Dog/cat-origin quinolone-resistant Streptococcus agalactiae isolates with point mutations in quinolone resistance-determining regions: Relatedness with clonal complex 10

2021 ◽  
Author(s):  
Takahiro Maeda ◽  
Yuzo Tsuyuki ◽  
Mieko Goto ◽  
Haruno Yoshida ◽  
Tomohiro Fujita ◽  
...  
Keyword(s):  
Streptococcus Agalactiae ◽  
Clonal Complex ◽  
Point Mutations ◽  
Quinolone Resistance

scholarly journals Mechanisms of quinolone resistance and implications for human and animal health

2010 ◽  
Vol 64 (3-4) ◽  
pp. 277-285
Author(s):  
Maja Velhner ◽  
Gordana Kozoderovic ◽  
Zora Jelesic ◽  
Igor Stojanov ◽  
Radomir Ratajac ◽  
...  
Keyword(s):  
Veterinary Medicine ◽  
Antimicrobial Resistance ◽  
Protein Interactions ◽  
Bacterial Infections ◽  
Animal Health ◽  
Point Mutations ◽  
Inhibitory Effect ◽  
Quinolone Resistance ◽  
Topoisomerase Iv ◽  
Target Enzyme

Quinolone antibiotics have been widely used in human and veterinary medicine. This has caused the development of resistance and difficulties in the treatment of complicated bacterial infections in humans. The resistance to quinolones develops due to chromosome mutations and it can also be transferred by plasmids. The target enzyme for quinolones in Gram-negative bacteria is Gyrasa A, while the target enzyme in Grampositive bacteria is mostly topoisomerase IV. Gyrase A consists of two subunits encoded by genes gyrA and gyrB. The function of the enzyme is to introduce negative super coiling in DNA and therefore is essential for the replication of bacteria. Quinolone resistance develops if point mutations at 83 and/or 87 codon are introduced on gyrA. Establishing a minimal inhibitory concentration (MIC) to this group of antimicrobials will reveal possible mutations. Recently it was discovered that quinolone resistance is transmittable by plasmid termed PMQR (plasmid mediated quinolone resistance). The target gene marked qnr encodes a pentapeptide repeat family protein. Pentapeptide repeats form sheets, involved in protein-protein interactions. Qnr protein binds to GyrA protecting the enzyme from the inhibitory effect of ciprofloxacin. The distribution of qnr related resistance is higher in humans than in animals. In poultry, however, this type of resistance is present more than in other animals. Plasmid mediated resistance contributes to the faster spread of quinolone resistance. Proper food handling will significantly contribute to decreasing the risk from infection to which people are exposed. In medical and veterinary laboratories antimicrobial resistance monitoring in clinical and environmental isolates is advised. Since correlation between antibiotics application and antimicrobial resistance is often suggested, antimicrobial use must be under strict control of the authorities both in human and in veterinary medicine. .

scholarly journals Mutational Analysis of Quinolone-Resistant Determining Region gyrA and parC Genes in Quinolone-Resistant ESBL-Producing E. Coli

2021 ◽  
Vol 20 (3) ◽  
Author(s):  
Hairul Aini Hamzah ◽  
Rahmatullah Sirat ◽  
Mohammed Imad A. Mustafa Mahmud ◽  
Roesnita Baharudin
Keyword(s):  
Mutational Analysis ◽  
Single Point ◽  
Point Mutations ◽  
Multidrug Resistant ◽  
Quinolone Resistance ◽  
Resistant Bacteria ◽  
Single Point Mutation ◽  
Phenotypic Resistance ◽  
Drug Effectiveness ◽  
E Coli

 Introduction: Co-resistance to quinolones among extended spectrum β[1]lactamase (ESBL)-producing E. coli commonly occurs in clinical settings. Quinolones act on DNA gyrase and DNA topoisomerase enzymes, which are coded by gyrA and parC genes, thus any mutation to the genes may affect the drug effectiveness. The objective of the study was to characterize gyrA and parC genes in quinolone-resistant E. coli isolates and correlated the mutations with their phenotypic resistance. Materials and Methods: Thirty-two quinolone-resistant (QR) and six quinolone-sensitive (QS) ESBL-E. coli isolates were identified by antibiotic susceptibility and minimum inhibitory concentration tests. Bioinformatics analysis were conducted to study any mutations occurred in the genes and generate their codon compositions. Results: All the QR ESBL-E. coli isolates were identified as multidrug-resistant bacteria. A single point mutation in the quinolone resistance-determining region (QRDR) of gyrA, at codon 83, caused the substitution amino acid Ser83Leu. It is associated with a high level of resistance to nalidixic acid. However, double mutations Ser83Leu and Asp87Asn in the same region were significantly linked to higher levels of resistance to ciprofloxacin. Cumulative point mutations in gyrA and/or in parC were also correlated significantly (p<0.05) to increased resistance to ciprofloxacin. Conclusion: Together, the findings showed that the mutations in gyrA and parC genes handled the institution of intrinsic quinolone resistance in the ESBL-E. coli isolates. Thus, vigilant monitoring for emergence of new mutation in resistance genes may give an insight into dissemination of QR ESBL-E. coli in a particular region.

