacin MICs; a S467N mutation in GyrB was identified in one isolate. We report that zoliflodacin has excellent in vitro activity against clinical gonococcal isolates, including those with high-level resistance to ciprofloxacin, azithromycin and extended spectrum cephalosporins.

scholarly journals PREVALENCE OF DRUG RESISTANT HIV STRAINS IN HIV-INFECTED PATIENTS OF REPRODUCTIVE AGE

2016 ◽  
Vol 72 (2) ◽  
pp. 8-13
Author(s):  
N. Babii
Keyword(s):  
Reverse Transcriptase ◽  
Reproductive Age ◽  
Drug Resistant ◽  
Resistance Mutations ◽  
Reverse Transcriptase Inhibitors ◽  
Nonnucleoside Reverse Transcriptase Inhibitors ◽  
High Prevalence ◽  
High Level ◽  
Drug Resistant Strains ◽  
Level Resistance

The prevalence of drug resistant HIV strains among HIV-positive reproductive aged persons with ineffective antiretroviral therapy (ART) was assessed. The prevalence of drug resistant strains of HIV was 73.8% in the group of women and 89.29% in the group of men (totally in 80.0% of patients). In the spectrum of drug resistance mutations (DRMs) the most prevalent mutation associated with high-level resistance to nucleoside reverse transcriptase inhibitors was substitution M184V (80.36%); in addition, the high prevalence of K65R (26.79%) was indicated. The most common mutations causing a high-level resistance to nonnucleoside reverse transcriptase inhibitors were G190S/A (57.14%), Y181C (37.50%), K101E (33.93%). The DRMs to protease inhibitors were indicated with significantly less frequent (5.36%).

scholarly journals Infective Endocarditis Complicated with Progressive Heart Failure due to β-Lactamase-Producing Cardiobacterium hominis

2000 ◽  
Vol 38 (5) ◽  
pp. 2015-2017 ◽  
Author(s):  
Po-Liang Lu ◽  
Po-Ren Hsueh ◽  
Chien-Ching Hung ◽  
Lee-Jene Teng ◽  
Tsrang-Neng Jang ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Infective Endocarditis ◽  
Aortic Valve ◽  
Blood Isolate ◽  
Severe Aortic Regurgitation ◽  
Progressive Heart Failure ◽  
Resistance To Penicillin ◽  
High Level ◽  
Level Resistance

We describe a 66-year-old woman with infective endocarditis due toCardiobacterium hominis whose condition, complicated by severe aortic regurgitation and congestive heart failure, necessitated aortic valve replacement despite treatment with ceftriaxone followed by ciprofloxacin. The blood isolate of C. hominis produced β-lactamase and exhibited high-level resistance to penicillin (MIC, ≧256 μg/ml) and reduced susceptibility to vancomycin (MIC, 8 μg/ml).

scholarly journals Transferable high-level trimethoprim resistance among isolates ofEscherichia colifrom urinary tract infections in Ontario, Canada

1992 ◽  
Vol 109 (3) ◽  
pp. 473-481 ◽  
Author(s):  
N. Harnett
Keyword(s):  
Nalidixic Acid ◽  
Antimicrobial Agents ◽  
Acid Resistance ◽  
The Public ◽  
E Coli ◽  
High Level ◽  
Tract Infections ◽  
K 12 ◽  
Level Resistance ◽  
Nalidixic Acid Resistance

SUMMARYOf 1171 isolates ofEscherichia coliisolated from urine samples at the Public Health Laboratory, Toronto, Ontario, Canada, between May 1990 and December 1991, 120 (10·3%) were resistant to trimethoprim (TMP), cotrimoxazole (TMP/SMX), sulfamethoxazole (SMX) and other antimicrobial agents; 110 of the 120 isolates (91·7%) were resistant to four or more agents. The majority of resistant isolates (91·7%) exhibited high-level resistance (MIC > 1000 mg/L) to TMP. The MIC of TMP/SMX for all 120 isolates was > 2·0/38·0 mg/L and for SMX > 1024 mg/L. High-level resistances were also present among the β-lactam antimicrobials with MICs ranging from 16- > 256 mg/L. Forty-three of 120 TMP-resistant (35·8%) isolates conjugally transferred TMP-resistance toE. coliK-12. Co-transfer of several other resistances was observed. SMX cotransferred from 86% of the 43 donors and β-lactams together with SMX cotransferred from 70%. Nalidixic acid resistance was present among 22 (18·3%) of the 120 resistant isolates, however, nalidixic acid resistance was not transferred toE. coliK-12.

Canadian national survey of prevalence of antimicrobial resistance among clinical isolates of Streptococcus pneumoniae. Canadian Bacterial Surveillance Network.

