Many diseases have both sexual and nonsexual transmission routes, and
closely related diseases often differ in their degree of sexual transm
ission. We investigate the evolution of transmission mode as a functio
n of host social and mating structure using a model in which disease t
ransmission is explicitly dependent on the numbers of sexual and nonse
xual contacts (which are themselves a function of population density)
and per-contact infection probabilities. Most generally, and in the ab
sence of tradeoffs between the degree of sexual transmission and effec
ts on host fecundity and mortality, nonsexual transmission is favored
above the social-sexual crossover point (the host density at which the
number of nonsexual contacts exceeds the number of sexual contacts),
while sexual transmission is favored below this point. When changes in
allocation to the two transmission modes are accompanied by changes i
n mortality or fecundity, both mixed and pure transmission strategies
can be favored. If invading genotypes differ substantially from reside
nt genotypes, genetic polymorphism in transmission mode is possible. T
he evolutionary outcomes are predictable from a knowledge of the equil
ibrium population sizes in relation to the social-sexual crossover poi
nt. Our results also show that predictions about dynamic outcomes, bas
ed on rates of invasion for single pathogens into healthy populations,
do not adequately describe the resulting disease prevalence nor predi
ct the subsequent evolutionary dynamics; once invasion of a pathogen h
as occurred, the conditions for spread of a second pathogen are themse
lves altered. If the host is considered as a single resource, our resu
lts show that two pathogens may coexist on a single resource ii they u
se that resource differentially and have differential feedbacks on res
ource abundance; such resource feedback effects map be present in othe
r biological systems.