Development of a rapid assay for screening point mutations associated with quinolone resistance in the Pseudomonas aeruginosa parC gene

2000 ◽  
Vol 6 (1) ◽  
pp. 26-29 ◽  
Author(s):  
Takashi Deguchi ◽  
Masayoshi Yamaha ◽  
Masahiro Nakano ◽  
Mitsuru Yasuda ◽  
Yoshinori Nishino ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Point Mutations ◽  
Quinolone Resistance ◽  
Rapid Assay

scholarly journals First Streptococcus agalactiae Isolates Highly Resistant to Quinolones, with Point Mutations in gyrA and parC

2003 ◽  
Vol 47 (11) ◽  
pp. 3605-3609 ◽  
Author(s):  
Yoshiaki Kawamura ◽  
Hiromitsu Fujiwara ◽  
Noriko Mishima ◽  
Yuko Tanaka ◽  
Ayako Tanimoto ◽  
...  
Keyword(s):  
Amino Acid ◽  
Sequence Analysis ◽  
Amino Acid Sequence ◽  
Streptococcus Agalactiae ◽  
Double Point ◽  
Point Mutations ◽  
Comparative Sequence Analysis ◽  
Hemolytic Streptococcus ◽  
Beta Hemolytic Streptococcus ◽  
Resistant Strains

ABSTRACT Three isolates of Streptococcus agalactiae highly resistant to multiple fluoroquinolones were isolated in Japan. Compared with susceptible strains of S. agalactiae, these quinolone-resistant strains had double point mutations within the quinolone resistance-determining regions of gyrA and parC; Ser-81 was changed to Leu (TCA → TTA) in the amino acid sequence deduced from gyrA, and Ser-79 was changed to Phe (TCC → TTC) in the amino acid sequence deduced from parC. Comparative sequence analysis revealed the possibility of gene transfer between S. agalactiae and another beta-hemolytic streptococcus, Streptococcus difficile.

scholarly journals Increased quinolone resistance among typhoid Salmonella isolated from Egyptian patients

2014 ◽  
Vol 8 (05) ◽  
pp. 661-665 ◽  
Author(s):  
Fatma O.I. Saleh ◽  
Hazem A Ahmed ◽  
Rasha M.M. Khairy ◽  
Sayed F. Abdelwahab
Keyword(s):  
Enteric Fever ◽  
Point Mutations ◽  
Quinolone Resistance ◽  
Limited Data ◽  
Gyra Gene ◽  
Egyptian Patients ◽  
Resistance Patterns ◽  
Stool Samples ◽  
Gyra Mutation ◽  
Over Time

Introduction: Typhoid fever is endemic in Egypt; and quinolones are the empirical treatment of choice. There are very limited data reporting quinolone resistance among Egyptian typhoidal Salmonella isolates. We previously reported that all typhoidal Salmonella were sensitive to quinolones. This study aimed to isolate and identify typhoidal Salmonella from cases suffering from enteric fever at Minia Governorate, Egypt, determine their quinolone resistance patterns, compare them to those reported 20 years ago, and test gyrA mutation as a possible mechanism for quinolone resistance. Methodology: Stool samples from Widal-positive subjects were screened by culture on suitable media and were identified biochemically. The identified isolates were tested for resistance against three representatives of the first three quinolone generations, namely nalidixic acid (NAL), levofloxacin (LEV), and norfloxacin (NOR). The gyrA gene was amplified and sequenced to detect point mutation(s) conferring quinolone resistance. Results: Out of 230 stool samples (from patients with Widal anti-O titers of ≥ 1/160), 40 isolates were S. enterica serovar Typhi (97.5%) and Paratyphi A (2.5%). Six (15%) isolates were resistant to at least one of the quinolones, compared to 0% in 1993. In this regard, 15%, 7.5%, and 2.5% of the isolates were resistant to NAL, both NAL and LEV, and all three quinolones tested, respectively. Sequencing of the gyrA gene revealed point mutations at position 83 and/or 87 of the gyrA gene only among the resistant isolates. Conclusion: There has been an increase in quinolone-resistant typhoidal Salmonella in Egypt over time.

scholarly journals Epidemic and molecular characterization of fluoroquinolone-resistant Shigella dysenteriae 1 isolates from calves with diarrhea

