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

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.