Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early Acanthamoeba keratitis was diagnosed in two soft contact lens wearers. Both patients had initially been diagnosed as having herpes simplex keratitis and treated with antiherpes drugs. In one patient, slit-lamp examination disclosed dendritiform epithelial keratitis, subepithelial opacities, linear stromal infiltrate along the corneal nerve (radial keratoneuritis), and marked swelling and hyperemia of the limbal conjunctiva. Acanthamoeba castellanii was cultured from the corneal scrapings and contact lens case. The second patient also showed dendritiform keratitis and subepithelial opacities, with swelling of the limbal conjunctiva. Cultures were positive for A. polyphaga from the contact lens case, but negative from the corneal scrapings. The patients were cured of Acanthamoeba keratitis with medical therapy consisting of topical fluconazole and miconazole, systemic fluconazole, and topical corticosteroids. Recognition of distinctive characteristics of the clinical findings in early Acanthamoeba keratitis can lead to the early diagnosis of the disease.
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PMID:[Two cases of early Acanthamoeba keratitis]. 831 77

To study the role of the host inflammatory response in Pseudomonas aeruginosa keratitis, rabbits were made leukopenic with intravenous injections of cyclophosphamide and dexamethasone. Twenty-four hr later, keratitis was initiated in all rabbits with an intrastromal injection of 1,000 log phase P. aeruginosa strain 27853. Slit lamp examination of eyes showed that leukopenic rabbits had significantly less (P < 0.0001) ocular pathology at 16, 22, and 27 hr postinfection. The number of viable bacteria recovered from corneas of leukopenic rabbits was the same as the number recovered from nonleukopenic rabbits (P = 0.95). These results suggest that the host inflammatory response significantly contributes to the overall ocular pathology associated with P. aeruginosa keratitis, but does not influence the survival of the infecting organism in the cornea at the height of the infection.
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PMID:Pseudomonas aeruginosa keratitis in leukopenic rabbits. 834 69

This study was conducted to determine the therapeutic efficacy of 3.0 mg/ml ciprofloxacin administered concurrently with one of two salts of prednisolone for the treatment of experimental pseudomonal keratitis. Rabbit corneas were injected intrastromally with Pseudomonas aeruginosa ATCC strain 27853. Sixteen hr after injection, rabbits were randomly divided into four treatment groups (3 rabbits, 6 eyes per group): 1) ciprofloxacin plus prednisolone acetate; 2) ciprofloxacin plus prednisolone phosphate; 3) ciprofloxacin only; 4) untreated. Signs of inflammation were graded in a masked fashion by slit lamp examination (SLE) and by estimating polymorphonuclear leukocyte (PMN) numbers in corneas 27 hr after injection. SLE scores and PMN numbers were significantly lower (P < 0.02) in eyes receiving either salt of prednisolone plus ciprofloxacin compared to the untreated controls. In contrast, SLE scores and PMN numbers were not significantly different in eyes treated with ciprofloxacin alone, compared to untreated controls (P > 0.13). No viable bacteria were recovered from any eye treated with ciprofloxacin (groups 1, 2, and 3). Ciprofloxacin concentrations in the aqueous humor of eyes in groups 1, 2, and 3 were greater than 15-fold higher than the MIC for P. aeruginosa 27853. These results suggest that either salt of prednisolone, when combined with ciprofloxacin, reduces ocular inflammation without affecting the antimicrobial efficacy of the antibiotic.
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PMID:Prednisolone acetate or prednisolone phosphate concurrently administered with ciprofloxacin for the therapy of experimental Pseudomonas aeruginosa keratitis. 834 70

Keratitis solaris is caused by ultraviolet radiation in the range 200-320 nm. The threshold dose for keratitis solaris is 40 J/m2 for short-term exposure. We measured the emission spectra of 22 sunbeds in the range 250-500 nm with a high-resolution double monochromator and calculated the exposure times for the threshold dose of keratitis solaris. Depending on the type of lamp used, the exposure times ranged from 90 s to 3.5 h. Lamps with short exposure times for keratitis solaris can induce keratitis solaris if protective goggles are not used (e.g., to achieve a uniform tan of the eye area) and if the eyes are opened briefly several times, perhaps, to look at a watch. Generally, sunbed users have no way of ascertaining the lamp type or its emission spectrum and of determining the exposure time for the threshold dose of keratitis solaris.
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PMID:Keratitis solaris and sunbeds. 875 41

The effect of basic fibroblast growth factor (bFGF) on the evolution of herpes simplex virus (HSV) infection in eyes of rabbits was investigated. Rabbit eyes were infected with HSV-1 by a non-invasive inoculation and treated for 7 days with an eye drop solution containing either bovine bFGF (50 ng; three times daily), or bFGF diluent as control. The treatment started 2 hr, 24 hr or 96 hr post-inoculation (p.i.). Follow-up of clinical disease parameters, such as conjunctivitis, epithelial keratitis, stromal disease, corneal neovascularization and of viral isolation continued for 17 days. The most significant difference between bFGF and control treatments was observed in the development of stromal keratitis. The incidence of stromal disease in the bFGF treated group (2/16 eyes) was significantly lower than in the control group (11/12 eyes) (P = 0.0001), when bFGF was administered 2 hr or 24 hr p.i. The severity of the disease developed in the bFGF treated eyes was also milder than in the control eyes (determined by serial slit-lamp clinical examinations and by histologic sections). Such effect was not demonstrated if the treatment started 96 hr p.i. The same duration of viral shedding was obtained with bFGF treated eyes (2 hr, 24 hr, or 96 hr p.i.) and control eyes. Neither HSV-1-infected, nor sham-inoculated bFGF-treated eyes demonstrated increased neovascularization of the cornea, as compared with the corresponding vehicle-treated control eyes. This study demonstrates that bFGF treatment (starting 2-24 hr p.i.) decreased the occurrence and severity of herpetic stromal keratitis, without subsequent aggravation of corneal vascularization. This beneficial anti-inflammatory effect of bFGF may have future application in the treatment of the most devastating stage of herpetic corneal infection.
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PMID:Moderation of herpetic stromal keratitis by basic fibroblast growth factor. 898 54