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Mingze Cao ◽  
Weiwei Wang ◽  
Liwei Zhang ◽  
Guanhui Liu ◽  
Xuzheng Zhou ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Virulence Genes ◽  
Point Mutations ◽  
Multidrug Resistant ◽  
Gansu Province ◽  
Quinolone Resistance ◽  
Shigella Dysenteriae ◽  
Fluoroquinolone Resistance ◽  
And Control

Abstract Background The widespread distribution of antimicrobial-resistant Shigella has become a recurrent challenge in many parts of the developing world. Previous studies indicate that the host of Shigella has expanded from humans to animals. This study aimed to investigate the prevalence of fluoroquinolone resistance and associated molecular characterization of S. dysenteriae 1 isolated from calves. Results All 38 unduplicated S. dysenteriae 1 isolates were collected from calves in Gansu Province from October 2014 to December 2016. According to MLST and PFGE analysis, these isolates were separated into 4 and 28 genotypes, respectively. The most common STs identified were ST228 (34.21%, 13/38) and ST229 (39.47%, 15/38), which were first found in the present study. All isolates harbored virulence genes, and the incidence of the seven virulence genes were ipaH (100%), ipaBCD (92.11%), stx (73.68%), ial (57.89%), sen (28.95%), set1A and set1B (0%). According to the results of antimicrobial susceptibilities, 76.32% (29/38) were resistant to fluoroquinolone and showed multidrug resistance. In a study on the polymorphism of quinolone resistance–determining region (QRDR) of gyrA/B and parC/E genes, we identified two mutations in gyrA (Ser83 → Leu and Asp87 → Asn) and parC (Ser80 → Ile and Ser83 → Leu), respectively. Among them, 55.17% (16/29) of resistant strains had the gyrA point mutations (Ser83 → Leu) and parC point mutation (Ser83 → Leu). Moreover, 41.38% (12/29) of isolates had all five point mutations of gyrA and parC. In addition, the prevalence of the plasmid-mediated quinolone resistance (PMQR) determinant genes was also investigated. All 29 fluoroquinolone-resistant isolates were positive for the aac (6′)-Ib-cr gene but negative for qepA, except for SD001. In addition, only 6 (20.69%, 6/29) isolates harbored the qnr gene, including two with qnrB (6.90%, 2/29) and four with qnrS (13.79%, 4/29). Conclusion Given the increased common emergence of multidrug resistant isolates, uninterrupted surveillance will be necessary to understand the actual epidemic burden and control this infection.

scholarly journals Epidemic and molecular characterization of fluoroquinolone-resistant Shigella dysenteriae 1 isolates from calves with diarrhea

2020 ◽  
Author(s):  
Mingze Cao ◽  
Weiwei Wang ◽  
Liwei Zhang ◽  
Guanhui Liu ◽  
Xuzheng Zhou ◽  
...  
Keyword(s):  
Molecular Characterization ◽  
Virulence Genes ◽  
Point Mutations ◽  
Multidrug Resistant ◽  
Gansu Province ◽  
Quinolone Resistance ◽  
Shigella Dysenteriae ◽  
Fluoroquinolone Resistance ◽  
And Control

Abstract Background: The widespread distribution of antimicrobial-resistant Shigella has become a recurrent challenge in many parts of the developing world. Previous studies indicate that the host of Shigella has expanded from humans to animals. This study aimed to investigate the prevalence of fluoroquinolone resistance and associated molecular characterization of S. dysenteriae 1 isolated from calves. Results: All 38 unduplicated S. dysenteriae 1 isolates were collected from calves in Gansu Province from October 2014 to December 2016. According to MLST and PFGE analysis, these isolates were separated into 4 and 28 genotypes, respectively. The most common STs identified were ST228 (34.21%, 13/38) and ST229 (39.47%, 15/38), which were first found in the present study. All isolates harbored virulence genes, and the incidence of the seven virulence genes were ipaH (100%), ipaBCD (92.11%), stx (73.68%), ial (57.89%), sen (28.95%), set1A and set1B (0%). According to the results of antimicrobial susceptibilities, 76.32% (29/38) were resistant to fluoroquinolone and showed multidrug resistance. In a study on the polymorphism of quinolone resistance–determining region (QRDR) of gyrA/B and parC/E genes, we identified two mutations in gyrA (Ser83→Leu and Asp87→Asn) and parC (Ser80→Ile and Ser83→Leu), respectively. Among them, 55.17% (16/29) of resistant strains had the gyrA point mutations (Ser83→Leu) and parC point mutation (Ser83→Leu). Moreover, 41.38% (12/29) of isolates had all five point mutations of gyrA and parC. In addition, the prevalence of the plasmid-mediated quinolone resistance (PMQR) determinant genes was also investigated. All 29 fluoroquinolone-resistant isolates were positive for the aac(6’)-Ib-cr gene but negative for qepA, except for SD001. In addition, only 6 (20.69%, 6/29) isolates harbored the qnr gene, including two with qnrB (6.90%, 2/29) and four with qnrS (13.79%, 4/29). Conclusion: Given the increased common emergence of multidrug resistant isolates, uninterrupted surveillance will be necessary to understand the actual epidemic burden and control this infection.