1996 ◽  
Vol 40 (9) ◽  
pp. 2190-2193 ◽  
Author(s):  
A E Simor ◽  
M Louie ◽  
D E Low
Keyword(s):  
Streptococcus Pneumoniae ◽  
Antimicrobial Agents ◽  
Clinical Isolates ◽  
Beta Lactam ◽  
Surveillance Network ◽  
Antibiotic Resistant ◽  
Intermediate Resistance ◽  
Resistant Strains ◽  
High Level ◽  
Level Resistance

The antimicrobial susceptibilities of 1,089 clinical isolates of Streptococcus pneumoniae obtained from 39 laboratories across Canada between October 1994 and August 1995 were determined. A total of 91 isolates (8.4%) demonstrated intermediate resistance (MIC, 0.1 to 1.0 microgram/ml) and 36 (3.3%) had high-level resistance (MIC, > or = 2.0 micrograms/ml) to penicillin. Penicillin-resistant strains were more likely to have been recovered from normally sterile sites (P = 0.005) and to be cross-resistant to several beta-lactam and non-beta-lactam antimicrobial agents (P < 0.05). These results indicate that there has been a recent significant increase in the prevalence of antibiotic-resistant S. pneumoniae in Canada.

scholarly journals Genetic Analyses of Mutations Contributing to Fluoroquinolone Resistance in Clinical Isolates ofStreptococcus pneumoniae

2001 ◽  
Vol 45 (12) ◽  
pp. 3517-3523 ◽  
Author(s):  
L. M. Weigel ◽  
G. J. Anderson ◽  
R. R. Facklam ◽  
F. C. Tenover
Keyword(s):  
Amino Acid ◽  
Antimicrobial Agents ◽  
Clinical Isolates ◽  
Fluoroquinolone Resistance ◽  
Cross Resistance ◽  
Genetic Analyses ◽  
High Level ◽  
Susceptibility Profiles ◽  
Level Resistance

ABSTRACT Twenty-one clinical isolates of Streptococcus pneumoniae showing reduced susceptibility or resistance to fluoroquinolones were characterized by serotype, antimicrobial susceptibility, and genetic analyses of the quinolone resistance-determining regions (QRDRs) of gyrA,gyrB, parC, and parE. Five strains were resistant to three or more classes of antimicrobial agents. In susceptibility profiles for gatifloxacin, gemifloxacin, levofloxacin, moxifloxacin, ofloxacin, sparfloxacin, and trovafloxacin, 14 isolates had intermediate- or high-level resistance to all fluoroquinolones tested except gemifloxacin (no breakpoints assigned). Fluoroquinolone resistance was not associated with serotype or with resistance to other antimicrobial agents. Mutations in the QRDRs of these isolates were more heterogeneous than those previously reported for mutants selected in vitro. Eight isolates had amino acid changes at sites other than ParC/S79 and GyrA/S81; several strains contained mutations in gyrB, parE, or both loci. Contributions to fluoroquinolone resistance by individual amino acid changes, including GyrB/E474K, ParE/E474K, and ParC/A63T, were confirmed by genetic transformation of S. pneumoniae R6. Mutations in gyrB were important for resistance to gatifloxacin but not moxifloxacin, and mutation of gyrAwas associated with resistance to moxifloxacin but not gatifloxacin, suggesting differences in the drug-target interactions of the two 8-methoxyquinolones. The positions of amino acid changes within the four genes affected resistance more than did the total number of QRDR mutations. However, the effect of a specific mutation varied significantly depending on the agent tested. These data suggest that the heterogeneity of mutations will likely increase as pneumococci are exposed to novel fluoroquinolone structures, complicating the prediction of cross-resistance within this class of antimicrobial agents.

scholarly journals Induction of Multidrug Resistance Mechanism in Escherichia coli Biofilms by Interplay between Tetracycline and Ampicillin Resistance Genes

2009 ◽  
Vol 53 (11) ◽  
pp. 4628-4639 ◽  
Author(s):  
Thithiwat May ◽  
Akinobu Ito ◽  
Satoshi Okabe
Keyword(s):  
Escherichia Coli ◽  
Antibiotic Resistance ◽  
Resistance Genes ◽  
Antimicrobial Agents ◽  
Efflux Pump ◽  
Marker Genes ◽  
Ampicillin Resistance ◽  
High Level ◽  
Biofilm Development ◽  
Level Resistance

ABSTRACT Biofilms gain resistance to various antimicrobial agents, and the presence of antibiotic resistance genes is thought to contribute to a biofilm-mediated antibiotic resistance. Here we showed the interplay between the tetracycline resistance efflux pump TetA(C) and the ampicillin resistance gene (bla TEM-1) in biofilms of Escherichia coli harboring pBR322 in the presence of the mixture of ampicillin and tetracycline. E. coli in the biofilms could obtain the high-level resistance to ampicillin, tetracycline, penicillin, erythromycin, and chloramphenicol during biofilm development and maturation as a result of the interplay between the marker genes on the plasmids, the increase of plasmid copy number, and consequently the induction of the efflux systems on the bacterial chromosome, especially the EmrY/K and EvgA/S pumps. In addition, we characterized the overexpression of the TetA(C) pump that contributed to osmotic stress response and was involved in the induction of capsular colanic acid production, promoting formation of mature biofilms. However, this investigated phenomenon was highly dependent on the addition of the subinhibitory concentrations of antibiotic mixture, and the biofilm resistance behavior was limited to aminoglycoside antibiotics. Thus, marker genes on plasmids played an important role in both resistance of biofilm cells to antibiotics and in formation of mature biofilms, as they could trigger specific chromosomal resistance mechanisms to confer a high-level resistance during biofilm formation.

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