High macrolides and fluoroquinolones resistance rate in Mycoplasma genitalium in southern Tenerife

Abstract

Introduction. Mycoplasma genitalium (MG) is a recognized sexually transmitted pathogen. Increasing resistance to main lines of treatment (macrolides and quinolones) justifies a genetic study of mutations to improve cure rates. Material and methods. A total of 8,508 samples from April 2018 to July 2022 were processed using AllplexTM STI Essential Assay. In MG positive cases 23S rRNA V domain, gyrA and parC genes were studied. Mutations detected were checked to assess their clinical significance and medical records were reviewed to obtain demographic and treatment information. Results. Resistance study was performed on 92 samples (65 men and 27 women). In relation to the genotypic study, 28 patients presented mutations to macrolides (30.43%). Most common was A2059G (18.48%). For quinolones, 5 patients (5.43%) had clinically relevant mutations in parC gene. Of note was a patient with G295 mutation in gyrA associated with G248T in parC. Thirty subjects underwent a test of cure (TOC). Azithromycin was the most common empirical regimen and moxifloxacin the main alternative. Conclusions. High rate of resistance in our environment evidences the need for targeted therapy by genotypic study of macrolide resistance, supported by the detection of mutations in parC and gyrA to predict quinolones susceptibility and the use of TOC to evaluate treatment response

Azithromycin and moxifloxacin resistance determinants in Mycoplasma genitalium in Lleida, Spain

“…The main mutation detected in Azi-R-MG in the present study has been A2059G (55/95, 57.9%), which was the most frequent in the fore-mentioned report (55.6%). Our results are similar to those performed in other Spanish areas: a study performed in Tenerife (Canary Islands, Spain) found that 17 out of 28 samples have the A2059G mutation [ 11 ], and in a report from the south of Spain, the same mutation was described in the 50% of Azi-R-MG samples [ 9 ].…”

“…The main parC mutation detected was G248T (19/26), which agrees with previously reports [ 3 , 7 , 10 ]. In our study, we only evaluated the parC gene, although some studies reported that resistance to moxifloxacin is also due to mutations in gyrA gene [ 11 , 14 , 15 ].…”

“…The main conclusion reported in our study is that the concerning resistance to azithromycin and the increasing resistance to the second line treatment (moxifloxacin), correlated with treatment failure and the persistence of MG infection. As we previously mentioned, we did not evaluate the gyrA gene by sequencing for moxifloxacin resistance, unlike other studies [ 11 , 14 ]. More studies with a larger number of samples to relate combinations of mutations responsible for azithromycin and/or moxifloxacin treatment failure are needed.…”

“…Azithromycin inhibits protein synthesis and its resistance is associated with mutations in the region V of the 23S rRNA gene, being the point mutations at positions 2058 and 2059 the most frequent ones [ 7 ]. Azithromycin-resistant MG (Azi-R-MG) has been reported worldwide in the last years [ 2 , 5 , 8 - 11 ]. On the other hand, mutations in the parC and/or gyrA are responsible for moxifloxacin-resistant MG (Moxi-R-MG) [ 12 ].…”

“…On the other hand, mutations in the parC and/or gyrA are responsible for moxifloxacin-resistant MG (Moxi-R-MG) [ 12 ]. Novel technologies to detect these mutations which include real-time PCR are excellent options to characterize these mechanisms when sequencing is not available [ 11 ]. The evaluation of acquired moxifloxacin resistance has been conducted in several studies, but the sample size evaluated is still not sufficient [ 1 - 3 , 7 ].…”