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

• Published in: Clinical infectious diseases Vol. 70; no. 5; pp. 805 - 810
• Main Authors: Li, Yang, Su, Xiaohong, Le, Wenjing, Li, Sai, Yang, Zhaoyan, Chaisson, Christine, Madico, Guillermo, Gong, Xiangdong, Reed, George W, Wang, Baoxi, Rice, Peter A
• Format: Journal Article
• Language: English
• Published: US Oxford University Press 14.02.2020
• Subjects: and Commentaries; Anti-Bacterial Agents - pharmacology; Anti-Bacterial Agents - therapeutic use; DNA, Bacterial; Drug Resistance, Bacterial; Humans; Macrolides - pharmacology; Macrolides - therapeutic use; Male; Mycoplasma genitalium - genetics; Mycoplasma Infections - drug therapy; Mycoplasma Infections - epidemiology; RNA, Ribosomal, 23S - genetics; Urethritis - drug therapy; Urethritis - epidemiology; urethritis; macrolide/quinolone resistance; Mycoplasma genitalium
• ISSN: 1058-4838; 1537-6591; 1537-6591
• DOI: 10.1093/cid/ciz294

Abstract Background Mycoplasma genitalium (MG) causes symptomatic urethritis in men, and can infect alone or together with other sexually transmitted infection (STI) agents. 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. 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. 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. Mycoplasma genitalium (MG) can be the only cause of symptomatic urethritis in men who have taken ineffective antibiotics. In Nanjing, China, nearly 90% of MG infections were resistant to macrolides (and fluoroquinolones), implicating possible antibiotic selection that resulted in persistent infection.