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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  Francisella tularensis  ( Ft ), the causative agent of tularemia. Additionally, few studies have identified genes/proteins required for  Ft  to infect, persist, and replicate in ticks. To answer questions about vector competence and  Ft  transmission by ticks, we infected  Dermacentor variabilis  ( Dv ) ,   Amblyomma americanum  ( Aa ), and  Haemaphysalis longicornis  ( Hl;  invasive species from Asia) ticks with  Ft , finding that although  Aa  ticks initially become infected with 1 order of magnitude higher  Ft ,  Ft  replicated more robustly in  Dv  ticks, and did not persist in  Hl  ticks. In transmission studies, both  Dv  and  Aa  ticks efficiently transmitted  Ft  to naïve mice, causing disease in 57% and 46% of mice, respectively. Of four putative  Ft  chitinases,  FTL1793  is the most conserved among  Francisella  sp. We generated a Δ FTL1793  mutant and found that Δ FTL1793  was deficient for infection, persistence, and replication in ticks. Recombinant  FTL1793  exhibited chitinase activity in vitro, suggesting that  FTL1793  may provide an alternative energy source for  Ft  in ticks. Taken together,  Dv  ticks appear to pose a greater risk for harboring and transmitting tularemia and  FTL1793  plays a major role in promoting tick infections by  Ft .

A Francisella tularensis Chitinase Contributes to Bacterial Persistence and Replication in Two Major U.S. Tick Vectors