BMC Infectious Diseases. 15:61.
Background: The diversity of pathogen strains is often overlooked, even though it is fundamental in medical, epidemiological or evolutionary perspectives. In the bacteria Borrelia burgdorferi s.s., responsible for Lyme disease, it is assumed that diversity of Outer surface protein C (OspC) gene is the product of selection to evade the immune system, explaining why wild hosts and tick vectors are often coinfected. We tested this hypothesis by conducting controlled mouse sequential coinfection by two of three selected OspC strains (type A, K and N) in nine groups (AA, AK, AN, KA, KK, KN, NA, NK, NN). We assessed competition between strains as the frequency of organ infection by the primary and the secondary strains, and the transmission of bacteria to naïve ticks through four xenodiagnoses. We measured generalist and strain-specific immunoglobulin G, characteristic of the acquired immune response.
Results: We found that regardless of the identity of the strains, the secondary strains were virtually not transmitted to ticks, whereas primary strains were well transmitted. The mechanism was the absence of dispersion into organs by the secondary strain. The immune response developed against the primary strain was inefficient at clearing the bacteria; however, regardless of the identity of the strains, the immune response against the secondary strain for both the specific and generalist antibodies was inexistent.
Conclusions: The strong inhibitory priority effect that we observed suggests that the diversity of strains would disappear quickly if not all conditions are met in nature. The acquired immune response does not seem to be the physiological mechanism responsible for this exclusion. We suggest that rather than to immune response from hosts, some specific ecological conditions such as host diversity and tick phenology are the mechanisms that maintain the diversity of OspC strains in wild population of Borrelia burgdorferi.