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Vicki L Krause

Publications and source records attributed to Vicki L Krause.

8 recordsLinked to original sources

Invasive Streptococcus dysgalactiae subspecies equisimilis compared with Streptococcus pyogenes in Australia, 2011-23, and the emergence of a multi-continent stG62647 lineage: a retrospective clinical and genomic epidemiology study.

BACKGROUND: Streptococcus dysgalactiae subspecies equisimilis (SDSE) is closely related to Streptococcus pyogenes, with overlapping disease manifestations. We compared the clinical and genomic epidemiology of invasive SDSE with invasive S pyogenes across different settings in Australia and phylogenetically contextualised the SDSE sequences within a global cohort of genomes. METHODS: In this retrospective clinical and genomic epidemiology study, cases of invasive SDSE isolated from normally sterile sites were identified and whole-genome sequenced across five hospital networks in temperate southeast Australia (Melbourne and Sydney) and the tropical Top End of the Northern Territory. SDSE disease incidence, case demographics, clinical outcomes, and longitudinal lineage dynamics were compared between southeast Australia and the Top End and to co-collected invasive S pyogenes cases in each region. SDSE genomes and lineages were also contextualised within 1166 global SDSE sequences. Genomic transmission clusters (not necessarily direct transmission) were inferred between isolates from different individuals by single-linkage clustering at a single nucleotide polymorphism threshold of less than or equal to seven for SDSE and less than or equal to five for S pyogenes based on previous transmission analyses. FINDINGS: Between Jan 1, 2011, and Feb 28, 2023, there were 693 invasive SDSE cases and 995 invasive S pyogenes cases. Invasive SDSE occurred almost exclusively in adults. The overall invasive SDSE incidence in southeast Australia was similar to invasive S pyogenes (incidence rate ratio [IRR] 1&#xb7;15, 95% CI 0&#xb7;91-1&#xb7;46; p=0&#xb7;26) and increased over the study period (IRR 1&#xb7;06 per year, 95% CI 1&#xb7;05-1&#xb7;08; p<0&#xb7;0001) from 1&#xb7;30 cases per 10&#x2009;000 admissions in 2011 to 3&#xb7;72 cases per 10&#x2009;000 admissions in the first 2 months of 2023 (95% CI 2&#xb7;13-6&#xb7;07). In southeast Australia, where stringent COVID-19 non-pharmaceutical interventions (NPIs) were implemented between 2020 and 2021, the SDSE incidence plateaued during 2020-21 but did not significantly decline (IRR 1&#xb7;09 compared with 2017-19, 95% CI 0&#xb7;88-1&#xb7;35; p=0&#xb7;47). By contrast, S pyogenes incidence substantially declined in 2020-21 in southeast Australia (IRR 0&#xb7;35 compared to 2017-19, 95% CI 0&#xb7;22-0&#xb7;52; p=0&#xb7;017). In the Top End, SDSE incidence was lower than S pyogenes (IRR 0&#xb7;24, 95% CI 0&#xb7;19-0&#xb7;31; p<0&#xb7;0001). However, crude incidence remained higher than southeast Australia (crude IRR 1&#xb7;24, 95% CI 1&#xb7;07-1&#xb7;42; p=0&#xb7;0037) and disproportionately affected First Nations Australians in the Top End compared with non-First Nations individuals (IRR 3&#xb7;36, 95% CI 2&#xb7;33-4&#xb7;85; p<0&#xb7;0001). Comparing 2020-21 with 2017-19, there was no decline in SDSE (IRR 1&#xb7;27, 95% CI 0&#xb7;73-2&#xb7;24; p=0&#xb7;45) or S pyogenes (IRR 0&#xb7;97, 95% CI 0&#xb7;80-1&#xb7;18; p=0&#xb7;81) incidence in the Top End, which did not implement prolonged stringent COVID-19 NPIs. Analysing the available genomes of invasive cases and in lineages for which more than or equal to five invasive cases occurred, only 24 (6%) of 384 SDSE cases were assigned to genomic transmission clusters, compared with 271 (52%) of 524 S pyogenes cases. An stG62647 lineage encompassed 113 (26%) of 436 sequenced SDSE genomes. Analysis of available SDSE sequences from Australia, western Europe, and North America inferred concurrent international expansion of the stG62647 lineage in all three regions between 1990 and 2005. INTERPRETATION: We identified a substantial burden of invasive SDSE, dominated by the emergent stG62647 lineage. The contrasting epidemiology between species in the different Australian regions, during COVID-19 NPIs, and genomic infection patterns indicates transmission dynamic, pathogen population, and host-pathogen interaction differences between SDSE and S pyogenes and indicates implications for disease control measures. FUNDING: Australian National Health and Medical Research Council.

