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During the 2008-2012 pertussis epidemic in Australia, pertactin (Prn)-negative Bordetella pertussis emerged. We analyzed 78 isolates from the 2013-2017 epidemic and documented continued expansion of Prn-negative ptxP3 B. pertussis strains. We also detected a filamentous hemagglutinin-negative and Prn-negative B. pertussis isolate.

Objectives: Despite high pertussis vaccination coverage, Australia experienced a prolonged epidemic in 2008-2012. The predominant Bordetella pertussis genotype harboured pertussis toxin promoter allele, ptxP3, and pertactin gene allele, prn2. The emergence and expansion of prn non-expressing isolates (Prn negative), were also observed. We aimed to investigate the microevolution and genomic diversity of epidemic B. pertussis isolates., Methods: We sequenced 22 B. pertussis isolates collected in 2008-2012 from two states of Australia which are geographically widely separated. Ten of the 22 were Prn negative isolates with three different modes of silencing of prn (prn::IS481F, prn::IS481R and prn::IS1002). Five pre-epidemic isolates were also sequenced for comparison., Results: Five single nucleotide polymorphisms were common in the epidemic isolates and differentiated them from pre-epidemic isolates. The Australian epidemic isolates can be divided into five lineages (EL1-EL5) with EL1 containing only Prn negative isolates. Comparison with global isolates showed that three lineages remained geographically and temporally distinct whereas two lineages mixed with isolates from 2012 UK outbreak., Conclusion: Our results suggest significant diversification and the microevolution of B. pertussis within the 2008-2012 Australian epidemic., (Copyright © 2016 The British Infection Association. Published by Elsevier Ltd. All rights reserved.)

Acellular vaccines against Bordetella pertussis were introduced in Australia in 1997. By 2000, these vaccines had replaced whole-cell vaccines. During 2008-2012, a large outbreak of pertussis occurred. During this period, 30% (96/320) of B. pertussis isolates did not express the vaccine antigen pertactin (Prn). Multiple mechanisms of Prn inactivation were documented, including IS481 and IS1002 disruptions, a variation within a homopolymeric tract, and deletion of the prn gene. The mechanism of lack of expression of Prn in 16 (17%) isolates could not be determined at the sequence level. These findings suggest that B. pertussis not expressing Prn arose independently multiple times since 2008, rather than by expansion of a single Prn-negative clone. All but 1 isolate had ptxA1, prn2, and ptxP3, the alleles representative of currently circulating strains in Australia. This pattern is consistent with continuing evolution of B. pertussis in response to vaccine selection pressure.

Australia is experiencing a prolonged epidemic of pertussis that began in 2008. A total of 194 Bordetella pertussis isolates collected from 2008 through 2010 were typed by single-nucleotide polymorphism (SNP) analysis, by multilocus variable number tandem repeats analysis, and by fim3, prn, and ptxP sequence analyses. Strains with 2 closely related SNP profiles carrying prn2 and ptxP3 from the recently emerged SNP cluster I predominated. The data suggest increasing selection among the B. pertussis population in Australia in favor of strains carrying prn2 and ptxP3 under the pressure of acellular vaccine-induced immunity.