Posted by: oikosasa | January 22, 2014

Vectors’ role in pathogen dynamics

If  a vector prefers uninfected hosts or infected hosts – how does that affect the pathogen’s spread? Find out in the Early View paper “Vector preference and host defense against infection interact to determine disease dynamics” by Adam R. Zeilinger and Matthew P. Daugherty. Here’s a short version of the paper:

Pathogen spread is greatly influenced by the way that vectors choose which host to feed upon.  Epidemiologists have recognized that many vectors make feeding choices based on whether the host is infected with the pathogen or not.  For example, some mosquito species prefer to feed on animals (including humans) that are infected with malaria over malaria-free animals.  Conversely, the glassy-winged sharpshooter—which spreads the causal pathogen of Pierce’s disease among grapevines—prefers healthy plants.

Grapevine1

At the same time, epidemiologists have also recognized that hosts vary in their susceptibility to a disease.  Some hosts are resistant to infection, meaning that the pathogen replicates poorly in them.  Other hosts are tolerant to the disease, meaning that the pathogen can replicate but the host simply does not express disease.  Resistance and tolerance are both forms of defense against a pathogen.

While vector feeding preference and host defense are clearly important for the spread of a pathogen, we were interested in understanding how the two factors may interact to influence pathogen spread.  To begin to understand the relationships between vector preference and host defense, we used a series of mathematical models, similar to SIR models widely used in epidemiology.  The models simulate the spread of a pathogen in interacting host and vector populations under different scenarios for vector preference and host defense.

Grapevine2

We found that host resistance curbed pathogen spread, regardless of whether vectors preferred or avoided disease symptoms.  However, differences in vector behavior resulted in highly divergent effects if hosts were tolerant, with the greatest pathogen spread occurring if vectors avoided symptoms.  This occurs because, by masking infection, tolerance causes more vectors to inadvertently come into contact with infected hosts and acquire the pathogen.  Furthermore, we extended our model to a two-patch model, in which two host populations with differing defenses were connected by vector movement.  The outcomes from those scenarios support the idea that host defense impacts pathogen spillover, with a greater potential for tolerant host to be pathogen sources relative to resistant host types.

These results highlight the importance of understanding both vector feeding behavior and the precise form of host defense in predicting pathogen spread.  This may be particularly important for integrated disease management for agricultural crops.  For example, given that the glassy-winged sharpshooter prefers disease-free grapevines, breeding new grapevine varieties that are tolerant to Pierce’s disease may lead to unexpectedly high disease spread among nearby susceptible grapevine varieties.

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