A minimal genome and absent bacterial cell wall renders Mycoplasma hominis inherently resistant to most antimicrobials except lincosamides, tetracyclines and fluoroquinionlones. Often dismissed as a commensal (except where linked to preterm birth), it causes septic arthritis in immunodeficient patients and is increasingly associated with transplant failure (particularly lung) accompanying immunosuppression. We examined antimicrobial susceptibility (AST) on strains archived between 2005-2015 submitted to the Public Health England reference laboratory and determined the underlying mechanism of resistance by whole genome sequencing (WGS). Archived M. hominis strains included 32/115 from invasive infection (sepsis, CSF, peritoneal and pleural fluid) over the 10-year period (6.4% of all samples submitted between 2010-2015 were positive). No clindamycin resistance was detected, while two strains were resistant to moxifloxacin and levofloxacin (resistance mutations: S83L or E87G in gyrA and S81I or E84V in parC). One of these strains and 11 additional strains were tetracycline resistant, mediated by tet(M) carried within an integrative conjugative element (ICE) consistently integrated at the somatic rumA gene; however, the ICEs varied widely in 5-19 associated accessory genes. WGS analysis showed tet(M)-carrying strains were not clonal, refuting previous speculation that the ICE was broken and immobile. We found tet(M)-positive and -negative strains (including the multi-resistant 2015 strain) to be equally susceptible to tigecycline and josamycin, however, the British National Formulary does not include guidance for these. Continued M. hominis investigation and AST surveillance (especially immunocompromised patients) is warranted, and expansion of the limited therapeutics needs to be expanded in the UK.
Often dismissed as a commensal, Mycoplasma hominis is an increasingly prominent target of research due to its role in septic arthritis and organ transplant failure in immunosuppressed patients, particularly lung transplantation. As a mollicute, its highly reductive genome and structure render it refractile to most forms of treatment and growing levels of resistance to the few sources of treatment left, such as fluoroquinolones. We examined antimicrobial susceptibility (AST) to fluoroquinolones on 72 isolates and observed resistance in three (4.1%), with corresponding mutations in the quinolone resistance-determining region (QRDR) of S83L or E87G in gyrA and S81I or E85V in parC. However, there were high levels of polymorphism identified between all isolates outside of the QRDR, indicating caution for a genomics-led approach for resistance screening, particularly as we observed a further two quinolone-susceptible isolates solely containing gyrA mutation S83L. However, both isolates spontaneously developed a second spontaneous E85K parC mutation and resistance following prolonged incubation in 4 mg/L levofloxacin for an extra 24–48 h. Continued AST surveillance and investigation is required to understand how gyrA QRDR mutations predispose M. hominis to rapid spontaneous mutation and fluoroquinolone resistance, absent from other susceptible isolates. The unusually high prevalence of polymorphisms in M. hominis also warrants increased genomics’ surveillance.
This article examines the way that non-clinical support services are provided in healthcare settings through outsourcing partnerships. The integrated support services model and benefits to patient experience and safety as well as organizational efficiency and effectiveness are explored through an examination of services at a busy urban community hospital.
Dans le présent article, l'auteur examine le mode de prestation des services de soutien non cliniques dans les établissements de santé par des partenariats de sous-traitance. Il examine le modèle des services de soutien intégrés et ses avantages pour l'expérience et la sécurité des patients ainsi que pour l'efficience et l'efficacité organisationnelles dans un hôpital général urbain achalandé.
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