294 research outputs found

    Potential impact of climate change on emerging vector-borne and other infections in the UK

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    Abstract Climate is one of several causes of disease emergence. Although half or more of infectious diseases are affected by climate it appears to be a relatively infrequent cause of human disease emergence. Climate mostly affects diseases caused by pathogens that spend part of their lifecycle outside of the host, exposed to the environment. The most important routes of transmission of climate sensitive diseases are by arthropod (insect and tick) vectors, in water and in food. Given the sensitivity of many diseases to climate, it is very likely that at least some will respond to future climate change. In the case of vector-borne diseases this response will include spread to new areas. Several vector-borne diseases have emerged in Europe in recent years; these include vivax malaria, West Nile fever, dengue fever, Chikungunya fever, leishmaniasis, Lyme disease and tick-borne encephalitis. The vectors of these diseases are mosquitoes, sand flies and ticks. The UK has endemic mosquito species capable of transmitting malaria and probably other pathogens, and ticks that transmit Lyme disease. The UK is also threatened by invasive mosquito species known to be able to transmit West Nile, dengue, chikungunya and Zika, and sand flies that spread leishmaniasis. Warmer temperatures in the future will increase the suitability of the UK’s climate for these invasive species, and increase the risk that they may spread disease. While much attention is on invasive species, it is important to recognize the threat presented by native species too. Proposed actions to reduce the future impact of emerging vector-borne diseases in the UK include insect control activity at points of entry of vehicles and certain goods, wider surveillance for mosquitoes and sand flies, research into the threat posed by native species, increased awareness of the medical profession of the threat posed by specific diseases, regular risk assessments, and increased preparedness for the occurrence of a disease emergency

    Effect of temperature and relative humidity on the development times and survival of Synopsyllus fonquerniei and Xenopsylla cheopis, the flea vectors of plague in Madagascar

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    Acknowledgements We would like to thank Dr Lila Rahalison and Jocelyn Ratovonjato for their advice and help during the experiment. We are grateful to the staff of the Plague Unit and the Medical Entomology Unit at the Institut Pasteur de Madagascar, particularly Dr Nohal Elissa. Without their expertise this study would not have been possible. Sincere thanks to Mr Tojo Ramihangihajason for his technical assistance. We are indebted to the Institut Pasteur de Madagascar for an internal grant which facilitated additional laboratory research. Two Wellcome Trust fellowships supported ST during this work (081705 and 095171).Peer reviewedPublisher PD

    Local dispersal of palaearctic Culicoides biting midges estimated by mark-release-recapture

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    Background: Farm to farm movement of Culicoides midges is believed to play a critical role in the spread of bluetongue (BT), Schmallenberg and other midge-borne diseases. To help understand and predict the spread of diseases carried by midges, there is a need to determine their dispersal patterns, and to identify factors contributing to the direction taken and distance travelled. Methods: The dispersal of Obsoletus Group members was studied on 19 farms around Bala, north Wales. Field-collected Culicoides were trapped in a black-light (OVI) trap and self-marked in the collecting vessel, using micronized fluorescent dust. Culicoides were released at a central farm and OVI traps set on 18 surrounding farms, at distances of 1 to 4 km. The study was repeated using six colours of fluorescent dust over an 18 day period. Results: An estimated 61,062 (95% CI = 56,298-65,830) marked Culicoides were released during the study and 12 (0.02%) Culicoides were recaptured. Of the females recaptured, six were C. obsoletus/scoticus, two C. dewulfi, two C. pulicaris and one C. festivipennis. The male was C. obsoletus. Recaptures occurred 1–2.5 km from the release site, with greatest numbers at 2.5 km. Most recaptures were 2 nights post-release; none were more than 3 nights post-release. Two females were recovered at 1.5 km on the night of release and one male at 1 km two nights post-release. The mean distance travelled (MDT) for males was 1 km, females was 2.21 km, and all recaptured Culicoides was 2.15 km. Recaptures were made both downwind and upwind of the prevailing wind direction during the trapping periods, highlighting possible passive and active dispersal of Culicoides between farms. Conclusions: This is the first study to demonstrate farm to farm movement of the main Palaearctic BT vector species, the Obsoletus Group. Such movement has disease control implications in terms of the vectoral movement of disease between farms. The results suggest that Culicoides control measures applied at an infected farm (trapping or killing Culicoides) will reduce risk of spread to neighbouring farms by lessening the number of Culicoides dispersing from that farm, as well as reducing transmission at the source farm itself

    Modelling bluetongue virus transmission between farms using animal and vector movements.

