Potential influence on pathogenesis, biology, and evolution from the bdr gene families of Lyme disease and relapsing fever spirochetes are discussed. Recent progress in characterization of Borrelia bdr genes and possible influence it has on evolution of the Borrelia genome are considered. The genome is unique among bacterial genomes with a linear chromosome and a series of circular and linear plasmids.
Species of the genus Borrelia cause human and animal infections, including Lyme disease, relapsing fever, and epizootic bovine abortion. The borrelial genome is unique among bacterial genomes in that it is composed of a linear chromosome and a series of linear and circular plasmids. The plasmids exhibit significant genetic redundancy and carry 175 paralogous gene families, most of unknown function. Homologous alleles on different plasmids could influence the organization and evolution of the Borrelia genome by serving as foci for interplasmid homologous recombination. The plasmid-carried Borrelia direct repeat (bdr) gene family encodes polymorphic, acidic proteins with putative phosphorylation sites and transmembrane domains. These proteins may play regulatory roles in Borrelia. We describe recent progress in the characterization of the Borrelia bdr genes and discuss the possible influence of this gene family on the biology, pathogenesis, and evolution of the Borrelia genome.( Burgdorfer W, Barbour AG, Hayes SF (2004))
Species of the genus Borrelia cause human and animal infections. In North America, Lyme disease and endemic relapsing fever pose the greatest threat to human health and have received the most attention of the borrelial diseases. Approximately 14,000 cases of Lyme disease are reported in the United States each year; however, the actual number of cases may be 10-fold higher. Lyme disease was not recognized as a distinct clinical entity in North America until the 1970s. The causative agent, a previously uncharacterized spirochete transmitted through the bite of infected ticks of the Ixodes ricinus complex........................
