Trophic interactions and population growth rates: describing patterns and identifying mechanisms

While the concept of population growth rate has been of central importance in the development of the theory of population dynamics, few empirical studies consider the intrinsic growth rate in detail, let alone how it may vary within and between populations of the same species. In an attempt to link theory with data we take two approaches. First, we address the question ''what growth rate patterns does theory predict we should see in time-series?'' The models make a number of predictions, which in general are supported by a comparative study between time-series of harvesting data from 352 red grouse populations. Variations in growth rate between grouse populations were associated with factors that reflected the quality and availability of the main food plant of the grouse. However, while these results support predictions from theory, they provide no clear insight into the mechanisms influencing reductions in population growth rate and regulation. In the second part of the paper, we consider the results of experiments, first at the individual level and then at the population level, to identify the important mechanisms influencing changes in individual productivity and population growth rate. The parasitic nematode Trichostrongylus tenuis is found to have an important influence on productivity, and when incorporated into models with their patterns of distribution between individuals has a destabilizing effect and generates negative growth rates. The hypothesis that negative growth rates at the population level were caused by parasites was demonstrated by a replicated population level experiment. With a sound and tested model framework we then explore the interaction with other natural enemies and show that in general they tend to stabilize variations in growth rate. Interestingly, the models show selective predators that remove heavily infected individuals can release the grouse from parasite-induced regulation and allow equilibrium populations to rise. By contrast, a tick-borne virus that killed chicks simply leads to a reduction in the equilibrium. When humans take grouse they do not appear to stabilize populations and this may be because many of the infective stages are available for infection before harvesting commences. In our opinion, an understanding of growth rates and population dynamics is best achieved through a mechanistic approach that includes a sound experimental approach with the development of models. Models can be tested further to explore how the community of predators and others interact with their prey.     

A stochastic model for extinction and recurrence of epidemics: estimation and inference for measles outbreaks

Epidemic dynamics pose a great challenge to stochastic modelling because chance events are major determinants of the size and the timing of the outbreak. Reintroduction of the disease through contact with infected individuals from other areas is an important latent stochastic variable. In this study we model these stochastic processes to explain extinction and recurrence of epidemics observed in measles. We develop estimating functions for such a model and apply the methodology to temporal case counts of measles in 60 cities in England and Wales. In order to estimate the unobserved spatial contact process we suggest a method based on stochastic simulation and marginal densities. The estimation results show that it is possible to consider a unified model for the UK cities where the parameters depend on the city size. Stochastic realizations from the dynamic model realistically capture the transitions from an endemic cyclic pattern in large populations to irregular epidemic outbreaks in small human host populations.     

Whole-genome analysis of human influenza A virus reveals multiple persistent lineages and reassortment among recent H3N2 viruses

Understanding the evolution of influenza A viruses in humans is important for surveillance and vaccine strain selection. We performed a phylogenetic analysis of 156 complete genomes of human H3N2 influenza A viruses collected between 1999 and 2004 from New York State, United States, and observed multiple co-circulating clades with different population frequencies. Strikingly, phylogenies inferred for individual gene segments revealed that multiple reassortment events had occurred among these clades, such that one clade of H3N2 viruses present at least since 2000 had provided the hemagglutinin gene for all those H3N2 viruses sampled after the 2002–2003 influenza season. This reassortment event was the likely progenitor of the antigenically variant influenza strains that caused the A/Fujian/411/2002-like epidemic of the 2003–2004 influenza season. However, despite sharing the same hemagglutinin, these phylogenetically distinct lineages of viruses continue to co-circulate in the same population. These data, derived from the first large-scale analysis of H3N2 viruses, convincingly demonstrate that multiple lineages can co-circulate, persist, and reassort in epidemiologically significant ways, and underscore the importance of genomic analyses for future influenza surveillance.     

The effects of strain heterology on the epidemiology of equine influenza in a vaccinated population

We assess the effects of strain heterology (strains that are immunologically similar but not identical) on equine influenza in a vaccinated population. Using data relating to individual animals, for both homologous and heterologous vaccinees, we estimate distributions for the latent and infectious periods, quantify the risk of becoming infected in terms of the quantity of cross-reactive antibodies to a key surface protein of the virus (haemagglutinin) and estimate the probability of excreting virus (i.e. becoming infectious) given that infection has occurred. The data suggest that the infectious period, the risk of becoming infected (for a given vaccine-induced level of cross-reactive antibodies) and the probability of excreting virus are increased for heterologously vaccinated animals when compared with homologously vaccinated animals. The data are used to parameterize a modified susceptible, exposed, infectious and recovered/resistant (SEIR) model, which shows that these relatively small differences combine to have a large effect at the population level, where populations of heterologous vaccinees face a significantly increased risk of an epidemic occurring.     

