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Rapid Increase in Pertactin-deficient Bordetella pertussis Isolates, Australia

Identifieur interne : 001887 ( Ncbi/Curation ); précédent : 001886; suivant : 001888

Rapid Increase in Pertactin-deficient Bordetella pertussis Isolates, Australia

Auteurs : Connie Lam ; Sophie Octavia ; Lawrence Ricafort ; Vitali Sintchenko ; Gwendolyn L. Gilbert ; Nicholas Wood ; Peter Mcintyre ; Helen Marshall ; Nicole Guiso ; Anthony D. Keil ; Andrew Lawrence ; Jenny Robson ; Geoff Hogg ; Ruiting Lan

Source :

RBID : PMC:3966384

Abstract

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.


Url:
DOI: 10.3201/eid2004.131478
PubMed: 24655754
PubMed Central: 3966384

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PMC:3966384

Le document en format XML

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<p>Acellular vaccines against
<italic>Bordetella pertussis</italic>
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
<italic>B. pertussis</italic>
isolates did not express the vaccine antigen pertactin (prn). Multiple mechanisms of prn inactivation were documented, including IS
<italic>481</italic>
and IS
<italic>1002</italic>
disruptions, a variation within a homopolymeric tract, and deletion of the
<italic>prn</italic>
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
<italic>B. pertussis</italic>
not expressing prn arose independently multiple times since 2008, rather than by expansion of a single prn-negative clone. All but 1 isolate had
<italic>ptxA1</italic>
,
<italic>prn2</italic>
, and
<italic>ptxP3</italic>
, the alleles representative of currently circulating strains in Australia. This pattern is consistent with continuing evolution of
<italic>B. pertussis</italic>
in response to vaccine selection pressure.</p>
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