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Table 2 Genetic resistance determinants for ceftriaxone, cefixime and ciprofloxacin in Neisseria gonorrhoeae isolates from India (n=40), Pakistan (n=18), and Bhutan (n=7) in 2007–2011

From: Antimicrobial susceptibility and genetic characteristics of Neisseria gonorrhoeae isolates from India, Pakistan and Bhutan in 2007–2011

Antimicrobial (Susceptibility, % of isolates) penAmosaic allele A501 altered PBP2 allele mtrR promoter (A-deletion/T-insertion) MtrR coding region (G45D) penB (alterations in G101/A102) gyrA (alterations in S91 and D95) parC (alterations in D86, S87, S88, E91 and A92)
Ceftriaxone (S, 100%) Nonea Nonea 42%/4.6%b 11% D/G (26%), G/S (20%), K/D (18%), K/N (9.2%), N/D (6.2%), K/G (4.6%), G/N (4.6%), N/G (1.5%), G/G (1.5%) ND ND
Cefixime (S, 100%) Nonea Nonea 42%/4.6%b 11% D/G (26%), G/S (20%), K/D (18%), K/N (9.2%), N/D (6.2%), K/G (4.6%), G/N (4.6%), N/G (1.5%), G/G (1.5%) ND ND
Ciprofloxacin (R, 93.8%) ND ND 44%/4.9%b 11% D/G (28%), G/S (20%), K/D (15%), K/N (9.8%), N/D (6.6%), K/G (4.9%), G/N (4.9%), N/G (1.6%), G/G (1.6%) S91F (100%), D86N (3.3%), S87N (4.9%), S87I (1.6%), S87R (1.6%), E91G (36%), E91K (15%), E91Q (4.9%)
D95N (46%), D95G (41%), D95A (10%), D95Y (1.6%)
Ciprofloxacin (I, 6.2%) ND ND None None K/D (75%), G/S (25%) S91F (100%) None
       D95G (100%)  
  1. S, susceptible; I, intermediate susceptible; R, resistant; ND, not determined because the resistance determinants do not evidently affect this antimicrobial.
  2. aThe identified penicillin-binding protein 2 (PBP2) alleles were IX (n=22), II (n=19), XIX (n=12), IV (n=7), Modified-XIV (n=3), XII (n=1), and XXXV (n=1). All these PBP2 alleles, with exception of PBP2 XXXV, contain an insertion of aspartate in amino acid position 345 (D345a), which explains the high level of intermediate susceptibility and resistance to penicillin among the isolates [11, 28].
  3. bOne additional isolate (from Pakistan) displayed the recently described C-to-T transition mutation 120 bp upstream of the mtrC start codon, termed mtr 120, that results in a novel consensus −10 element and generation of a novel promoter for mtrCDE transcription. This mutation also results in an over-expression of the MtrCDE efflux pump [29].