Azadeh Safarchi1, Sophie Octavia1, Sunny Z Wu1, Sandeep Kaur1, Vitali Sintchenko2, Gwendolyn L Gilbert2, Nicholas Wood3, Peter McIntyre3, Helen Marshall4, Anthony D Keil5, Ruiting Lan6. 1. School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, New South Wales, Australia. 2. Centre for Infectious Diseases and Microbiology - Public Health, Institute of Clinical Pathology and Medical Research, Pathology West, Westmead Hospital, New South Wales, Australia; Marie Bashir Institute for Infectious Diseases and Biosecurity, The University of Sydney, New South Wales, Australia. 3. National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases (NCIRS), The Children's Hospital at Westmead, Westmead, New South Wales 2145, Australia; Discipline of Paediatrics and Child Health, University of Sydney, The Children's Hospital at Westmead, Westmead, New South Wales 2145, Australia; Department of Microbiology and Infectious Diseases, The Children's Hospital at Westmead, New South Wales, Australia. 4. Vaccinology and Immunology Research Trials Unit, Women's and Children's Hospital and School of Medicine and Robinson Research Institute, University of Adelaide, South Australia, Australia. 5. Department of Microbiology, PathWest Laboratory Medicine WA, Princess Margaret Hospital for Children, Perth, Australia. 6. School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, New South Wales, Australia. Electronic address: r.lan@unsw.edu.au.
Abstract
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.
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.
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