JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. Ecological Society of America is collaborating with JSTOR to digitize, preserve and extend access to Ecology. Abstract.Using simple analytical models of the probability of disease transmission and a spatially explicit computer simulation of the spread of the aphid-transmitted barley yellow dwarf virus, we examined the effect of vector preference for diseased or healthy hosts on the spread of an economically important plant pathogen. Our analytical models indicate that the effect of vector preference for diseased plants on the probability of disease spread depends on the frequency of diseased plants in the population. In a non-spatial environment with a high frequency of diseased plants, disease spread is favored by vectors preferring healthy plants. With a low frequency of diseased plants, disease spread is favored by vectors preferring diseased plants.The effect of vector preference depends on the amount of persistence exhibited by the disease. For persistently transmitted diseases, the vector remains infective for a long period after visiting a diseased host. Persistence increases the rate of spread for a vector preferring healthy hosts more than it increases the rate of spread for a vector preferring diseased hosts.Using a Markov chain model of disease transmission, we have shown that an increase in the spatial patchiness of the disease can lead to a decrease in the rate of disease spread by a vector capable of moving only limited distances. The effect of spatial disease structure depends on the preference behavior exhibited by the vector.Our spatially explicit computer simulation explored the effect of frequency, persistence, and spatial structure in a dynamic model. All of these factors were shown to be important in describing the impact of vector disease preference on epidemiology. Many of our results contrast with the assumption found in the agricultural literature that a preference for diseased plants leads to an increase in disease spread.These results may have implications for the evolution of pathogen-modified vector behavior and/or host attractiveness. Explicit knowledge of the interaction between spatial dynamics and vector preference will improve our ability to model epidemics and predict the spread of infectious diseases.

Transmission bottlenecks occur in pathogen populations when only a few individual pathogens are transmitted from one infected host to another in the initiation of a new infection. Transmission bottlenecks can dramatically affect the evolution of virulence in rapidly evolving pathogens such as RNA viruses. Characterizing pathogen diversity with the quasispecies concept, we use analytical and simulation methods to demonstrate that severe bottlenecks are likely to drive down the virulence of a pathogen because of stochastic loss of the most virulent pathotypes, through a process analogous to Muller's ratchet. We investigate in this process the roles of host population size, duration of within-host viral replication, and transmission bottleneck size. We argue that the patterns of accumulation of deleterious mutation may explain differing levels of virulence in vertically and horizontally transmitted diseases.

The pteropod Limacina helicina frequently experiences seasonal exposure to corrosive conditions (Ωar  < 1) along the US West Coast and is recognized as one of the species most susceptible to ocean acidification (OA). Yet, little is known about their capacity to acclimatize to such conditions. We collected pteropods in the California Current Ecosystem (CCE) that differed in the severity of exposure to Ωar conditions in the natural environment. Combining field observations, high-CO2 perturbation experiment results, and retrospective ocean transport simulations, we investigated biological responses based on histories of magnitude and duration of exposure to Ωar < 1. Our results suggest that both exposure magnitude and duration affect pteropod responses in the natural environment. However, observed declines in calcification performance and survival probability under high CO2 experimental conditions do not show acclimatization capacity or physiological tolerance related to history of exposure to corrosive conditions. Pteropods from the coastal CCE appear to be at or near the limit of their physiological capacity, and consequently, are already at extinction risk under projected acceleration of OA over the next 30 years. Our results demonstrate that Ωar exposure history largely determines pteropod response to experimental conditions and is essential to the interpretation of biological observations and experimental results.