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INTRODUCTION

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Cat scratch disease (CSD) is a ubiquitous, self-limited infection characterized by prolonged regional lymphadenitis and often an inoculation site papule, usually after a cat’s (frequently a kitten’s) scratch or bite, and caused primarily by Bartonella henselae. In 10% to 20% of cases, the lymph node will suppurate. In a minority of cases (approximately 10%), a wide range of extranodal manifestations collectively known as atypical CSD may occur, including fever of unknown origin (FUO), as well as visceral, neurologic, and ocular involvement. In immune-competent individuals, prognosis is generally good, but infection may be life-threatening and its manifestations different in the immunocompromised.

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PATHOGENESIS AND EPIDEMIOLOGY

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Bartonellae are fastidious, slow-growing, pleomorphic gram-negative Proteobacteria related to Brucella. All Bartonella species can be cultured on cell-free media (eg, rabbit-heart infusion or chocolate agar plates). Results are optimized if media are fresh. Culture of B henselae may require several weeks of incubation before colonies can be detected. Routine bacterial cultures in the clinical microbiology laboratory are not likely to detect Bartonella growth. Although B henselae frequently can be isolated from infected cats, sensitivity of blood or lymph node cultures is extremely low in immunocompetent patients with CSD. Therefore, cultures are not recommended for the routine diagnosis of most CSD cases. B bacilliformis, B quintana, and B henselae are the most important human pathogens; rarely, other Bartonella species also cause human disease.

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CSD was clinically recognized in the early 20th century and was first described in 1950 by Debré. In 1983, organisms were visualized by silver staining of CSD lymph nodes. Finally, in the 1990s, B henselae was proven to be the major cause of CSD—epidemiologically, serologically, by culture, and by molecular methods. The pathogenesis of CSD is poorly understood, and the reasons some patients develop typical CSD with localized infection and regional necrotizing granulomatous adenitis while others develop serious atypical disease, presumably due to bloodborne dissemination with visceral or other end-organ involvement, are not clear. Bacterial and host factors play a role. B henselae strains particularly associated with human disease (eg, ST1 genotype) or with only cat infection (eg, ST7 genotype) were identified. The type and severity of the host immune response to infection also modify the clinical picture. Immunocompromised individuals, especially those with cell-mediated immune deficiency, either congenital or acquired (particularly HIV-AIDS but also solid organ transplant patients), are at risk of developing severe or atypical disease. Bartonella infection has also been increasingly reported in patients treated with biological immune modulators such as monoclonal antibodies (eg, infliximab, tocilizumab). B henselae, like other Bartonellae, interacts with endothelial cells and is capable of inducing angiogenesis. B henselae can induce a Th1 inflammatory response, and interferon-γ and nitric oxide play important roles. Dendritic cells and humoral immunity also play a role in the host response to B henselae.

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CSD occurs worldwide and is prevalent in warm and humid climates. In temperate zones, CSD occurs primarily during fall ...

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