scholarly journals Relationship between the severity of acne vulgaris and antimicrobial resistance of bacteria isolated from acne lesions in a hospital in Japan

2014 ◽  
Vol 63 (5) ◽  
pp. 721-728 ◽  
Author(s):  
Keisuke Nakase ◽  
Hidemasa Nakaminami ◽  
Yuko Takenaka ◽  
Nobukazu Hayashi ◽  
Makoto Kawashima ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Acne Vulgaris ◽  
Normal Skin ◽  
Resistance Mechanisms ◽  
University Hospital ◽  
23S Rrna ◽  
Rrna Gene ◽  
Severe Acne ◽  
23S Rrna Gene

Propionibacterium acnes and Staphylococcus epidermidis are normal skin inhabitants that are frequently isolated from lesions caused by acne, and these micro-organisms are considered to contribute to the inflammation of acne. In the present study, we examined the antimicrobial susceptibilities and resistance mechanisms of P. acnes and S. epidermidis isolated from patients with acne vulgaris in a university hospital in Japan from 2009 to 2010. Additionally, we analysed the relationship between the antimicrobial resistance of P. acnes and the severity of acne vulgaris. Some P. acnes strains (18.8 %; 13/69) were resistant to clindamycin. All strains had a mutation in the 23S rRNA gene, except for one strain that expressed erm(X) encoding a 23S rRNA methylase. Tetracycline-resistant P. acnes strains were found to represent 4.3 % (3/69) of the strains, and this resistance was caused by a mutation in the 16S rRNA gene. Furthermore, three strains with reduced susceptibility to nadifloxacin (MIC = 16 µg ml−1) were detected. When analysing the correlation between the antimicrobial resistance of P. acnes and S. epidermidis, more than 80 % of the patients who carried clindamycin-resistant P. acnes also carried clindamycin-resistant S. epidermidis. However, no epidemic strain that exhibited antimicrobial resistance was detected in the P. acnes strains when analysed by PFGE. Therefore, our results suggest that the antimicrobial resistance of P. acnes is closely related to antimicrobial therapy. Additionally, those P. acnes strains tended to be frequently found in severe acne patients rather than in mild acne patients. Consequently, the data support a relationship between using antimicrobial agents and the emergence of antimicrobial resistance.

scholarly journals Drug Resistance Mechanisms ofMycoplasma pneumoniaeto Macrolide Antibiotics

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Xijie Liu ◽  
Yue Jiang ◽  
Xiaogeng Chen ◽  
Jing Li ◽  
Dawei Shi ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Resistance Mechanisms ◽  
23S Rrna ◽  
Macrolide Antibiotics ◽  
Rrna Gene ◽  
Site Mutation ◽  
23S Rrna Gene ◽  
Resistant Strains ◽  
Domain V ◽  
The 16S Rrna Gene

Throat swabs from children with suspectedMycoplasma pneumoniae(M. pneumoniae) infection were cultured for the presence ofM. pneumoniaeand its species specificity using the 16S rRNA gene. Seventy-sixM. pneumoniaestrains isolated from 580 swabs showed that 70 were erythromycin resistant with minimum inhibitory concentrations (MIC) around 32–512 mg/L. FiftyM. pneumoniaestrains (46 resistant, 4 sensitive) were tested for sensitivity to tetracycline, ciprofloxacin, and gentamicin. Tetracycline and ciprofloxacin had some effect, and gentamicin had an effect on the majority ofM. pneumoniaestrains. Domains II and V of the 23S rRNA gene and the ribosomal protein L4 and L22 genes, both of which are considered to be associated with macrolide resistance, were sequenced and the sequences were compared with the corresponding sequences in M129 registered with NCBI and the FH strain. The 70 resistant strains all showed a 2063 or 2064 site mutation in domain V of the 23S rRNA but no mutations in domain II. Site mutations of L4 or L22 can be observed in either resistant or sensitive strains, although it is not known whether this is associated with drug resistance.

