Oral Presentation Australian Society for Microbiology Annual Scientific Meeting 2018

Molecular epidemiology of the 2013-2017 pertussis epidemic in Australia (#130)

Alice(Zheng) Xu 1 , Sophie Octavia 1 , Laurence Don Wai Luu 1 , Michael Payne 1 , Verlaine Timms 2 , Alfred Chin Yen Tay 3 , Anthony Keil 4 , Vitali Sintchenko 2 , Ruiting Lan 1
  1. UNSW, Randwick, NSW, Australia
  2. Centre for Infectious Diseases and Microbiology–Public Health, Institute of Clinical Pathology and Medical Research, Sydney, NSW, Australia
  3. Marie Bashir Institute for Infectious Diseases and Biosecurity, The University of Sydney, Sydney, NSW, Australia
  4. Department of Microbiology, Path West Laboratory Medicine WA, Perth, WA, Australia

Background: Pertussis (whooping cough) is a vaccine preventable disease caused by the bacterium Bordetella pertussis. Despite high vaccine coverage, pertussis has re-emerged to cause epidemic level disease. Our prior studies have shown a rapid increase in the proportion of B. pertussis isolates not expressing PRN (PRN-negative) during the 2008-2012 epidemic. As a new pertussis epidemic occurred in 2015 and to further our understanding of pertussis epidemiology, we characterised Australian B. pertussis isolates from 2013-2017, and compared their molecular characteristics with isolates from the 2008-2012 epidemic.


Methods: Whole-genome sequencing was performed on 78 clinical isolates collected from 2013-2017 to detect single-nucleotide polymorphisms (SNPs) in virulence genes and to determine their SNP profiles (SP). Together with previous 27 previously sequenced Australian B. pertussis isolates, a total of 105 isolates were analysed to determine their phylogenetic relationships. Western immunoblotting was performed to detect the expression of pertussis toxin (PTX), PRN and Filamentous haemagglutinin (FHA) proteins.


Results: The 78 isolates were typed into two SPs: SP13 (SNP cluster I, ptxP3, 96.15% [75/78]) and SP18 (non-cluster I, ptxP1, 3.85% [3/78]). The majority (75/78, 96.15%) of the SP13 isolates had the prn2 and fim3A allele. Three non-cluster I SP18 isolates genotyped as ptxP1-fim3A*-prn1. The frequency of ptxP and fim3 alleles were higher than those observed during the last epidemic. For PRN, 89.74% (70/78) of the isolates were found to be PRN-negative. By contrast, the percentage of PRN-negative isolates increased from 5.13% in 2008 to 77.78% in 2012. One novel PRN inactivation mechanism and a novel fim2-3 allele were also found in this study. Importantly, we detected the first FHA-negative B. pertussis isolate in Australia.


Conclusion: The Australian 2013-2017 pertussis epidemic was predominantly caused by PRN-negative isolates, with local and interstate expansion. Our results suggest that B. pertussis continues to evolve under vaccine-induced selective pressure.