Mycoplasma hominis is one of the smallest pathogens responsible for a diverse range of infections, including non-gonococcal urethritis, infertility, chorioamnionitis, adverse pregnancy outcomes and neonatal diseases (Ahmed et al., 2021). M. hominis lacks the cell wall and hydrolyzes arginine as its major energy source (Pereyre et al., 2009). It has one of the smallest genomes among self-replicating organisms (0.54–0.83 Mbp) and exhibits a low G + C content (26.5%−27.4%). As a commensal of the genital tract, approximately 21–53% of asymptomatic sexually active women are colonized with M. hominis (Waites et al., 2012), it sometimes contributes to urogenital tract infections, including conditions like pelvic inflammation and cervicitis. However, its typical impact involves surface infections of the genital tract mucosa, with rare instances of tissue and bloodstream invasion. Extragenital invasive infections caused by M. hominis are rare and unable to be identified through conventional bacteriological culture methods. M. hominis is challenging to detect promptly and exhibits resistance to commonly used antimicrobial agents. This resistance leads to patients postponing treatment, thereby posing a potential threat to their lives. Moreover, M. hominis has been reported to cause septic arthritis (Luttrell et al., 1994), central nervous system (CNS) infections (Reissier et al., 2016), mediastinitis (Le Guern et al., 2015, Grancini et al., 2016), infective endocarditis (Givone et al., 2020) and abscess formation, particularly in postoperative patients and immunocompromised patients (Meyer and Clough, 1993, Adams et al., 2020).

Antibiotics active against M. hominis are restricted to those that disrupt protein synthesis and DNA replication. However, due to the intrinsic resistance to 14- and 15-membered macrolides, the only effective antibiotics against M. hominis are fluoroquinolones, tetracyclines, and 16-membered macrolides. Bacterial resistance to fluoroquinolone is associated with genetic mutations in DNA gyrase (GyrA and GyrB) and/or the topoisomerase IV complex (ParC and ParE) (Drlica and Zhao, 1997). The resistance of M. hominis to 16-membered macrolides can be related to substitutions in domain II or V of 23S rRNA and/or in the ribosomal proteins L4 and L22 (Pereyre et al., 2002, Pereyre et al., 2006). The emergence of antibiotic resistance in M. hominis has raised global public health concerns, as reported in various countries and regions (Kong et al., 2016, Kasprzykowska et al., 2018, Choi et al., 2018, Meygret et al., 2018, Ozturk et al., 2019, Shao et al., 2021). China and Korea showed an increasing rate of resistance to fluoroquinolones, while the susceptibility to tetracycline remains high (Kong et al., 2016, Choi et al., 2018, Shao et al., 2021). In Turkey and Poland, a notable degree of resistance to tetracycline has been observed (Kasprzykowska et al., 2018, Ozturk et al., 2019). Besides, the annual decrease in antibiotic susceptibility rates of M. hominis to pristinamycin has been documented in Korea from 2016 to 2018 (Lee and Yang, 2020). In this study, we report the first genome sequence of a M. hominis isolate recovered from extra-urogenital cystic abscess in China to underline the antimicrobial resistance and virulence mechanisms of this emerging pathogen.