Emergence and dissemination of three mild outbreaks of Neisseria gonorrhoeae with high-level resistance to azithromycin in Barcelona, 2016–18

2020 ◽  
Author(s):  
P Salmerón ◽  
A Moreno-Mingorance ◽  
J Trejo ◽  
R Amado ◽  
B Viñado ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Neisseria Gonorrhoeae ◽  
23S Rrna ◽  
Phylogenomic Analysis ◽  
Rrna Gene ◽  
Snp Analysis ◽  
Enhanced Resolution ◽  
23S Rrna Gene ◽  
High Level ◽  
Level Resistance

Abstract Background Neisseria gonorrhoeae (NG) isolates with high-level azithromycin resistance (HL-AziR) have emerged worldwide in recent decades, threatening the sustainability of current dual-antimicrobial therapy. Objectives This study aimed to characterize the first 16 NG isolates with HL-AziR in Barcelona between 2016 and 2018. Methods WGS was used to identify the mechanisms of antimicrobial resistance, to establish the MLST ST, NG multiantigen sequence typing (NG-MAST) ST and NG sequence typing for antimicrobial resistance (NG-STAR) ST and to identify the clonal relatedness of the isolates with other closely related NG previously described in other countries based on a whole-genome SNP analysis approach. The sociodemographic characteristics of the patients included in the study were collected by comprehensive review of their medical records. Results Twelve out of 16 HL-AziR isolates belonged to the MLST ST7823/NG-MAST ST5309 genotype and 4 to MLST ST9363/NG-MAST ST3935. All presented the A2059G mutation in all four alleles of the 23S rRNA gene. MLST ST7823/NG-MAST ST5309 isolates were only identified in men who have sex with women and MLST ST9363/NG-MAST ST3935 were found in MSM. Phylogenomic analysis revealed the presence of three transmission clusters of three different NG strains independently associated with sexual behaviour. Conclusions Our findings support the first appearance of three mild outbreaks of NG with HL-AziR in Spain. These results highlight the continuous capacity of NG to develop antimicrobial resistance and spread among sexual networks. The enhanced resolution of WGS provides valuable information for outbreak investigation, complementing the implementation of public health measures focused on the prevention and dissemination of MDR NG.

scholarly journals Atypical Mutation in Neisseria gonorrhoeae 23S rRNA Associated with High-Level Azithromycin Resistance.

2020 ◽  
Author(s):  
Cau D. Pham ◽  
Evelyn Nash ◽  
Hsi Liu ◽  
Matthew W. Schmerer ◽  
Samera Sharpe ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Genetic Analysis ◽  
Neisseria Gonorrhoeae ◽  
23S Rrna ◽  
Rrna Gene ◽  
Neisseria Gonorrhoea ◽  
23S Rrna Gene ◽  
High Level ◽  
Azithromycin Resistance

A2059G mutation in the 23S rRNA gene is the only reported mechanism conferring high-level azithromycin resistance (HL-AZMR) in Neisseria gonorrhoea. Through U.S. gonococcal antimicrobial resistance surveillance projects, we identified four HL-AZMR gonococcal isolates lacking this mutational genotype. Genetic analysis revealed an A2058G mutation of 23S rRNA alleles in all four isolates. In vitro selected gonococcal strains with homozygous A2058G recapitulated the HL-AZMR phenotype. Taken together, we postulate that A2058G mutation confers HL-AZMR in N. gonorrhoeae.

scholarly journals Delayed Development of Linezolid Resistance in Staphylococcus aureus following Exposure to Low Levels of Antimicrobial Agents

2008 ◽  
Vol 52 (6) ◽  
pp. 1940-1944 ◽  
Author(s):  
Keith Miller ◽  
Alexander J. O'Neill ◽  
Mark H. Wilcox ◽  
Eileen Ingham ◽  
Ian Chopra
Keyword(s):  
Staphylococcus Aureus ◽  
Homologous Recombination ◽  
Antimicrobial Agents ◽  
Suppressive Effect ◽  
23S Rrna ◽  
Rrna Gene ◽  
Selection Window ◽  
23S Rrna Gene ◽  
Resistant Mutants ◽  
Selection Of