scholarly journals An international invasive meningococcal disease outbreak due to a novel and rapidly expanding serogroup W strain, Scotland and Sweden, July to August 2015

2016 ◽  
Vol 21 (45) ◽  
Author(s):  
Jay Lucidarme ◽  
Kevin J Scott ◽  
Roisin Ure ◽  
Andrew Smith ◽  
Diane Lindsay ◽  
...  
Keyword(s):  
Meningococcal Disease ◽  
Clonal Complex ◽  
Point Mutations ◽  
Case Fatality ◽  
Transcriptional Regulator ◽  
The Novel ◽  
The Past ◽  
The United Kingdom ◽  
Genomic Typing ◽  
Close Contacts

The 23rd World Scout Jamboree in 2015 took place in Japan and included over 33,000 scouts from 162 countries. Within nine days of the meeting ending, six cases of laboratory-confirmed invasive serogroup W meningococcal disease occurred among scouts and their close contacts in Scotland and Sweden. The isolates responsible were identical to one-another by routine typing and, where known (4 isolates), belonged to the ST-11 clonal complex (cc11) which is associated with large outbreaks and high case fatality rates. Recent studies have demonstrated the need for high-resolution genomic typing schemes to assign serogroup W cc11 isolates to several distinct strains circulating globally over the past two decades. Here we used such schemes to confirm that the Jamboree-associated cases constituted a genuine outbreak and that this was due to a novel and rapidly expanding strain descended from the strain that has recently expanded in South America and the United Kingdom. We also identify the genetic differences that define the novel strain including four point mutations and three putative recombination events involving the horizontal exchange of 17, six and two genes, respectively. Noteworthy outcomes of these changes were antigenic shifts and the disruption of a transcriptional regulator.

scholarly journals Fluoroquinolone resistance of Staphylococcus epidermidis isolated from healthy conjunctiva and analysis of their mutations in quinolone-resistance determining region

2020 ◽  
Author(s):  
Jung Youb Kang ◽  
Woonhyung Lee ◽  
Bo Hyeon Jeong ◽  
Indal Park ◽  
Sang Joon Lee
Keyword(s):  
Staphylococcus Epidermidis ◽  
Point Mutations ◽  
Gene Mutations ◽  
Resistance Rate ◽  
Quinolone Resistance ◽  
Fluoroquinolone Resistance ◽  
Dilution Method ◽  
Multiple Point ◽  
Positive Rate ◽  
Resistant Strains

Abstract Background: S. epidermidis is the most common pathogen in postoperative endophthalmitis and causes various infectious eye diseases. However, there is very little information on fluoroquinolone antibiotic resistance to S. epidermidis identified in conjunctival microbe and analysis of related genes. Here, the authors investigated the rate of resistance to fluoroquinolones of Staphylococcus epidermidis isolated from normal conjunctival microbes and mutations in the quinolone-resistance determining region (QRDR).Methods: 377 eye samples from 187 patients who underwent intravitreal injection and cataract surgery were included. Before the procedure, specimens were taken from the bilateral lower conjunctival sacs using a cotton swab and cultured. The cultures were identified and gyrA, gyrB, parC, and parE gene mutations of QRDR were confirmed by DNA extraction from resistant strains of S. epidermidis with a micro-dilution method using ciprofloxacin, levofloxacin, and moxifloxacin.Results: The culture positive rate was 61.8% (231) for 374 eye samples. Of the 303 total strains cultured, S. epidermidis was the most common with 33.7% (102). Ten types of gene mutations were observed in the resistant S. epidermidis of 21 strains. One-point mutation was observed mainly in gyrA and parC, and a small number of mutations were observed in parE in the form of a double point mutations. When there were multiple point mutations in both gyrA and parC, the highest minimum inhibitory concentration (MIC) was observed.Conclusions: The quinolone resistance rate of S. epidermidis increased in comparison with previous studies, and resistant S. epidermidis showed mostly QRDR mutations, which were mainly found in gyrA and parC, and showed strong resistance when mutated in both genes.

Dominance of clonal complex 10 among the levofloxacin-resistant Streptococcus agalactiae isolated from bacteremic patients in a Korean hospital

2014 ◽  
Vol 20 (8) ◽  
pp. 509-511 ◽  
Author(s):  
Hyejin Ryu ◽  
Yeon-Joon Park ◽  
Yong-kyun Kim ◽  
Jiyoung Chang ◽  
Jin Kyung Yu
Keyword(s):  
Streptococcus Agalactiae ◽  
Clonal Complex
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