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A case of cat-scratch disease (CSD) complicated by reversible encephalopathy is presented. Neurological complications of CSD are uncommon. Laboratory and radiological examinations were negative. There was complete recovery.
To clarify the clinical manifestations of cat scratch disease (CSD), we evaluated a total of 130 seropositive patients with CSD. The patients' ages ranged from 1 to 68 years; 103 (79.2%) were under 18 years of age. CSD occurred predominantly in the fall and winter months. Regional lymphadenopathy was noted in 110 (84.6%) of the cases, and the most common sites were the neck (33%), axillary (27%), and inguinal (18%) regions. One hundred of the patients (77%) had general symptoms, such as fever, headache, and malaise. The clinical manifestations of CSD showed a wide spectrum from typical or classical CSD, with regional lymphadenopathy, to atypical or systemic CSD. Of the 130 cases, 103 (79.2%) were typical CSD and 27 (20.8%) were atypical CSD. Atypical cases of CSD were commonly reported as fever of unknown origin (37.0%), neuroretinitis (22.2%), encephalopathy (14.8%), hepatosplenic granuloma (11.1%), and Parinaud's oculoglandular syndrome (7.4%). Fever of unknown origin or prolonged fever lasting more than 14 days was evident in 27 (20.8%) of the 130 cases in this study. Eleven of the 27 cases lacked lymphadenopathy. Our findings suggest that CSD is not a rare disease in Japan. The indirect fluorescent antibody (IFA) test to detect Bartonella species may provide a prompt diagnosis of CSD and facilitate appropriate therapy.
UNLABELLED: Cat-scratch disease is a well-known cause of regional adenopathy in immunocompetent children. Rarely, patients may present with symptoms simulating a neoplastic disease. The case of a 12-year-old boy with fever, swelling of the chest wall and hepatosplenic nodules is reported. Histological analysis of biopsy specimen obtained from the chest wall lesion and the liver revealed granulomatous reaction without malignant cells. Serological investigations were positive for Bartonella species. The symptoms and the lesions disappeared after oral antibiotic therapy (ciprofloxacin) was started. The patient remained symptom-free 12 months later. CONCLUSION: The present case emphasizes the wide spectrum of clinical manifestations associated with cat-scratch disease which should be investigated as differential diagnosis of manifestations suggesting a neoplastic disease in children.
The diagnosis of cat-scratch disease is based on history and clinical symptoms. We present a case of a 4-year-old girl admitted to our unit with suspicion of histiocytosis X after histologic evaluation of a submandibular lymph node biopsy. On the basis of history, clinical features and histologic reevaluation, the diagnosis of cat-scratch disease was made.
A male homosexual (positive for the human immunodeficiency virus) with a recent cat scratch developed fever, epitrochlear and axillary lymphadenopathy, and retinitis. Subsequently, he developed skin (epitheloid hemangioma) and mucosal lesions (Kaposi's sarcoma), multiple liver abscesses, and pleural effusion. Warthin-Starry stains and/or electron micrographs of lymph nodes and skin lesions demonstrated bacilli characteristic of those associated with cat-scratch disease. Cultures of lymph node, pleural fluid, and liver abscess specimens yielded organisms believed to be the causative agent of cat-scratch disease. We believe that disseminated cat-scratch disease may become an indicator of opportunistic infection signaling acquired immunodeficiency syndrome in a patient who is positive for the human immunodeficiency virus.
PURPOSE: To describe the clinical characteristics of patients with cat scratch disease during the last 2 years. METHODS: Clinical characteristics and anterior and posterior segment manifestations were reviewed in five patients who were serologically diagnosed as having cat scratch disease. RESULTS: Four women and one man were examined. Their ages ranged from 7 to 60 years. Each patient had a markedly elevated serum anti-Bartonella henselae antibody titer. Visual symptoms developed 2 weeks or less after the onset of systemic symptoms. Lymphadenopathy was detected in one of five patients. Neuroretinitis was found in 4 patients, and papillitis in 1 patient. Seven eyes showed retinochoroidal exudates. Anterior uveitis was observed in three eyes. Four patients received systemic corticosteroids. CONCLUSION: The ocular manifestations of cat scratch disease include neuroretinitis, papillitis, retinochoroidal exudates, and anterior uveitis.
