Abstract
BackgroundPhenotypic fluoroquinolone resistance was first reported in Western Kenya in 2009 and later in Coastal Kenya and Nairobi. Until recently gonococcal fluoroquinolone resistance mechanisms in Kenya had not been elucidated. The aim of this paper is to analyze mutations in both gyrA and parC responsible for elevated fluoroquinolone Minimum Inhibitory Concentrations (MICs) in Neisseria gonorrhoeae (GC) isolated from heterosexual individuals from different locations in Kenya between 2013 and 2017.MethodsAntimicrobial Susceptibility Tests were done on 84 GC in an ongoing Sexually Transmitted Infections (STI) surveillance program. Of the 84 isolates, 22 resistant to two or more classes of antimicrobials were chosen for analysis. Antimicrobial susceptibility tests were done using E-test (BioMerieux) and the results were interpreted with reference to European Committee on Antimicrobial Susceptibility Testing (EUCAST) standards. The isolates were sub-cultured, and whole genomes were sequenced using Illumina platform. Reads were assembled de novo using Velvet, and mutations in the GC Quinolone Resistant Determining Regions identified using Bioedit sequence alignment editor. Single Nucleotide Polymorphism based phylogeny was inferred using RaxML.ResultsDouble GyrA amino acid substitutions; S91F and D95G/D95A were identified in 20 isolates. Of these 20 isolates, 14 had an additional E91G ParC substitution and significantly higher ciprofloxacin MICs (p = 0.0044*). On the contrary, norfloxacin MICs of isolates expressing both GyrA and ParC QRDR amino acid changes were not significantly high (p = 0.82) compared to MICs of isolates expressing GyrA substitutions alone. No single GyrA substitution was found in the analyzed isolates, and no isolate contained a ParC substitution without the simultaneous presence of double GyrA substitutions. Maximum likelihood tree clustered the 22 isolates into 6 distinct clades.ConclusionSimultaneous presence of amino acid substitutions in ParC and GyrA has been reported to increase gonococcal fluoroquinolone resistance from different regions in the world. Our findings indicate that GyrA S91F, D95G/D95A and ParC E91G amino acid substitutions mediate high fluoroquinolone resistance in the analyzed Kenyan GC.
Highlights
Phenotypic fluoroquinolone resistance was first reported in Western Kenya in 2009 and later in Coastal Kenya and Nairobi
A 2018 publication focused on sex workers and Men who have Sex with Men (MSM) from Coastal Kenya found that S91F, D95G/A, and F504 L GyrA amino acid substitutions were associated with fluoroquinolone resistance [14]
A total of 583 symptomatic cases comprising of 332 males and 251 females were enrolled from four geographic locations in Kenya (Nairobi, Coastal Kenya, Nyanza, and Rift Valley) between 2013 and 2017
Summary
Phenotypic fluoroquinolone resistance was first reported in Western Kenya in 2009 and later in Coastal Kenya and Nairobi. Since the 1970s, a small number of studies have reported both chromosomal and plasmid mediated gonococcal penicillin and tetracycline resistance in Kenya [5,6,7,8,9]. These reports led to the introduction of fluoroquinolones as the first line of drugs for gonorrhea treatment in 1993 [10]. Fluoroquinolone resistance was reported in western Kenya in 2009 [11], Coastal Kenya in 2011 and 2012 [12, 13], and Nairobi in 2012 [12] These findings formed the basis for revision of national treatment guidelines in 2013. A 2018 publication focused on sex workers and Men who have Sex with Men (MSM) from Coastal Kenya found that S91F, D95G/A, and F504 L GyrA amino acid substitutions were associated with fluoroquinolone resistance [14]
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