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2311. Atypical Cat Scratch Disease Presentations

BACKGROUND: Cat scratch disease (CSD) is caused by B henselae, a Gram-negative intracellular bacilli which is transmitted to humans via cat bite/scratch. Typical CSD presents as regional lymphadenopathy and fever. However, there are multiple atypical presentations of cat scratch disease that have be...

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Detalles Bibliográficos
Autores principales: Comisford, Ross, Spaeth-Cook, Aliza, Erdem, Guliz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6254191/
http://dx.doi.org/10.1093/ofid/ofy210.1964
Descripción
Sumario:BACKGROUND: Cat scratch disease (CSD) is caused by B henselae, a Gram-negative intracellular bacilli which is transmitted to humans via cat bite/scratch. Typical CSD presents as regional lymphadenopathy and fever. However, there are multiple atypical presentations of cat scratch disease that have been reported including prolonged fever, absence of lymphadenopathy and systemic complications such hepatosplenic disease, osteomyelitis, Parinaud oculoglandular syndrome, neuroretinitis, encephalitis, and bacillary angiomatosis among other rare presentations. The aim of this study was to review the frequency, presentation, and treatment outcomes of aytpical CSD presentations at Nationwide Children’s Hospital (Columbus OH). METHODS: This was a retrospective study performed at Nationwide Children’s Hospital, Columbus, OH. EMR of patients were reviewed between January 2010 and March 2017 using ICD9 or ICD 10 codes for CSD. Patients were identified on the basis of compatible clinical presentation and confirmatory serological test or PCR results for B. henselae. Clinical, radiological, and histopathological findings were collected RESULTS: A total of 204 patients were serologically diagnosed as having cat scratch disease between January 2010 and July 2017. Of the 204 cases, 166 (81%) had typical CSD and 38 (18.6%) had atypical CSD. Of the atypical manifestations, 20 (52%) patients had no lymphadenopathy, 12 (31%) had osteomyelitis, 12 (31%) patients had hepatic and/or splenic microabscesses, 4 (10.5%) had osteomyelitis and hepatic/splenic involvement, 3 (1.5%) had encephalitis, 2 (5.2%) had neuroretinitis, and there was one case each (2.6%) of Parinaud oculoglandular syndrome, uveitis, pulmonary cavitary lesion, myocarditis, and endocarditis. Fever of unknown origin was present in 28 (75.6%) of the atypical CSD cases. The median duration of antibiotic treatment was 25 days (IQR 31) and median duration of illness in patients with atypical CSD was 51 days (IQR 56). The majority of patients were treated with dual antibiotic therapy that included rifampin. CONCLUSION: In children with fever of unknown origin, serologic testing for CSD should be performed even in the absence of lymphadenopathy and a search for underlying systemic complications is recommended for prompt diagnosis and appropriate treatment. DISCLOSURES: All authors: No reported disclosures.