Nearly 100 years after the first report of tick-borne tularemia, questions remain about the tick vector(s) that pose the greatest risk for transmitting (), the causative agent of tularemia. Additionally, few studies have identified genes/proteins required for to infect, persist, and replicate in ticks. To answer questions about vector competence and transmission by ticks, we infected () (), and ( invasive species from Asia) ticks with , finding that although ticks initially become infected with 1 order of magnitude higher , replicated more robustly in ticks, and did not persist in ticks. In transmission studies, both and ticks efficiently transmitted to naïve mice, causing disease in 57% and 46% of mice, respectively. Of four putative chitinases, is the most conserved among sp. We generated a Δ mutant and found that Δ was deficient for infection, persistence, and replication in ticks. Recombinant exhibited chitinase activity in vitro, suggesting that may provide an alternative energy source for in ticks. Taken together, ticks appear to pose a greater risk for harboring and transmitting tularemia and plays a major role in promoting tick infections by .