Humans↗

Temporal and geographical lineage dynamics of invasive Streptococcus pyogenes in Australia from 2011 to 2023: a retrospective, multicentre, clinical and genomic epidemiology study.

BACKGROUND: Defining the temporal dynamics of invasive Streptococcus pyogenes (group A Streptococcus) and differences between hyperendemic and lower-incidence regions provides crucial insights into pathogen evolution and, in turn, informs preventive measures. We aimed to examine the clinical and temporal lineage dynamics of S pyogenes across different disease settings in Australia to improve understanding of drivers of pathogen diversity. METHODS: In this retrospective, multicentre, clinical and genomic epidemiology study, we identified cases of invasive S pyogenes infection from normally sterile sites between Jan 1, 2011, and Feb 28, 2023. Data were collected from five hospital networks across low-incidence regions in temperate southeast Australia and the hyperendemic, tropical, and largely remote Top End of the Northern Territory of Australia. The crude incidence rate ratio (IRR) of bloodstream S pyogenes infection comparing the Top End and southeast Australia and in First Nations people compared with non-First Nations people was estimated by quasi-Poisson regression. We estimated odds ratios (ORs) of intensive care unit (ICU) admission, in-hospital mortality, and 30-day mortality for the Top End versus southeast Australia using logistic regression. Retrieved and successfully sequenced isolates were assigned lineages at whole-genome resolution. Temporal trends in the composition of co-circulating lineages were compared between the two regions. We used an S&#x2009;pyogenes-specific multistrain simulated transmission model to examine the relationship between host population-specific parameters and observed pathogen lineage dynamics. The prevalence of accessory genes (those present in 5-95% of all genomes) was compared across geographies and temporal periods to investigate genomic drivers of diversity. FINDINGS: We identified 500 cases of invasive S pyogenes infection in patients in the Top End and 495 cases in patients in southeast Australia. The crude IRR of bloodstream infection for the Top End compared with southeast Australia was 5&#xb7;97 (95% CI 4&#xb7;61-7&#xb7;73) across the entire study period; in the Top End, infection disproportionately affected First Nations people compared with non-First Nations people (5&#xb7;41, 4&#xb7;28-6&#xb7;89). The odds of in-hospital mortality (OR 0&#xb7;43, 95% CI 0&#xb7;26-0&#xb7;70), 30-day mortality (0&#xb7;38, 0&#xb7;23-0&#xb7;63), and ICU admission (0&#xb7;42, 0&#xb7;30-0&#xb7;59) were lower in the Top End than in southeast Australia. Longitudinal lineage analysis of 642 S pyogenes genomes identified waves of replacement with distinct lineages in the Top End, whereas southeast Australia had a small number of dominant lineages that persisted and cycled in frequency. The transmission model qualitatively reproduced a similar pattern of replacement with distinct lineages when using a high transmission rate, small population size, and high levels of human movement-characteristics similar to those of communities in the hyperendemic Top End. Using a lower transmission rate, larger population size, and lower levels of migration similar to those of communities in urbanised southeast Australia, the transmission model qualitatively reproduced a pattern of dominant lineages that cycled in frequency. Despite distinct circulating lineages, the prevalence of accessory genes in the bacterial population was maintained across geographies and temporal periods. INTERPRETATION: In a hyperendemic setting, the replacement of distinct S pyogenes lineages occurred in waves, which could be linked to the disproportionate burden of disease and sparse human population in this setting. The maintenance of bacterial gene frequency could be consistent with multilocus selection. These findings suggest that lineage-specific interventions-such as vaccines under development-should consider disease setting and, without broad cross-protection, might lead to lineage replacement. FUNDING: National Health and Medical Research Council, and Leducq Foundation.

