Neisseria gonorrhoeae arthritis in a patient with systemic lupus: resistance and virulence profiles

In this study, we describe a case report of gonococcal arthritis in a Systemic Lupus Erythematosus patient. Although several mechanisms favor disseminated gonococcal infection (DGI) in patients immunosup-pressed by SLE, this association is rarely reported in literature. We performed whole genome sequencing (WGS) of the etiologic agent involved and molecular analysis using a global collection of Neisseria gonorrhoeae strains. Ours is the only sample derived from synovial fluid identified in this collection, the others being from the usual anatomical sites. Antimicrobial susceptibility was determined by disk diffusion and Etest, and WGS was conducted to determine multilocus sequence typing profiles, group isolates based on core genome single nucleotide polymorphisms (SNP), and identify virulence genes and antimicrobial resistance determinants. The N. gonorrhoeae samples in the global collection were highly heterogeneous. The SNP tree had a total 19,532 SNPs in 320 samples. Our sample displayed resistance to ciprofloxacin (MIC = 2 mg/mL) and tetracycline (zone diameter = 0 mm) belonged to ST 1588 and was not closely related to any isolate in the global collection of N. gonorrhoeae strains. The isolate had genetic features related to beta-lactam, tetracycline and quinolone resistance. Seventy-one virulence genes were identified in our sample, belonging to the following classes: adherence, efflux pump, immune modulator, invasion, iron uptake, protease and stress adaptation. Moreover, no virulence genes for immune evasion and toxin were identified.(c) 2022 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.

Automated summary

This study presents a rare case of gonococcal arthritis in a patient with Systemic Lupus Erythematosus (SLE). Whole genome sequencing (WGS) and molecular analysis were performed on the etiologic agent, which was found to be resistant to ciprofloxacin and tetracycline. The isolate had genetic features related to beta-lactam, tetracycline, and quinolone resistance, and 71 virulence genes were identified.