80 research outputs found

    Finding the ‘Who’ in Whooping Cough: Vaccinated Siblings are Important Pertussis Sources in Infants 6 Months of Age and Under

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    Objectives: To describe the epidemiology of pertussis, and to identify changes in the source of pertussis in infants 6 months of age and under, during the 2008–2012 epidemic in south metropolitan Perth. Design and setting: Analysis of all pertussis cases notified to the South Metropolitan Population Health Unit and recorded on the Western Australian Notifiable Infectious Disease Database over the study period. Information on the source of pertussis was obtained from enhanced surveillance data. Results: Notification rates were highest in the 5–9 years age group, followed by the 0–4 years and 10–14 years age groups. There was a significant increase in the proportion of known sources who were siblings from the early epidemic period of 2008–2010, compared with the peak epidemic period of 2011–2012 (14.3% versus 51.4%, p = 0.002). The majority of sibling sources were fully vaccinated children aged 2 and 3 years. Conclusions: The incidence of pertussis was highest in children aged 12 years and under in this epidemic. At its peak, siblings were the most important sources of pertussis in infants 6 months and younger, particularly fully vaccinated children aged 2 and 3 years. Waning immunity before the booster at 4 years may leave this age group susceptible to infection. Even if cocooning programs could achieve full vaccination coverage of parents and ensure all siblings were fully vaccinated according to national schedules, waning immunity in siblings could provide a means for ongoing transmission to infants. Recent evidence suggests that maternal antenatal vaccination would significantly reduce the risk of pertussis in infants 3 months of age and under

    Community-associated Clostridium difficile infection in emergency department patients in Western Australia

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    Clostridium difficile infection (CDI) is primarily associated with hospitalised patients, however, community-associated CDI (CA-CDI) has increased in Australia. We aimed to investigate the epidemiology and outcomes of CA-CDI cases presenting to hospital emergency departments in Western Australia (WA). A retrospective case-control study of CA-CDI cases presenting at six emergency departments in WA from July 2013 to June 2014 was performed. Clinical signs, recent medication, hospitalisations and potential risk factors for CA-CDI were investigated for cases (n = 34) and unmatched controls (n = 62) who were infected with another gastrointestinal pathogen, including Campylobacter spp., Salmonella spp., Aeromonas spp., Shigella sonnei and Escherichia coli O157. Elevated white cell count (31.3% vs 8.2%, p < 0.01), female gender (67.6% vs 41.9%, p < 0.05), age =65 years (41.2% vs 21.0%, p < 0.05) and antimicrobial use in the previous month (41.2% vs 11.3%, p < 0.01) were significantly more frequent among cases compared to controls. After multivariable analysis, antibiotic use (odds ratio 8.49, 95% confidence interval 2.75–26.21) and age =65 years (3.03, 1.05–8.75) were significantly associated with CA-CDI. Ribotype (RT) 014/020 was most common (40.7%) among 27 C. difficile isolates followed by RTs 002 (14.8%), 001, 056 and 244 (all 7.4%). CA-CDI was associated with advanced age and recent antibiotic use compared to those infected with other gastrointestinal pathogens. RT 014 has also recently been found at high prevalence in public lawn spaces, and previously RT 014 strains from humans and pigs in Australia were closely genetically related, suggesting CA-CDI may be linked with these community reservoirs

    Campylobacter-associated hospitalisations in an Australian provincial setting

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    Background: Campylobacter spp. infections are a globally important cause of enterocolitis, causing substantial morbidity. Capturing accurate information on hospitalisations is challenging and limited population-level data exist to describe the clinico-epidemiological characteristics of hospitalised cases. Methods: Hospital administrative and laboratory datasets were linked to identify Campylobacter-associated hospitalisations between 2004 and 2013. Accuracy of morbidity coding was assessed using laboratory diagnosis as a gold standard, with health department surveillance data used to calculate population-based rates. Additional patient-level data were collected via review of medical records. Descriptive statistics were used to assess changes in rates and proportions and to assess relationships between key variables including age, length of stay, comorbidity and complications. Results: In total 685 Campylobacter-associated hospital admissions were identified, with the sensitivity of morbidity coding 52.8% (95% CI 48.9–56.7%). The mean annual rate of hospitalisation was 13.6%. Hospitalisation rates were higher for females across most age-groups, while for both genders marked increases were observed for those aged ≥60 years. Median admission age was 39.5 years, with an average length of stay of 3.5 days. Comorbidities were present in 34.5% (237/685) of admissions, with these patients more likely to develop electrolyte disturbances, hypotension, renal impairment or acute confusion (all p < 0.001). Bacteraemia and acute kidney injury were observed in 4.1% (28/ 685) and 3.6% (23/685) of admissions, respectively. Inpatient mortality was low (0.15%). Conclusion: Under reporting of Campylobacter-associated hospitalisations is substantial but can be improved through data linkage. We observed demographic differences among those hospitalised but further work is needed to determine risk factors and predictors for hospitalisation.The National Health and Medical Research Council provided funding to authors CM [APP107490] and MK [APP1145997]

