49 resultados para Insects as carriers of disease.

em Deakin Research Online - Australia


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Over the past 30 years, heathland and open forest communities in south-eastern Australia dominated by Xanthorrhoea australis R.Br. have been severely affected by disease caused by Phytophthora cinnamomi Rands. The disease has caused a sharp decline in numbers of individuals within populations of X. australis; however, the etiology of the disease is unclear. The characteristics and disease symptoms induced by P. cinnamomi were analysed within nine mature X. australis plants that had been removed from the field. Seven plants showed typical disease symptoms that ranged from chlorotic leaves through to plant death. Plants showing disease symptoms had different numbers of infected roots, ranging from 0% in one dead plant, 40% infected roots in a plant showing yellowing of leaf tips and 67 and 86%, respectively, in two plants with severe chlorosis. There was variation within the roots, with some infected close to the stem while others were infected at more distal regions. Within stems of all plants, P. cinnamomi was difficult to isolate but was found in the desmium and stem apex and was associated with massive lesions within the central area of the stem. The symptoms of disease in X. australis are caused by a combination of damage to tissues of the roots and stem that may lead to a reduction in water and mineral transport throughout the plant.

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The extent of disease caused by Phytophthora cinnamomi was determined within vegetation communities of Wilsons Promontory National Park. Aerial survey of visible symptoms by helicopter and systematic survey along all roads and tracks followed by isolation of the pathogen from soil found that in total 551 ha of moist foothill forest, heath and heathy woodland broad vegetation types were affected by the disease. P. cinnamomi was isolated from 93% of sites that, based on the presence of visible symptoms, were expected to yield the pathogen. The species-rich heathy woodland was most affected with 6.5% of the total area of this type showing symptoms of disease. The size of infestation ranged from 229 ha on the slopes of the Vereker Range in the north to less than 1 ha along the Sealers Cove Walking Track in the south. The potential for disease to spread into uninfested vegetation was estimated for all sites from which P. cinnamomi was isolated. Eight of 18 sites where evidence of disease was found were estimated to have a high potential for further disease spread. This study indicates that even though the disease may be waning in some areas of the Park, the pathogen is active and easily isolated from others and provides a continuing threat to susceptible vegetation communities.

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The nucleotide sequence of the Brachyspira hyodysenteriae ftnA gene, encoding a putative ferritin protein (FtnA), was determined. Analysis of the sequence predicted that this gene encoded a protein of 180 amino acids. RT-PCR and Western blot showed that the ftnA gene was expressed in B. hyodysenteriae, and evidence suggests that FtnA stores iron rather than haem. ftnA was delivered as DNA and recombinant protein vaccines in a mouse model of B. hyodysenteriae infection. Vaccine efficacy was monitored by caecal pathology and quantification of B. hyodysenteriae numbers in the caeca of infected mice by real-time PCR.

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This paper summarises the findings of an empirical investigation of some of the technical and social assumptions on which the disability adjusted life year (DALY) is based. The objectives of the study were to examine the notion that the burden of disease is broadly similar without regard to country, environment, gender or socio-economic status and to develop detailed descriptions of the experiences of the burden of disease as they related to these contextual factors. The study was a multi-factorial exploratory study employing qualitative and quantitative techniques to obtain data on the effects of country (development), environment (urban versus rural), gender and socio-economic status on people with paraplegia. The data provided an extensive and detailed compilation of context rich descriptions of living with paraplegia. Striking features of the data were the differences between countries with respect to the impact of the health conditions on functioning and highlight a context in which paraplegia of like clinical severity can be fatal in one environment and not in another. While there has been some focus on the control of social determinants of disease, there has been little work on the social determinants of the severity of disease. The underlying assumptions of the DALY, which ignore context in the assessment of the burden of disease, risk exacerbating inequalities by undervaluing the burden of disease in less-developed countries. There is a need to continue to subject the development of indicators to rigorous debate to determine a balance between the assumption of a global “average social milieu” and the treatment of each individual as belonging to their own context in the assessment of population health in order for indicators to be meaningful cross-culturally.

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Objective:
To quantify the burden of disease and injury for the Aboriginal and non-Aboriginal populations in the Northern Territory.

Design and setting:
Analysis of Northern Territory data for 1 January 1994 to 30 December 1998 from multiple sources.

Main outcome measures:
Disability-adjusted life-years (DALYs), by age, sex, cause and Aboriginality.

Results:
Cardiovascular disease was the leading contributor (14.9%) to the total burden of disease and injury in the NT, followed by mental disorders (14.5%) and malignant neoplasms (11.2%). There was also a substantial contribution from unintentional injury (10.4%) and intentional injury (4.9%). Overall, the NT Aboriginal population had a rate of burden of disease 2.5 times higher than the non-Aboriginal population; in the 35-54-year age group their DALY rate was 4.1 times higher. The leading causes of disease burden were cardiovascular disease for both Aboriginal men (19.1%) and women (15.7%) and mental disorders for both non-Aboriginal men (16.7%) and women (22.3%).

Conclusions:
A comprehensive assessment of fatal and non-fatal conditions is important in describing differentials in health status of the NT population. Our study provides comparative data to identify health priorities and facilitate a more equitable distribution of health funding.


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Objective: To investigate the sources of cross-national variation in disability-adjusted life-years (DALYs) in the European Disability
Weights Project.

Methods
: Disability weights for 15 disease stages were derived empirically in five countries by means of a standardized procedure and the cross-national differences in visual analogue scale (VAS) scores were analysed. For each country the burden of dementia in women, used as an illustrative example, was estimated in DALYs. An analysis was performed of the relative effects of cross-national variations in demography, epidemiology and disability weights on DALY estimates.

