The article discusses the unique intracellular lifestyle of *Coxiella burnetii*, the causative agent of Q fever. Unlike other intracellular pathogens, *Coxiella* thrives in the harsh environment of the phagolysosome, a compartment typically hostile to bacterial intruders. The bacterium's ability to survive and replicate in this environment is facilitated by its interaction with the autophagic pathway, which stalls phagosome maturation and promotes the development of a spacious parasitophorous vacuole (PV). The PV acquires lysosomal characteristics such as an acidic pH and acid hydrolases, yet *Coxiella* manages to thrive within this hostile environment. The bacterium synthesizes proteins that mediate these processes, including a type IV secretion system (T4SS) that delivers effector proteins to the host cytosol. The article also explores the role of lipopolysaccharide (LPS) phase variation in *Coxiella* virulence and the use of various model systems to study *Coxiella*-host interactions. Additionally, it discusses the mechanisms by which *Coxiella* resists the bactericidal elements of the phagolysosome and the potential benefits of its interactions with autophagy. The article concludes by highlighting unresolved questions about *Coxiella*'s morphological differentiation, the role of autophagy, and the nature of its T4SS effectors.The article discusses the unique intracellular lifestyle of *Coxiella burnetii*, the causative agent of Q fever. Unlike other intracellular pathogens, *Coxiella* thrives in the harsh environment of the phagolysosome, a compartment typically hostile to bacterial intruders. The bacterium's ability to survive and replicate in this environment is facilitated by its interaction with the autophagic pathway, which stalls phagosome maturation and promotes the development of a spacious parasitophorous vacuole (PV). The PV acquires lysosomal characteristics such as an acidic pH and acid hydrolases, yet *Coxiella* manages to thrive within this hostile environment. The bacterium synthesizes proteins that mediate these processes, including a type IV secretion system (T4SS) that delivers effector proteins to the host cytosol. The article also explores the role of lipopolysaccharide (LPS) phase variation in *Coxiella* virulence and the use of various model systems to study *Coxiella*-host interactions. Additionally, it discusses the mechanisms by which *Coxiella* resists the bactericidal elements of the phagolysosome and the potential benefits of its interactions with autophagy. The article concludes by highlighting unresolved questions about *Coxiella*'s morphological differentiation, the role of autophagy, and the nature of its T4SS effectors.