Neisseria gonorrhoeae-derived outer membrane vesicles package β-lactamases to promote antibiotic resistance

Subhash Dhital, Pankaj Deo, Manasa Bharathwaj, Kristy Horan, Joshua Nickson, Mohammad Azad, Isabella Stuart, Seong H Chow, Sachith D Gunasinghe, Rebecca Bamert, Jian Li, Trevor Lithgow, Benjamin P. Howden, Thomas Naderer

Research output: Contribution to journalArticleResearchpeer-review

13 Citations (Scopus)

Abstract

Neisseria gonorrhoeae causes the sexually transmitted disease gonorrhoea. The treatment of gonorrhoea is becoming increasingly challenging, as N. gonorrhoeae has developed resistance to antimicrobial agents routinely used in the clinic. Resistance to penicillin is wide-spread partly due to the acquisition of β-lactamase genes. How N. gonorrhoeae survives an initial exposure to β-lactams before acquiring resistance genes remains to be understood. Here, using a panel of clinical isolates of N. gonorrhoeae we show that the β-lactamase enzyme is packaged into outer membrane vesicles (OMVs) by strains expressing blaTEM-1B or blaTEM-106, which protects otherwise susceptible clinical isolates from the β-lactam drug amoxycillin. We characterized the phenotypes of these clinical isolates of N. gonorrhoeae and the time courses over which the cross-protection of the strains is effective. Imaging and biochemical assays suggest that OMVs promote the transfer of proteins and lipids between bacteria. Thus, N. gonorrhoeae strains secret antibiotic degrading enzymes via OMVs enabling survival of otherwise susceptible bacteria.

Original languageEnglish
Article numberuqac013
Number of pages11
JournalmicroLife
Volume3
DOIs
Publication statusPublished - 29 Jul 2022

Keywords

  • antimicrobial resistance
  • gonorrhoea
  • lactamase
  • OMV
  • secretion system
  • TEM-1

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