the pharynx is not an ideal site for N. gonorrhoeae growth. From the routine examinations of commercial sex workers during January–March 2009, 40 N. gonorrhoeae were isolated in the clinic, but no other ceftriaxoneresistant strains were isolated. There is no evidence of dissemination of this strain in Kyoto. Three independent molecular subtyping methods indicated that the ceftriaxone-resistant H041 strain was N. gonorrhoeae, and it might originate from an ST7363 cefixime-resistant N. gonorrhoeae clone. There are several possible mechanisms for the acquisition of resistance, including formation of a new mosaic type penA allele as penA-X cefixime resistance and acquisition of an extended-spectrum β-lactamase gene. The H041 strain did not produce β-lactamase in a nitrocephin test. Further molecular analysis is needed to elucidate the precise mechanism of the ceftriaxone resistance of the H041 strain. The emergence of ceftriaxone-resistant N. gonorrhoeae raises concerns for controlling gonorrhea because ceftriaxone is widely recommended and the first-line treatment for gonorrhea around the world. N. gonorrhoeae has a potential to gain an extraordinarily high MIC to ceftriaxone. Surveillance for ceftriaxone-resistant N. gonorrhoeae should be strengthened. Acknowledgment We thank Hiroko Matsuoka for her technical assistance. This study was supported by grantsin-ai
To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.