ABSTRACT The development of resistance to linezolid (LZD) in gram-positive bacteria depends on the mutation of a single 23S rRNA gene, followed by homologous recombination and gene conversion of the other alleles. We sought to inhibit this process in Staphylococcus aureus using a range of antibacterial agents, including some that suppress recombination. A model for the rapid selection of LZD resistance was developed which allowed the selection of LZD-resistant mutants with G2576T mutations in all five copies of the 23S rRNA gene following only 5 days of subculture. The emergence of LZD-resistant isolates was delayed by exposing cultures to low concentrations of various classes of antibiotics. All antibiotic classes were effective in delaying the selection of LZD-resistant mutants and, with the exception of fusidic acid (FUS) and rifampin (RIF), prolonged the selection window from 5 to ∼15 days. Inhibitors of DNA processing were no more effective than any other class of antibiotics at suppressing resistance development. However, the unrelated antimicrobials FUS and RIF were particularly effective at preventing the emergence of LZD resistance, prolonging the selection window from 5 to 25 days. The enhanced suppressive effect of FUS and RIF on the development of LZD resistance was lost in a recA-deficient host, suggesting that these drugs affect recA-dependent recombination. Furthermore, FUS and RIF were shown to be effective inhibitors of homologous recombination of a plasmid into the staphylococcal chromosome. We suggest that RIF or FUS in combination with LZD may have a role in preventing the emergence of LZD resistance.

Molecular mechanisms of macrolide and fluoroquinolone resistance among Korean isolates of Mycoplasma genitalium over a period of five years 2014–2019

2021 ◽  
Vol 70 (11) ◽  
Author(s):  
Yumi Seo ◽  
Heeyoon Park ◽  
Gilho Lee
Keyword(s):  
Genetic Diversity ◽  
Antimicrobial Resistance ◽  
Type Species ◽  
Mycoplasma Genitalium ◽  
Quinolone Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Content Type ◽  
Link Type ◽  
23S Rrna Gene

Antimicrobial resistance in Mycoplasma genitalium has become a global issue, and certain groups have a higher probability of acquiring resistant strains. Little is known about the genetic diversity and characteristics of the antimicrobial resistance-determining sites (ARDSs) of M. genitalium in the Korean population. Therefore, we examined the genetic diversity of the ARDSs of M. genitalium-positive urogenital samples obtained from Korean females (G1) and males (G2) visiting primary care clinics and DNA samples from referred males (G3) with persistent urethritis. From 2014 to 2019, 54 patients from G1, 86 patients from G2, and 68 patients from G3 were included in the study. Sanger sequencing was performed on the 2058/2059 sites in the 23S rRNA gene and quinolone resistance-determining regions (QRDRs) of M. genitalium . The rates of mutation in G1, G2, and G3 were 1.85, 5.81, and 48.53 %, respectively, for A2059G in the 23S rRNA gene (P<0.001); 1.85, 0, and 17.78 %, respectively, for M95R or I in gyrA (P<0.001); 0, 0, and 31.11 %, respectively, for D99N or G in gyrA (P<0.001); and 7.41, 16.28, and 30 %, respectively, for S83R or N or I in parC (P=0.015). A2059G significantly increased the risk of mutations at the gyrA95, gyrA99, and parC83 sites (all P<0.01). In conclusion, although the genetic diversity of the ARDSs of M. genitalium was variable among the groups, it was generally lower in isolates with macrolide resistance and higher in isolates with quinolone resistance in Korea compared with the isolates in other countries. The G3 group demonstrated increased genetic diversity at the A2059G, gyrA95, gyrA99, and parC83 sites.

scholarly journals Antimicrobial susceptibility and clarithromycin resistance patterns of Helicobacter pylori clinical isolates in Vietnam

