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

<i>Nocardia</i> species are opportunistic pathogens causing nocardiosis, often misdiagnosed as tuberculosis or nontuberculous mycobacterial infections, leading to inappropriate treatment. This study evaluates the <i>in vitro</i> activity of common and potential antimicrobials, including Trimethoprim-sulfamethoxazole, Amikacin, Oxazolidinones (Linezolid, Tedizolid, Contezolid), Fluoroquinolones (Moxifloxacin, Levofloxacin, Sitafloxacin), Rifampicin, and Fidaxomicin against 51 clinical <i>Nocardia</i> 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 <i>Nocardia</i> species. Fidaxomicin exhibited significant activity (88.24%), contrasting with Rifampicin's limited effect. A high prevalence of the <i>gyrA</i> Ser83Ala mutation was identified in resistant <i>Nocardia</i> 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.