Oropharyngeal Neisseria gonorrhoeae infections: should women be routinely tested?

Oropharyngeal infection with Neisseria gonorrhoeae is important: it is harder to treat than anogenital infection and the oropharynx provides a niche for the development of antimicrobial resistance. Additionally, since oropharyngeal N gonorrhoeae infections are usually asymptomatic, they can easily remain undetected, providing a reservoir of infection that facilitates onward transmission. Emerging evidence suggests that in addition to oral sex, oropharyngeal infection might be transmitted through kissing

Lessons learnt from ceftriaxone-resistant gonorrhoea in the UK and Australia.

Neisseria gonorrhoeae, the causative pathogen of gonorrhoea, has shown impressive agility in developing resistance to successive classes of antimicrobials used for therapy, leading to a progressive reduction in available treatment options. Ceftriaxone is the last-line treatment option for gonorrhoea, and many countries recommend dual therapy with ceftriaxone (250–1000 mg) in combination with azithromycin (1–2 g). However, since the introduction of dual therapy, the global prevalence of azithromycin resistance has increased. Additionally, the extensively drug-resistant N gonorrhoeae FC428 clone, which is associated with ceftriaxone resistance and intermediate resistance to azithromycin, has been reported to have spread internationally, with epidemiological links to the Asia-Pacific region

What’s left in the cupboard? Older antimicrobials for treating gonorrhoea

Background: Neisseria gonorrhoeae has developed resistance to all antimicrobials used to treat gonorrhoea, with even ceftriaxone being undermined. It is therefore important to examine any potential to redeploy older antimicrobials routinely used for other infections to treat ceftriaxone-resistant gonococcal infections. Objectives: We examined the susceptibility of N. gonorrhoeae to aztreonam, chloramphenicol, co-trimoxazole, fosfomycin, piperacillin/tazobactam and rifampicin. Methods: N. gonorrhoeae isolates (n = 94) were selected to include a range of antimicrobial susceptibilities: 58 were collected in the Gonococcal Resistance to Antimicrobials Surveillance Programme; 17 were clinical isolates referred to the PHE reference laboratory; and 19 were control strains. MICs were determined by agar dilution for the six study antimicrobials and for ceftriaxone and azithromycin as comparators. Results: There was correlation between piperacillin/tazobactam and ceftriaxone MICs, but all five isolates with high ceftriaxone MICs (>0.5 mg/L) were inhibited by piperacillin/tazobactam at 0.06–0.5 mg/L. Aztreonam MICs for ceftriaxone-resistant isolates exceeded those of ceftriaxone. Among non-β-lactams, fosfomycin and co-trimoxazole had low, tightly clustered MICs, suggesting widespread susceptibility, rifampicin split the collection into highly susceptible and highly resistant groups and chloramphenicol had a wide MIC distribution. Conclusions: Although unsuitable for empirical use, piperacillin/tazobactam, fosfomycin, co-trimoxazole, rifampicin and, possibly, chloramphenicol could be considered for individual patients with ceftriaxone-resistant gonococcal infection once MICs are known. Wider surveillance of the susceptibility of N. gonorrhoeae to these agents is needed, along with clinical trials and the establishment of clinical breakpoints for N gonorrhoeae