Humans↗

Invasive pneumococcal disease in Australia, 2004.

There were 2,375 cases of invasive pneumococcal disease (IPD) notified to the National Notifiable Diseases Surveillance System in Australia in 2004; a notification rate of 11.8 cases per 100,000 population. The rate varied between states and territories and by geographical region with the highest rates in the Northern Territory. Invasive pneumococcal disease was reported most frequently in children aged less than 5 years (55.4 cases per 100,000 population). Enhanced surveillance for IPD was carried out in all states and territories, in 2004, providing additional data on 2,023 (85%) cases. The overall rate of IPD in Indigenous Australians was 3.2 times the rate in non-Indigenous Australians. There were 154 deaths attributed to IPD resulting in an overall case fatality rate of 7.6 per cent. Rates of IPD in the Indigenous and non-Indigenous under 2-year-old population were similar in 2004 (91.5 and 93.6 cases per 100,000 population, respectively) following a targeted introduction of the 7-valent pneumococcal conjugate vaccine (7vPCV) in mid-2001 for Indigenous infants and children. Serotypes of isolates were identified from 80 per cent of all notified cases, with 72 per cent of isolates belonging to serotypes represented in the 7vPCV and 91 per cent in the 23-valent polysaccharide pneumococcal vaccine (23vPPV). Comparison of serotypes in the 7vPCV target population showed that the rate of IPD due to 7vPCV serotypes decreased by 74 per cent between 2001-02 and 2003-04. Of 216 isolates with reduced penicillin susceptibility, 83 per cent belonged to pneumococcal serotypes in the 7vPCV and 95 per cent in the 23vPPV.

Adolescent↗

Tuberculosis notifications in Australia, 2004.

The National Notifiable Disease Surveillance System received 1,076 tuberculosis (TB) notifications in 2004, of which 1,043 were new cases and 33 were relapses. The incidence of TB in Australia has remained at a stable rate since 1985 and was 5.4 cases per 100,000 population in 2004. The high-incidence groups remain people born overseas and Indigenous Australians at 21.7 and 8.1 cases per 100,000 population, respectively. By contrast, the incidence of TB in the non-Indigenous Australian-born population was 1.0 cases per 100,000 population. Comparison of the 2004 TB notification data against the performance indicators set by National Tuberculosis Advisory Committee highlights that enhanced TB control measures should be considered among these high-risk groups.

Adolescent↗

Melioidosis epidemiology and risk factors from a prospective whole-population study in northern Australia.

OBJECTIVES: The aims of this study were to describe the epidemiology of melioidosis in tropical northern Australia and to assess the importance of defined risk factors. METHODS: The data were taken from a 14-year prospective study of 364 cases of melioidosis in the 'Top End' of the Northern Territory. A whole-population logistic regression model was used to estimate the crude and adjusted relative risk (RR) for the defined risk factors. RESULTS: The mean age of the study population was 46.8 years, 264 (72.5%) were male, 178 (49%) were aboriginal Australians and 59 (16.2%) died from melioidosis. Average annual incidence was 19.6 cases per 100 000 population, with an estimated rate of 260 cases per 100,000 diabetics per year. Using a whole-population logistic regression model, the estimated crude and adjusted RR [95% confidence intervals (CI)] for melioidosis were 6.3 (5.1-7.8) and 4.0 (3.2-5.1) for those aged > or = 45 years, 2.3 (1.8-2.9) and 2.4 (1.9-3.0) for males, 2.9 (2.3-3.5) and 3.0 (2.3-4.0) for aboriginal Australians, 21.2 (17.1-26.3) and 13.1 (9.4-18.1) for diabetics, 2.7 (2.2-3.4) and 2.1 (1.6-2.6) for those with excess alcohol consumption, 6.8 (5.4-8.6) and 4.3 (3.4-5.5) for chronic lung disease and 6.7 (4.7-9.6) and 3.2 (2.2-4.8) for chronic renal disease, respectively. CONCLUSIONS: Diabetes, excess alcohol intake, chronic renal disease and chronic lung disease are each independent risk factors for melioidosis. In tropical northern Australia, male sex, aboriginal ethnicity and age of > or = 45 years are also independent predictors for melioidosis. Impaired polymorph function may be critical in the predisposition to melioidosis.

