Abstract
Neisseria meningitidis is the causative agent of invasive meningococcal disease (IMD). The BEXSERO® vaccine which is used to prevent serogroup B disease is composed of four sub-capsular protein antigens supplemented with an outer membrane vesicle. Since the sub-capsular protein antigens are variably expressed and antigenically variable amongst meningococcal isolates, vaccine coverage can be estimated by the meningococcal antigen typing system (MATS) which measures the propensity of the strain to be killed by vaccinated sera. Whole genome sequencing (WGS) which identifies the alleles of the antigens that may be recognised by the antibody response could represent, in future, an alternative estimate of coverage. In this study, WGS of 278 meningococcal isolates responsible for 62% of IMD in Western Australia from 2000–2014 were analysed for association of genetic lineage (sequence type [ST], clonal complex [cc]) with BEXSERO® antigen sequence type (BAST) and MATS to predict the annual vaccine coverage. A hyper-endemic period of IMD between 2000–05 was caused by cc41/44 with the major sequence type of ST-146 which was not predicted by MATS or BAST to be covered by the vaccine. An increase in serogroup diversity was observed between 2010–14 with the emergence of cc11 serogroup W in the adolescent population and cc23 serogroup Y in the elderly. BASTs were statistically associated with clonal complex although individual antigens underwent antigenic drift from the major type. BAST and MATS predicted an annual range of 44–91% vaccine coverage. Periods of low vaccine coverage in years post-2005 were not a result of the resurgence of cc41/44:ST-146 but were characterised by increased diversity of clonal complexes expressing BASTs which were not predicted by MATS to be covered by the vaccine. The driving force behind the diversity of the clonal complex and BAST during these periods of low vaccine coverage is unknown, but could be due to immune selection and inter-strain competition with carriage of non-disease causing meningococci.
Highlights
Neisseria meningitidis is the causative agent of invasive meningococcal disease (IMD)
Prevalence and Distribution of serogroup and multi-locus sequence typing (MLST) clonal complexes Of the 447 notified cases of IMD in Western Australia (WA), the serogroup was determined for 436 isolates
In WA, cc41/44:sequence type (ST)-146 was the predominant cause of IMD in children
Summary
Neisseria meningitidis (the meningococcus) is the causative agent of invasive meningococcal disease (IMD). IMD is characterised by meningitis and/or fatal septicaemia. Meningococci expressing capsule serogroups A, B, C, W, Y and X are most often associated with outbreaks [2, 3]. Conjugated polysaccharide vaccines of A, C, W and Y serogroups elicit herd immunity and have suppressed disease worldwide [4]. Because serogroup B polysaccharide mimics human antigens, a vaccine using sub-capsular protein antigens has been licensed for the control of serogroup B disease. The BEXSERO1 vaccine (previously known as 4CMenB) (Novartis) incorporates factor H binding protein (fHbp), Neisseria adhesin A (NadA), Neisserial Heparin-Binding Antigen (NHBA) and Porin antigen A (PorA) [5]
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