Cat-scratch disease (CSD) is a clinical syndrome that usually presents as a self-limiting lymphadenopathy associated with a cat scratch or bite. Commonly affecting children and young adults, it has a worldwide distribution. In temperate climates, higher rates are reported in the autumn and winter, which can be attributed to the seasonal breeding of the domestic cat. The organism responsible was identified in 1983, having eluded detection for 50 years. Initially, Afipia felis was thought to be the cause; however, subsequent study failed to confirm a link. During the 1990s, it was demonstrated conclusively that Rochalimaea henselae, later reclassified as Bartonella henselae, was the cause of CSD. B. henselae has been isolated from bacteraemic cats, with transmission among cats thought to be via the cat flea. Although other Bartonella species are transmitted by arthropod vectors, it is unlikely that the cat flea is involved directly in human infection, but plays a role in amplifying the reservoir. B. henselae is difficult to culture, and either serology or the polymerase chain reaction are considered to be the best methods of detection. Genetic variation occurs amongst B. henselae strains, perhaps explaining the inconsistency of some diagnostic techniques. A separate serogroup (Marseilles) has been reported in a seronegative patient with CSD, and B. clarridgeiae has the potential to cause the disease. Atypical presentation is seen in up to 25% of cases, and manifests itself as ocular involvement, encephalopathy, granulomatous hepatitis, hepatosplenic infection, endocarditis and osteomyelitis. The majority of CSD cases resolve spontaneously and do not require antibiotic treatment. In complicated CSD, treatment with trimethoprim-sulphamethoxazole, ciprofloxacin or azithromycin is recommended, with gentamicin being reserved for the severely ill patient.