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Disease may play a critical role in invasions by nonnative plants and animals that currently threaten global biodiversity. For example, a generalist viral pathogen has been recently implicated in one of the most extensive plant invasions worldwide, the invasion and domination of California's perennial grasslands by exotic annual grasses. To date, disease has never been quantitatively assessed as a cause of this invasion. Using a model with field-estimated parameters, we demonstrate that pathogen presence was necessary to reverse competitive outcome and to allow exotic annual grass invasion and dominance. Although pathogen-induced reversal of a competitive hierarchy has been suggested as a mechanism of species invasion, here we quantitatively demonstrate the importance of this phenomenon by using field-derived parameters in a dynamical model. Pathogen-mediated reversals in competitive balance may be critically important for understanding past, and predicting future, invasions. barley yellow dwarf virus | California grassland | disease ecology | integrodifference model | invasion

Parasitism is the most common animal lifestyle, yet food webs rarely include parasites. The few earlier studies have indicated that including parasites leads to obvious increases in species richness, number of links, and food chain length. A less obvious result was that adding parasites slightly reduced connectance, a key metric considered to affect food web stability. However, reported reductions in connectance after the addition of parasites resulted from an inappropriate calculation. Two alternative corrective approaches applied to four published studies yield an opposite result: parasites increase connectance, sometimes dramatically. In addition, we find that parasites can greatly affect other food web statistics, such as nestedness (asymmetry of interactions), chain length, and linkage density. Furthermore, whereas most food webs find that top trophic levels are least vulnerable to natural enemies, the inclusion of parasites revealed that mid-trophic levels, not low trophic levels, suffered the highest vulnerability to natural enemies. These results show that food webs are very incomplete without parasites. Most notably, recognition of parasite links may have important consequences for ecosystem stability because they can increase connectance and nestedness. connectance | parasitism | trophic | predation | trematode

The population structure of social species has important consequences for both their demography and transmission of their pathogens. We develop a metapopulation model that tracks two key components of a species' social system: average group size and number of groups within a population. While the model is general, we parameterize it to mimic the dynamics of the Yellowstone wolf population and two associated pathogens: sarcoptic mange and canine distemper. In the initial absence of disease, we show that group size is mainly determined by the birth and death rates and the rates at which groups fission to form new groups. The total number of groups is determined by rates of fission and fusion, as well as environmental resources and rates of intergroup aggression. Incorporating pathogens into the models reduces the size of the host population, predominantly by reducing the number of social groups. Average group size responds in more subtle ways: infected groups decrease in size, but uninfected groups may increase when disease reduces the number of groups and thereby reduces intraspecific aggression. Our modeling approach allows for easy calculation of prevalence at multiple scales (within group, across groups, and population level), illustrating that aggregate population-level prevalence can be misleading for group-living species. The model structure is general, can be applied to other social species, and allows for a dynamic assessment of how pathogens can affect social structure and vice versa. [ABSTRACT FROM AUTHOR]

It is extremely likely that the malaria vaccines currently in development will be used in conjunction with treated bednets and other forms of malaria control. The interaction of different intervention methods is at present poorly understood in a disease such as malaria where immunity is more complex than for other pathogens that have been successfully controlled by vaccination. Here we develop a general mathematical model of malaria transmission to examine the interaction between vaccination and bednets. Counterintuitively, we find that the frailty ofmalaria immunity will potentially cause both synergistic and antagonistic interactions between vaccination and the use of bednets. We explore the conditions that create these tensions, and outline strategies that minimize their detrimental impact. Our analysis specifically considers the three leading vaccine classes currently in development: preerythrocytic (PEV), blood stage (BSV), and transmission blocking (TBV). We find that the combination of BSV with treated bednets can lead to increased morbidity with no added value in terms of elimination; the interaction is clearly antagonistic. In contrast, there is strong synergy between PEV and treated bednets that may facilitate elimination, although transient stages are likely to increase morbidity. The combination of TBV with treated bednets is synergistic, lowering both morbidity and elimination thresholds. Our results suggest that vaccines will not provide a straightforward solution to malaria control, and that future programs need to consider the synergistic and antagonistic interactions between vaccines and treated bednets. [ABSTRACT FROM AUTHOR]

In this article, the authors reflect on the article by K. P. Paaijmans and colleagues concerning the effects of climate change on malaria risk. They indicate the authors' findings that diurnal fluctuations in temperature can modify the external incubation period of the parasite, in relation to estimates based on the coarser temporal resolution of daily mean temperature. They emphasize that the authors' work underlines the need to understand malaria biology and its interaction with climate.

Morbilliviruses cause many diseases of medical and veterinary importance, and although some (e.g., measles and rinderpest) have been controlled successfully, others, such as canine distemper virus (CDV), are a growing concern. A propensity for host-switching has resulted in CDV emergence in new species, including endangered wildlife, posing challenges for controlling disease in multispecies communities. CDV is typically associated with domestic dogs, but little is known about its maintenance and transmission in species-rich areas or about the potential role of domestic dog vaccination as a means of reducing disease threats to wildlife. We address these questions by analyzing a long-term serological dataset of CDV in lions and domestic dogs from Tanzania's Serengeti ecosystem. Using a Bayesian state-space model, we show that dynamics of CDV have changed considerably over the past three decades. Initially, peaks of CDV infection in dogs preceded those in lions, suggesting that spill-over from dogs was the main driver of infection in wildlife. However, despite dog-to-lion transmission dominating cross-species transmission models, infection peaks in lions became more frequent and asynchronous from those in dogs, suggesting that other wildlife species may play a role in a potentially complex maintenance community. Widespread mass vaccination of domestic dogs reduced the probability of infection in dogs and the size of outbreaks but did not prevent transmission to or peaks of infection in lions. This study demonstrates the complexity of CDV dynamics in natural ecosystems and the value of long-term, large-scale datasets for investigating transmission patterns and evaluating disease control strategies.