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Volume 20, Number 4—April 2014

Research

Rapid Increase in Pertactin-deficient Bordetella pertussis Isolates, Australia

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, and Ruiting LanComments to Author 
Author affiliations: University of New South Wales, Sydney, New South Wales, Australia (C. Lam. S. Octavia, L. Ricafort, R. Lan); University of Sydney, Sydney (V. Sintchenko, G.L. Gilbert); Westmead Hospital, Sydney, (V. Sintchenko, N. Wood, P. McIntyre); University of Adelaide, Adelaide, South Australia, Australia (H. Marshall); Institut Pasteur, Paris, France (N. Guiso); Princess Margaret Hospital for Children, Perth, Western Australia, Australia (A.D. Keil); Women’s and Children’s Hospital, Adelaide (A. Lawrence); Sullivan Nicolaides Pathology, Brisbane, Queensland, Australia (J. Robson); University of Melbourne, Parkville, Victoria, Australia (G. Hogg)

Main Article

Figure 3

Variations in protactin (prn) gene of prn-negative Bordetella pertussis isolates, Australia, 2008–2012, Ninety-six B. pertussis isolates were identified as prn negative. Eighty of these isolates had 1 of 4 mechanisms of prn disruption: IS481 (in forward and reverse directions) and IS1002, which were inserted at the ACTAGG motif within prn, or an extended homopolymeric tract of G residues (n = 1). Lower case letters indicate residues that are conserved in all IS disruptions, and red letters indic

Figure 3. . . Variations in protactin (prn) gene of prn-negative Bordetella pertussis isolates, Australia, 2008–2012, Ninety-six B. pertussis isolates were identified as prn negative. Eighty of these isolates had 1 of 4 mechanisms of prn disruption: IS481 (in forward and reverse directions) and IS1002, which were inserted at the ACTAGG motif within prn, or an extended homopolymeric tract of G residues (n = 1). Lower case letters indicate residues that are conserved in all IS disruptions, and red letters indicate differences in IS disruptions. Positions of nucleotides have been numbered relative to the first start codon of sequence AJ011092 (17). The prn gene of 2 isolates was not amplified by PCR with a combination of primers from published studies (1519), which indicated a deletion of the entire gene. Sixteen isolates that had no gene disruptions were also observed.

Main Article

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