A Commentary in mBio this week discusses how new findings on Coxiella burnetii, the causative agent of Q fever, paves the way for future progress in understanding this zoonotic disease.
First discovered in Australia, Q fever is most often contracted from cattle, goats and sheep or from infected meat and milk products. C. burnetii is an unusual intracellular pathogen: it is the only bacterium known to replicate within a vacuole that resembles a phagolysosome. (Note: the phagolysosome is kind of a killing room. It’s a combination of a phagosome, a compartment for killing and digesting pathogens, and a lysosome, an organelle containing enzymes for breaking down wastes and other materials. And yet C. burnetii not only survives in these compartments, it replicates.)
Recent finding show that the Dot/Icm Type 4 Secretion System (T4SS) is necessary for the bacterium to be able to renovate a lysosome into a mature Coxiella-containing vacuole.
In a study in the July/August issue of mBio, researchers proved that when C. burnetii lacks this T4SS, it isn’t picky about what kind of vacuole it inhabits. Beare et al. got the pathogen to replicate in a different kind of vacuole entirely: one that was created by the protozoan parasite Leishmania amazonensis.
The authors of this week’s Commentary say this says something important about how C. burnetii uses T4SS to take advantage of human cells. The cohort of Dot/Icm effector proteins are not the necessary aspect of T4SS, but rather the collective action of those effector proteins, which creates the phagolysosome. In other words, C. burnetii needs a home within human or animal cells, and anything resembling a phagolysosome will do. Advances in genetic analyses will help move studies of the Dot/Icm effector functions forward to figure out more about how the Coxiella-containing vacuole is created.