often
employ the agar bead model of respiratory infection, where
bacteria are embedded in agar beads prior to instillation into
murine lungs [31]. Animals develop nonlethal pulmonary disease,
and viable bacteria may be recovered from lungs for 2–
3 weeks. However, because phage killing depends on unobstructed
access of phages to their bacterial target, we chose to
employ a model of acute infection that avoids encasing bacteria
in agar. In a series of preliminary experiments, we determined
that when inoculated into the lungs of mice via intratracheal
instillation, B. cenocepacia causes nonlethal pulmonary disease
and can be recovered for up to 7 days, thus providing a tractable
model to assess the relative efficacy of anti-infective treatments.
We also chose to use B. cenocepacia strain AU0728, which was
recovered from respiratory culture of a patient with cystic fibrosis,
and is a representative of the B. cenocepacia Midwest clone,
a lineage that accounts for a great deal of infection among patients
with cystic fibrosis in the United States [32]. Furthermore,
our previous work with AU0728 indicates that it is multidrugresistant
and capable of robust biofilm formation in vitro (unpublished
data) and thus ought to provide for a rigorous test
of novel anti-infective therapies.