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We took a genetic approach to test the hypothesis that virulence toward OS cockroaches at 37^{$\circ$}C mimics virulence toward mammals. We examined the virulence of a small panel of \textit{F. tularensis} LVS mutants that are attenuated in other model systems. DsbA and DipA are both associated with the normal structure and function of the \textit{F. tularensis} membrane and their loss results in severe attenuation in mammals \cite{25257164, 23840797}. DeoB is a metabolic protein (a phosphopentomutase) required for cellular invasion and virulence toward macrophages, dendritic cells, and chick embryos in \textit{F. tularensis} \cite{18842136, 20385757} and virulence toward mice in the closely related \textit{Francisella novicida} \cite{17389372}. Finally, IglC is a virulence factor encoded on the \textit{Francisella} pathogenicity island that is required for intracellular survival and virulence toward mice \cite{23185631, 25115488, 12770718}. We found that mutants lacking each of these proteins are also attenuated in OS cockroaches (\textbf{Table 1}). Since these proteins play essential roles in distinct components of the \textit{F. tularensis} virulence program, this finding supports the idea that \textit{F. tularensis} uses similar mechanisms to evade immune clearance and cause disease in extremely diverse host organisms. Thus, the OS cockroach model should be useful in identifying additional regulators and effectors of \textit{F. tularensis} pathogenesis.  Since \textit{F. tularensis} is considered a facultative intracellular pathogen, we sought to determine the proportion of bacteria that were located in intracellular and extracellular compartments throughout infection of OS cockroaches. As seen in \textbf{Figure 4}, intracellular bacteria can be recovered as early as six hours post injection, indicating successful invasion of OS cockroach  cells. The intracellular population continues to grow throughout the infection process, as does the total bacterial population. Initially, we were surprised that the majority of the bacterial population at each time point was located in the extracellular environment, as judged by sensitivity to gentamicin. However, our results are similar to what others have observed for \textit{F. novicida} in \textit{D. melanogaster} \cite{20865166}. Since hemocoel-injected gentamicin rescued OS cockroaches from lethality (\textbf{Table 2}), the extracellular \textit{F. tularensis} population appears to be essential to the infection process, as has been recently suggested elsewhere \cite{22795971}. While the intracellular phase of \textit{F. tularensis} pathogenesis is well-appreciated, our findings suggest that the OS cockroach may be a useful model for elucidating the mechanisms by which \textit{F. tularensis} survives, grows, and moves within the extracellular environment. Host immune function is not static; it can vary dramatically across developmental stages in wax worms and other lepidopterans \cite{17198709, 25730277, 18076108} and fruit flies \cite{24828474, 22808242}. Importantly, Meylaers, et al, found that wax worm immunity dramatically increases as larvae progress through the wandering stage, in which they are typically used, and enter pupation \cite{17198709}. We therefore sought to determine if OS cockroach susceptibility to \textit{F. tularensis} LVS varied by developmental stage. We determined the killing kinetics and LD_{50}s of \textit{F. tularensis} LVS against juvenile, adult female, and adult male OS cockroaches. The susceptibility pattern of juveniles (which we used for all other experiments reported here) and adult females were highly similar. In comparison, adult males showed enhanced susceptibility, with a shorter median time-to-death (\textbf{Figure 4}) and a lower LD_{50} (\textbf{Table 1}). The reason for increased susceptibility in adult males is currently unknown and could result from either decreased resistance to \textit{F. tularensis} or decreased tolerance to damage that occurs during infection. Interestingly, Horn, et al, found that the phagocytic ability of \textit{D. melanogaster} hemocytes, migratory cells similar in function to mammalian macrophages, decreases with age \cite{24828474} and it will be interesting to examine this and other possible causes of the increased susceptibility that we observed in adult males. Revealing these causes may illuminate key host factors that differentiate protective and unprotective immune responses to \textit{F. tularensis} infection, information that could aid in developing a much-needed safe and effective vaccine.