Findings
: Cross-national comparison of VAS scores showed almost identical ranking orders. After standardization for population size and age structure of the populations, the DALY rates per 100 000 women ranged from 1050 in France to 1404 in the Netherlands. Because of uncertainties in the epidemiological data, the extent to which these differences reflected true variation between countries was difficult to estimate. The use of European rather than country-specific disability weights did not lead to a significant change in the burden of disease estimates for dementia.

Conclusions
: Sound epidemiological data are the first requirement for burden of disease estimation and relevant between-countries comparisons. DALY estimates for dementia were relatively insensitive to differences in disability weights between European countries.

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Disease caused by the soilborne plant pathogen Phytophthora cinnamomi causes long-term floristic and structural changes in native vegetation communities in Australia. Key components of the management of this disease are to know where it occurs and the rate at which it spreads. The distribution of P. cinnamomi has generally been assessed as locality points of infestation and mapping the extent of diseased vegetation in any area is difficult and costly. This study was undertaken in P. cinnamomi-infested heathland communities in southern Victoria, Australia, where the symptoms of P. cinnamomi arise as a mosaic within healthy vegetation. We investigated the potential to improve the efficiency and effectiveness of mapping and monitoring vegetation affected by P. cinnamomi using digital multi-spectral imaging. This technique was developed for the purposes of monitoring vegetation and provides a single, seamless ortho-rectified digital image over the total area of interest. It is used to spatially quantify small differences in the characteristics of vegetation. In this study, the symptoms of disease caused by P. cinnamomi infestation were related to differences in the imagery and were used to map areas of infestation. Comparison of the digital multi-spectral imaging indications with on-ground observations gave moderate accuracy between the datasets (κ = 0.49) for disease and healthy indications. This study demonstrates the ability of the technique to determine disease extent over broad areas in native vegetation and provides a non-invasive, cost effective tool for management.

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A role for α4 and β7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood-brain barrier has not been determined. In the present paper, it is shown that an antibody directed against MAdCAM-1, the preferential ligand for α4β7, effectively prevented the development of a progressive, non-remitting, form of EAE, actively induced by injection of myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) autoantigen. Combinational treatment with both anti-MAdCAM-1, VCAM-1, and intercellular adhesion molecule-1 (ICAM-1) (ligand for integrin lymphocyte function-associated antigen (LFA)-1) mAbs led to more rapid remission than that obtained with anti-MAdCAM-1 antibody alone. However, neither MAdCAM-1 monotherapy, nor combinational antibody blockade was preventative when administered late in the course of disease progression. In conclusion, MAdCAM-1 plays a major contributory role in the progression of chronic EAE and is a potential therapeutic target for the treatment of MS. Critically, antivascular addressin therapy must be given eaA role for alpha4 and beta7 integrins in mediating leucocyte entry into the central nervous system in the multiple sclerosis (MS)-like disease experimental autoimmune encephalomyelitis (EAE) has been demonstrated. However, the individual contributions of their respective ligands mucosal addressin cell adhesion molecule-1 (MAdCAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-cadherin expressed on the blood-brain barrier has not been determined. In the present paper, it is shown that an antibody directed against MAdCAM-1, the preferential ligand for alpha4beta7, effectively prevented the development of a progressive, non-remitting, form of EAE, actively induced by injection of myelin oligodendrocyte glycoprotein peptide (MOG(35-55)) autoantigen. Combinational treatment with both anti-MAdCAM-1, VCAM-1, and intercellular adhesion molecule-1 (ICAM-1) (ligand for integrin lymphocyte function-associated antigen (LFA)-1) mAbs led to more rapid remission than that obtained with anti-MAdCAM-1 antibody alone. However, neither MAdCAM-1 monotherapy, nor combinational antibody blockade was preventative when administered late in the course of disease progression. In conclusion, MAdCAM-1 plays a major contributory role in the progression of chronic EAE and is a potential therapeutic target for the treatment of MS. Critically, antivascular addressin therapy must be given early in the course of disease prior to the establishment of irreversible damage if it is to be effective, as a single treatment modality.

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The report measures mortality, disability, illness and injury arising from over 170 diseases and injuries. Burden of disease analysis gives a unique perspective on health

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This report provides an overview of results from the Australian Burden of Disease and Injury Study undertaken by the AIHW during 1998 and 1999. The Study uses the methods developed for the Global Burden of Disease Study, adapted to the Australian context and drawing extensively on Australian sources of population health data. It provides a comprehensive assessment of the amount of ill health and disability, the ‘burden of disease’ in Australia in 1996.

Mortality, disability, impairment, illness and injury arising from 176 diseases, injuries and risk factors are measured using a common metric, the Disability-Adjusted Life Year or DALY. One DALY is a lost year of ‘healthy’ life and is calculated as a combination of years of life lost due to premature mortality (YLL) and equivalent ‘healthy’ years of life lost due to disability (YLD). This report provides estimates of the contribution of fatal and non-fatal health outcomes to the total burden of disease and injury measured in DALYs in Australia in 1996.

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An overview of the results of the Australian Burden of Disease (ABD) study is presented. The ABD study was the first to use methodology developed for the Global Burden of Disease study to measure the burden of disease and injury in a developed country. In 1996, mental disorders were the main causes of disability burden, responsible for nearly 30% of total years of life lost to disability (YLD), with depression accounting for 8% of the total YLD. Ischaemic heart disease and stroke were the main contributors to the disease burden disability-adjusted life years (DALYs), together causing nearly 18% of the total disease burden. Risk factors such as smoking, alcohol consumption, physical inactivity, hypertension, high blood cholesterol, obesity and inadequate fruit and vegetable consumption were responsible for much of the overall disease burden in Australia. The lessons learnt from the ABD study are discussed, together with methodological issues that require further attention.