Environmental Drivers of the Spatiotemporal Dynamics of Respiratory Syncytial Virus in the United States

Epidemics of respiratory syncytial virus (RSV) are known to occur in wintertime in temperate countries including the United States, but there is a limited understanding of the importance of climatic drivers in determining the seasonality of RSV. In the United States, RSV activity is highly spatially structured, with seasonal peaks beginning in Florida in November through December and ending in the upper Midwest in February-March, and prolonged disease activity in the southeastern US. Using data on both age-specific hospitalizations and laboratory reports of RSV in the US, and employing a combination of statistical and mechanistic epidemic modeling, we examined the association between environmental variables and state-specific measures of RSV seasonality. Temperature, vapor pressure, precipitation, and potential evapotranspiration (PET) were significantly associated with the timing of RSV activity across states in univariate exploratory analyses. The amplitude and timing of seasonality in the transmission rate was significantly correlated with seasonal fluctuations in PET, and negatively correlated with mean vapor pressure, minimum temperature, and precipitation. States with low mean vapor pressure and the largest seasonal variation in PET tended to experience biennial patterns of RSV activity, with alternating years of “early-big” and “late-small” epidemics. Our model for the transmission dynamics of RSV was able to replicate these biennial transitions at higher amplitudes of seasonality in the transmission rate. This successfully connects environmental drivers to the epidemic dynamics of RSV; however, it does not fully explain why RSV activity begins in Florida, one of the warmest states, when RSV is a winter-seasonal pathogen. Understanding and predicting the seasonality of RSV is essential in determining the optimal timing of immunoprophylaxis.     

Antischistosomal activity of a calcium channel antagonist on schistosomula and adult Schistosoma mansoni worms

Current schistosomiasis control strategies are largely based on chemotherapeutic agents and a limited number of drugs are available today. Praziquantel (PZQ) is the only drug currently used in schistosomiasis control programs. Unfortunately, this drug shows poor efficacy in patients during the earliest infection phases. The effects of PZQ appear to operate on the voltage-operated Ca2+channels, which are located on the external Schistosoma mansoni membrane. Because some Ca2+channels have dihydropyridine drug class (a class that includes nifedipine) sensitivity, an in vitro analysis using a calcium channel antagonist (clinically used for cardiovascular hypertension) was performed to determine the antischistosomal effects of nifedipine on schistosomula and adult worm cultures. Nifedipine demonstrated antischistosomal activity against schistosomula and significantly reduced viability at all of the concentrations used alone or in combination with PZQ. In contrast, PZQ did not show significant efficacy when used alone. Adult worms were also affected by nifedipine after a 24 h incubation and exhibited impaired motility, several lesions on the tegument and intense contractility. These data support the idea of Ca2+channels subunits as drug targets and favour alternative therapeutic schemes when drug resistance has been reported. In this paper, strong arguments encouraging drug research are presented, with a focus on exploring schistosomal Ca2+channels.     

New Approaches with Different Types of Circulating Cathodic Antigen for the Diagnosis of Patients with Low Schistosoma mansoni Load

Background

Schistosomiasis mansoni is a debilitating and sometimes fatal disease. Accurate diagnosis plays a key role in patient management and infection control. However, currently available parasitological methods are laborious and lack sensitivity. The selection of target antigen candidates has turned out to be a promising tool for the development of more sensitive diagnostic methods. In our previous investigations, the use of crude antigens led to false-positive results. Recently, focus has been given to highly purified Schistosoma mansoni antigens, especially to circulating antigens.

Method

Thus, our main goal was to test different types of circulating cathodic antigen glycoprotein (CCA), as “crude antigen,” the protein chain of recombinant CCA and two individual peptides. These schistosome proteins/peptides were tested in a new diagnostic method employing immunomagnetic separation based on the improvement of antigen–antibody binding.

Principal Findings

Use of recombinant CCA as a diagnostic antigen allowed us to develop a diagnostic assay with high sensitivity and specificity with no false-negative results. Interestingly, the “crude antigen” worked as a good marker for control of cure after praziquantel treatment.

Conclusions/Significance

Our new diagnostic method was superior to enzyme-linked immunosorbent assay in diagnosing low endemicity patients.