Pain caused by bacterial infection is generally considered to be a secondary consequence of immune activation, but findings recently published in Nature indicate that bacteria are capable of directly activating nociceptor sensory neurons. Chiu et al. found that Staphylococcus aureus infection could still produce hyperalgesia in mice when key immune response pathways were inactivated. S. aureus seems to activate nociceptors via factors such as N-formyl peptides and the pore-forming toxin α-haemolysin.