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 in Australia. The largest epidemic spanned between 2008 - 2012 and peaked in 2011 with 39,000 cases. Our prior studies have shown that B. pertussis isolates deficient in the expression of the vaccine antigen, pertactin (Prn), have emerged and expanded during the 2008 - 2012 epidemic. As a new pertussis epidemic occurred in NSW in 2015 and to further our understanding of pertussis epidemiology, we characterised Australian B. pertussis isolates from 2013 - 2016, and compared their molecular characteristics with isolates from the 2008 - 2012 epidemic.
Methods: A total of 69 isolates from Western Australia and New South Wales were collected from 2013 to 2016. Real-time PCR was used for detecting the single-nucleotide polymorphisms (SNPs) of the virulence genes ptxP3 and fim3 and to determine SNP profiles (SP). Western immunoblotting was used to detect the expression of pertussis toxin (Ptx), Prn and Filamentous haemagglutinin (Fha) proteins.
Results: SNP typing revealed that all except three isolates belonged to SNP cluster I and these strains all belonged to SP13. In contrast, the 2008 – 2012 epidemic was dominated by three SPs, SP13, SP14 and SP16. Similarly, by ptxP typing, 96% (66 out of 69) of the isolates were ptxP3, compared with 86% (167/194) of the isolates being ptxP3 in the 2008 – 2012 epidemic. All except one ptxP3 isolate carried the fim3A allele, and only one isolate had fim3B. All except five isolates (93% [64/69]) did not express Prn. In comparison, during the 2008–2012 epidemic, 30% (96/320) of all isolates and 78% (28/36) of the 2012 isolates were Prn negative.
Conclusion: Prn deficient strains continue to expand in Australia, showing continuing evolution of epidemic pertussis in Australia. It is critical that we continue to monitor vaccine antigen deficient strains of this re-emerging disease.