Adolescent↗

Melioidosis in northern Australia, 2001-02.

Melioidosis, caused by the gram negative bacterium Burkholderia pseudomallei, is endemic in northern Australia. Using data collated from centres in Western Australia, the Northern Territory and Queensland, this report describes the epidemiology of this disease between 1 November, 2001 and 31 October, 2002. There were 47 cases seen during this period with an average annual incidence of 5.8 cases per 100,000 population. In Indigenous Australians, an incidence of 25.5 cases per 100,000 population was seen. The timing and location of cases was generally correlated with rainfall across northern Australia. A case-cluster in a Queensland community was associated with post-cyclonic flooding. Risk factors included diabetes, alcohol-related problems and renal disease. Pneumonia (51%) was the most common clinical diagnosis. The mortality rate attributable to melioidosis was 21 per cent, although a number of other patients died of underlying disease. Despite improvements in recognition and treatment, melioidosis is still associated with a high morbidity and mortality, particularly in Indigenous Australians.

Adolescent↗

Rainfall and vector mosquito numbers as risk indicators for mosquito-borne disease in central Australia.

There have been 5 confirmed cases of Murray Valley encephalitis virus (MVE) infection in the Alice Springs region during the high rainfall years of 1999/00 and 2000/01, compared with one case in the preceding 9 years. There also appeared to be an increased prevalence of Ross River virus (RR) infection in the Alice Springs and Tennant Creek regions associated with high rainfall. This paper presents an analysis of summer rainfall from 1990/91 to 2000/01, numbers of seroconversion of sentinel chickens to MVE, and RR cases in both regions. In Alice Springs where summer rainfall (December to February) and average vector numbers in the December to March period are closely correlated, the analysis also included mosquito vector numbers and MVE cases. Summer rainfall over 100 mm was significantly associated with sentinel chicken seroconversions to MVE. From December to March there was also a significant association of average vector numbers (> or = 300) with seroconversions in sentinel chickens following high summer rainfall. MVE appears enzootic in the Tennant Creek region and epizootic in the Alice Springs region. In Alice Springs during December to March, there was a significant association of RR cases with rainfall over 100 mm and with average vector numbers over 300. There was also a significant correlation of summer rainfall with RR cases in Tennant Creek. Summer rainfall is a new and good early indicator of high risk for both MVE and RR disease in the Alice Springs locality and RR in the Tennant Creek locality. Although similar relationships between rainfall and vector abundance, and disease incidence probably exist in other areas of central Australia, rainfall and vector abundance thresholds will probably vary according to local climatic and environmental conditions.

Alphavirus Infections↗

Prevention of opportunistic infections in immunosuppressed patients in the tropical top end of the Northern Territory.

The population of the Top End of the Northern Territory has a high incidence of several infections of particular significance in the immunosuppressed. The following protocol for evaluation and treatment of patients prior to immunosuppression was developed in order to reduce the incidence of serious opportunistic infections. The infections discussed are Strongyloides stercoralis, tuberculosis, scabies, chronic hepatitis B, melioidosis and other bacterial infections. We recommend that all patients planned to receive more than 0.5 mg/kg/day of prednisolone for >14 days, or any more potent immunosuppressive drug, be evaluated and treated according to this protocol. Details of the rationale, evidence base, and proposed investigations and therapy for such patients are discussed.

AIDS-Related Opportunistic Infections↗