    Validation of questions designed for investigation of gastroenteritis

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    Background: Health departments routinely investigate cases of gastroenteritis through interviews to determine the source of infection. However, validation studies of dietary questionnaires typically focus on quantities consumed and don't assess questions designed to identify sources of foodborne illness. We aimed to assess the accuracy and reliability of information collected by surveys of food history recall for gastroenteritis investigations. Methods: A questionnaire was developed to investigate the sources of foodborne gastroenteritis in Australia, with questions on food exposures selected for validation. Fifty-five participants photographed all foods consumed and food receipts obtained during a seven-day observation period. These photographs were uploaded to an online survey or emailed to the researcher. Participants were contacted 14 days later for a telephone interview about foods consumed in the seven-day period. Questionnaire responses were compared to uploaded photographs. Kappa statistics (κ) and 95% confidence intervals were calculated. Sixty-two questions were assessed, including those targeting foods considered high-risk for foodborne gastroenteritis. Potential risk factors covered by these questions included: meats (poultry, beef, pork, and deli meats), the state of poultry purchased (raw versus precooked), and the number of meals eaten outside of the home. Results: Several questions targeting high-risk foods were found to have substantial-to-almost perfect agreement (κ ≥ 0.610) between what was eaten and what was reported by participants, with most questions showing at least a moderate level of agreement (κ = 0.410–0.600). Questions regarding exposure to different types of meat showed a high level of consistency. The only question with poor participant recall (κ < 0.000) was that relating to consumption of undercooked beef or veal. Conclusion: Several questions designed for investigation of gastroenteritis were found to provide at least a moderate level of accurate and reliable recall, even after a delay until interview. These questions are suitable for investigating sources of foodborne gastroenteritis

    Aetiology-Specific Estimates of the Global and Regional Incidence and Mortality of Diarrhoeal Diseases Commonly Transmitted through Food

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    Diarrhoeal diseases are major contributors to the global burden of disease, particularly in children. However, comprehensive estimates of the incidence and mortality due to specific aetiologies of diarrhoeal diseases are not available. The objective of this study is to provide estimates of the global and regional incidence and mortality of diarrhoeal diseases caused by nine pathogens that are commonly transmitted through foods.We abstracted data from systematic reviews and, depending on the overall mortality rates of the country, applied either a national incidence estimate approach or a modified Child Health Epidemiology Reference Group (CHERG) approach to estimate the aetiology-specific incidence and mortality of diarrhoeal diseases, by age and region. The nine diarrhoeal diseases assessed caused an estimated 1.8 billion (95% uncertainty interval [UI] 1.1-3.3 billion) cases and 599,000 (95% UI 472,000-802,000) deaths worldwide in 2010. The largest number of cases were caused by norovirus (677 million; 95% UI 468-1,153 million), enterotoxigenic Escherichia coli (ETEC) (233 million; 95% UI 154-380 million), Shigella spp. (188 million; 95% UI 94-379 million) and Giardia lamblia (179 million; 95% UI 125-263); the largest number of deaths were caused by norovirus (213,515; 95% UI 171,783-266,561), enteropathogenic E. coli (121,455; 95% UI 103,657-143,348), ETEC (73,041; 95% UI 55,474-96,984) and Shigella (64,993; 95% UI 48,966-92,357). There were marked regional differences in incidence and mortality for these nine diseases. Nearly 40% of cases and 43% of deaths caused by these nine diarrhoeal diseases occurred in children under five years of age.Diarrhoeal diseases caused by these nine pathogens are responsible for a large disease burden, particularly in children. These aetiology-specific burden estimates can inform efforts to reduce diarrhoeal diseases caused by these nine pathogens commonly transmitted through foods

