Michelle Clarke1, Peter B McIntyre2, Christopher C Blyth3, Nick Wood2, Sophie Octavia4, Vitali Sintchenko5, Lynne Giles6, Helen Quinn7, Verity Hill8, Gabrielle Hanly9, Ruiting Lan10, Helen S Marshall11. 1. School of Public Health, University of Adelaide, Adelaide, SA 5000, Australia; Discipline of Paediatrics, Women's and Children's Hospital, North Adelaide, SA 5006, Australia; School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia. 2. National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases (NCIRS), The Children's Hospital at Westmead, Westmead, NSW, 2145, Australia; Discipline of Paediatrics and Child Health, University of Sydney, The Children's Hospital at Westmead, Westmead, NSW, 2145, Australia; Department of Microbiology and Infectious Diseases, The Children's Hospital at Westmead, NSW, Australia. 3. School of Paediatrics and Child Health, University of Western Australia, WA, Australia; Department of Infectious Diseases, Princess Margaret Hospital for Children, WA, Australia; Wesfarmers Centre for Vaccines and Infectious Diseases, Telethon Kids Institute, WA, Australia; Department of Microbiology, Princess Margaret Hospital, PathWest Laboratory Medicine, WA, Australia. 4. School of Biotechnology and Biomolecular Sciences, University of New South Wales, NSW, Australia. 5. Sydney Emerging Infectious Diseases and Biosecurity Institute, The University of Sydney, NSW, Australia; Centre for Infectious Diseases and Microbiology (CIDM) Public Health, Sydney West LHD and Pathology West, NSW, Australia. 6. School of Public Health, University of Adelaide, Adelaide, SA 5000, Australia; Robinson Research Institute, University of Adelaide, SA 5000, Australia. 7. National Centre for Immunisation Research and Surveillance of Vaccine Preventable Diseases (NCIRS), The Children's Hospital at Westmead, Westmead, NSW, 2145, Australia; Discipline of Paediatrics and Child Health, University of Sydney, The Children's Hospital at Westmead, Westmead, NSW, 2145, Australia. 8. Discipline of Paediatrics, Women's and Children's Hospital, North Adelaide, SA 5006, Australia. 9. School of Paediatrics and Child Health, University of Western Australia, WA, Australia. 10. School of Biotechnology and Biomolecular Sciences, University of New South Wales, NSW, Australia. Electronic address: r.lan@unsw.edu.au. 11. School of Public Health, University of Adelaide, Adelaide, SA 5000, Australia; Discipline of Paediatrics, Women's and Children's Hospital, North Adelaide, SA 5006, Australia; School of Medicine, University of Adelaide, Adelaide, SA 5000, Australia; Robinson Research Institute, University of Adelaide, SA 5000, Australia. Electronic address: Helen.marshall@adelaide.edu.au.
Abstract
OBJECTIVES: Changes in circulating Bordetella pertussis genotypes, including a novel pertussis toxin promoter ptxP3 allele and absence of pertactin (Prn) antigen, have been reported from several countries but limited data on relative severity are available. We compared markers of disease severity in children with B. pertussis infection due to strains of differing genotype. METHODS: Culture confirmed cases presenting to tertiary paediatric hospitals in three Australian states between 2008 and 2012 were classified as severe if they required a hospital stay greater than seven days, were admitted to intensive care, or if death occurred. Associations between age, vaccination, genotype and severity were assessed. RESULTS: Of 199 pertussis cases, 81 (41%) were <3 months, including 32/39 (82%) of severe cases. The proportion of isolates from these cases that were Prn deficient increased markedly between 2008 and 2012. Of B. pertussis isolates, the proportion considered severe was similar for Prn positive (27/128, 21%) and Prn deficient (12/71, 17%) cases but only 1/22 (4.5%) of non ptxP3 cases were severe versus 38/177 (21.4%) ptxP3 positive. Adjusting for ptxP type, vaccination status and age, disease severity was not significantly associated with Prn status (RRA: 0.95, [0.57-1.56]; p = 0.83). CONCLUSIONS: In children, we found no relationship between Prn status and markers of severe pertussis. An increased proportion of severe disease in isolates with the ptxP3 allele was observed.
OBJECTIVES: Changes in circulating Bordetella pertussis genotypes, including a novel pertussis toxin promoter ptxP3 allele and absence of pertactin (Prn) antigen, have been reported from several countries but limited data on relative severity are available. We compared markers of disease severity in children with B. pertussis infection due to strains of differing genotype. METHODS: Culture confirmed cases presenting to tertiary paediatric hospitals in three Australian states between 2008 and 2012 were classified as severe if they required a hospital stay greater than seven days, were admitted to intensive care, or if death occurred. Associations between age, vaccination, genotype and severity were assessed. RESULTS: Of 199 pertussis cases, 81 (41%) were <3 months, including 32/39 (82%) of severe cases. The proportion of isolates from these cases that were Prn deficient increased markedly between 2008 and 2012. Of B. pertussis isolates, the proportion considered severe was similar for Prn positive (27/128, 21%) and Prn deficient (12/71, 17%) cases but only 1/22 (4.5%) of non ptxP3 cases were severe versus 38/177 (21.4%) ptxP3 positive. Adjusting for ptxP type, vaccination status and age, disease severity was not significantly associated with Prn status (RRA: 0.95, [0.57-1.56]; p = 0.83). CONCLUSIONS: In children, we found no relationship between Prn status and markers of severe pertussis. An increased proportion of severe disease in isolates with the ptxP3 allele was observed.
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