Plasmid-mediated streptomycin and sulfamethoxazole resistance in Shigella flexneri 3a

Shigellosis is a major cause of diarrhoea-related morbidity and mortality, especially in children in developing countries such as India. Recently, it was estimated that 91 million individuals worldwide contract shigellosis each year. The emergence and dissemination of multidrug-resistant strains of Shigella is now an emerging global health problem. During the past two decades, much attention was given to re-evaluation of treatment recommendations. In the present study, we investigated a clinical strain of Shigella flexneri 3a with multiple drug resistance. This strain was resistant to ampicillin, chloramphenicol, co-trimoxazole (trimethoprim/sulfamethoxazole), nalidixic acid, streptomycin, sulfamethoxazole, tetracycline and trimethoprim. However, it was susceptible to 46.7% of drugs tested, i.e. azithromycin, ceftriaxone, ciprofloxacin, gentamicin, kanamycin, norfloxacin and ofloxacin. A 6.3-kb plasmid was cured from this strain using acridine orange. Following curing, it was observed that 87% of drug resistance loci of S. flexneri 3a are chromosomal and 13% are plasmid-encoded. This 6.3-kb plasmid was involved in streptomycin and sulfamethoxazole resistance in S. flexneri 3a strain, which was confirmed by the disk diffusion method. Clonality was confirmed by pulse-field gel electrophoresis (PFGE). This study contributes to our knowledge on acquired drug resistance in one of the most common Shigella spp., S. flexneri 3a, which will enable better understanding of effective clinical management of shigellosis.