Multilocus sequence typing of Borrelia hermsii isolates reveals its divergence into two major genomic groups (GG), but no differences in transmission efficiency or host pathogenicity are associated with these genotypes. To compare GGI and GGII in the tick-host infection cycle, we first determined if spirochetes from the two groups could superinfect the tick vector Ornithodoros hermsi. We infected mice with isolates from each group and fed ticks sequentially on these mice. We then fed the infected ticks on naive mice and measured GGI and GGII spirochete densities in vector and host, using quantitative PCR of genotype-specific chromosomal DNA sequences. Sequential feedings resulted in dual tick infections, showing that GGI or GGII primary acquisition did not block superinfection by a secondary agent. On transmission to naive mice at short intervals after acquisition, ticks with primary GGI and secondary GGII spirochete infections caused mixed GGI and GGII infections in mice. However, ticks with primary GGII and secondary GGI spirochete infections caused only GGII infections with all isolate pairs examined. At longer intervals after acquisition, the exclusion of GGI by GGII spirochetes declined and cotransmission predominated. We then examined GGI and GGII spirochetemia in mice following single inoculation and coinoculation by needle and found that GGI spirochete densities were reduced on multiple days when coinoculated with GGII. These findings indicate that dual GGI-GGII spirochete infections can persist in ticks and that transmission to a vertebrate host is dependent on the order of tick acquisition and the interval between acquisition and transmission events.
Borrelia hermsii is the primary agent of tick-borne relapsing fever in western North America, where it persists in enzootic cycles involving the argasid (soft tick) vector Ornithodoros hermsi and diverse vertebrate hosts (1). Argasid ticks are predominately nest dwelling and feed at each immature stage and multiple times as adults, with the potential for acquisition and transmission of multiple spirochete genotypes (2). As rapid feeders, their occasional infestation of humans is rarely discovered, and spirochete isolation from ticks involved in transmission is virtually unreported. Spirochete DNA analysis from clinical samples, rodent hosts, and ticks indicates divergence into two major B. hermsii genomic groups (GGI and GGII), based on the 16S-23S rRNA gene intergenic spacer (2, 3) and multilocus sequence typing (4). The latter study demonstrated that GGI and GGII isolates are distributed throughout the range of the vector. Clinical isolates from a western Montana site showed sympatry of GGI and GGII spirochetes within a microenvironment where the disease is endemic (4, 5), suggesting that ticks may be exposed to spirochetes of both genotypes during their life cycle. Tick vectors and mammalian hosts can show significant heterogeneity in pathogen populations, as shown by studies on B. burgdorferi sensu lato and sensu stricto isolates (6-8) and Anaplasma ma...