scholarly journals 961. Prevalence and Macrolide Resistance of Mycoplasma genitalium After Initiation of HIV Preexposure Prophylaxis

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S29-S29
Author(s):  
Jens Van Praet ◽  
Sanne Steyaert ◽  
Stefaan Vandecasteele ◽  
Barbara Van Den Bergh ◽  
Hilde Mahieu ◽  
...  
Keyword(s):  
Mycoplasma Genitalium ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Sexually Transmitted ◽  
Preexposure Prophylaxis ◽  
23S Rrna Gene ◽  
Resistant Strains ◽  
Taqman Array

Abstract Background Recent evidence shows that patients using HIV preexposure prophylaxis (PrEP) have an increased rate of bacterial sexually transmitted infections (STIs), including syphilis, chlamydia, and gonorrhea. The rate of Mycoplasma genitalium infections and the susceptibility of M. genitalium in patients on PrEP have been less well described. Methods We studied all patients who started on PrEP in the AZ Sint-Jan Hospital Bruges from January 6, 2017 to January 4, 2019. Patients were screened for M. genitalium and other bacterial STIs with rectal swabs, pharyngeal swabs, first-voided urine and blood collections at baseline and quarterly intervals after initiating PrEP. TaqMan array card technology was used to detect M. genitalium and determine macrolide-resistance mediating mutations in the region V of the 23S rRNA gene (A2058G, A2059G, A2058C, and others). Patients with an STI were treated based on a national guideline. Proportions were estimated using a Generalized Estimating Equations model with independent correlation structure. Results A total of 136 males and 1 female (median age, 40 years (interquartile range (IQR), 20–79)) were included in the study. All men were gay or bisexual. The median follow-up time was 11.3 months (IQR, 4.7–15.3). In total, 117 patients (85%) used PrEP daily at their last visit. The estimated proportion of patients with M. genitalium at baseline, 3 months, 6 months, 9 months, and 12 months was 7% (95% CI 4–13), 12% (95% CI 7–20), 7% (95% CI 4–15), 6% (3–15), and 6% (2–15). Thirty-two patients (23%) tested at least once positive for M. genitalium during the study period. The estimated percentage of macrolide resistance increased from 40% (95% CI 16–70) at baseline to 71% (95% CI 44–89), 67% (95% CI 27–92), 80% (95% CI 31–97), and 75% (95% CI 24–97) at 3 months, 6 months, 9 months, and 12 months, respectively. Conclusion After initiation of PrEP, the prevalence of M. genitalium in our cohort at quarterly screening was not increased compared with baseline. However, a nonsignificant trend of an increased percentage of macrolide-resistant strains was observed. Disclosures All Authors: No reported Disclosures.

Mycoplasma genitalium acquisition and macrolide resistance after initiation of HIV pre-exposure prophylaxis in men who have sex with men

2020 ◽  
Vol 96 (6) ◽  
pp. 396-398 ◽  
Author(s):  
Jens Tomas Van Praet ◽  
Sanne Steyaert ◽  
Stefaan Vandecasteele ◽  
Barbara Van Den Bergh ◽  
Hilde Mahieu ◽  
...  
Keyword(s):  
Mycoplasma Genitalium ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Younger Age ◽  
23S Rrna Gene ◽  
Sex With Men ◽  
Taqman Array ◽  
Exposure Prophylaxis

