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.

scholarly journals A novel, double mutation in DNA gyrase A of Escherichia coli conferring resistance to quinolone antibiotics.

1997 ◽  
Vol 41 (1) ◽  
pp. 85-90 ◽  
Author(s):  
Q C Truong ◽  
J C Nguyen Van ◽  
D Shlaes ◽  
L Gutmann ◽  
N J Moreau
Keyword(s):  
Escherichia Coli ◽  
Nalidixic Acid ◽  
Acid Resistance ◽  
Gyra Gene ◽  
Double Mutation ◽  
E Coli ◽  
Quinolone Antibiotics ◽  
Gyrase A ◽  
Level Resistance ◽  
Nalidixic Acid Resistance

A spontaneous Escherichia coli mutant, named Q3, resistant to nalidixic acid was obtained from a previously described clinical isolate of E. coli, Q2, resistant to fluoroquinolones but susceptible to nalidixic acid (E. Cambau, F. Bordon, E. Collatz, and L. Gutmann, Antimicrob. Agents Chemother. 37:1247-1252, 1993). Q3 harbored the mutation Asp82Gly in addition to the Gly81Asp mutation of Q2. The different mutations leading to Gly81Asp, Asp82Gly, and Gly81AspAsp82Gly were introduced into the gyrA gene harbored on plasmid pJSW102, and the resulting plasmids were introduced into E. coli KNK453 (gyrAts) by transformation. The presence of Asp82Gly or Gly81Asp alone led to a low-level resistance to fluoroquinolones but not to nalidixic acid resistance. When both mutations were present, resistance to both nalidixic acid and fluoroquinolones was expressed. Purified gyrases of the different mutants showed similar rates of supercoiling. Dominance of the various gyrA mutant alleles harbored on plasmids was examined. The susceptibility to quinolones associated with wild-type gyrA was always dominant. The susceptibility to nalidixic acid expressed by the Gly81Asp mutant was dominant, while that expressed by the Asp82Gly mutant was recessive. From these results, we hypothesize that some amino acids within the quinolone resistance-determining region of gyrase A are more important for the association of subunits rather than for the activity of the holoenzyme.

scholarly journals Escherichia coli from community-acquired urinary tract infections resistant to fluoroquinolones and extended-spectrum beta-lactams

2007 ◽  
Vol 1 (03) ◽  
pp. 257-262 ◽  
Author(s):  
Samuel Kariuki ◽  
Gunturu Revathi ◽  
John Corkill ◽  
John Kiiru ◽  
Joyce Mwituria ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Nalidixic Acid ◽  
Urinary Tract Infections ◽  
Acid Resistance ◽  
Beta Lactam ◽  
E Coli ◽  
Extended Spectrum ◽  
Tract Infections ◽  
Multiple Drugs

Background: Uropathogenic Escherichia coli are increasingly becoming resistant to flouroquinolones and to other commonly available antimicrobials. We sought to investigate the genetic basis for fluoroquinolone and extended spectrum beta-lactam (ESBL) resistance in 17 fluoroquinolone-resistant (MIC of levofloxacin and ciprofloxacin >32 μg/ml) E. coli isolated from patients with urinary tract infections (UTIs). Methods: We applied PCR and Pulsed Field Gel Electrophoresis (PFGE) to characterize resistance genes and to determine clonal relatedness of strains, respectively. Results: Twelve of the 17 E. coli were resistant to multiple drugs, including ampicillin, co-amoxyclav, cefotaxime, ceftriaxone, ceftazidime and gentamicin and nalidixic acid and produced plasmid-mediated CTX-M-15 type ESBLs and CMY-2 AmpC type enzymes. The other 5 E. coli that were non-ESBL-producing were multiply resistant to ampicillin, nitrofurantoin, cefoxitin, nalidixic acid. Resistance to fluoroquinolones resulted from a combination of the presence of qnrA, qnrB, ciprofloxacin acetylating enzyme designated aac(6’)-1b-cr, and mutations in the two amino acid substitutions; 83 Serine (TCG) to Leucine (TTG) and 87 Aspartic acid (GAC) to Asparagine (AAC). Conclusion: Antibiogram patterns and PFGE of E. coli showed that these were community acquired UTI caused by pockets of clonally-related and some discreet strain types. Plasmid-mediated CTX-M-15 beta-lactamases and CMY-2 AmpC enzymes and fluoroquinolone resistant E. coli are becoming increasingly prevalent in hospitals in Kenya, posing a major challenge in the management of UTIs.

