Publication | Open Access
Rapid Increase in Pertactin-deficient<i>Bordetella pertussis</i>Isolates, Australia
171
Citations
31
References
2014
Year
VaccinationVaccine DevelopmentBordetella PertussisMedicineZoonotic DiseasePathogenesisImmunologyVaccine TargetImmunodominanceB. Pertussis IsolatesEmerging Infectious DiseaseInfection ControlRapid IncreaseClinical Infectious DiseasePrecision VaccinologyClinical MicrobiologyEpidemiologyB. Pertussis
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.
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