Molecular sub-typing of plasmids harbouring quinolone resistance genes in Salmonella strains

Abstract

Salmonella spp are the most frequent causative agents of foodborne disease. Clinical manifestations of human infections with Salmonella spp. cause from mild to severe gastroenteritis intestinal and extra-intestinal infections such as bacteremia, sepsis and meningitis, including typhoid fever. Antimicrobial therapy is essential for immunocompromised patients, the elderly or children, or in severe cases or invasive caused by Salmonella, and ciprofloxacin (fluorquinolone) is recommended as the drug of first choice for treatment. The resistance to fluorquinolones is still rare in Salmonella spp. However, in recent decades the emergence and spread of resistance to nalidixic acid (quinolone first generation) associated with reduced susceptibility to ciprofloxacin among Salmonella serotypes, it has become of great interest public health, interfering directly in response to clinical treatment. The multidrug resistance in Salmonella has been increased due to the indiscriminate use of antimicrobial agents in the treatment and prophylaxis human and veterinary medicine. In this paper we will study 47 Salmonella strains, harbouring plasmids-mediated quinolone resistance genes (oqxA/B, qnrB19 and aac(6') lb-cr) from human infections cases and non human origin (mostly food), isolated in the state of São Paulo. The aim of this study is the typing of plasmids using conjugation/transformation tests, assign to incompatibility groups by PCR-based replicon typing, a plasmid multilocus sequence typing (pMLST) was developed to verify the dissemination of antimicrobial resistance and plasmid diversity, as well as we will perform the sequencing of plasmids to analyze the organization and composition of plasmids, analyze the association with other resistance genes, and genomic comparisons. The results contribute to knowledge about the molecular mechanisms of resistance to fluorquinolones among Salmonella strains, to reduce the selection pressure and prevent the emergence of resistant clones (AU)