We present a case of a cat-scratch disease (CSD) presenting with typical (primary lesion and regional lymphadenitis) and rare (purulent lymphadenitis and maculopapular rash) symptoms and positive epidemiological data. Laboratory blood test showed normal values for routine parameters, except for mild leukocytosis (L 12.4 x 10(9)), elevated erythrocyte sedimentation rate (SE 65/h) and moderately elevated asparta e-aminotransferase and alanine-aminotransferase values (AST/ALT 48/90), fibrinogen (5.3 g/L) and C-reactive protein (CRP 85 mg/L). Cytological analysis of lymph node content revealed granulomatous inflammation in the first sample, and purulent inflammation in the second sample. In paired serum samples, collected on the 15th and 29th day from the onset of disease, antibodies IgG (titre 4096/8192) and IgM (titre 80/40) to Bartonella henselae were detected by using an indirect immunofluorescence assay (IFA). Antibiotic therapy with azithromycin (1 x 500 mg per os/5 days) was administered. Purulent lymphadenitis and rash, although a rare clinical manifestation in CSD, are significant clinical findings in differentiating CSD from other febrile illnesses accompanied with rash and lymphadenitis.
The spectrum of illness attributed to cat-scratch disease (CSD) continues to expand. Although a common cause of cervical adenitis in children, CSD has not been associated as a cause of deep fascial space infections of the head and neck. We describe a child with extensive parapharyngeal adenitis and abscesses due to CSD confirmed by histological and serological evaluations.
We report a case of cat-scratch disease neuroretinitis for which systemic and ocular investigations proved the responsibility of Bartonella henselae. An 11-year-old boy was referred to the hospital in November 2002 for severe visual loss in the left eye over the preceding 2 weeks. At the same time, he also developed a flu-like illness. The best corrected acuity in the left eye was counting fingers at 30 cm. Posterior segment examination on the left eye showed an optic disk edema with papillary and peripapillary hemorrhages and serous retinal detachment, mild vitreous inflammation, and two little perivascular white spots. The medical history was unremarkable except for a cat scratch on his left forearm 2 months before. Four weeks of antibiotic therapy including oral rifampin and doxycycline was used. Bartonella henselae immunoglobulin M were first detected with Bartonella henselae immunoglobulin G testing negative at this time. A 3-week serum showed immunoglobulin M seroreversion, while Bartonella henselae immunoglobulin G appeared. Other causes of optic disk edema with macular star were excluded by biological data. Bartonella antibodies to both Bartonella henselae and Bartonella clarridgeiae were detected in the cat. Ophthalmic follow-up showed progressive resorption of the neuroretinitis and the visual acuity increased to 5/10. The significance of this case report lies in the reminder that this pathology can be the cause of neuroretinitis; the prognosis can be improved by earlier treatment.
A case of cat-scratch disease in an 8 year-old girl is reported. The inoculation injury followed by regional lymphadenopathy was typical of Parinaud syndrome. This patient also had vertebral lesions on scintigraphy, x-rays and CT scan. While the oculoglandular localization spontaneously improved within a few weeks, osteomyelitic lesions remained grossly unchanged after almost 2 years of follow-up.
We report five cases of cat-scratch disease encephalopathy (CSDE), with a brief review of the literature in English, in which only 96 patients of CSDE have been described up to the present. The Gram-negative bacilli demonstrated by Warthin-Starry or Dieterle silver stains are regarded as the causative agent of CSDE. Administration of antibiotics is recommended. The onset of CSDE is usually acute and the prognosis favorable.
The infective agent responsible for cat scratch disease, Bartonella henselae, is a rare cause of hepatic granulomatosis in immunocompetent adults. Clinical features include a prolonged fever or more typical symptoms such as lymphadenopathy associated with painful hepatomegaly and a fever following a cat scratch or bite. Images of micronodular hepatosplenic lesions on abdominal ultrasonography or computed tomography scan along with epithelioid granulomas in a liver biopsy can suggest this diagnosis. It is established with a serology by indirect immunofluorescence or by ELISA and/or the presence of Bartonella henselae DNA evidenced by PCR in the liver biopsy. We report two cases of hepatosplenic localizations of cat scratch disease in a 41-year-old woman and a 44-year-old man presenting asthenia and fever associated with a biological inflammatory syndrome and elevated liver enzymes.
Our objective was to describe the imaging features of lymphadenopathy at the medial epitrochlear region as frequently seen in cat-scratch disease (CSD) and to compare these features with those seen in non-CSD. Ten patients (four males and six females) presented with a subcutaneous soft tissue mass at the medial epitrochlear region. Three patients were younger than 15 years. Magnetic resonance imaging was performed in all patients. All lesions turned out to be regional lymphadenopathy instead of soft tissue neoplasm. They were caused by benign disorders in eight cases, including seven CSD and one other infection, and in two cases by metastatic disease. All lesions, except for three benign ones, were solitary. On MRI, high signal intensity (SI) strands in the surrounding soft tissue on T2-weighted images (WI) were present in all cases. Three cases of CSD showed homogeneous SI on both T1- and T2WI. After contrast administration, a moderate, homogeneous enhancement was seen. The other seven lesions, except for one metastasis, had both solid and liquid components. Liquid components showed high SI on T2WI without enhancement, whereas solid components had intermediate SI on T2WI and marked enhancement after contrast administration. Pathological findings in seven patients, including four with CSD, supported the tentative diagnosis made on MRI. One of two patients with CSD had positive serological test. Cat-scratch disease is a major cause of a soft tissue swelling at the medial epitrochlear region. Identification of lymphadenopathy and its presentation on MRI may be helpful in eliciting an animal-scratch history and achieving diagnostic and therapeutic aims in patients without primary cancer.
