Contribution of gelatinase, serine protease, and fsr to the pathogenesis of Enterococcus faecalis endophthalmitis - PubMed (original) (raw)

Contribution of gelatinase, serine protease, and fsr to the pathogenesis of Enterococcus faecalis endophthalmitis

Michael Engelbert et al. Infect Immun. 2004 Jun.

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.

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Figures

FIG. 1.

FIG. 1.

Intraocular growth of E. faecalis wild-type strains OG1RF and TX 5266 (OG1RF Δ_fsrB_), TX 5264 (GelE− SprE+), TX 5243 (GelE+ SprE−), and TX 5128 (GelE− SprE−) in vivo.

FIG. 2.

FIG. 2.

Retinal function after intraocular infection with E. faecalis OG1RF and the mutants TX 5266 (OG1RF Δ_fsrB_), TX 5264 (GelE− SprE+), TX 5243 (GelE+ SprE−), and TX 5128 (GelE− SprE−). Rabbits were injected with 100 CFU, and retinal function was assessed at 24, 36, and 48 h after injection. Percent retinal function was defined as the ratio of the B-wave amplitude of the infected eye to the B-wave amplitude of the saline-injected contralateral eye. Error bars represent the standard errors of the mean. *, statistically significant result in comparison to results for the wild type, OG1RF (P < 0.05, two-tailed t test for unequal variances); †, statistically significant difference in results for TX 5264 (GelE− SprE+) and TX 5243 (GelE+ SprE−) at 24 h (P < 0.05).

FIG. 3.

FIG. 3.

Thin-section histopathology (representative slides, hematoxylin and eosin stain). (a) Saline-injected control eye. The vitreous (V) with some extracellular matrix and no inflammatory cells, the internal limiting membrane (arrow labeled ILM), the retina with intact nuclear and plexiform layers (R), the choroid (C), and the sclera (S) can be clearly discerned. (b) Infection with E. faecalis OG1RF after 48 h, showing marked vitreal polymorphonuclear infiltrate, cystoid changes in the ganglionic cell layer, decreased nuclear density of the inner and outer nuclear layers, mild subretinal polymorphonuclear infiltrate, and overall loss of structural integrity. (c) Infection with TX 5266 (OG1RF Δ_fsrB_) after 48 h, showing mild vitreal polymorphonuclear infiltrate, preserved structure of all retinal layers, and no subretinal inflammatory infiltrate. (d) Infection with TX 5128 (GelE− SprE−) after 48 h. The appearance is similar to that after infection with TX 5266 (OG1RF Δ_fsrB_). Note the bacterial clusters on the internal limiting membrane (arrow labeled BC). (e) Infection with TX 5243 (GelE+ SprE−) after 48 h. The appearance is similar to that after infection with the wild type, OG1RF. (f) Infection with TX 5264 (GelE− SprE+) after 48 h, with marked vitreal inflammation, mild to moderate retinal and subretinal infitration, and relatively preserved retinal structure.

FIG. 4.

FIG. 4.

Histopathological results. Numerical scores ranging from 0 (normal) to 4 (most severe) were assigned to each slide according to a standardized grading system. The mean was significantly higher for the OG1RF-infected group than for the mutant-infected groups (P < 0.02). The apparent differences between the means for individual mutants are not statistically significant.

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