ObjectivesRecent evidence shows that patients using HIV pre-exposure prophylaxis (PrEP) have an increased rate of bacterial STIs, including syphilis, chlamydia and gonorrhoea. Our study aimed to describe the acquisition and the susceptibility for macrolides of Mycoplasma genitalium in men who have sex with men (MSM) on PrEP.MethodsWe studied all MSM who started PrEP in the AZ Sint-Jan Hospital Bruges from 1 June 2017 to 31 March 2019 with at least one follow-up visit. Patients were screened for M. genitalium and other STIs with pooled rectal swabs, pharyngeal swabs and first-voided urine, and blood samples at baseline and quarterly intervals after initiating PrEP. TaqMan Array Card technology was used to detect M. genitalium and determine macrolide-resistance mediating mutations in region V of the 23S rRNA gene (A2058G, A2059G, A2058C and others). Patients with an STI were treated based on a national guideline.Results131 MSM (median age 40 years, range 20–79) were included in the study. The median follow-up time was 12 months (IQR 6.1–17). Baseline prevalence of M. genitalium was 6.9% and incidence rate after PrEP initiation was 28.8 per 100 person-years (95% CI 21.7 to 37.2), without significant differences in proportions between the first four quarterly intervals. All but one acquisitions were asymptomatic. Younger age and positivity for M. genitalium at baseline were significantly associated with incident M. genitalium acquisition. The observed proportion of macrolide resistance increased not significantly from 44% at baseline to 57%–86% after PrEP initiation. None of the 27 macrolide-resistant M. genitalium acquisitions could be linked to azithromycin exposure in the three preceding months.ConclusionsAfter initiation of PrEP, we found a stable incidence of almost exclusively asymptomatic M. genitalium. However, a non-significant trend of an increased percentage of macrolide-resistant strains was observed.

scholarly journals Molecular Basis of Macrolide Resistance inCampylobacterStrains Isolated from Poultry in South Korea

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Bai Wei ◽  
Min Kang
Keyword(s):  
Molecular Mechanisms ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Campylobacter Coli ◽  
Erythromycin Resistance ◽  
23S Rrna Gene ◽  
Ribosomal Protein L22 ◽  
Resistant Strains ◽  
Azithromycin Resistance

We investigated the molecular mechanisms underlying macrolide resistance in 38 strains ofCampylobacterisolated from poultry. Twenty-seven strains were resistant to azithromycin and erythromycin, five showed intermediate azithromycin resistance and erythromycin susceptibility, and six showed azithromycin resistance and erythromycin susceptibility. FourCampylobacter jejuniand sixCampylobacter colistrains had azithromycin MICs which were 8–16 and 2–8-fold greater than those of erythromycin, respectively. The A2075G mutation in the 23S rRNA gene was detected in 11 resistant strains with MICs ranging from 64 to ≥ 512μg/mL. Mutations including V137A, V137S, and a six-amino acid insertion (114-VAKKAP-115) in ribosomal protein L22 were detected in theC. jejunistrains. Erythromycin ribosome methylase B-erm(B) was not detected in any strain. All strains except three showed increased susceptibility to erythromycin with twofold to 256-fold MIC change in the presence of phenylalanine arginine ß-naphthylamide (PAßN); the effects of PAßN on azithromycin MICs were limited in comparison to those on erythromycin MICs, and 13 strains showed no azithromycin MIC change in the presence of PAßN. Differences between azithromycin and erythromycin resistance and macrolide resistance phenotypes and genotypes were observed even in highly resistant strains. Further studies are required to better understand macrolide resistance inCampylobacter.

scholarly journals In VitroActivity of the New Fluoroketolide Solithromycin (CEM-101) against Macrolide-Resistant and -Susceptible Mycoplasma genitalium Strains

2014 ◽  
Vol 58 (6) ◽  
pp. 3151-3156 ◽  
Author(s):  
Jørgen Skov Jensen ◽  
Prabhavathi Fernandes ◽  
Magnus Unemo
Keyword(s):  
Clinical Trials ◽  
Sexually Transmitted Infections ◽  
Antimicrobial Agents ◽  
Mycoplasma Genitalium ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Content Type ◽  
Sexually Transmitted

