Determinants of Emergence of Antibiotic-Resistant Neisseria gonorrhoeae

Abstract

Studies were carried out to evaluate the prevalence and risk factors for antibiotic-resistant Neisseria gonorrhoeae infections. Monthly surveillance of gonococcal isolates showed the prevalence of gonococci with high-level, plasmid-mediated tetracycline resistance (TRNG) to be about 15% for three consecutive 6-mo periods. Over the same period, the prevalence of gonococci with chromosomally mediated resistance to penicillin G steadily increased, from 0% to 9% and then to 21%. From April to July 1987, while chromosomally mediated penicillin resistance was rapidly increasing, a more intensive study was conducted. Patients infected with TRNG reported significantly more lifetime sexual partners (P less than .05) but otherwise resembled patients infected with antibiotic-sensitive gonococci. Patients infected with chromosomally mediated penicillin-resistant gonococci differed from other patients. In addition to reporting more lifetime partners (P less than .05), patients with chromosomally mediated penicillin-resistant gonorrhea were more likely to be older (P less than .05) and more often reported past episodes of gonorrhea (P less than .05), greater numbers of recent sexual partners (P less than .05), new sexual partners (P less than .05), prostitute contact (P = .06), and parenteral drug use or sexual partners who were drug users (P = .07). The introduction of antibiotic-resistant N. gonorrhoeae into communities may be attributable to a subset of patients who practice "risky behaviors" and who could be targeted for disease intervention activities.

Prevalence of and Associated Risk Factors for Fluoroquinolone-Resistant Neisseria gonorrhoeae in California, 2000-2003

“…In our population, recent antibiotic use was associated with QRNG; however, only a minority of patients reported fluoroquinolone use. Similar associations with tetracycline, penicillin, and fluoroquinolone resistance have been identified in the United States and The Philippines [32][33][34]; however, other risk analyses have not demonstrated this association [30,[35][36][37][38][39]. The process of developing resistance is multifactorial, and antimicrobials used to treat infections other than STDs may well have a larger role in causing resistance in N. gonorrhoeae than does use of antimicrobials for gonococcal infection.…”

Development Frequency of Penicillinase-producing Neisseria Gonorrhoeae (Jung-gu Community Health Center in Seoul, 1994-1998)

“…Its resistance development toward antibiotics and its further spread has several factors. Antibiotic-resistance is usually involved with the introduction of new strains to a community through infection and its spread in high risk groups [17][18][19][20] . Its medications may add resistance to a part of strains through selective pressure 11,[21][22][23] .…”

“…Its medications may add resistance to a part of strains through selective pressure 11,[21][22][23] . In addition, non-compliancy of the patients and self-treatment may promote its development 17,19,20,23 . Antibiotic-resistance varies in regions a great deal.…”

Unique Gonococcal Phenotype Associated with Asymptomatic Infection in Men and with Erroneous Diagnosis of Nongonococcal Urethritis

“…Large epidemics caused by gonococci with distinctive phenotypic properties such as nutritional requirements (auxotype) and serovar class have sometimes been associated with distinctive host behavioral factors. For example, a large epidemic of b-lactamase-producing gonococci in Seattle, caused by a single auxotype/serovar class, was associated with cocaine use [3]; other outbreaks in Baltimore and in Ohio have been associated with other factors linked to core group membership [4,5].Two gonococcal auxotypes-1 requiring arginine, hypoxanthine, and uracil (AHU) and 1 requiring proline, citrulline, and uracil-have previously been linked to clinically mild or inapparent infection [6,7]. It has been hypothesized that the epidemic spread of such strains could be linked to prolonged duration of infectiousness, because of the frequent absence of symptoms that would have prompted health-care seeking [8].…”

“…Large epidemics caused by gonococci with distinctive phenotypic properties such as nutritional requirements (auxotype) and serovar class have sometimes been associated with distinctive host behavioral factors. For example, a large epidemic of b-lactamase-producing gonococci in Seattle, caused by a single auxotype/serovar class, was associated with cocaine use [3]; other outbreaks in Baltimore and in Ohio have been associated with other factors linked to core group membership [4,5].…”