Diversity and host specificity of Borrelia burgdorferi's outer surface protein C (ospC) alleles in synanthropic mammals, with a notable ospC allele U absence from mixed infections

Interactions among pathogen genotypes that vary in host specificity may
affect overall transmission dynamics in multi-host systems. Borrelia
burgdorferi, a bacterium that causes Lyme disease, is typically
transmitted among wildlife by Ixodes ticks. Despite the existence of many
alleles of B. burgdorferi’s sensu stricto outer surface protein C (ospC)
gene, most human infections are caused by a small number of ospC alleles
[“human infectious alleles” (HIAs)], suggesting variation in host
specificity associated with ospC. To characterize the wildlife host
association of B. burgdorferi’s ospC alleles, we used metagenomics to
sequence ospC alleles from 68 infected individuals belonging to eight
mammalian species trapped at three sites in suburban New Brunswick, New
Jersey (USA). We found that multiple allele (“mixed”) infections were
common. HIAs were most common in mice (Peromyscus spp.) and only one HIA
was detected at a site where mice were rarely captured. OspC allele U was
exclusively found in chipmunks (Tamias striatus), and although a
significant number of different alleles were observed in chipmunks,
including HIAs, allele U never co-occurred with other alleles in mixed
infections. Our results suggest that allele U may be excluding other
alleles, thereby reducing the capacity of chipmunks to act as reservoirs
for HIAs.