    Un nuevo morbillivirus de la neumonía equina y su transmisión a humanos

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    En Septiembre 22 y 23 de 1994, las autoridades veterinarias en Queensland y en el CSIRO Laboratorio Australiano de Salud Animal («Australian Animal Health Laboratory») fueron avisados de un brote de enfermedad respiratoria aguda en caballos en un establo en Brisbane, suburbio de Hendra. El entrenador de los caballos había sido hospitalizado por una enfermedad respiratoria y estuvo en condición crítica. En ese momento, la causa de enfermedad de los caballos era incierta y cualquier nexo entre la enfermedad humana y equina era un pensamiento improbable. Se investigaron causas de envenenamiento, enfermedad exótica, virósica, y bacteriana. EL historial de los caballos en este aspecto fue considerada importante; (Figura 1) dos semanas antes de la enfermedad del entrenador, el 7 de Septiembre, dos caballos habían sido llevados al Hendra desde un establo de pre-carrera en Cannon Hill (6 km). Uno de éstos, una yegua preñada, enfermó y murió en 2 días. El otro caballo fue trasladado luego y nunca llegó a enfermarse. Por el 26 de Septiembre, 13 caballos habían muerto: la yegua; otros 10 caballos en el establo de Hendra; un caballo, que tuvo contacto muy cercano con caballos en el establo de Hendra, en una propiedad vecina; y uno que había sido transportado desde el establo a otro sitio (150 km). Cuatro caballos de Hendra y otros tres (uno en un establo adyacente, uno llevado a Kenilworth, y uno a Samford) se consideraron que habían estado expuestos y se habían recuperado de la enfermedad. Algunos de estos caballos fueron asintomáticos. Nueve caballos de Hendra habían permanecido inafectados. Los caballos enfermos estaban anoréxicos, deprimidos, comúnmente febriles (temperatura hasta 41ºC), mostraron tasa respiratoria elevada, y llegaron a estar atáxicos. Una descarga nasal espumosa ocurrió antes de la muerte.Facultad de Ciencias Veterinaria

    Un nuevo morbillivirus de la neumonía equina y su transmisión a humanos

    Get PDF
    En Septiembre 22 y 23 de 1994, las autoridades veterinarias en Queensland y en el CSIRO Laboratorio Australiano de Salud Animal («Australian Animal Health Laboratory») fueron avisados de un brote de enfermedad respiratoria aguda en caballos en un establo en Brisbane, suburbio de Hendra. El entrenador de los caballos había sido hospitalizado por una enfermedad respiratoria y estuvo en condición crítica. En ese momento, la causa de enfermedad de los caballos era incierta y cualquier nexo entre la enfermedad humana y equina era un pensamiento improbable. Se investigaron causas de envenenamiento, enfermedad exótica, virósica, y bacteriana. EL historial de los caballos en este aspecto fue considerada importante; (Figura 1) dos semanas antes de la enfermedad del entrenador, el 7 de Septiembre, dos caballos habían sido llevados al Hendra desde un establo de pre-carrera en Cannon Hill (6 km). Uno de éstos, una yegua preñada, enfermó y murió en 2 días. El otro caballo fue trasladado luego y nunca llegó a enfermarse. Por el 26 de Septiembre, 13 caballos habían muerto: la yegua; otros 10 caballos en el establo de Hendra; un caballo, que tuvo contacto muy cercano con caballos en el establo de Hendra, en una propiedad vecina; y uno que había sido transportado desde el establo a otro sitio (150 km). Cuatro caballos de Hendra y otros tres (uno en un establo adyacente, uno llevado a Kenilworth, y uno a Samford) se consideraron que habían estado expuestos y se habían recuperado de la enfermedad. Algunos de estos caballos fueron asintomáticos. Nueve caballos de Hendra habían permanecido inafectados. Los caballos enfermos estaban anoréxicos, deprimidos, comúnmente febriles (temperatura hasta 41ºC), mostraron tasa respiratoria elevada, y llegaron a estar atáxicos. Una descarga nasal espumosa ocurrió antes de la muerte.Facultad de Ciencias Veterinaria