scholarly journals Adaptation of Esherichia coli to Antiobiotic Cycling via Single Nucleotide Polymorphisms

2017 ◽  
Vol 14 (1) ◽  
Author(s):  
Samuel Hager ◽  
Ellen Jensen ◽  
Timothy Johnson ◽  
David Mitchell
Keyword(s):  
Escherichia Coli ◽  
Minimum Inhibitory Concentration ◽  
Nalidixic Acid ◽  
Inhibitory Concentration ◽  
Acid Resistance ◽  
Penicillin G ◽  
Single Nucleotide ◽  
E Coli ◽  
Esherichia Coli ◽  
Nalidixic Acid Resistance

Bacteria are quick to adapt and evolve, especially under the effects of selective pressures from chemical antibiotics. In addition, bacteria may develop resistance to antibiotics from multiple classes simultaneously, making their eradication from the human body particularly challenging. This study aims to demonstrate that bacterial multiple-drug resistance can be developed and retained in a laboratory setting. Escherichia coli B was grown in tryptic soy broth in the presence of a small, increasing concentration of streptomycin. This exposure resulted in a strain of E. coli, which had an increased minimum inhibitory concentration (MIC) towards streptomycin, or “resistance.” This resistant strain was then grown in like manner in nalidixic acid and then penicillin G. The result was a strain that became resistant to streptomycin and nalidixic acid, and increasingly resistant to nalidixic acid after penicillin G exposure. Additionally, the bacteria retained resistance to streptomycin and nalidixic acid even after exposure to those chemicals ceased. Genome sequencing and comparison to E. coli B reference strain REL606 revealed the emergence of point mutations with each exposure to an antibiotic. Of particular interest is a mutation associated with the appearance of nalidixic acid resistance. Base pair 4,553,488 was changed from adenine to guanine, resulting in a change from aspartate to glycine in the protein helicase. Previous studies have not indicated mutations to this locus as nalidixic acid resistance conferring. Thus, this mutation may be a novel mutation conferring E. coli B nalidixic acid resistance. Since the region of the mutated helicase is functionally undefined, a mechanism is not apparent. Further research needs to be done to confirm this hypothesis and illuminate a mechanism. KEYWORDS: Bacteria; Escherichia coli; Evolution; Antibiotic Resistance; Nalidixic Acid; Streptomycin; Point Mutation; Single-nucleotide Polymorphism; Helicase; Minimum Inhibitory Concentration

scholarly journals Similarities between Salmonella Enteritidis isolated from humans and captive wild animals in South Africa

2014 ◽  
Vol 8 (12) ◽  
pp. 1615-1619 ◽  
Author(s):  
Anthony Marius Smith ◽  
Husna Ismail ◽  
Maryke M Henton ◽  
Karen H Keddy ◽  
GERMS-SA Surveillance Network
Keyword(s):  
South Africa ◽  
Nalidixic Acid ◽  
Salmonella Enteritidis ◽  
Antimicrobial Agents ◽  
Acid Resistance ◽  
Diarrhoeal Disease ◽  
Common Source ◽  
Wild Animals ◽  
Animal Isolates ◽  
Nalidixic Acid Resistance

