In vitro activity of fluoroquinolone and the gyrA gene mutation in Helicobacter pylori strains isolated from children

1 Department of Microbiology, Miyagi University, 1 Gakuen, Taiwa-cho, Miyagi, 981-3298, Japan 2 Department of Pediatrics, Tohoku University School of Medicine, 1-1, Seiryo-machi, Aoba-ku, Sendai, Japan 3 Department of Respiratory Oncology and Molecular Medicine, Institute of Development, Ageing and Cancer, Tohoku University, 4-1, Seiryo-machi, Aoba-ku, Sendai, Japan Correspondence Shigeru Fujimura hujimura{at}myu.ac.jp Received February 25, 2004 Accepted May 27, 2004 Resistance to antibiotics, especially clarithromycin, is the major cause of the failure to eradicate Helicobacter pylori . There are few studies in children concerning fluoroquinolone activity against H. pylori . Primary resistance to antibiotics including fluoroquinolones was studied in 55 H. pylori strains isolated from Japanese children. DNA sequences of the gyrA gene in fluoroquinolone-resistant strains were determined. Twelve strains (21.8 %) were resistant to clarithromycin and three (5.5 %) were resistant to both levofloxacin and ciprofloxacin. Out of 12 clarithromycin-resistant strains, 11 (91.7 %) were susceptible to levofloxacin and ciprofloxacin. Sequence analysis in three fluoroquinolone-resistant strains showed point mutations of the gyrA gene at G271A, G271T and A272G, indicating mutations of the codon Asp91 in the fluoroquinolone-resistance-determining region of the DNA gyrase. The results suggest that fluoroquinolones should be considered as an option for second- or third-line H. pylori eradication therapy in children.