H F Gidding1, L McCallum2, P Fathima3, H C Moore4, T L Snelling5, C C Blyth6, S Jayasinghe7, C Giele8, N de Klerk9, R M Andrews10, P B McIntyre11. 1. School of Public Health and Community Medicine, UNSW Medicine, The University of New South Wales, Sydney, NSW, Australia; National Centre for Immunisation Research and Surveillance, Westmead, NSW, Australia. Electronic address: hgidding@unsw.edu.au. 2. School of Public Health and Community Medicine, UNSW Medicine, The University of New South Wales, Sydney, NSW, Australia. Electronic address: lisa.mccallum@doh.health.nsw.gov.au. 3. Wesfarmers Centre of Vaccines and Infectious Diseases, Telethon Kids Institute, The University of Western Australia, Perth, WA, Australia. Electronic address: Parveen.Fathima@telethonkids.org.au. 4. Wesfarmers Centre of Vaccines and Infectious Diseases, Telethon Kids Institute, The University of Western Australia, Perth, WA, Australia. Electronic address: hannah.moore@telethonkids.org.au. 5. Wesfarmers Centre of Vaccines and Infectious Diseases, Telethon Kids Institute, The University of Western Australia, Perth, WA, Australia; Department of Infectious Diseases, Princess Margaret Hospital, Perth, WA, Australia; Menzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia; School of Public Health, Curtin University, Perth, WA, Australia. Electronic address: Tom.Snelling@telethonkids.org.au. 6. Wesfarmers Centre of Vaccines and Infectious Diseases, Telethon Kids Institute, The University of Western Australia, Perth, WA, Australia; Department of Infectious Diseases, Princess Margaret Hospital, Perth, WA, Australia; School of Medicine, University of Western Australia, Perth, WA, Australia; Department of Microbiology, PathWest Laboratory Medicine WA, Princess Margaret Hospital, Perth, WA, Australia. Electronic address: christopher.blyth@uwa.edu.au. 7. National Centre for Immunisation Research and Surveillance, Westmead, NSW, Australia; Discipline of Child and Adolescent Health, Medical School, University of Sydney, Sydney, Australia. Electronic address: sanjay.jayasinghe@health.nsw.gov.au. 8. Communicable Disease Control Directorate, Department of Health Western Australia, Perth, WA, Australia. Electronic address: Carolien.Giele@health.wa.gov.au. 9. Wesfarmers Centre of Vaccines and Infectious Diseases, Telethon Kids Institute, The University of Western Australia, Perth, WA, Australia. Electronic address: Nick.deKlerk@telethonkids.org.au. 10. Menzies School of Health Research, Charles Darwin University, Darwin, Northern Territory, Australia; National Centre for Epidemiology and Population Health, Australian National University, Canberra, Australian Capital Territory, Australia. Electronic address: ross.andrews@menzies.edu.au. 11. National Centre for Immunisation Research and Surveillance, Westmead, NSW, Australia; Discipline of Child and Adolescent Health, Medical School, University of Sydney, Sydney, Australia; School of Public Health, Medical School, University of Sydney, Sydney, Australia. Electronic address: peter.mcintyre@health.nsw.gov.au.
