POLYMORPHISM IN SEXUAL VERSUS NONSEXUAL DISEASE TRANSMISSION

Pathogens causing sexually transmitted diseases (STDs) often consist o f related strains that cause nonsexually transmitted, or 'ordinary inf ectious', diseases (OIDs). We use differential equation models of sing le populations to derive conditions under which a genetic variant with one (e.g. sexual) transmission mode can invade and successfully displ ace a genetic variant with a different (e.g. non-sexual) transmission mode. Invasion by an STD is easier if the equilibrium population size in the presence of an OID is smaller; conversely an OID can invade mor e easily if the equilibrium size of the population with the STD is lar ger. Invasion of an STD does not depend on the degree of sterility cau sed by the infection, but does depend on the added mortality caused by a resident OID. In contrast, the ability of an OID to invade a popula tion at equilibrium with an STD decreases as the degree of sterility c aused by the STD increases. When equilibrium population sizes for a po pulation infected with an STD are above the point at which non-sexual contacts exceed sexual contacts (the sexual-social crossover point) an d when equilibrium population sizes for an OID are below this point, t here can be a stable genetic polymorphism for transmission mode. This is most likely when the STD is mildly sterilizing, and the OID causes low or intermediate levels of added mortality. Because we assume the s trains are competitively equivalent and there are no heterogeneities a ssociated with the transmission process, the polymorphism is maintaine d by density-dependent selection brought about by pathogen effects on population size.