1. Academic Validation
  2. In Vitro Activity of Sulfamethoxazole-Trimethoprim, Amikacin, Oxazolidinones, Fluoroquinolones and Fidaxomicin against Isolates of Nocardia

In Vitro Activity of Sulfamethoxazole-Trimethoprim, Amikacin, Oxazolidinones, Fluoroquinolones and Fidaxomicin against Isolates of Nocardia

  • ACS Omega. 2025 Oct 27;10(44):52289-52295. doi: 10.1021/acsomega.5c02351.
Chaohong Wang 1 2 Yiheng Shi 1 Ming Wei 3 Jun Yan 1 Sibo Long 1 Guanglu Jiang 4 Yan Zhao 1 Hairong Huang 4 Li Gu 3 Xinting Yang 5 Hao Li 6 Guirong Wang 1
Affiliations

Affiliations

  • 1 Department of Clinical Laboratory, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Institute, Beijing 101149, China.
  • 2 Department of Clinical Laboratory, Ningbo No.2 Hospital, Ningbo, Zhejiang 315099, China.
  • 3 Department of Infectious Diseases and Clinical Microbiology, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
  • 4 National Clinical Laboratory on Tuberculosis, Beijing Key Laboratory for Drug Resistant Tuberculosis Research, Beijing Chest Hospital, Capital Medical University, Beijing Tuberculosis and Thoracic Tumor Institute, Beijing 101149, China.
  • 5 Tuberculosis Department, Beijing Chest Hospital, Capital Medical University, Beijing 101149, China.
  • 6 College of Veterinary Medicine, China Agricultural University, Beijing 100107, China.
Abstract

Nocardia species are opportunistic pathogens causing nocardiosis, often misdiagnosed as tuberculosis or nontuberculous mycobacterial infections, leading to inappropriate treatment. This study evaluates the in vitro activity of common and potential antimicrobials, including Trimethoprim-sulfamethoxazole, Amikacin, Oxazolidinones (Linezolid, Tedizolid, Contezolid), Fluoroquinolones (Moxifloxacin, Levofloxacin, Sitafloxacin), Rifampicin, and Fidaxomicin against 51 clinical Nocardia isolates. Minimum inhibitory concentrations (MICs) were determined using the AlamarBlue assay, revealing that Linezolid exhibited significant efficacy against all isolates, while Trimethoprim-sulfamethoxazole and Amikacin showed 92.16% sensitivity. Sitafloxacin demonstrated superior efficacy among Fluoroquinolones, with variations across Nocardia species. Fidaxomicin exhibited significant activity (88.24%), contrasting with Rifampicin's limited effect. A high prevalence of the gyrA Ser83Ala mutation was identified in resistant Nocardia strains, correlating with reduced Fluoroquinolone susceptibility. These findings highlight the need for tailored treatment strategies based on species-specific susceptibility and resistance profiles and suggest Fidaxomicin and Sitafloxacin as promising options. Further clinical validation is warranted to optimize therapeutic outcomes.

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