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 671 ◽  
Author(s):  
Camelia Quek ◽  
Son T. Pham ◽  
Kieu T. Tran ◽  
Binh T. Pham ◽  
Loc V. Huynh ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Antimicrobial Resistance ◽  
Antimicrobial Susceptibility ◽  
Susceptibility Testing ◽  
23S Rrna ◽  
Rrna Gene ◽  
Clarithromycin Resistance ◽  
Resistance Patterns ◽  
23S Rrna Gene ◽  
H Pylori

Helicobacter pylori is a gastric pathogen that causes several gastroduodenal disorders such as peptic ulcer disease and gastric cancer.  Eradication efforts of H. pylori are often hampered by antimicrobial resistance in many countries, including Vietnam.  Here, the study aimed to investigate the occurrence of antimicrobial resistance among H. pylori clinical isolates across 13 hospitals in Vietnam.  The study further evaluated the clarithromycin resistance patterns of H. pylori strains.  In order to address the study interests, antimicrobial susceptibility testing, epsilometer test and PCR-based sequencing were performed on a total of 193 strains isolated from patients, including 136 children (3–15 years of age) and 57 adults (19–69 years of age).  Antimicrobial susceptibility testing showed that the overall resistance to amoxicillin, clarithromycin, levofloxacin, metronidazole, and tetracycline was 10.4%, 85.5%, 24.4%, 37.8%, and 23.8% respectively.  The distribution of minimum inhibitory concentrations (MICs) of clarithromycin-resistant strains was 85.5% with MIC >0.5 μg/mL.  The majority of the clarithromycin resistant isolates (135 of 165 subjects) have MICs ranging from 2 μg/mL to 16 μg/mL.  Furthermore, sequencing detection of mutations in 23S rRNA gene revealed that strains resistant and susceptible to clarithromycin contained both A2143G and T2182C mutations.  Of all isolates, eight clarithromycin-resistant isolates (MIC >0.5 μg/mL) had no mutations in the 23S rRNA gene.  Collectively, these results demonstrated that a proportion of clarithromycin-resistant H. pylori strains, which are not related to the 23S rRNA gene mutations, could be potentially related to other mechanisms such as the presence of an efflux pump or polymorphisms in the CYP2C19 gene.  Therefore, the present study suggests that providing susceptibility testing prior to treatment or alternative screening strategies for antimicrobial resistance is important for future clinical practice.  Further studies on clinical guidelines and treatment efficacy are pivotal for successful eradication of H. pylori infection.

scholarly journals МОНГОЛ ХҮНИЙ БАТГА ҮҮСГЭГЧ, ЭМГЭГШҮҮЛЭГЧИЙГ ТОДОРХОЙЛСОН ДҮН

2017 ◽  
pp. 56-64
Author(s):  
Оюунбилэг Н ◽  
Энхцацрал М ◽  
Болортуяа Б ◽  
Даваапүрэв Б ◽  
Чинзориг Р ◽  
...  
Keyword(s):  
Acne Vulgaris ◽  
Normal Skin ◽  
Research Result ◽  
Chronic Inflammatory Disease ◽  
The Body ◽  
Rrna Gene ◽  
Severe Acne ◽  
Demodex Mite ◽  
Staphylococcus Capitis ◽  
Complete Condition

