Infection with the major etiologic agent of CSD, B henselae, most commonly presents as lymphadenitis of 1 or more nodes. This can be accompanied by systemic symptoms such as low-grade fever, headache, sore throat, and malaise. Other clinical manifestations of B henselae infection include cat-scratch encephalitis, Parinaud oculoglandular syndrome, hepatic and splenic granulomas, fever of unknown origin, osteomyelitis, bacillary angiomatosis and peliosis, endocarditis, pneumonia, bacteremia, and sepsis.1 The incubation period from the time of the cat scratch to the appearance of lymphadenopathy varies from 12 to 62 days.2 This suggests that the kitten scratch that occurred 3 days prior to the onset of our patient's symptoms was not directly related to his illness. It is possible that he may have had previously unrecalled scratches from other cats in the home. Osteolytic lesions have been reported in association with CSD as early as 1954.3 Since then, several published articles have reported similar findings.4- 7 However, in these cases all of the bone lesions were imaged via radiography or CT scan. Reports of patients having bone lesions in association with CSD detected by MRI or radionuclide bone scan are fewer still.8- 9 Wilson and Castillo8 described a patient with CSD in whom vertebral bone marrow abnormalities were detected by MRI. However, these abnormalities correlated with those demonstrated on a subsequent radionuclide bone scan. In our patient there was no correlation between the bone lesions demonstrated by MRI and by radionuclide bone scan. In addition, CT failed to reveal any bone abnormalities in our patient. It is possible that MRI is more sensitive to the early bone marrow changes that can occur with CSD than either radionuclide bone scan or CT. Further studies to determine this may be indicated.