Clarke M.,University of Adelaide |
Clarke M.,Womens and Childrens Hospital |
McIntyre P.B.,The Childrens Hospital at Westmead |
McIntyre P.B.,University of Sydney |
And 20 more authors.
Journal of Infection | Year: 2016
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. © 2015 The British Infection Association.
Watts M.R.,Center for Infectious Diseases and Microbiology Public Health |
Watts M.R.,Pathology West Institute for Clinical Pathology |
Watts M.R.,University of Sydney |
Chan R.C.F.,Concord Repatriation General Hospital |
And 18 more authors.
Emerging Infectious Diseases | Year: 2014
The insect microsporidian Anncaliia algerae was first described in 2004 as a cause of fatal myositis in an immunosuppressed person from Pennsylvania, USA. Two cases were subsequently reported, and we detail 2 additional cases, including the only nonfatal case. We reviewed all 5 case histories with respect to clinical characteristics, diagnosis, and management and summarized organism life cycle and epidemiology. Before infection, all case-patients were using immunosuppressive medications for rheumatoid arthritis or solid-organ transplantation. Four of the 5 case-patients were from Australia. All diagnoses were confirmed by skeletal muscle biopsy; however, peripheral nerves and other tissues may be infected. The surviving patient received albendazole and had a reduction of immunosuppressive medications and measures to prevent complications. Although insects are the natural hosts for A. algerae, human contact with water contaminated by spores may be a mode of transmission. A. algerae has emerged as a cause of myositis, particularly in coastal Australia.
Lowbridge C.,Public Health Officer Training Program |
Lowbridge C.,University of New South Wales |
McIntyre P.B.,Childrens Hospital |
McIntyre P.B.,University of Sydney |
And 5 more authors.
Vaccine | Year: 2015
Introduction: Significant reductions in invasive pneumococcal disease (IPD) following 7-valent pneumococcal conjugate vaccine (7vPCV) are well documented, but population-level data comparing different schedules are sparse. We compared data from long-term stable surveillance in one Australian region (3 primary doses (3 + 0) schedule) with similar data from England and Wales (2 + 1 schedule) and the United States (3 + 1 schedule). Methods: Incidence rate ratios (IRRs) for all, vaccine type, and non-vaccine type IPD were calculated by age-group, using comparable case definitions and time periods post 7vPCV introduction. Results: At baseline, the % of IPD due to 7vPCV serotypes (VT) disease in children <5 years was 88% in Greater Sydney (GS), 83% in the United States (US), and 74% in England and Wales (E&W). IRR for VT IPD <5 years in GS was 0.05 (0.02-0.09), for ≥65 years was 0.15 (0.12-0.19) and for all ages 0.12 (0.10-0.13). In the US, IRR for VT IPD was lower in each age group, and for all ages the 95% CI of the IRR (0.06 (0.05-0.07)), did not overlap with GS or E&W (0.14 (0.11-0.18)). In contrast, the IRR for IPD due to any serotype did not differ between sites for any age group or overall. Conclusions: Differences in direct and indirect reductions in VT IPD with a "3 + 0″ 7vPCV schedule versus "2 + 1″ or "3 + 1″ were small. All 3 countries moved to 13vPCV by 2011; data post 13vPCV will be important to assess IPD impact using more similar baseline incidence and comparison periods. © 2015 Elsevier Ltd.