Bacteria of the genus Bartonella inhabit the red blood cells of many mammals, including humans, and are transmitted by blood-sucking arthropod vectors. Different species of Bartonella are associated with different mammalian host species, to which they have adapted and normally do not cause any symptoms. Incidental infection of other hosts is however often followed by various disease symptoms, and several Bartonella species are considered as emerging human pathogens.
In this work, I have studied the genomic diversity within and between different Bartonella species, with focus on the feline-associated human pathogen B. henselae and its close relatives, the similarly feline-associated B. koehlerae and the trench-fever agent B. quintana which is restricted to humans.
In B. henselae, the overall variability in sequence and genome content was modest and well correlated, suggesting low levels of intra-species recombination in the core genome. The variably present genes were located in the prophage and the genomic islands, which are also absent from B. quintana and B. koehlerae, indicating multiple independent excision events. In contrast, diversity of genome structures was immense and probably associated with rearrangements between the repeated genomic islands located around the terminus of replication, possibly to avoid the host’s immune system. In both B. henselae and the mouse-associated species B. grahamii a large portion of the chromosome was manifold amplified in long-time cultures and packaged into phage particles, allowing for different recombination rates for different chromosomal regions.
In B. quintana, diversity was studied by sequencing non-coding spacers. The low variability might be due to the recent emergence of this species. Surprisingly, also this species displayed high variability in genome structures, despite its lack of repeated sequences.
The results indicate that genome rearrangements and gain or loss of mobile elements are major mechanisms of evolution in Bartonella.