Levels of Mycoplasma genitalium Antimicrobial Resistance Differ by Both Region and Gender in the State of Queensland, Australia: Implications for Treatment Guidelines

Abstract

Mycoplasma genitaliumis frequently associated with urogenital and rectal infections, with the number of cases of macrolide-resistant and quinolone-resistantM. genitaliuminfection continuing to increase. In this study, we examined the levels of resistance to these two common antibiotic treatments in geographically distinct locations in Queensland, Australia. Samples were screened for macrolide resistance-associated mutations using a commercially available kit (ResistancePlus MG; SpeeDx), and quinolone resistance-associated mutations were identified by PCR and DNA sequencing. Comparisons between antibiotic resistance mutations and location/gender were performed. The levels ofM. genitaliummacrolide resistance were high across both locations (62%). Quinolone resistance mutations were found in ∼10% of all samples, with a number of samples harboring mutations conferring resistance to both macrolides and quinolones. Quinolone resistance was higher in southeast Queensland than in north Queensland, and this was consistent in both males and females (P = 0.007). TheM. genitaliumisolates in rectal swab samples from males harbored high levels of macrolide (75.9%) and quinolone (19%) resistance, with 15.5% harboring resistance to both classes of antibiotics. Overall, the lowest observed level of resistance was to quinolones in females from north Queensland (1.6%). These data highlight the high levels of antibiotic resistance inM. genitaliumisolates within Queensland and the challenges faced by sexually transmitted infection clinicians in managing these infections. The data do, however, show that the levels of antibiotic resistance may differ between populations within the same state, which has implications for clinical management and treatment guidelines. These findings also support the need for ongoing antibiotic resistance surveillance and tailored treatment.

Macrolide and fluoroquinolone associated mutations in Mycoplasma genitalium in a retrospective study of male and female patients seeking care at an STI Clinic in Guangzhou, China, 2016-2018.

“…NC_000908.2) was used as a reference strain. Amino acid changes in the QRDRs of the gyrA and parC genes in this study were compared with previous studies [6,24,26,33,38,41].…”

“…The uoroquinolone moxi oxacin, another medication extensively used as a second-line bactericidal, has a cure rate approaching 100% in infections with susceptible strains [36]. In recent years, the e cacy of moxi oxacin failure rate has also been noted, rst in Japan [7] and later in Australia [37][38][39]. The elimination rate of moxi oxacin for M. genitalium infection has decreased from 100% to 89% since 2010 [37].…”

“…AMR studies of uoroquinolone resistance in M. genitalium DNA tend to amplify the quinolone-resistance determining region (QRDR) of the gyrA gene and the corresponding region of the parC gene from M. genitalium DNA [47]. Antibiotic resistance of M. genitalium to both macrolides and quinolones have been found in Japan, Australia, and New Zealand since 2008 [33,38,44,48,49]. This disturbing trend suggests that the AMR dilemma attributable to M. genitalium is spreading and becoming even more virulent [33,44,48,49].…”

Molecular Typing of Mycoplasma genitalium-Positive Specimens Discriminates between Persistent and Recurrent Infections in Cases of Treatment Failure and Supports Contact Tracing

“…Nonetheless, few studies have assessed the role of these different scenarios in treatment failure. Investigating the molecular epidemiology of M. genitalium may shed light on these events and improve control of this infection [4,5].…”

Molecular detection of Mycoplasma genitalium in endocervical swabs and associated rates of macrolide and fluoroquinolone resistance in Hong Kong

“…Although the populations have differed among studies, similarly high rates of macrolide resistance (Table 4). 3,[23][24][25][26][27][28] Several studies also demonstrated consistent increases in resistance rates over time. 3,28,29 All mutations detected in this study have been described previously; while C184T (Pro62Ser) in parC is of unknown significance, others are known to confer antibiotic resistance leading to higher minimal inhibitory concentrations and treatment failure.…”