Rapid increase in pertactin-deficient Bordetella pertussis isolates, Australia.

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 (Pm). Multiple mechanisms of Prn inactivation were documented, including IS481 and IS 1002 disruptions, a variation within a homopolymeric tract, and deletion of the pm gene. The mechanism of lack of expression of Pm in 16 (17%) isolates could not be determined at the sequence level. These findings suggest that B. pertussis not expressing Pm 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.