Introduction: Salmonella is well recognized as an aetiological agent of gastrointestinal and diarrhoeal disease. Salmonella enterica serotype Enteritidis (Salmonella Enteritidis) is one of the commonest serotypes associated with foodborne illness. In South Africa, we compared Salmonella Enteritidis strains isolated from humans with gastroenteritis and strains isolated from captive wild animals, between June 2011 and July 2012. Methodology: Bacteria were phenotypically characterized using standard microbiological techniques. Genotypic relatedness of isolates was investigated by pulsed-field gel electrophoresis (PFGE) analysis. Results: a diversity of 27 PFGE patterns amongst 196 human non-invasive isolates was shown; two PFGE patterns predominated and accounted for 74% of all human isolates. Human isolates showed a 12% prevalence rate for nalidixic acid resistance. Animal isolates from 5 different sources were investigated. With the exception of an isolate from a ground hornbill, all animal isolates (jaguar, crocodile, lion and poultry) showed PFGE pattern matches to a human isolate. Animal isolates showed susceptibility to all antimicrobial agents tested, with the exception of nalidixic acid resistance in isolates from the lion and poultry source. Conclusions: Our data showed similarities between Salmonella Enteritidis strains isolated from humans and captive wild animals, suggesting a probable common source for strains from humans and animals.

scholarly journals Detection of Plasmid-Mediated qnr Genes Among the Clinical Quinolone-Resistant Escherichia coli Strains Isolated in Tehran, Iran

2018 ◽  
Vol 12 (1) ◽  
pp. 248-253 ◽  
Author(s):  
Reza Ranjbar ◽  
Sajjad S. Tolon ◽  
Mehrdad Sami ◽  
Reza Golmohammadi
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Nalidixic Acid ◽  
Treatment Options ◽  
Bacterial Genome ◽  
Multidrug Resistant ◽  
Documentation System ◽  
E Coli ◽  
High Level ◽  
Tract Infections

Background:Escherichia coliis one of the most important bacterial agents to cause urinary tract infections. Inappropriate and unnecessary administration of antibiotics has led to an increase in the appearance of multidrug-resistantE. coliisolates, limiting treatment options. The increase in a number of resistant strains of bacteria is a major concern of health authorities worldwide.Objective:The purpose of this study was to determine the presence of theqnrgenes amongE. coliisolated from UTIs of patients in Baqiyatallah hospital in Tehran province, Iran.Method:Clinical urine samples of patients with suspected urinary tract infection were collected by standard methods in sterile disposable containers. After analysis of urine, microscopic observations and culture analysis, the bacterial genome was extracted by boiling method. PCR for detection ofqnrgenes includingqnrA,qnrBandqnrSwas done by specific primers, then PCR products were run using gel electrophoresis and visualized by gel documentation system.Results:In the present study among the 95 isolates, 60 strains were resistant to nalidixic acid. PCR showed that 92 strains were positive forqnrS. TheqnrAandqnrBgenes were not found among the clinical isolates.Conclusion:Our finding indicates a high level of resistance against nalidixic acid amongE. coliisolates recovered from the patients with UTI. Also, the high frequency ofqnrSimposes the importance of survey of molecular and genetic analysis of mechanisms of quinolone resistance inE. colistrains.

scholarly journals The life and times of the Enterococcus.

1990 ◽  
Vol 3 (1) ◽  
pp. 46-65 ◽  
Author(s):  
B E Murray
Keyword(s):  
Antimicrobial Agents ◽  
Acquired Resistance ◽  
Active Agent ◽  
Bactericidal Effect ◽  
Human Pathogens ◽  
A Cell ◽  
High Level ◽  
Tract Infections ◽  
Level Resistance ◽  
Resistance Traits

