Figure 1. A spiral computed tomographic scan of the abdomen shows 4 well-defined, hypodense, hepatic lesions (arrows) with peripheral contrast enhancement. There is also a large area of low attentuation in the posterior segment of the right lobe of the liver.
Figure 2. The single photon emission computed tomographic technetium Tc 99m sulfur colloid liver-spleen scan shows inhomogeneous uptake of tracer in the right lobe with focal areas (arrowheads) of absent tracer uptake corresponding to the spiral computed tomographic abnormalities.
Cat-scratch disease (CSD) is caused by an argyrophilic, gram-negative, pleomorphic bacillus known as Bartonella (Rochalimaea) henselae. The diagnosis is made when 3 of the 4 following criteria are satisfied: (1) history of cat contact, associated with skin or eye inoculation, (2) positive CSD skin test, (3) normal laboratory study findings for other causes of lymphadenopathy, and (4) characteristic histopathologic features in the biopsy specimen of the involved skin or lymph node.1
The disease typically presents a fever and regional lymphadenopathy located adjacent to the inoculated site within 2 weeks after exposure to the cat. The cat is usually less than 1 year of age. The inoculated site appears as a papule 3 to 5 days after exposure and becomes vesicular and crusty. The involved lymph nodes may remain enlarged for months. Axillary lymphadenopathy is common because the hands and arms are the usual sites of inoculation. Other sites include the cervical and the inguinal regions. The histopathologic feature of the involved lymph node is a granuloma with central necrosis, infiltrating neutrophils, and lymphoid hyperplasia. The course of the disease is self-limited and seldom needs medical therapy. About 10% to 12% of the patients have unusual presentations making the diagnosis less obvious.2 Granulomatous hepatitis presenting with fever and abdominal pain, with or without lymphadenopathy, has been reported in the past.3,4 Rare presentations of CSD include Parinaud oculoglandular syndrome, acute encephalopathy,5 osteolytic lesions,6 transverse myelitis,7 neuroretinitis, aseptic meningitis,8 thrombocytopenic purpura, atypical pneumonia, and erythema nodosum.2 Gastrointestinal manifestations of CSD may include granulomatous splenitis and appendicitis.9 Atypical presentations may mimic other serious illnesses, such as lymphoma, tuberculosis, and malignancies. If the diagnosis of CSD is not considered early on, unnecessary, extensive and costly workup may ensue.
Of particular interest in this case is the extensive radiologic workup of the suspicious hepatic hypoechoic lesions found on the ultrasound film. With the findings of the computed tomographic, liver-spleen, and tagged red blood cell scans, we were able to rule out cystic lesions, benign nodular hyperplasia and hemangioma, respectively. Hepatocellular adenoma was considered as a possibility due to the detection of multiple cold defects on the liver-spleen scan. An open liver biopsy was performed. Operative findings revealed multiple nodules and histology showed necrotizing granulomas with special staining suspicious for CSD. The liver tissue was positive by DNA polymerase chain reaction for B henselae. Enzyme-linked immunosorbent assay serologies for B henselae were also positive.
The disease is self-limiting and seldom needs antibiotic therapy. However, in some cases of extensive lymphadenopathy and liver-spleen involvement, intravenous gentamicin has been used with success.10,11 In another study, ciprofloxacin has been shown to be an effective therapy for CSD.12
Accepted for publication December 16, 1996.
Reprints: Theodore Hall, MD, Radiological Science BL-428, CHS, 10833 Le Conte Ave, Los Angeles, CA 90095.
Radiological Case of the Month. Arch Pediatr Adolesc Med. 1998;152(1):88. doi: