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A Francisella tularensis Chitinase Contributes to Bacterial Persistence and Replication in Two Major U.S. Tick
Brenden G Tully1, Jason F Huntley1
1Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA.
Abstract:
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 ΔFTL1793 mutant and found that ΔFTL1793 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.
Insights
Dermacentor variabilis ticks pose a greater risk for transmitting tularemia. The Francisella tularensis gene FTL1793 is crucial for Ft infection, persistence, and replication in ticks.
Area of Science:
- Microbiology
- Vector-borne diseases
- Genetics
Background:
- Tularemia, caused by Francisella tularensis (Ft), is a tick-borne disease with ongoing questions about transmission vectors.
- Limited understanding exists regarding the genes and proteins essential for Ft survival and replication within ticks.
Purpose of the Study:
- To investigate the vector competence of three tick species for Ft transmission.
- To identify Ft genes critical for infection, persistence, and replication in ticks.
Main Methods:
- Infection of Dermacentor variabilis (Dv), Amblyomma americanum (Aa), and Haemaphysalis longicornis (Hl) ticks with Ft.
- Transmission studies of Ft-infected ticks to naïve mice.
- Generation and analysis of a Ft mutant lacking the FTL1793 gene (ΔFTL1793).
Main Results:
- Ft replicated more robustly in Dv ticks and did not persist in Hl ticks, despite higher initial infection in Aa ticks.
- Both Dv and Aa ticks efficiently transmitted Ft to mice, causing disease.
- The ΔFTL1793 mutant showed deficiencies in infection, persistence, and replication in ticks, while recombinant FTL1793 exhibited chitinase activity.
Conclusions:
- Dermacentor variabilis ticks represent a significant risk for harboring and transmitting tularemia.
- The Ft gene FTL1793 plays a critical role in facilitating Ft infection and survival within ticks, potentially by providing an alternative energy source.