Abstract
BACKGROUND: Most studies use indirect cohort or case-control methods to estimate vaccine effectiveness (VE) of 7- and 13-valent pneumococcal conjugate vaccines (PCV7 and PCV13) against invasive pneumococcal disease (IPD). Neither method can measure the benefit vaccination programs afford the unvaccinated and many studies were unable to estimate dose-specific VE. We linked Australia's national immunisation register with health data from two states to calculate IPD incidence by vaccination status and VE for a 3 + 0 PCV schedule (doses at 2, 4, 6 months, no booster) among a cohort of 1.4 million births. METHODS: Births records for 2001-2012 were probabilistically linked to IPD notifications, hospitalisations, deaths, and vaccination history (available until December 2013). IPD rates in vaccinated and unvaccinated children <2 years old were compared using Cox proportional hazards models (adjusting for potential confounders), with VE = (1 - adjusted hazard ratio) × 100. Separate models were performed for all-cause, PCV7, PCV13 and PCV13-non-PCV7 serotype-specific IPD, and for Aboriginal and non-Aboriginal children. RESULTS: Following introduction of universal PCV7 in 2005, rates of PCV7 serotype and all-cause IPD in unvaccinated children declined 89.5% and 61.4%, respectively, to be similar to rates in vaccinated children. Among non-Aboriginal children, VEs for 3 doses were 94.2% (95%CI: 81.9-98.1) for PCV7 serotype-specific IPD, 85.6% (95%CI: 60.5-94.8) for PCV13-non-PCV7 serotype-specific IPD and 80.1% (95%CI: 59.4-90.3) for all-cause IPD. There were no statistically significant differences between the VEs for 3 doses and for 1 or 2 doses against PCV13 and PCV13-non-PCV7 serotype-specific IPD, or between Aboriginal and non-Aboriginal children. CONCLUSION: Our population-based cohort study demonstrates that >90% coverage in the first year of a universal 3 + 0 PCV program provided high population-level protection, predominantly attributable to strong herd effects. The size of the cohort enabled calculation of robust dose-specific VE estimates for important population sub-groups relevant to vaccination policies internationally.
BACKGROUND: Most studies use indirect cohort or case-control methods to estimate vaccine effectiveness (VE) of 7- and 13-valent pneumococcal conjugate vaccines (PCV7 and PCV13) against invasive pneumococcal disease (IPD). Neither method can measure the benefit vaccination programs afford the unvaccinated and many studies were unable to estimate dose-specific VE. We linked Australia's national immunisation register with health data from two states to calculate IPD incidence by vaccination status and VE for a 3 + 0 PCV schedule (doses at 2, 4, 6 months, no booster) among a cohort of 1.4 million births. METHODS: Births records for 2001-2012 were probabilistically linked to IPD notifications, hospitalisations, deaths, and vaccination history (available until December 2013). IPD rates in vaccinated and unvaccinated children <2 years old were compared using Cox proportional hazards models (adjusting for potential confounders), with VE = (1 - adjusted hazard ratio) × 100. Separate models were performed for all-cause, PCV7, PCV13 and PCV13-non-PCV7 serotype-specific IPD, and for Aboriginal and non-Aboriginal children. RESULTS: Following introduction of universal PCV7 in 2005, rates of PCV7 serotype and all-cause IPD in unvaccinated children declined 89.5% and 61.4%, respectively, to be similar to rates in vaccinated children. Among non-Aboriginal children, VEs for 3 doses were 94.2% (95%CI: 81.9-98.1) for PCV7 serotype-specific IPD, 85.6% (95%CI: 60.5-94.8) for PCV13-non-PCV7 serotype-specific IPD and 80.1% (95%CI: 59.4-90.3) for all-cause IPD. There were no statistically significant differences between the VEs for 3 doses and for 1 or 2 doses against PCV13 and PCV13-non-PCV7 serotype-specific IPD, or between Aboriginal and non-Aboriginal children. CONCLUSION: Our population-based cohort study demonstrates that >90% coverage in the first year of a universal 3 + 0 PCV program provided high population-level protection, predominantly attributable to strong herd effects. The size of the cohort enabled calculation of robust dose-specific VE estimates for important population sub-groups relevant to vaccination policies internationally.
Authors: Shabir A Madhi; Eleonora Aml Mutsaerts; Alane Izu; Welekazi Boyce; Sutika Bhikha; Benit T Ikulinda; Lisa Jose; Anthonet Koen; Amit J Nana; Andrew Moultrie; Lucy Roalfe; Adam Hunt; David Goldblatt; Clare L Cutland; Jeffrey R Dorfman Journal: Lancet Infect Dis Date: 2020-08-25 Impact factor: 25.071