ABSTRACTMycoplasma genitaliumhas become well established as an etiological agent of sexually transmitted infections, but due to its fastidious growth requirements, only a fewM. genitaliumstrains are available to determine the MICs of currently used and new antimicrobial agents. Recent clinical trials have suggested that treatment with azithromycin has decreasing efficacy due to an increasing prevalence of macrolide resistance, and alternative treatment with moxifloxacin is similarly under pressure from emerging resistance. Thus, there is an urgent need for new antimicrobials. Thein vitroactivity of the newly developed fluoroketolide solithromycin (CEM-101) was evaluated against a collection of 40M. genitaliumstrains, including 15 with high-level macrolide resistance and 5 multidrug-resistant strains with resistance to both macrolides and quinolones. Furthermore, the MIC of solithromycin was correlated with mutations in the 23S rRNA gene and in the genes encoding ribosomal proteins L4 and L22. Thein vitroresults showed that solithromycin has activity againstM. genitaliumsuperior to that of other macrolides, doxycycline, and fluoroquinolones. Accordingly, this new fluoroketolide might be an effective option for treatment ofM. genitaliuminfections. However, the efficacy of solithromycin in clinical trials with follow-up for test of cure and detection of genotypic and phenotypic resistance needs to be evaluated prior to widespread use. In a phase 2 clinical trial, solithromycin was highly effective as a single oral dose againstC. trachomatisandNeisseria gonorrhoeae, suggesting that solithromycin could be a treatment option for several sexually transmitted infections, including in syndromic treatment of urethral and vaginal discharge.

scholarly journals Macrolide Resistance in Mycoplasma genitalium in Singapore

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S104-S104 ◽  
Author(s):  
Timothy Barkham ◽  
Wen Ying Tang ◽  
Siti Aminah Mansoor ◽  
Martin Tze-Wei Chio
Keyword(s):  
Direct Detection ◽  
Bacterial Genome ◽  
Mycoplasma Genitalium ◽  
Clinical Diagnostics ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Resistance Mutations ◽  
Transmitted Infection ◽  
Sexually Transmitted

Abstract Background Mycoplasma genitalium was first reported as a cause of non-gonococcal urethritis in 1980. It has progressed from being an ‘emerging’ sexually transmitted infection (STI) to an accepted STI. Prevalence of infection has been reported as the Netherlands 4.5%, Sweden 6.3%, UK 1.2% and France 4%. M. genitalium has the smallest known bacterial genome and was the second bacterial genome fully sequenced. It has minimal requirements and is said to approach the minimum possible for a living cell. It is extremely fastidious; only a few strains have been cultured worldwide. Diagnosis relies on direct detection. It does not have a cell wall so it is not susceptible to antibiotics such as penicillins and cephalosporins. Therapy depends on fluoroquinolones and macrolides but resistance to macrolides has been widely reported: 13% France, 18% Sweden, 40% UK, Australia and Denmark, 100% Greenland, 30% Japan. Methods Ethics approval was granted. DNA extracts left over after routine clinical diagnostics at the Department of STI Control (DSC) Clinic, Kelantan Lane, Singapore were harvested. DNA had been extracted on a Cobas 4800 instrument (Roche) from urine and urethral swabs collected for testing for Chlamydia trachomatis (CT) and Neisseria gonorrhoeae (NG). A 2-plex real-time PCR assay targeting the pdhD and mgpB genes was used to screen for M. genitalium. Samples were deemed positive if both targets were detected. If only one target was detected, the sample was retested; if reactive in either target upon retest, the sample was considered positive for M. genitalium. Positive DNA preps were then screened for macrolide resistance mutations after Sanger sequencing of the 23S rRNA gene. Results 368 anonymised DNA elutes from 254 urines and 114 urethral swabs were collected between May and July 2016. One hundred eighty-four were CT/NG positive and 184 were CT/NG negative. Sixteen (4.3%) were positive for M. genitalium. Four (25%) of these 16 samples contained macrolide resistance associated mutations; A2058T (x2), A2058G (x1), and A2059G (x1). Conclusion M. genitalium was detected in 4.3% of samples. Macrolide resistance mutations were detected in 25%, similar to international rates. Some guidelines recommend testing for resistance to guide therapy and to perform a test of cure. Disclosures All authors: No reported disclosures.