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    Bluetongue is a notifiable disease of ruminants which, in 2007, occurred for the first time in England. We present the first model for bluetongue that explicitly incorporates farm to farm movements of the two main hosts, as well as vector dispersal. The model also includes a seasonal vector to host ratio and dynamic restriction zones that evolve as infection is detected. Batch movements of sheep were included by modelling degree of mixing at markets. We investigate the transmission of bluetongue virus between farms in eastern England (the focus of the outbreak). Results indicate that most parameters affecting outbreak size relate to vectors and that the infection generally cannot be maintained without between-herd vector transmission. Movement restrictions are effective at reducing outbreak size, and a targeted approach would be as effective as a total movement ban. The model framework is flexible and can be adapted to other vector-borne diseases of livestock

    Two-Host, Two-Vector Basic Reproduction Ratio (R-0) for Bluetongue

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    Mathematical formulations for the basic reproduction ratio (R (0)) exist for several vector-borne diseases. Generally, these are based on models of one-host, one-vector systems or two-host, one-vector systems. For many vector borne diseases, however, two or more vector species often co-occur and, therefore, there is a need for more complex formulations. Here we derive a two-host, two-vector formulation for the R (0) of bluetongue, a vector-borne infection of ruminants that can have serious economic consequences; since 1998 for example, it has led to the deaths of well over 1 million sheep in Europe alone. We illustrate our results by considering the situation in South Africa, where there are two major hosts (sheep, cattle) and two vector species with differing ecologies and competencies as vectors, for which good data exist. We investigate the effects on R (0) of differences in vector abundance, vector competence and vector host preference between vector species. Our results indicate that R (0) can be underestimated if we assume that there is only one vector transmitting the infection (when there are in fact two or more) and/or vector host preferences are overlooked (unless the preferred host is less beneficial or more abundant). The two-host, one-vector formula provides a good approximation when the level of cross-infection between vector species is very small. As this approaches the level of intraspecies infection, a combination of the two-host, one-vector R (0) for each vector species becomes a better estimate. Otherwise, particularly when the level of cross-infection is high, the two-host, two-vector formula is required for accurate estimation of R (0). Our results are equally relevant to Europe, where at least two vector species, which co-occur in parts of the south, have been implicated in the recent epizootic of bluetongue

    Domesticated animals and human infectious diseases of zoonotic origins: Domestication time matters

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    The rate of emergence for emerging infectious diseases has increased dramatically over the last century, and research findings have implicated wildlife as an importance source of novel pathogens. However, the role played by domestic animals as amplifiers of pathogens emerging from the wild could also be significant, influencing the human infectious disease transmission cycle. The impact of domestic hosts on human disease emergence should therefore be ascertained. Here, using three independent datasets we showed positive relationships between the time since domestication of the major domesticated mammals and the total number of parasites or infectious diseases they shared with humans. We used network analysis, to better visualize the overall interactions between humans and domestic animals (and amongst animals) and estimate which hosts are potential sources of parasites/pathogens for humans (and for all other hosts) by investigating the network architecture. We used centrality, a measure of the connection amongst each host species (humans and domestic animals) in the network, through the sharing of parasites/pathogens, where a central host (i.e. high value of centrality) is the one that is infected by many parasites/pathogens that infect many other hosts in the network. We showed that domesticated hosts that were associated a long time ago with humans are also the central ones in the network and those that favor parasites/pathogens transmission not only to humans but also to all other domesticated animals. These results urge further investigation of the diversity and origin of the infectious diseases of domesticated animals in their domestication centres and the dispersal routes associated with human activities. Such work may help us to better understand how domesticated animals have bridged the epidemiological gap between humans and wildlife. (Résumé d'auteur

    Distinct spread of DNA and RNA viruses among mammals amid prominent role of domestic species

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    AimEmerging infectious diseases arising from pathogen spillover from mammals to humans constitute a substantial health threat. Tracing virus origin and predicting the most likely host species for future spillover events are major objectives in One Health disciplines.We assessed patterns of virus sharing among a large diversity of mammals, including humans and domestic species.LocationGlobal.Time periodCurrent.Major taxa studiedMammals and associated viruses.MethodsWe used network centrality analysis and trait-based Bayesian hierarchical models to explore patterns of virus sharing among mammals. We analysed a global database that compiled the associations between 1,785 virus species and 725 mammalian host species as sourced from automatic screening of meta-data accompanying published nucleotide sequences between 1950 and 2019.ResultsWe show that based on current evidence, domesticated mammals hold the most central positions in networks of known mammal-virus associations. Among entire host-virus networks, Carnivora and Chiroptera hold central positions for mainly sharing RNA viruses, whereas ungulates hold central positions for sharing both RNA and DNA viruses with other host species. We revealed strong evidence that DNA viruses were phylogenetically more host specific than RNA viruses. RNA viruses exhibited low functional host specificity despite an overall tendency to infect phylogenetically related species, signifying high potential to shift across hosts with different ecological niches. The frequencies of sharing viruses among hosts and the proportion of zoonotic viruses in hosts were larger for RNA than for DNA viruses.Main conclusionsAcknowledging the role of domestic species in addition to host and virus traits in patterns of virus sharing is necessary to improve our understanding of virus spread and spillover in times of global change. Understanding multi-host virus-sharing pathways adds focus to curtail disease spread
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