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Background Neglected tropical diseases are responsible for considerable morbidity and mortality in low-income populations. International efforts have reduced their global burden, but transmission is persistent and case-finding-based interventions rarely target asymptomatic individuals. Methods We develop a generic mathematical modeling framework for analyzing the dynamics of visceral leishmaniasis in the Indian sub-continent (VL), gambiense sleeping sickness (gHAT), and Chagas disease and use it to assess the possible contribution of asymptomatics who later develop disease (pre-symptomatics) and those who do not (non-symptomatics) to the maintenance of infection. Plausible interventions, including active screening, vector control, and reduced time to detection, are simulated for the three diseases. Results We found that the high asymptomatic contribution to transmission for Chagas and gHAT and the apparently high basic reproductive number of VL may undermine long-term control. However, the ability to treat some asymptomatics for Chagas and gHAT should make them more controllable, albeit over relatively long time periods due to the slow dynamics of these diseases. For VL, the toxicity of available therapeutics means the asymptomatic population cannot currently be treated, but combining treatment of symptomatics and vector control could yield a quick reduction in transmission. Conclusions Despite the uncertainty in natural history, it appears there is already a relatively good toolbox of interventions to eliminate gHAT, and it is likely that Chagas will need improvements to diagnostics and their use to better target pre-symptomatics. The situation for VL is less clear, and model predictions could be improved by additional empirical data. However, interventions may have to improve to successfully eliminate this disease. [ABSTRACT FROM AUTHOR]

Lyme disease is the most common tick-borne disease in temperate regions of North America, Europe and Asia, and the number of reported cases has increased in many regions as landscapes have been altered. Although there has been extensive work on the ecology and epidemiology of this dis- ease in both Europe and North America, substantial uncertainty exists about fundamental aspects that determine spatial and temporal variation in both disease risk and human incidence, which hamper effective and efficient pre- vention and control. Here we describe areas of consensus that can be built on, identify areas of uncertainty and outline research needed to fill these gaps to facilitate predictive models of disease risk and the development of novel disease control strategies. Key areas of uncertainty include: (i) the precise influence of deer abundance on tick abundance, (ii) how tick popu- lations are regulated, (iii) assembly of host communities and tick-feeding patterns across different habitats, (iv) reservoir competence of host species, and (v) pathogenicity for humans of different genotypes of Borrelia burgdor- feri. Filling these knowledge gaps will improve Lyme disease prevention and control and provide general insights into the drivers and dynamics of this emblematic multi-host-vector-borne zoonotic disease. This article is part of the themed issue 'Conservation, biodiversity and infectious disease: scientific evidence and policy implications'. [ABSTRACT FROM AUTHOR]

Phocine distemper virus (PDV) was first recognized in 1988 following a massive epidemic in harbor and grey seals in north-western Europe. Since then, the epidemiology of infection in North Atlantic and Arctic pinnipeds has been investigated. In the western North Atlantic endemic infection in harp and grey seals predates the European epidemic, with relatively small, localized mortality events occurring primarily in harbor seals. By contrast, PDV seems not to have become established in European harbor seals following the 1988 epidemic and a second event of similar magnitude and extent occurred in 2002. PDV is a distinct species within the Morbillivirus genus with minor sequence variation between outbreaks over time. There is now mounting evidence of PDV-like viruses in the North Pacific/Western Arctic with serological and molecular evidence of infection in pinnipeds and sea otters. However, despite the absence of associated mortality in the region, there is concern that the virus may infect the large Pacific harbor seal and northern elephant seal populations or the endangered Hawaiian monk seals. Here, we review the current state of knowledge on PDV with particular focus on developments in diagnostics, pathogenesis, immune response, vaccine development, phylogenetics and modeling over the past 20 years. [ABSTRACT FROM AUTHOR]

Background The risk posed by ticks as vectors of disease is typically assessed by blanket-drag sampling of host-seeking individuals. Comparisons of peak abundance between plots -- either in order to establish their relative risk or to identify environmental correlates -- are often carried out by sampling on one or two occasions during the period of assumed peak tick activity. Methods This paper simulates this practice by 're-sampling' from model datasets derived from an empirical field study. Re-sample dates for each plot are guided by either the previous year's peak at the plot, or the previous year's peak at a similar, nearby plot. Results from single, double and three-weekly sampling regimes are compared. Results Sampling on single dates within a two-month window of assumed peak activity has the potential to introduce profound errors; sampling on two dates (double sampling) offers greater precision, but three-weekly sampling is the least biased. Conclusions The common practice of sampling for the abundance of host-seeking ticks on single dates in each plot-year should be strenuously avoided; it is recommended that field acarologists employ regular sampling throughout the year at intervals no greater than three weeks, for a variety of epidemiological studies. [ABSTRACT FROM AUTHOR]

We present a susceptibles-exposed-infectives (SEI)model to analyze the effects of seasonality on epidemics, mainly of rabies, in a wide range of wildlife species. Model parameters are cast as simple allometric functions of host body size. Via nonlinear analysis, we investigate the dynamical behavior of the disease for different levels of seasonality in the transmission rate and for different values of the pathogen basic reproduction number (R0) over a broad range of body sizes. While the unforced SEI model exhibits long-term epizootic cycles only for large values of R0, the seasonal model exhibits multiyear periodicity for small values of R0. The oscillation period predicted by the seasonal model is consistent with those observed in the field for different host species. These conclusions are not affected by alternative assumptions for the shape of seasonality or for the parameters that exhibit seasonal variations. However, the introduction of host immunity (which occurs for rabies in some species and is typical of many other wildlife diseases) significantly modifies the epidemic dynamics; in this case, multiyear cycling requires a large level of seasonal forcing. Our analysis suggests that the explicit inclusion of periodic forcing in models of wildlife disease may be crucial to correctly describe the epidemics of wildlife that live in strongly seasonal environments. [ABSTRACT FROM AUTHOR]

The article discusses research being done on hyperinfectivity in cholera. It references a study by D. M. Hartley et al published in the 2006 issue of "PLoS Medicine" journal. The study proposes an epidemiological model for the dynamics of cholera that explicitly incorporates a hyperinfectious stage of the pathogen Vibrio cholerae. It notes that the importance of sanitary conditions and clean water for cholera prevention and eradication has been known for a long time.

Through the work of international public health organizations and advancements in the biological and technological sciences, substantial progress has been made in our ability to prevent, control, locally eliminate, and in one case eradicate infectious diseases. Yet each successful control or local elimination has been met with the emergence of new pathogens, the evolution of novel strains, or different epidemiological circumstances that have limited or reversed control methods. To respond to the increasing threat of emerging infectious diseases and bioterrorism it is vital that we design and implement efficient programs that prevent and control infectious pathogen transmission. The theoretical tools of ecology and epidemiology may be the cornerstone in constructing future programs aimed at preventing and controlling infectious diseases throughout the world. [ABSTRACT FROM AUTHOR]

Pathogens that can infect multiple host species will have different dynamics than pathogens that are restricted to a single species of host. This article examines the conditions for establishment and long-term population dynamic behavior of pathogens that infect multiple species of hosts. The article attempts to address three major questions in this area: First, under which conditions will increases in the diversity of host species buffer infectious disease outbreaks, and under which conditions will host diversity amplify disease outbreaks? Second, under what conditions is it possible to control an infectious agent by focusing control against only one host species? Third, what role does host species diversity play in maintaining pathogen persistence? The answers to these questions supply some important general insights into the role that biodiversity plays in buffering humans and other species against new and emerging pathogens. [ABSTRACT FROM AUTHOR]