scholarly journals Ribosomal Mutations as the Main Cause of Macrolide Resistance in Campylobacter jejuni and Campylobacter coli

2011 ◽  
Vol 55 (12) ◽  
pp. 5939-5941 ◽  
Author(s):  
Mirva Lehtopolku ◽  
Pirkko Kotilainen ◽  
Marjo Haanperä-Heikkinen ◽  
Ulla-Maija Nakari ◽  
Marja-Liisa Hänninen ◽  
...  
Keyword(s):  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
Campylobacter Coli ◽  
Resistance Mutations ◽  
Content Type ◽  
Amino Acid Insertion ◽  
23S Rrna Gene ◽  
Ribosomal Protein L22 ◽  
Resistant Strains

ABSTRACTThe aim of this study was to examine macrolide resistance mutations inCampylobacterspecies. In 76 strains studied, point mutation A to G at position 2059 of the 23S rRNA gene was detected in 30 of the 33 erythromycin-resistant strains. An amino acid insertion in the ribosomal protein L22 was found in one resistant strain without a 23S rRNA mutation. The A2059G mutation is the main cause of macrolide resistance inCampylobacterspecies.

scholarly journals Clinical case of failure of josamycin in a patient with urethritis caused by Mycoplasma genitalium

2018 ◽  
Vol 94 (4) ◽  
pp. 55-59 ◽  
Author(s):  
L. M. Zubareva ◽  
I. A. Eydel’shteyn ◽  
A. V. Romanov ◽  
V. V. Evstaf’ev ◽  
R. S. Kozlov
Keyword(s):  
Antibiotic Resistance ◽  
Molecular Genetic ◽  
Mycoplasma Genitalium ◽  
23S Rrna ◽  
Routine Practice ◽  
Rrna Gene ◽  
First Line ◽  
Sexually Transmitted ◽  
23S Rrna Gene ◽  
Unknown Status

Mycoplasma genitalium is one of the obligate pathogens that cause sexually transmitted diseases. To detect this pathogen in routine practice, only molecular genetic methods are used that are also used to identify the resistance of MGE to antibiotics. The first-line drugs for the treatment of diseases caused by MGE, are tetracycline and macrolides. In recent years, many countries have increasingly recorded cases of unsuccessful therapy macrolides. Mutations that confer antibiotic resistance to macrolides for Mycoplasm genitalium are concentrated in nucleotide positions 2058 and 2059 in region V of the 23S rRNA gene. Unknown status of macrolide resistance M. genitalium can lead to the development of a persistent infection. We describe the first reported cases of clinical josamycin treatment failure from patient with ure - thritis. The reason for antibiotic resistance was a mutation in the 23S rRNA of MGE as a nucleotide substitution in position A2058G.

Mycoplasma genitalium and its resistance to azithromycin in incarcerated men from Far North Queensland

Sexual Health ◽  
2014 ◽  
Vol 11 (6) ◽  
pp. 587 ◽  
Author(s):  
Gemma Maree Daley ◽  
Darren B. Russell ◽  
Sepehr N. Tabrizi ◽  
Jimmy Twin ◽  
William J. H. McBride
Keyword(s):  
Mycoplasma Genitalium ◽  
Macrolide Resistance ◽  
Urine Samples ◽  
23S Rrna ◽  
Rrna Gene ◽  
Far North ◽  
Incarcerated Men ◽  
23S Rrna Gene

This study examined the prevalence of Mycoplasma genitalium in incarcerated men from Far North Queensland as well as the prevalence of macrolide resistance in identified isolates. Overall, eight out of 140 [5.71% (95% CI 1.82–9.60)] urine samples tested positive and two out of eight (25%) samples carried a mutation in the 23S rRNA gene associated with macrolide resistance.

scholarly journals A Novel SimpleProbe PCR Assay for Detection of Mutations in the 23S rRNA Gene Associated with Macrolide Resistance in Mycoplasma genitalium in Clinical Samples