    Entry Screening for Infectious Diseases in Humans

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    In response to the severe acute respiratory syndrome (SARS) pandemic of 2003 and the influenza pandemic of 2009, many countries instituted border measures as a means of stopping or slowing the spread of disease. The measures, usually consisting of a combination of border entry/exit screening, quarantine, isolation, and communications, were resource intensive, and modeling and observational studies indicate that border screening is not effective at detecting infectious persons. Moreover, border screening has high opportunity costs, financially and in terms of the use of scarce public health staff resources during a time of high need. We discuss the border-screening experiences with SARS and influenza and propose an approach to decision-making for future pandemics. We conclude that outbreak-associated communications for travelers at border entry points, together with effective communication with clinicians and more effective disease control measures in the community, may be a more effective approach to the international control of communicable diseases

    Rainfall and sentinel chicken seroconversions predict human cases of Murray Valley encephalitis in the north of Western Australia

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    Background Murray Valley encephalitis virus (MVEV) is a flavivirus that occurs in Australia and New Guinea. While clinical cases are uncommon, MVEV can cause severe encephalitis with high mortality. Sentinel chicken surveillance is used at many sites around Australia to provide an early warning system for risk of human infection in areas that have low population density and geographical remoteness. MVEV in Western Australia occurs in areas of low population density and geographical remoteness, resulting in logistical challenges with surveillance systems and few human cases. While epidemiological data has suggested an association between rainfall and MVEV activity in outbreak years, it has not been quantified, and the association between rainfall and sporadic cases is less clear. In this study we analysed 22 years of sentinel chicken and human case data from Western Australia in order to evaluate the effectiveness of sentinel chicken surveillance for MVEV and assess the association between rainfall and MVEV activity. Methods Sentinel chicken seroconversion, human case and rainfall data from the Kimberley and Pilbara regions of Western Australia from 1990 to 2011 were analysed using negative binomial regression. Sentinel chicken seroconversion and human cases were used as dependent variables in the model. The model was then tested against sentinel chicken and rainfall data from 2012 and 2013.Results Sentinel chicken seroconversion preceded all human cases except two in March 1993. Rainfall in the prior three months was significantly associated with both sentinel chicken seroconversion and human cases across the regions of interest. Sentinel chicken seroconversion was also predictive of human cases in the models. The model predicted sentinel chicken seroconversion in the Kimberley but not in the Pilbara, where seroconversions early in 2012 were not predicted. The latter may be due to localised MVEV activity in isolated foci at dams, which do not reflect broader virus activity in the region. Conclusions We showed that rainfall and sentinel chickens provide a useful early warning of MVEV risk to humans across endemic and epidemic areas, and that a combination of the two indicators improves the ability to assess MVEV risk and inform risk management measures

    Clostridium difficile Infections amongst Patients with Haematological Malignancies: A Data Linkage Study

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    OBJECTIVES: Identify risk factors for Clostridium difficile infection (CDI) and assess CDI outcomes among Australian patients with a haematological malignancy. METHODS: A retrospective cohort study involving all patients admitted to hospitals in Western Australia with a haematological malignancy from July 2011 to June 2012. Hospital admission data were linked with all hospital investigated CDI case data. Potential risk factors were assessed by logistic regression. The risk of death within 60 and 90 days of CDI was assessed by Cox Proportional Hazards regression. RESULTS: There were 2085 patients of whom 65 had at least one CDI. Twenty percent of CDI cases were either community-acquired, indeterminate source or had only single-day admissions in the 28 days prior to CDI. Using logistic regression, having acute lymphocytic leukaemia, neutropenia and having had bacterial pneumonia or another bacterial infection were associated with CDI. CDI was associated with an increased risk of death within 60 and 90 days post CDI, but only two deaths had CDI recorded as an antecedent factor. Ribotyping information was available for 33 of the 65 CDIs. There were 19 different ribotypes identified. CONCLUSIONS: Neutropenia was strongly associated with CDI. While having CDI is a risk factor for death, in many cases it may not be a direct contributor to death but may reflect patients having higher morbidity. A wide variety of C. difficile ribotypes were found and community-acquired infection may be under-estimated in these patients
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