Host-diversity in the transmission of vector-borne disease: an epidemiologic model

Martin Eichner , 1994
Technical report, German Accademic Exchange Service (DAAD)

Harvard School of Public Health, Boston, U.S.A.

Abstract

The proposed model rationalizes the force of transmission of a zoonotic vector-borne pathogen in the presence of an array of vertebrate populations that are more or less attractive to the vector but differ in competence for the pathogen. A set of differential equations is used to represent these dynamic host-vector-pathogene interactions. The pathogen under consideration produces effective but transient immunity in vertebrate hosts. To provide for the feeding cycle of the vector population, the model assumes a ``resting period'' in which these vector arthropods cease questing for hosts.

At the endemic equilibrium of the infection, the density of infective vectors or vertebrates depends on many parameters of each of these populations. The density of vertebrate hosts critically affects pathogen perpetuation, and particular changes in host density can lead to counter-intuitive outcomes. Changes in the density of a vertebrate host population either increase or decrease prevalence of infection in coexisting populations and in the original population as well. Perpetuation would fail due to a dilution effect, if the vertebrate reservoir population becomes excessively dense or the vector sparse. If the vector feeds on incompetent hosts as well as competenet hosts, perpetuation would require a certain minimum density of vertebrate reservoir hosts as well as a reduced maximum density. Perpetuation would fail due to zooprophylaxis, if a vector-attractive, but incompetent host population becomes excessively dense.

These theoretical considerations warn against ill-considered public health interventions designed to reduce the density of potenential vertebrate hosts of a vector-borne pathogen.