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Mycoplasma genitalium in Symptomatic Male Urethritis: Macrolide Use Is Associated With Increased Resistance.

Authors :
Li Y
Su X
Le W
Li S
Yang Z
Chaisson C
Madico G
Gong X
Reed GW
Wang B
Rice PA
Source :
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America [Clin Infect Dis] 2020 Feb 14; Vol. 70 (5), pp. 805-810.
Publication Year :
2020

Abstract

Background: Mycoplasma genitalium (MG) causes symptomatic urethritis in men, and can infect alone or together with other sexually transmitted infection (STI) agents.<br />Methods: The prevalence of MG and other STIs was determined in 1816 men with symptomatic urethritis. Resistance of MG to macrolides and fluoroquinolones was determined by sequencing; the impact of recent antimicrobial usage on the distribution of MG single or mixed infections was determined.<br />Results: Overall, prevalence of MG infection was 19.7% (358/1816). Fifty-four percent (166/307) of MG infections occurred alone in the absence of other STI agents. Men with single MG infection self-administered or were prescribed antibiotics more often in the 30 days prior to enrollment than subjects with urethritis caused by MG coinfection (P < .0001). Higher rates (96.7%) of infection with macrolide resistance in MG were identified in men who had taken macrolides prior to enrollment (P < .03). Overall, 88.9% (303/341) of 23S ribosomal RNA (rRNA) genes contained mutations responsible for macrolide resistance; 89.5% (308/344) of parC and 12.4% (42/339) of gyrA genes had mutations responsible for fluoroquinolone resistance. Approximately 88% (270/308) of MG had combined mutations in 23S rRNA and parC genes; 10.4% (32/308) had mutations in all 3 genes.<br />Conclusions: MG was the single pathogen identified in 11% of men with symptomatic urethritis. Overall, nearly 90% of MG infections were resistant to macrolides and fluoroquinolones. Men who took macrolides in the 30 days prior to enrollment had higher rates (97%) of macrolide-resistant MG. Resistance was associated with numerous mutations in 23SrRNA, parC, and gyrA genes.<br /> (© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.)

Details

Language :
English
ISSN :
1537-6591
Volume :
70
Issue :
5
Database :
MEDLINE
Journal :
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
Publication Type :
Academic Journal
Accession number :
30972419
Full Text :
https://doi.org/10.1093/cid/ciz294