The pain associated with bacterial infections such as those caused by Staphylococcus aureus was thought to be caused by immune mediators. A new study, however, shows that in mice, S. aureus activates nociceptor sensory neurons directly. Bacteria-derived pain-mediating molecules such as N-formylated peptides produced alterations in intracellular calcium and action potentials in these neurons. Furthermore, the hyperalgesia caused by S. aureus infection was correlated with bacterial load rather than the intensity of the immune response and was mediated by NaV1.8-expressing nociceptors.