1) The sequencing of the QRDR of the gyrA (GenBank accession no

1). The sequencing of the QRDR of the gyrA (GenBank accession no. GQ495079) gene indicated a mutation in codon 83, which resulted in the substitution of serine to isoleucine. The sequencing of the QRDR of the parC (GenBank accession no. GQ495081) gene revealed a mutation in codon 85, which resulted in the substitution of serine to leucine. However, no mutations were detected in QRDR of gyrB and parE genes. Tetracycline, ciprofloxacin and co-trimoxazole are the most important drugs considered for the treatment of cholera (Amita et al., 2003; Khan et al., 2003; Sack et al., 2004). Furazolidone was found to be effective clinically in treating cholera in children (Rabbani Opaganib et al.,

1991). The MCV09 showed resistance to 10 antibiotics including the common drugs used for the treatment of diarrhoeal diseases. All O1 strains examined from Kerala since 1999 were resistant to co-trimoxazole, streptomycin, nalidixic acid and polymixin B and furazolidone (Sabeena et al., 2001; Sabu et al., 2007). When compared with these data, the test strain showed additional resistance to ampicillin, furazolidone, tetracycline and ciprofloxacin. Hence, the selleckchem emergence of resistance to potent

antibiotics among toxigenic strains is a cause of great concern and it may create major problems in treating severe cases of diarrhoea when an antibiotic intervention is necessary. Since 1992, the majority of O1 and O139 strains isolated from India have exhibited uniform resistance to trimethoprim–sulphamethoxazole and streptomycin and a harboured SXT element (Waldor et al., 1996; Amita et al., 2003; Ramachandran

et al., 2007). The SXT element was also identified in Lenvatinib concentration non-O1/non-O139 strains of both environmental and clinical origin (Thungapathra et al., 2002; Mohapatra et al., 2008). Hence, it becomes highly relevant to examine the SXT and associated drug resistance genes in MCV09. The Int is required for integration and excision of SXT from chromosome and the C-terminal half (232–254 and 342–377 residues) is highly conserved (Hochhut & Waldor, 1999). The substitutions observed in the present investigation were not in conserved domains and therefore may not interfere with the function of Int. Ahmed et al. (2005) described a variant of SXT with typical antibiotic resistance genes from V. fluvialis isolated from Calcutta. They further compared the attP sites of V. fluvialis and MO10 and explained that the attP in the former is shorter and there is deletion of 144 bp and addition of 95 bp. When analysed, the sequence of attP from MCV09 also exhibited similar addition and deletion (data not shown). However, the 17-bp core sequences of MCV09 and all O1 strains differed from that of V. fluvialis and MO10 in a single nucleotide position (Fig. 3). No such changes in the attP attachment site and the 17-bp core site have been reported from SXT previously.

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