Disease transmission in filter feeders often occurs directly via filtration of waterborne pathogens. We explored the relationship between host density , pathogen dilution and disease risk using a compartmental model , which incorporates the effect of a dose-­‐response mechanism and the potential of a remote volume , adjacent to the local volume directly influenced by filtration , to modulate the infection process through diffusional exchange of particles with the local volume. We estimated the basic reproduction number R0 , a measure of disease risk that serves as a threshold parameter for disease outbreak. We identified two major mechanisms limiting epizootic development. The first , overfiltration , occurs when a dense assemblage of filter feeders effectively removes pathogens from the system by refiltering water many times over. In this case , each animal acquires on average a reduced number of particles , so that once the population rises above a certain initial population the maximal R0 is attained and remains constant. We also found epizootic development to be limited by a diffusive effect , where a large remote volume leads to a system with an effective mechanism to purge pathogens accessible to benthic filter feeders. Whether the epizootic develops (i. e. Ro >1) depends on the balance between the in vivo inactivation of pathogens and the rate of particle acquisition through filtering that determines whether the body burden of infective particles will exceed the infective dose. Preliminary 3-­‐D simulations using the hydrodynamic model ROMS coupled to a benthic model , confirm the overfiltration effect over a dense oyster reef resulting in turns in a reduction of downstream pathogen flux and a dilution of the disease risk both locally and in neighboring reefs .