Enterococci are important human pathogens that are increasingly resistant to antimicrobial agents. These organisms were previously considered part of the genus Streptococcus but have recently been reclassified into their own genus, called Enterococcus. To date, 12 species pathogenic for humans have been described, including the most common human isolates, Enterococcus faecalis and E. faecium. Enterococci cause between 5 and 15% of cases of endocarditis, which is best treated by the combination of a cell wall-active agent (such as penicillin or vancomycin, neither of which alone is usually bactericidal) and an aminoglycoside to which the organism is not highly resistant; this characteristically results in a synergistic bactericidal effect. High-level resistance (MIC, greater than or equal to 2,000 micrograms/ml) to the aminoglycoside eliminates the expected bactericidal effect, and such resistance has now been described for all aminoglycosides. Enterococci can also cause urinary tract infections; intraabdominal, pelvic, and wound infections; superinfections (particularly in patients receiving expanded-spectrum cephalosporins); and bacteremias (often together with other organisms). They are now the third most common organism seen in nosocomial infections. For most of these infections, single-drug therapy, most often with penicillin, ampicillin, or vancomycin, is adequate. Enterococci have a large number of both inherent and acquired resistance traits, including resistance to cephalosporins, clindamycin, tetracycline, and penicillinase-resistant penicillins such as oxacillin, among others. The most recent resistance traits reported are penicillinase resistance (apparently acquired from staphylococci) and vancomycin resistance, both of which can be transferred to other enterococci. It appears likely that we will soon be faced with increasing numbers of enterococci for which there is no adequate therapy.

Antimicrobial Resistance in Shigella flexneri and Shigella sonnei in Hong Kong, 1986 to 1995

1998 ◽  
Vol 42 (2) ◽  
pp. 440-443 ◽  
Author(s):  
Yiu-wai Chu ◽  
Elizabeth T. S. Houang ◽  
Donald J. Lyon ◽  
Julia M. Ling ◽  
Tak-keung Ng ◽  
...  
Keyword(s):  
Hong Kong ◽  
Antimicrobial Resistance ◽  
Nalidixic Acid ◽  
Antimicrobial Agents ◽  
Shigella Flexneri ◽  
Acid Resistance ◽  
Shigella Sonnei ◽  
Nalidixic Acid Resistance

ABSTRACT Three hundred and thirty-three Shigella isolates obtained in 1986 to 1995 were tested for their susceptibilities to 19 antimicrobial agents. Nalidixic acid resistance had emerged in 59.6% of Shigella flexneri isolates during 1994 to 1995, with all tested resistant isolates having the mutation in gyrAencoding the Ser-83 alteration. Multiresistance (resistance to four or more agents) was more common in S. flexneri than inShigella sonnei.

scholarly journals Susceptibility to patterns of ciprofloxacin among nalidixic acid-resistant Salmonella isolates collected in Banepa, Nepal from enteric fever patients

2016 ◽  
Vol 89 (2) ◽  
Author(s):  
Girija Roka ◽  
Subash Pandaya ◽  
Md. Reyad-ul Ferdous ◽  
Manson Pandey ◽  
Naba Raj Pokhrel ◽  
...  
Keyword(s):  
Nalidixic Acid ◽  
Salmonella Enterica ◽  
Enteric Fever ◽  
Inhibitory Concentration ◽  
Acid Resistance ◽  
Dilution Method ◽  
Disc Diffusion ◽  
Antimicrobial Sensitivity ◽  
Broth Dilution ◽  
Nalidixic Acid Resistance

The present study determined the susceptibility to ciprofloxacin of nalidixic acid resistant <em>Salmonella</em> (NARS) isolated from enteric fever patients at Scheer Memorial Hospital, Banepa, Nepal, from June 2012 to December 2012. The antimicrobial sensitivity to nalidixic acid and ciprofloxacin was determined using modified Kirby-Bauer disc diffusion and broth dilution method according to the guidelines of the Clinical and Laboratory Standard Institute. <em>Salmonella</em> was isolated from 34 out of 992 (3.43%) blood cultures collected during the study period, and 10 (29.4%) isolates were identified as <em>Salmonella enterica</em> serotype Typhi, while 24 (70.6%) were identified as <em>Salmonella enterica</em> serotype Paratyphi. Out of the total isolates, 31 (91.2%) were nalidixic acid-resistant <em>Salmonella</em> (NARS). Among NARS, the minimum inhibitory concentration values for ciprofloxacin ranged from 0.25 to 2 mg/L and were constantly higher than those shown by the nalidixic acid-susceptible <em>Salmonella</em>. Therefore, in typhoid <em>Salmonella</em> nalidixic acid resistance may be the indicator of decreased susceptibility to ciprofloxacin.

