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Clinical Microbiology Reviews, January 2002, p. 111-124, Vol. 15, No. 1
0893-8512/02/$04.00+0     DOI: 10.1128/CMR.15.1.111-124.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Bacterial Endophthalmitis: Epidemiology, Therapeutics, and Bacterium-Host Interactions

Michelle C. Callegan,1,2,3* Michael Engelbert,2 David W. Parke II,1,3 Bradley D. Jett,4 and Michael S. Gilmore1,2,3

Department of Ophthalmology,1 Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center,2 Molecular Pathogenesis of Eye Infections Research Center, Dean A. McGee Eye Institute, Oklahoma City,3 Department of Biology, Oklahoma Baptist University, Shawnee, Oklahoma4

Endophthalmitis is a severe inflammation of the interior of the eye caused by the introduction of contaminating microorganisms following trauma, surgery, or hematogenous spread from a distant infection site. Despite appropriate therapeutic intervention, bacterial endophthalmitis frequently results in visual loss, if not loss of the eye itself. Although the pathogenicity of bacterial endophthalmitis has historically been linked with toxin production during infection, a paucity of information exists as to the exact mechanisms of retinal toxicity and the triggers for induction of the intraocular immune response. Recently, research has begun to examine the bacterial and host molecular and cellular events that contribute to ocular damage during endophthalmitis. This review focuses on the causative agents and therapeutic challenges of bacterial endophthalmitis and provides current data from the analysis of the role of bacterial virulence factors and host inflammatory interactions in the pathogenesis of eye infections. Based on these and related studies, a hypothetical model for the molecular pathogenesis of bacterial endopthalmitis is proposed. Identifying and understanding the basic mechanisms of these bacterium-host interactions will provide the foundation for which novel, information-based therapeutic agents are developed in order to prevent vision loss during endophthalmitis.

* Corresponding author. Mailing address: Department of Ophthalmology DMEI 418, 608 Stanton L. Young Blvd., Oklahoma City, OK 73104. Phone: (405) 271-1084. Fax: (405) 271-8781. E-mail: michelle-callegan{at}ouhsc.edu.

Clinical Microbiology Reviews, January 2002, p. 111-124, Vol. 15, No. 1
0893-8512/02/$04.00+0     DOI: 10.1128/CMR.15.1.111-124.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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