Poster Presentation BACPATH 2017

Whole-genome Sequencing Reveals a New Cluster of Penicillin-resistant Serogroup W Neisseria meningitidis in Western Australia (#130)

Shakeel Mowlaboccus 1 2 , Keith A Jolley 3 , James E Bray 3 , Stanley Pang 4 5 , Yung Thin Lee 4 , Jane D Bew 6 , David J Speers 6 7 , Anthony D Keil 8 , Geoffrey W Coombs 4 5 , Charlene M Kahler 1 2 9
  1. Marshall Center for Infectious Diseases Research and Training, The University of Western Australia, Perth
  2. School of Biomedical Sciences, The University of Western Australia, Perth, Western Australia, Australia
  3. Department of Zoology, University of Oxford, Oxford, UK
  4. School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, Australia
  5. Department of Microbiology, PathWest Laboratory Medicine WA Fiona Stanley Hospital, Murdoch, Western Australia, Australia
  6. Department of Microbiology, PathWest Laboratory Medicine WA QEII Medical Centre, Perth, Western Australia, Australia
  7. School of Medicine and Pharmacology, The University of Western Australia, Perth, Western Australia, Australia
  8. Department of Microbiology, PathWest Laboratory Medicine WA Princess Margaret Hospital for Children, Perth, Western Australia, Australia
  9. Telethon Kids Institute, Perth, Western Australia, Australia

Neisseria meningitidis (meningococcus) causes invasive meningococcal disease (IMD) which has a mortality rate of 6%. Disease is most commonly caused by strains expressing capsule serogroups A, B, C, W, X or Y. Multi-locus sequence typing (MLST) classifies meningococci into genetic lineages termed clonal complexes (cc). Recent global outbreaks have been caused by meningococcal serogroup W belonging to cc11 (MenW:cc11). Although MenB has been the predominant cause of disease in Australia for decades, MenW predominated in 2016.

The aim was to analyse whole-genome sequences of invasive MenW:cc11 isolated in Western Australia (WA) and investigate changes in antibiotic susceptibility.

The genomic DNA of 19 MenW:cc11 strains isolated from patients in WA was sequenced using Illumina paired ends. Raw reads were assembled using Velvet Assembler and auto-tagged and curated using the BIGSdb genomics platform available from the PubMLST database.

In WA, the first MenW:cc11 case occurred in 2013. This was followed by two cases in 2014, three cases in 2015 and 13 cases in 2016. Four different sequence types (ST) were identified – ST-11 (n=11), ST-1287 (n=2), ST-3298 (n=1) and ST-12351 (n=5). All isolates possessed the P1.5,2:F1-1 PorA:FetA profile. Resistance to ciprofloxacin or rifampicin was not identified. However, variation in penicillin susceptibility was observed with 8 isolates showing high susceptibility (MIC=0.064 mg/L) compared to the remainder which were resistant (0.5 mg/L). Phylogenetic analysis of the core genomes identified two clusters, A and B. All isolates susceptible to penicillin fell in Cluster A and possessed the penA_59 allele. The penicillin-resistant meningococci, all isolated in 2016, fell in cluster B and possessed the penA_253 allele. Exchange of penA_59 for penA_253 in Cluster A isolates resulted in a significant increase in penicillin MIC.

In conclusion, core-genome analysis identified the emergence and expansion of a penicillin-resistant MenW:cc11 cluster in WA in 2016 which may impact treatment regimens.