CSD, caused by Bartonella henselae
, is a worldwide zoonosis associated with a variety of clinical manifestations. Typically, a nontender papule develops in the scratch line, three to 10 days after exposure, healing without scarring in two or three weeks. Regional lymphadenopathy follows in more than 80% of cases, but resolves usually within two to three months (7
). Atypical CSD are reported up to 25% of cases (8
). The manifestations of atypical CSD are fever of unknown origin, neuroretinitis, encephalopathy, hepatosplenic granuloma, juvenile rheumatoid arthritis. Nowadays, B. henselae
infection is regarded as a common cause among patients with fever of unknown origin (9
). Atypical presentations are considered as manifestations of Bartonella
infection rather than CSD. The epidemiological and clinical characteristics of CSD have been well delineated in countries other than Korea (2
). Epidemiological and clinical study of CSD in Korea is rare (10
). Domestic cats or dogs are the reservoirs for B. henselae
and it is transmitted through scratches or bites (7
). However, no history of animal contact can be elicited in small percentage of CSD patient.
Cat scratch disease is usually a self-limiting disease and does not require therapy. But, some patients with multi-system involvement may benefit from antibiotics treatment, so it is necessary to identify the organism rapidly by clinical laboratory assay. The diagnosis of CSD is made currently on the basis of clinical criteria in addition to a recent history of cat or dog exposure, a scratch or a flea bite plus bacteria culture, histologic examination of tissue biopsies and serologic test. Although serologic analysis by immunofluorescence or enzyme linked immnuosorbent assay is a useful tool for the diagnosis of B. henselae
infection, the specificity of serological assay has been questioned due to the cross reactivity between B. henselae
and other species (13
). Also antigenic variability within the species could partly explain inconsistent results in the serological diagnosis of CSD.
PCR assays appear to be very useful in confirming clinically suspected CSD and have advantage of rapid diagnosis with the reliability since it is independent on the patient's humoral response. Recent studies relied on PCR amplification to improve diagnosis of CSD (4
). Earlier assays targeted amplification of 16S rRNA gene which is present in all bacteria with species polymorphism (14
). PCR assay using the amplification of a portion of the citrate synthase gene (gltA
) followed by Taq
I restriction digest of the products is a sensitive tool for the detection of B. henselae
DNA in tissue biopsy specimens and pus aspirates from lymph nodes of patients with CSD, but require large amounts of clinical material. The pap 31
gene encodes a major protein associated with a phage from B. henselae
and allowed the classification of its strains into two clusters, B. henselae
Houston-1 and B. henselae
). Avidor et al. (14
) demonstrated that PCR diagnosis of CSD from fine needle aspiration and primary lesion specimens can be minimally invasive and highly accurate, so precluding the necessity for excision biopsy. In this case, antibody titer to B. henselae
was positive (1:64) and corresponding sequence to major genogroup B. henselae
Houston was detected by PCR analysis of lymph node tissue by fine needle aspiration. PCR offers a rapid and specific means to detect the organism directly from clinical specimens in CSD patients. And it is more sensitive than isolation when performed on suitable clinical samples such as fresh or frozen lymph node tissues.
In conclusion, when presented with lymphadenopathy, physicians should inquire about recent cat, dog, or pets contact and/or animal scratches considering the possibility of CSD.