Members of the genus Rickettsia are obligately intracellular vector-borne bacteria that cause acute febrile illness (1). Doxycycline is the drug of choice for all rickettsioses (2). To circumvent modes of tetracycline resistance, such as the emergence of efflux pumps and ribosomal protection produced by more typical bacteria (e.g., Staphylococcus aureus and members of the Enterobacteriaceae), new tetracycline-like derivatives—tigecycline, omadacycline, and eravacycline—have been developed (3, 4). There are no known naturally occurring tetracycline-resistant strains of Rickettsia. Considering the limited antibiotic exposure of their primary reservoirs (i.e., arthropods) and evolution through intense genome reduction (minimizing their genetic plasticity), it is unlikely that spontaneous tetracycline resistance of Rickettsia would occur. Considering the activity of these tetracycline-like agents against resistant but more typical pathogens, their empirical use is likely to expand. Thus, their usefulness against rickettsiae, the cause of empirically treated undifferentiated febrile illnesses, should be sought. Here, we describe the in vitro effectiveness of eravacycline, omadacycline, and tigecycline against pathogenic rickettsiae.