The skin is thin layer of tissue forming the natural outer covering of the body of a person, it is protected from some infections [1]. Skin’s naturally occurring microbes are Staphylococcus, Micrococcus, Corynebacterium, Brevibacteria, Propionibacteria and Acinetobacteria [2, 3]. Acnes caused by Propionibacterium acnes (P.acnes) infection but it is commensal with other microorganisms. Sometimes P.acnes identified in normal skin. P. acnes live deep within follicles oil-bag and pores, away from the surface of the skin. Elevated production of sebum by hyperactive sebaceous glands (sebaceous hyperplasia) or blockage of the follicle can cause P. acnes to grow and multiply. Acne is chronic inflammatory disease affecting the pilosebaceous follicle [18]. Skin infections are decreasing immunity of certain parts of the body.Acne severity correlated highly with increasing stress and harmful for self-confidence [4]. The most countries had study about their acne patient’s microflora and pathogenic microbes. Currently, our country has not been study yet. Therefore, we carried out research to determine the relationship between Mongolian samples of acne and acne causing their pathogenic microorganisms.We were interested microflora of Mongolian acne patients. We took samples by swab and obtained from 40 acne patients. The acne patients were 25 females and 15 males with teenagers of 57.5% and 25-52 years old of 42.5%. The samples were cultured on modified GAM agar (Nissui, Japan) under anaerobic conditions at 37°C for 96 hr. P. acnes was identified by PCR and the 16s rRNA gene sequences. Also the samples were cultured on Nutrient agar (Biolab, Hungary), Tryptose soy agar (Biolab, Hungary) in aerobic conditions at 37°C for 48 hr. Staphylococcus epidermidis, Staphylococcus aureus, Micrococcus spp, Staphylococcus capitis and Staphylococcus cohnii were identified by API-STAPH-IDENT (Biomerieux, France). We detected demodex mite by microscope.We were found demodex 45% of all patient. All patients had S.epidermidis, P.acnes had 30% of them, S.aureus in 47.5%, Micrococcus, spp in 27.5%, S.Capitis and S.Cohnii each 5%. We compared our research result with Germany, French, Indian and Japanese researcher’s similar studies. Whereas our research results were more than European acne patients such as P.acnes 16 percent and Staphylococcus 64 percent. However Mongolian acne patient’s microorganisms determined more than European acne patients, P.acnes determined 32 percent lower than Japan and Indian patients. Even though Staphylococcus was 47 percent more than their result.Our study shows in causing acne, especially severe acne is associated cases demodex mite, P. Acnes, S.epidermidis. And the strains of bacteria S.aureus, Micrococcus spp conditions from acne were related degree occur in acne but complications. Appearance acne bacteria S. capitis, S.cohnii samples, but only casually. Mongolian people causing acne, pathogenic species had a relatively high percent of people in other countries, S.epidermidis acne compared to the complete condition pathogenic type of acne vulgaris.

scholarly journals Development of a Microelectronic Chip Array for High-Throughput Genotyping of Helicobacter Species and Screening for Antimicrobial Resistance

2005 ◽  
Vol 10 (3) ◽  
pp. 235-245 ◽  
Author(s):  
James Z. Xing ◽  
Chris Clarke ◽  
Lijun Zhu ◽  
Stephan Gabos
Keyword(s):  
Antimicrobial Resistance ◽  
16S Rrna ◽  
Tetracycline Resistance ◽  
Rrna Genes ◽  
23S Rrna ◽  
Rrna Gene ◽  
Nucleotide Polymorphisms ◽  
23S Rrna Gene ◽  
23S Rrna Genes ◽  
H Pylori

A microelectronic array assay was developed to specifically genotype Helicobacter pylori versus Helicobacter heilmannii and to determine antimicrobial resistance. Helicobacter 16S rRNA and 23S rRNA genes were specifically generated with Helicobacter genus-specific primers, respectively. The single-nucleotide polymorphisms (SNPs) in 16S rRNA, 268T specific in the H. pylori sequence, and 263A specific in H. heilmannii were used as molecular markers for identification of H. pylori and H. heilmannii, respectively. A triple-base-pair resistant mutation, AGA965-967TTC in 16S rRNA, is known to be responsible for H. pylori tetracycline resistance and was detected to identify resistant strains. H. pylori macrolide resistance was determined by the identification of 3 defined mutations in the 23S rRNA gene using the same method. The assay could be directly used to detect H. pylori in feces. The assay performs multiple determinations, including identification of Helicobacter species and antibiotic resistances, on the same microelectronic platform and is highly amenable to the development of other DNA-based assays.

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