Michael Engelbert

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

SUMMARY 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.

The Enterococcus faecalis fsrB gene, a key component of the fsr quorum-sensing system, is associated with virulence in the rabbit endophthalmitis model.

ABSTRACT We used a rabbit endophthalmitis model to explore the role of fsrB, a gene required for the function of the fsr quorum-sensing system of Enterococcus faecalis, in pathogenicity. A nonpolar deletion mutant of fsrB had significantly reduced virulence compared to wild type. Complementation of mutation restored virulence. These data corroborate the role of fsrB in E. faecalis pathogenesis and suggest that the rabbit endophthalmitis model can be used to study the in vivo role of quorum sensing.

Contribution of Gelatinase, Serine Protease, and fsr to the Pathogenesis of Enterococcus faecalis Endophthalmitis

ABSTRACT Gelatinase and serine protease were found to contribute in concert to pathogenesis in a rabbit model of endophthalmitis. However, a mutant defective in the fsr regulator was observed to be more attenuated than a mutant rendered defective in the expression of gelatinase and serine protease as the result of a polar transposon insertion into the former. This increased attenuation suggests that there are possible additional pleiotropic effects of the defect in fsr on expression of traits contributing to the pathogenesis of enterococcal infection.

Immunology of Staphylococcal Biofilm Infections in the Eye: New Tools to Study Biofilm Endophthalmitis

Endophthalmitis is an important disease of the eye that is most frequently caused by postoperative and post-traumatic introduction of bacteria into the posterior segment of the eye. In the case of severe infections, visual acuity is greatly damaged or completely lost. Much work has focused on the ability of planktonic bacteria to cause infection and ocular damage while little work has focused on chronic infections in endophthalmitis mediated by the formation of bacterial biofilms on the surface of the lens. This review focuses on the interaction of Staphylococcus aureus and Staphylococcus epidermidis lens-associated biofilms in endophthalmitis. Additionally, this review highlights some relevant biofilm-immune system interactions and outlines a new in vivo mouse model to explore biofilm-related infections in endophthalmitis.

Imaging in the diagnosis and management of acute macular neuroretinopathy.

Acute macular neuroretinopathy (AMN) is a rare condition that was first described by Bos and Deutman in 1975.1 To date, 67 cases are reported in the English medical literature, all of which have been as single case reports or small case series. When AMN was first described, it was considered an excl