Antibiotic Resistance in Neisseria gonorrhoeae: Genetics and Mechanisms of Resistance

In recent years the emergence and spread of antibiotic resistance in Neisseria gonorrhoeae has increased markedly. Chromosomal resistance to penicillin and tetracycline is due to the effects of one or more mutations and is generally low-level. However, the effects of these mutations are additive. Thus, the level of resistance in strains with several mutations is often high enough to yield significant rates of treatment failure. Resistance to aminoglycosides (e.g., streptomycin and kanamycin) and spectinomycin, an aminocyclitol antibiotic is not due to the inactivation of the antibiotic but to an alteration in the sensitivity of the 30S ribosomal subunit to the drug. At least five beta-lactamase plasmids of N. gonorrhoeae have been described. Some of these plasmids can be mobilized by the 24.5-MDa gonococcal conjugative plasmid and transferred to other gonococcal strains. Gonococci have recently acquired high-level resistance to tetracycline due to the streptococcal tetM determinant. This determinant is located on a 25.2-MDa plasmid that possesses a considerable degree of homology with the 24.5-MDa conjugative plasmid. The 25.2-MDa plasmid has retained the ability to transfer beta-lactamase plasmids as well as to mobilize and transfer itself to suitable recipient strains.