You are here: Home Published Research Molecular characterization of fluoroquinolone resistance in nontypeable Haemophilus influenzae clinical isolates.

Carmen Puig, José M Tirado-Vélez, Laura Calatayud, Fe Tubau, Junkal Garmendia, Carmen Ardanuy, Sara Marti, Adela G de la Campa, and Josefina Liñares (2014)

Molecular characterization of fluoroquinolone resistance in nontypeable Haemophilus influenzae clinical isolates.

Antimicrobial agents and chemotherapy.

Nontypeable Haemophilus influenzae (NTHi) is a common cause of respiratory infections in adults, who are frequently treated with fluoroquinolones. The aims of this study were to characterize the genotypes of fluoroquinolone-resistant NTHi isolates and their mechanisms of resistance. Among 7267 H. influenzae isolates collected from adult patients (2000-2013), 28 (0.39%) were ciprofloxacin-resistant according to Clinical and Laboratory Standards Institute (CLSI) criteria. In addition, a nalidixic acid screening during 2010-2013 detected five (0.23%) isolates, which were ciprofloxacin-susceptible but nalidixic acid-resistant. Sequencing of their quinolone resistance-determinant regions and genotyping by pulse-field gel electrophoresis and multi locus sequence typing was performed in the 25 ciprofloxacin-resistant isolates available and in all five nalidixic acid-resistant isolates. In the NTHi studied, two mutations producing changes in two GyrA residues (Ser84, Asp88), and/or two ParC residues (Ser84, Glu88), were associated with increased fluoroquinolone MICs. Strains with one or two mutations (n=15) presented ciprofloxacin and levofloxacin MICs of 0.12-2 μg/ml while those with three or more mutations (n=15) presented MICs of 4-16 μg/ml. Long persistence of fluoroquinolone-resistant strains was observed in three COPD patients. High genetic diversity was observed among fluoroquinolone-resistant NTHi. Although fluoroquinolones are commonly used to treat respiratory infections, the proportion of resistant NTHi remains low. The nalidixic acid disk is a useful test for detecting the first changes in GyrA or in GyrA plus ParC among fluoroquinolone-susceptible strains which are a potential risk for the development of resistance under selective pressure by fluoroquinolone treatments.

 
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