YOSHIDA Atsushi
   Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine
   Position  
Article types Case report
Language English
Peer review Peer reviewed
Title Pulmonary infection due to fluoroquinolone-resistant Mycolicibacterium fortuitum: a case report.
Journal Formal name：BMC infectious diseases
Abbreviation：BMC Infect Dis
ISSN code：14712334/14712334
Domestic / ForeginForegin
Volume, Issue, Page 20(1),pp.866
Author and coauthor Kurokawa Kana, Harada Norihiro, Sasano Hitoshi, Takagi Haruhi, Takei Satomi, Nakamura Ayako, Kamada Keisuke, Yoshida Atsushi, Kikuchi Ken, Takahashi Kazuhisa
Publication date 2020/11
Summary BACKGROUND:Mycolicibacterium fortuitum is a species of the rapidly growing mycobacteria that can cause pulmonary infection. It is susceptible to multiple antibiotics both in vitro and in clinical practice, so that any combination of susceptible drugs is effective. However, we encountered a case of infection due to fluoroquinolone-resistant M. fortuitum. In this study, we report the case and describe the mechanism of resistance.CASE PRESENTATION:A 65-year-old man with a history of total gastrectomy and immunosuppressant treatment for rheumatoid arthritis developed a recurrence of pulmonary infection caused by M. fortuitum. He was treated with clarithromycin and levofloxacin as a first-line treatment, based on the favorable susceptibility at that time. After recurrence, a high minimum inhibitory concentration to fluoroquinolones was detected. DNA sequencing of the pathogen showed the substitution of serine for tryptophan at residue 83 in the gyrA gene. He was successfully treated with a combination of other antibiotics.CONCLUSION:This is the first report on the treatment of fluoroquinolone-resistant M. fortuitum and investigation of the mechanism of resistance. We suggest that the susceptibility test remains effective for determining the next line of treatment after a pathogen has acquired resistance, and resistance to fluoroquinolones in M. fortuitum can be attributed to a single change of amino acid.
DOI 10.1186/s12879-020-05596-1
PMID 33213390