Lyme disease is a major vector-borne bacterial disease in the USA. The disease is caused by Borrelia burgdorferi, and transmitted among hosts and humans, primarily by blacklegged ticks (Ixodes scapularis). The ~25 B. burgdorferi genotypes, based on genotypic variation of their outer surface protein C (ospC), can be phenotypically separated as strains that primarily cause human diseases – human invasive strains (HIS) – or those that rarely do – and are non-randomly associated with host species. The goal of this study was to examine the extent to which phenotypic outcomes of B. burgdorferi could be explained by the host communities fed upon by blacklegged ticks. In 2006 and 2009, we determined the host community composition based on abundance estimates of the vertebrate hosts, and collected host-seeking nymphal ticks in 2007 and 2010 to determine the ospC genotypes within infected ticks. We regressed instances of B. burgdorferi phenotypes on site-specific characteristics of host communities by constructing Bayesian hierarchical models that properly handled missing data. The models provided quantitative support for the relevance of host composition on Lyme disease risk pertaining to B. burgdorferi prevalence (i.e., overall nymphal infection prevalence, or NIP All ) and HIS prevalence among the infected ticks (NIP HIS ). In 2006, we found positive associations of the relative abundances of mice, of chipmunks, and of shrews with NIP All . We also found positive associations of NIP HIS with shrews, and with host community diversity (H’), but negative associations with mice, and with chipmunks. In 2009, the relative abundance of mice showed a positive association with NIP All , whereas the relative abundance of shrews and of H’ showed a negative association. With NIP HIS , only H’ showed a positive association, whereas the relative abundances of mice, of chipmunks, and of shrews, had negative associations. Our study highlights the variability between two years in the effects of host composition on B. burgdorferi genotypes. More importantly, our results highlight how disease risk inference, based on the role of host community, changes when we examine risk overall or at the phenotypic level. Long-term studies will be necessary to detect any consistent effects of host community composition on genotypic variation in the Lyme disease spirochetes.