BACKGROUND/PURPOSE: Bartonella henselaeis the causative agent of cat scratch disease (CSD), manifesting as fever and acute regional lymphadenopathy. Although serologic testing is the reference method for diagnosis, successful use of immunohistochemical (IHC) stain of regional lymph nodes for the diagnosis of CSD has been reported. To determine the characterization and diagnostic potential of IHC in lymphadenopathy of CSD, lymph nodes were excised from patients with suspected CSD for further evaluation. METHODS: Polyclonal antibody-based IHC studies were performed for the detection of B. henselae. Between January 2001 and December 2004, the reference laboratory of the Center for Disease Control, Taiwan, received a total of 377 sera from 352 reported suspected CSD cases. Twenty-three formalin-fixed paraffin-embedded lymph nodes from 16 patients and two skin biopsies from two patients suspected of having CSD were included in this study. Nine of them were serologically confirmed to have CSD and the others were seronegative but suspected to have CSD by the attending physicians. Seven lymph node specimens were obtained from tuberculosis patients for comparison. RESULTS: We demonstrated that the microorganisms existed in the cytoplasm of histiocytes within the granulomatous lesions in nine lymph nodes and one skin biopsy. Among the nine lymph nodes with IHC (+) stains, three were seronegative. On the other hand, three cases were IHC (+) and six cases were IHC (-) among nine seronegative patients. In addition, two seronegative patients with skin biopsy showed one IHC (+) and one IHC (-). CONCLUSION: IHC can contribute to the etiologic diagnosis of B. henselaelymphadenopathy when serology and molecular techniques are not available.
Bartonella henselae is the primary agent of cat scratch disease (CSD). In order to study the genetic variation of B. henselae and the correlation of the various genotypes with epidemiological and clinical findings, two seminested, groEL- and pap31-based PCR assays were carried out with specimens from 273 patients. Amplicons were sequenced to determine the genotype of the causative Bartonella species. Compared to our reference intergenic spacer region-based PCR, the groEL- and pap31-based assays were 1.7 and 1.9 times more sensitive, respectively. All 107 positive patients were infected with B. henselae; neither Bartonella clarridgeiae nor other species were detected. Based on the groEL and pap31 sequences, B. henselae amplicons were classified into two genogroups, Marseille and Houston-1, and into four variants, Marseille, CAL-1, Houston-1, and a new variant, ZF-1. Patients infected with either one or the other genogroup did not exhibit different epidemiological or clinical characteristics. Our study highlights the genotypic heterogeneity of B. henselae in patients with CSD.
Cat scratch disease (CSD) has been difficult to diagnose in animals because of the protracted clinical course of infection and the quiescent phases when the microbial culprit lies dormant. The causative agent in CSD appears to be multiple species and strains of Bartonella. Using polymerase chain reaction (PCR) techniques for amplification of highly variable regions of the 16S ribosomal RNA (rRNA) gene sequence, a very sensitive species- and strain-specific assay for CSD-causing Bartonella species was developed. PCR primers were designed to specifically amplify the 16S rRNA gene of Bartonella species but not of other microbial pathogens. This initial PCR was multiplexed with a universal primer set, based on conserved sequence regions in the 16S rRNA gene, that provides a 162-bp fragment in all species tested. Subsequently, 3 distinct nested PCR primer sets enabled the individual amplification and specific detection of Bartonella henselae type 1, B. henselae type II, and B. clarridgeae. Thus, this 2-step PCR procedure enabled the sensitive detection and identification of these species and the B. henselae genotype by exploiting minor sequences differences. Verification of these results were demonstrated with both sequencing and ligase chain reaction techniques. The diagnostic usefulness of this CSD test has been demonstrated by the analysis of specimens from control and infected cats. The diagnosis was confirmed and the specific B. henselae strain was correctly identified in peripheral blood specimens obtained from control and strain-specific CSD-infected cats. Such an accurate and sensitive diagnostic tool for the detection and identification of CSD causative agents should be a useful for the medical, veterinary, and scientific communities.
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