Rapid Poster Presentation BACPATH 2019

Serogroup W clonal complex 11 meningococci from Western Australia have increased invasive potential compared to other hyperinvasive lineages. (#33)

Edward Mikucki 1 , Shakeel Mowlaboccus 1 , Charlene Kahler 1
  1. The Marshall Centre for Infectious Diseases Research and Training, The University of Western Australia, Perth, WA, Australia

Serogroup W Neisseria meningitidis isolates from clonal complex 11 (MenW:cc11) are responsible for outbreaks of invasive meningococcal disease worldwide. In Western Australia, two distinct lineages of MenW:cc11 isolates have emerged since 2016, Cluster A and Cluster B, the latter of which is penicillin-resistant and was responsible for 81% of all MenW cases in WA since 2018.This study characterised the virulence of three Cluster A and three B representatives by investigating the expression of major known virulence determinants and comparing attachment and invasion into Detroit 562 epithelial cells. Immunoblots to detect expression of Opa and PilE surface antigens showed that these determinants were not phase-variable in all six MenW:cc11 isolates analysed. No differences in the genotype of the loci encoding the minor adhesins NadA, NhhA, fHbp, and App were observed among MenW:cc11 isolates, while the opcA locus was not detected in all isolates. Bioinformatics analysis of the whole genome revealed that all isolates were predicted to express the L2/L4 immunotype lipooligosaccharide which has a terminal lacto-N-neotetraose (LNT) moiety.  Tricine SDS-PAGE showed that all isolates had a LOS with a mass of 4.6 kDa consistent with a L2/L4 LOS, but only Cluster A isolates reacted with the 3F11 monoclonal antibody (MAb) that detects LNT. All three Cluster B isolates exhibited a 3F11-negative phenotype which is often the result of blocking MAb binding by terminal sialylation of the LNT. A comparison of three MenW:cc11 strains with a cc8 strain NMB found no significant difference in their ability to colonise Detroit 562 cells. However, two strains belonging to Cluster A displayed a significant 21.0- and 16.0-fold increase in invasion, respectively, compared to strain NMB. In conjunction with previous work, these results demonstrate a wide range of invasive potential amongst meningococcal lineages even when the expression of known virulence factors are accounted for. The factors contributing to the increased invasive potential of MenW:cc11 isolates from WA have yet to be identified.