gms | German Medical Science

102. Jahrestagung der DOG

Deutsche Ophthalmologische Gesellschaft e. V.

23. bis 26.09.2004, Berlin

Multifocal chorioretinitis and optic neuritis caused by Bartonella henselae

Meeting Abstract

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  • corresponding author K. Droutsas - Zentrum für Augenheilkunde, Philipps-Universität, Marburg; Zentrum für Augenheilkunde, Justus-Liebig-Universität, Gießen
  • C.H. Meyer - Zentrum für Augenheilkunde, Philipps-Universität, Marburg
  • S. Mennel - Zentrum für Augenheilkunde, Philipps-Universität, Marburg

Evidenzbasierte Medizin - Anspruch und Wirklichkeit. 102. Jahrestagung der Deutschen Ophthalmologischen Gesellschaft. Berlin, 23.-26.09.2004. Düsseldorf, Köln: German Medical Science; 2004. Doc04dogP 202

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dog2004/04dog693.shtml

Published: September 22, 2004

© 2004 Droutsas et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Objective

The etiopathology of posterior uveitis remains often despite meticulous diagnostic unclear. One of the possible pathogens is Bartonella henselae, a recently characterized and classified gramnegative rod.

Methods

A 41-year-old healthy female was referred because of recurrent posterior uveitis and optic neuritis OD of unknown cause. The initial event occured one year ago and was treated in another clinic with oral steroids and clindamycin. The visual acuity increaced from 0,05 to 1,0. An etiology could not be found. The serology for borrelia, lues and toxoplasma was negative. A tuberculosis and sarcoidosis could be excluded. At the initial presentation in our clinic the patient complained of an acute loss of vision OD.

Results

Ophthalmoscopy disclosed a mild temporal optic disc edema and multiple, subretinal white choroidal infiltrates at the posterior pole. A significant delay of the P100-response in VECP-testing confirmed the clinical diagnosis of an optic neuritis. The indirect fluorescend antibody test revealed positive IgG and negative IgM for Bartonella henselae. After therapy with oral steroids visual acuity increased from 0,5 to 0,8.

Conclusions

The classical manifestation of cat-scratch disease in the posterior segment is a neuroretinitis or a multifocal chorioretinitis. In these cases Bartonella h. should also be considered as a possible etiopathogen. Our case shows that a recurrent optic neuritis may play a significant role in visual loss in cat-scratch disease