scholarly journals The Small Noncoding DsrA RNA Is an Acid Resistance Regulator in Escherichia coli

2004 ◽  
Vol 186 (18) ◽  
pp. 6179-6185 ◽  
Author(s):  
Richard A. Lease ◽  
Dorie Smith ◽  
Kathleen McDonough ◽  
Marlene Belfort
Keyword(s):  
Escherichia Coli ◽  
Stress Response ◽  
Resistance Genes ◽  
Acid Resistance ◽  
Dna Arrays ◽  
E Coli ◽  
Specific Mrnas ◽  
Steady State Levels ◽  
Control Translation ◽  
K 12

ABSTRACT DsrA RNA is a small (87-nucleotide) regulatory RNA of Escherichia coli that acts by RNA-RNA interactions to control translation and turnover of specific mRNAs. Two targets of DsrA regulation are RpoS, the stationary-phase and stress response sigma factor (σs), and H-NS, a histone-like nucleoid protein and global transcription repressor. Genes regulated globally by RpoS and H-NS include stress response proteins and virulence factors for pathogenic E. coli. Here, by using transcription profiling via DNA arrays, we have identified genes induced by DsrA. Steady-state levels of mRNAs from many genes increased with DsrA overproduction, including multiple acid resistance genes of E. coli. Quantitative primer extension analysis verified the induction of individual acid resistance genes in the hdeAB, gadAX, and gadBC operons. E. coli K-12 strains, as well as pathogenic E. coli O157:H7, exhibited compromised acid resistance in dsrA mutants. Conversely, overproduction of DsrA from a plasmid rendered the acid-sensitive dsrA mutant extremely acid resistant. Thus, DsrA RNA plays a regulatory role in acid resistance. Whether DsrA targets acid resistance genes directly by base pairing or indirectly via perturbation of RpoS and/or H-NS is not known, but in either event, our results suggest that DsrA RNA may enhance the virulence of pathogenic E. coli.

scholarly journals SENSITIVITY AND RESISTANCE TO ANTIMICROBIAL AGENTS ESBL-PRODUCING AND NOT PRODUCING ESBL STRAINS OF E. COLI IN PATIENTS WITH URINARY TRACT INFECTION

2019 ◽  
Vol 64 (2) ◽  
pp. 104-110
Author(s):  
N. I. Dimitrova ◽  
T. D. Gasretova ◽  
E. L. Alutina ◽  
G. G. Kharseeva
Keyword(s):  
Urinary Tract ◽  
Antimicrobial Agents ◽  
Beta Lactamase ◽  
Test Results ◽  
Beta Lactams ◽  
Esbl Production ◽  
E Coli ◽  
Amoxicillin Clavulanate ◽  
Resistant Strains ◽  
Tract Infections

As a result of the conducted researches it is shown that 44.1% of urinary tract infections (UTIS) caused by E. coli are accounted for by producers of beta-lactamase of the extended spectrum of action (ESBL). Associated resistance to fluoroquinolones and co-trimoxazole was found in 93.3% of BLRS-producing E. coli strains. All studied strains regardless of ESBL production were sensitive to imipenem, the majority showed sensitivity to ertapenem, gentamicin and resistance to doxycycline. Not producing ESBL strains of E. coli were sensitive to fosfomycin. Comparison of data obtained during testing of isolated cultures on ESBL, study of their sensitivity and resistance to beta-lactams (amoxicillin/clavulanate, ceftazidime, ceftriaxone, cefotaxime, imipenem) indicates the need to test isolates for AmpC products. To this end, during the screening test for ESBL and the method of «double disks», along with cephalosporins of III generation, it is necessary to use a phenotypic test for sensitivity to cefepime. The use of test results of E. coli isolates isolated from patients with UTIS for the production of ESBL, ampC enzymes, carbapenemase and sensitivity to AMP will improve the effectiveness of antimicrobial therapy and will help to curb the formation and spread of antimicrobial-resistant strains.

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