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To the Editor-in-Chief
It has recently been reported that 13% of men who have sex with men (MSM) attending a sexual health clinic were coinfected with Chlamydia trachomatis and Mycoplasma genitalium in the rectum,1 a site that has been described as a reservoir for asymptomatic M. genitalium infection.2
Public Health England’s (PHE) reference laboratory detects mutations associated with macrolide and fluoroquinolone resistance in M. genitalium and the lymphogranuloma venereum (LGV) genovars of C. trachomatis. In 2018, 2491 specimens were submitted to the reference laboratory for M. genitalium resistance testing where local assays were unavailable (488/2491 (19.6%) M. genitalium positive). Only 16 (0.6%) were documented from ano-rectal sites, probably because UK guidelines do not recommend asymptomatic screening for M. genitalium.3 Due to the nature of LGV, rectal swabs from MSM are the specimen-type primarily received.
The following study aimed to inform about the prevalence of M. genitalium/C. trachomatis coinfections and the predicted M. genitalium antimicrobial resistance in specimens referred for LGV detection between 6 December 2018 and 9 January 2019 from laboratories across England and Wales. Residual genomic DNA from 250 C. trachomatis-positive clinical specimens (229/250, 91.6% male, 187/250, 74.8% aged >25 years, 212/250, 84.8% rectal swabs and 20/250, 8.0% LGV positive) was tested for the presence of M. genitalium. Testing was performed using a modified multiplex real-time PCR targeting intrinsic M. genitalium genes; MgPa and gap. M. genitalium 23S rRNA and parC genes were then amplified in positive specimens, followed by Sanger sequencing to ascertain genetic susceptibility to macrolide and fluoroquinolone antimicrobials, respectively.
M. genitalium-specific DNA was detected in 23/250 (9.2%) C. trachomatis-positive (1/23, 4.4% LGV positive) specimens tested. Mutations associated with resistance to macrolides were found in 60.9% M. genitalium-positive specimens (table 1). The S83R parC mutation, previously correlated with clinical treatment failure with fluoroquinolones,4 was detected in one specimen (1/23, 4.4%) and the D87V mutation,5 of unknown clinical significance, was detected in another specimen (table 1). A macrolide resistance-associated mutation in the 23S rRNA gene was also detected in the latter specimen.
The prevalence of M. genitalium/C. trachomatis coinfections in this study (9.2%) was slightly lower than has been previously reported (13%).1 However, a high prevalence of macrolide resistance was detected, comparable with that detected by the PHE reference service overall in 2018 (table 1). Further to this, evidence of resistance to fluoroquinolones was also found. Data on clinical presentation was unavailable; therefore, it is not possible to comment on how or if coinfection with M. genitalium contributed to presence of symptoms. In a recent report, only 6.7% of rectal M. genitalium infections were symptomatic; however, in a third of the specimens, another STI pathogen was also detected.6 Diagnosis and treatment of M. genitalium at this site, while there is a lack of clarity on the organisms natural history and sequalae, against a background of high resistance, could have a negative impact on antimicrobial stewardship and possible harm to the patient. Detection of high levels of macrolide resistance in these specimens re-enforces evidence for removal of single dose azithromycin from all STI management guidelines.
Handling editor Anna Maria Geretti
Contributors RP was responsible for the first draft of the letter; all authors commented and edited subsequent versions.
Funding This study was funded by PHE to inform reference service development.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Not commissioned; internally peer reviewed.
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