Submitted to: Environmental Entomology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 13, 2008
Publication Date: April 1, 2009
Citation: Sisterson, M.S. 2009. Transmission of Insect-Vectored Pathogens: Effects of Vector Fitness as a Function of Infectivity Status. Environmental Entomology. 38:345-355. Interpretive Summary: Epidemiology models provide the opportunity to systemically examine how different assumptions about a research system affect pathogen spread. In this project, assumptions about the effects of a pathogen on the survival and reproduction of an insect-vector were investigated using a set of compartmentalized differential equations. The model suggests that pathogens which increase the death rate of inoculative vectors may ultimately reduce disease incidence by reducing the proportion of vectors which were inoculative. With regards to birth-rate, the model suggests that pathogens which increase the birth rate of inoculative vectors will only influence disease incidence provided that the birth rate of pathogen-free vectors is only slightly greater than their death rate. Understanding how pathogen spread is affected by alterations in vector fitness due to infectivity status will aid in determining how such effects could be used by disease management programs.
Technical Abstract: The spread of insect vectored pathogens is dependent on the population dynamics of the vector. Epidemiology models typically assume that birth and death rates of pathogen-free and inoculative vectors are equal, an assumption which is not true for all pathosystems. Here a series of simple and general epidemiology models were used to explore how assumptions about birth and death rates of vectors based on their infectivity status influence disease incidence. With unequal death rates of pathogen-free and inoculative vectors, the death rate of pathogen-free vectors was more important in determining total vector density than the death rate of inoculative vectors. Thus, with fixed death rate of inoculative vectors, increasing the death rate of pathogen-free vectors reduced disease incidence by reducing vector density. In contrast, with fixed death rate of pathogen-free vectors, increasing the death rate of inoculative vectors did not reduce total vector density, but still decreased disease incidence. This occurred because inoculative vectors which died were replaced by pathogen-free vectors which in turn reduced the proportion of the vector population which carried the pathogen. With fixed birth rate of pathogen-free vectors, variation in the birth rate of inoculative vectors had little influence on disease incidence provided that the birth rate of pathogen-free vectors was much greater than their death rate. However, when the birth rate of pathogen-free vectors was only slightly greater than their death rate, large increases in the birth rate of inoculative vectors increased total vector density and in turn disease incidence. The results indicate that assumptions about the birth and death rates of vectors based on infectivity status can have important effects on the vector population which in turn effects disease incidence.