The Role of CCL Chemokines in Experimental Staphylococcus aureus Endophthalmitis.

Purpose: To test the hypothesis that (C-C motif) ligand 2 (CCL2) and CCL3 impact retinal function decline and inflammation during Staphylococcus aureus endophthalmitis.

Methods: Experimental endophthalmitis was initiated by intravitreal injection of 5000 colony-forming units of S. aureus into the eyes of C57BL/6J, CCL2-/-, or CCL3-/- mice.

Virulence-related genotypic differences among ocular and gastrointestinal isolates and the relationship to endophthalmitis pathogenesis.

Background: can cause self-limiting gastrointestinal infections, but when infecting the eye, can cause rapid and irreversible blindness. This study investigated whether clinical ocular and gastrointestinal isolates differed in terms of virulence-related genotypes and endophthalmitis virulence.

Methods: Twenty-eight ocular, gastrointestinal, and laboratory reference isolates were evaluated.

The Role of C-X-C Chemokines in Staphylococcus aureus Endophthalmitis.

Purpose: To test the hypothesis that the C-X-C chemokines CXCL1, CXCL2, and CXCL10 contribute to inflammation during Staphylococcus aureus endophthalmitis.

Methods: S. aureus endophthalmitis was induced by intravitreal injection of 5000 colony forming units of S.

Bloodstream Infection Associated with an Urticarial Exanthem.

. Capnocytophaga canimorsus is a fastidious, slow-growing, Gram-negative rod that is a commensal bacterium in normal gingival flora of canine and feline species. Infection with the organism may cause disease ranging from flu-like symptoms to disseminated intravascular coagulation (DIC), fulminant sepsis, meningitis, and endocarditis with an overall fatality rate of 6-26%.

The virulome in endophthalmitis.

is recognized as a causative agent of gastrointestinal syndromes, but can also cause a devastating form of intraocular infection known as endophthalmitis. We have previously reported that the PlcR/PapR master virulence factor regulator system regulates intraocular virulence, and that the S-layer protein (SlpA) contributes to the severity of endophthalmitis. To better understand the role of other virulence genes in endophthalmitis, expression of a subset of factors was measured at the midpoint of disease progression in a murine model of endophthalmitis by RNA-Seq.

ENDOPHTHALMITIS AFTER TRANSCONJUNCTIVAL PARS PLANA VITRECTOMY: A 6-year Experience Without Prophylactic Intraoperative Subconjunctival Antibiotics.

Purpose: This study aimed to investigate the incidence and risk factors of endophthalmitis after transconjunctival pars plana vitrectomy (PPV) without intraoperative subconjunctival antibiotics.

Design: Retrospective, consecutive case series at a single institution.

Methods: Consecutive cases of transconjunctival 25-gauge PPV without intraoperative subconjunctival antibiotics performed by three retina surgeons at a single surgical site at the Dean McGee Eye Institute from 2012 to 2018 were reviewed.

Expression of Virulence-Related Genes in an Ocular Infection-Related Environment.

produces many factors linked to pathogenesis and is recognized for causing gastrointestinal toxemia and infections. also causes a fulminant and often blinding intraocular infection called endophthalmitis. We reported that the PlcR/PapR system regulates intraocular virulence, but the specific factors that contribute to virulence in the eye remain elusive.

Targets of immunomodulation in bacterial endophthalmitis.

Bacterial infection of the posterior segment of the eye (endophthalmitis) leads to a robust host response that often results in irreversible damage to the layers of the retina, significant vision loss, and in some patients, enucleation of the globe. While a great deal of effort has gone into understanding the role of bacterial virulence factors in disease initiation and propagation, it is becoming increasingly clear that the host response to infection plays a major role in causing the damage associated with endophthalmitis. Researchers have identified the host receptors which detect infecting organisms and initiate the cascade of events that result in inflammation.

Disarming Pore-Forming Toxins with Biomimetic Nanosponges in Intraocular Infections.

Intraocular infections are prevalent after traumatic injuries or after common ocular surgeries. Infections cause inflammation that can damage the retina and architecture of the eye, often resulting in poor visual outcomes. Severe cases may result in blindness or require enucleation of the eye.

TLR4 modulates inflammatory gene targets in the retina during Bacillus cereus endophthalmitis.

Background: Endophthalmitis is a serious intraocular infection that frequently results in significant inflammation and vision loss. Because current therapeutics are often unsuccessful in mitigating damaging inflammation during endophthalmitis, more rational targets are needed. Toll-like receptors (TLRs) recognize specific motifs on invading pathogens and initiate the innate inflammatory response.

A Novel Biomimetic Nanosponge Protects the Retina from the Cytolysin.

Intraocular infections are a potentially blinding complication of common ocular surgeries and traumatic eye injuries. Bacterial toxins synthesized in the eye can damage intraocular tissue, often resulting in poor visual outcomes. causes blinding infections and is responsible for 8 to 17% of postoperative endophthalmitis cases.

The role of pili in Bacillus cereus intraocular infection.

Bacterial endophthalmitis is a potentially blinding intraocular infection. The bacterium Bacillus cereus causes a devastating form of this disease which progresses rapidly, resulting in significant inflammation and loss of vision within a few days. The outer surface of B.

Bloodstream-To-Eye Infections Are Facilitated by Outer Blood-Retinal Barrier Dysfunction.

The blood-retinal barrier (BRB) functions to maintain the immune privilege of the eye, which is necessary for normal vision. The outer BRB is formed by tightly-associated retinal pigment epithelial (RPE) cells which limit transport within the retinal environment, maintaining retinal function and viability. Retinal microvascular complications and RPE dysfunction resulting from diabetes and diabetic retinopathy cause permeability changes in the BRB that compromise barrier function.