Sexually transmitted infections (STI/SOA)

5 important questions on Sexually transmitted infections (STI/SOA)

What is the infection way of N. Gonorrhoea?

  1. Adherence to urogenital epithelium, OPA protein and type 4 pilli
  2. Competition with resident microbiota, nutrient acquisition and microcolony formation → Colonisation and invasion of epithelium
  3. Release of peptidoglycan, LOS and OMVs
  4. Cytokine, chemokine and inflammatory transcription factor activation
  5. Influx of neutrophils; adherence and phagocytosis of N. gonorrhoeae
  6. A neutrophil-rich purulent exudate facilitates transmission

Why is it difficult to treat N. Gonorrhoea?

Different classes of antibiotics resistance: current treatment is cephalosporins (inhibit the ribosome), resistance also occurred with it.
  1. Plasmid-mediated resistance
  2. Mutations in antibiotic binding site
  3. Mutations in topo-isomerases
  4. Overexpression of efflux pumps

Explain Mutations in antibiotic binding site

Inhibition of antibiotic influx
  • Mutation in penicillin-binding protein A (penA) and proin B (porB) lead to inhibited uptake of beta-lactams and cephalosporins
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Explain overexpression of efflux pumps

Overexpression of efflux pumps through mutation in gene promoters
  • Mutation in promoter of multi-drug resistance (mtr) gene involved in resistance to multiple antibiotics

Multi-locus sequence typing (MLST) surveillance technique

  • Sequence of 7 housekeeping genes that are genetically stable
  • Widely spear over the chromosome
  • Not under selective pressure
  • Not adjacent to outer membrane proteins and secreted or hypothetical proteins
  • Not on mobile elements


MLST types and antimicrobial resistance
  • Certain MLST types were found to be associated to antimicrobial resistance
  • Surveillance: MLST typing of circulating bacteria to get insight in resistance prevalence
  • Higher resolution: whole-genome sequencing



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