Microevolution of epidemic Australian <em>Bordetella pertussis</em> isolates — ASN Events
  1. Schedule
  2. Poster Session B
  3. Microevolution of epidemic Australian Bordetella pertussis isolates

Microevolution of epidemic Australian Bordetella pertussis isolates (#322)

Azadeh Safarchi 1 , Sophie Octavia 1 , Sandeep Kaur 1 , Vitali Sintchenko 2 , Gwendolyn L Gilbert 2 , Nicholas Wood Wood 2 , Peter McIntyre 2 , Helen Marshall 3 , Anthony D Keil 4 , Ruiting Lan 1
  1. University of New South Wales, Kingsford, Sydney, NSW, Australia
  2. Centre for Infectious Diseases and Microbiology, Institute of Clinical Pathology and Medical Research-Westmead Hospital, Sydney, New South Wales, Australia
  3. Vaccinology and Immunology Research Trials Unit-Women’s and Children’s Hospital and School of Paediatrics and Reproductive Health and Robinson Research Institute, University of Adelaide, Adelaide, South Australia, Australia
  4. Department of Microbiology,PathWest Laboratory Medicine WA, Princess Margaret Hospital for Children, Perth, Western Australia, Australia

Despite high pertussis vaccination coverage, Australia experienced a prolonged epidemic in 2008-2012. The predominant B. pertussis genotype harboured pertussis toxin promoter allele, ptxP3, and pertactin gene allele, prn2. The emergence and expansion of non-expressing prn isolates (Prn negative), was also observed. In this study, whole genome sequencing was used to investigate the evolution and genomic diversity of 22 epidemic B. pertussis isolates, including 10 Prn-negative strains with three different modes of inactivation (IS481F, IS481R and IS1002). Five pre-epidemic strains were also sequenced for comparison. Five single nucleotide polymorphisms (SNPs) were common in the epidemic isolates and differentiated them from pre-epidemic isolates. We found that virulence-associated genes had higher numbers of non-synonymous SNPs, indicating selection pressure driving their evolution and that isolates not expressing Prn were derived independently multiple times. We conclude that SNPs play an important role in the adaptation and microevolution of the 2008-2012 epidemic B. pertussis. 

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