2016 ◽  
Vol 54 (10) ◽  
pp. 2563-2567 ◽  
Author(s):  
Marianne Gossé ◽  
Hilde Lysvand ◽  
Brita Pukstad ◽  
Svein Arne Nordbø
Keyword(s):  
Melting Curve ◽  
Mycoplasma Genitalium ◽  
Curve Analysis ◽  
23S Rrna ◽  
Clinical Samples ◽  
Melting Curve Analysis ◽  
Rrna Gene ◽  
Content Type ◽  
23S Rrna Gene ◽  
Resistant Strains

Macrolide-resistant strains ofMycoplasma genitaliumare an increasing problem throughout the world, and the implementation of a rapid and sensitive assay for mutation detection to guide treatment is needed. Macrolide-resistant strains have been shown to contain base substitutions in positions 2058 and 2059 (Escherichia colinumbering) in region V of the 23S rRNA gene. In this study, we present a SimpleProbe PCR followed by melting curve analysis to differentiate between macrolide-resistant mutants and wild types. The assay was performed on 159Mycoplasma genitalium-positive samples, and the results were compared with DNA sequencing. We also looked at the prevalence of macrolide-resistant strains in a Norwegian population. Of 139 samples characterized successfully by sequencing, 54 (39%) were wild types and 85 (61%) were mutants, consisting of 59 (42%) A2059G, 24 (17%) A2058G, 1 (1%) A2058T, and 1 (1%) A2059C mutation. The melting curve analysis correctly differentiated between wild-type and mutant strains in all cases, but it could not identify the different mutant types. The SimpleProbe PCR proved to be a simple, rapid, and reliable method for the detection of macrolide-resistant isolates ofMycoplasma genitaliumin a clinical setting.

scholarly journals Detection of Macrolide Resistance in Mycoplasma pneumoniae by Real-Time PCR and High-Resolution Melt Analysis

2008 ◽  
Vol 52 (10) ◽  
pp. 3542-3549 ◽  
Author(s):  
Bernard J. Wolff ◽  
W. Lanier Thacker ◽  
Stephanie B. Schwartz ◽  
Jonas M. Winchell
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Rrna Gene ◽  
High Resolution Melt ◽  
23S Rrna Gene ◽  
Resistant Strains ◽  
V Region ◽  
Domain V

ABSTRACT Mycoplasma pneumoniae is a significant cause of community-acquired pneumonia, which is often empirically treated with macrolides or azalides such as erythromycin or azithromycin. Recent studies have discovered the existence of macrolide-resistant strains within the population that have been mapped to mutations within the domain V region of the 23S rRNA gene. Currently, identification of these resistant strains relies on time-consuming and labor-intensive procedures such as restriction fragment length polymorphism, MIC studies, and sequence analysis. The current study reports two distinct real-time PCR assays that can detect the A2063G or A2064G base mutation (A2058G or A2059G by Escherichia coli numbering) conferring macrolide resistance. By subjecting the amplicon of the targeted domain V region of the 23S rRNA gene to a high-resolution melt curve analysis, macrolide-resistant strains can quickly be separated from susceptible strains. Utilizing this method, we screened 100 clinical isolates and found 5 strains to possess mutations conferring resistance. These findings were concordant with both sequencing and MIC data. This procedure was also used successfully to identify both susceptible and resistant genotypes in 23 patient specimens. These patient specimens tested positive for the presence of M. pneumoniae by a separate real-time PCR assay, although the bacteria could not be isolated by culture. This is the first report of a real-time PCR assay capable of detecting the dominant mutations that confer macrolide resistance on M. pneumoniae, and these assays may have utility in detecting resistant strains of other infectious agents. These assays may also allow for clinicians to select appropriate treatment options more rapidly and may provide a convenient method to conduct surveillance for genetic mutations conferring antibiotic resistance.

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