We sought to determine whether there are unique findings in infections crystalline keratitis (ICK) examined by confocal microscopy and if confocal microscopy is predictive for bacteriology in ICK. A retrospective review of consecutive patients with a presumed diagnosis of ICK by slit-lamp examination was performed. These patients were then examined with confocal microscope and cultured. Sixteen patients were identified by biomicroscopy. Average age was 71 years; 12 of 16 patients were women; 10 of 16 had prior penetrating keratoplasty; and 12 of 16 were taking topical steroids. Confocal microscopy revealed a variable appearance to the crystals in the corneal stroma. Eight of 16 patients had distinct needle-like deposits at varying depths in the stroma, and eight had amorphous deposits grouped at different levels of the stroma. The results of confocal microscopic examination resembled the reported histopathology with clusters of deposits, but its current resolution does not allow identification of bacterial morphology. There was no correlation of morphology with culture results. Organisms were recovered in 12 of 16 patients by culture. In 10 of 16 patients, the infection was successfully treated with topical antibiotics, usually cefazolin. Crystal morphology of ICK can be observed by confocal microscopy. No pathognomonic, single pattern for this disease is seen with the confocal microscope. The latter may be an aid in determining the clinical response to treatment.
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PMID:Evaluation of infectious crystalline keratitis with confocal microscopy in a case series. 898 29

Staphylococcus aureus corneal infection results in extensive inflammation and tissue damage. Our previous studies of bacterial mutants have demonstrated a role for alpha-toxin in corneal virulence. This study analyzes, by genetic rescue experiments, the virulence of mutants affecting alpha-toxin and beta-toxin activity and demonstrates the ocular toxicity of these purified staphylococcal proteins. Three types of isogenic mutants were analyzed: (i) mutants specifically deficient in alpha-toxin (Hla) or beta-toxin (Hlb), (ii) a mutant deficient in both Hla and Hlb, and (iii) a regulatory mutant, deficient in the accessory gene regulator (agr), that produces reduced quantities of multiple exoproteins, including alpha- and beta-toxins. Plasmids coding for Hla and Hlb (pDU1212 and pCU1hlb, respectively) were used to restore toxin activity to mutants specifically deficient in each of these toxins. Either corneas were injected intrastromally with logarithmic-phase S. aureus or purified alpha- or beta-toxins were administered to normal eyes. Ocular pathology was evaluated by slit lamp examination and myeloperoxidase activity of infiltrating polymorphonuclear leukocytes. Corneal homogenates were cultured to determine the CFU per cornea. Eyes infected with the wild-type strain developed significantly greater corneal damage than eyes infected with Agr-, Hlb-, or Hla- strains. Epithelial erosions produced by parent strains were not produced by Agr- or Hla- strains. Hlb+ strains, unlike Hlb- strains, caused scleral edema. Plasmid pDU1212 restored corneal virulence to strain DU1090 (Hla-), and plasmid pCU1hlb restored corneal virulence to strain DU5719 (Hlb-). Application of purified alpha-toxin produced corneal epithelial erosions and iritis, while application of beta-toxin caused scleral inflammation. These studies confirm the role of alpha-toxin as a major virulence factor during S. aureus keratitis and implicate beta-toxin, a mediator of edema, as a lesser contributor to ocular damage.
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PMID:Specific roles of alpha-toxin and beta-toxin during Staphylococcus aureus corneal infection. 912 32

This is the first report of a severe case of Mycobacterium chelonae keratitis; it occurred in a 26-year-old man after he had undergone excimer laser photorefractive keratectomy for the correction of severe myopia, once the epithelium was already healed. The diagnosis was made by culture results and acid-fast staining of corneal scrapings. Topical ciprofloxacin sodium, 0.3 mg/mL, plus amikacin sodium, 10 mg/mL, and oral clarithromycin sodium led to remission of the ulceration after 3 months of therapy. Subsequent topical corticosteroid therapy led to complete visual recovery during 1 year of follow-up. There may be an increased risk of severe keratitis during the first postoperative months in eyes that have already undergone photorefractive keratectomy, due to the presence of some microepithelial defects symptomatically negative and not easily detectable by slit-lamp examination.
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PMID:Mycobacterium chelonae keratitis after excimer laser photorefractive keratectomy. 933 81

Herpetic stromal keratitis (HSK) is an immunoinflammatory lesion in the cornea of the eye set off by infection with herpes simplex virus (HSV). The disease appears to be orchestrated by CD4+ T cells of the Th1 phenotype but the identity of target antigens involved in HSK remains unknown. In this proposal, we investigated if the inhibition of T cell activation with the fusion protein CTLA4Ig would abrogate the disease process when administered systemically. BALB/c mice infected with HSV-1 (RE strain) by corneal scarification were injected intraperitoneally on a single occasion with CTLA4Ig or L6 control (IgG Fc) given on day 2, day 5, or day 8 postinfection. Lesions in CTLA4Ig-treated mice showed markedly reduced severity judged by both slit lamp biomicroscopy and histopathology if treated on day 2 or day 5. Treated animals also expressed minimal HSV-specific splenic T cell and humoral antibody responses. Judged by the profile of T cell and IgG subset responses, inhibition by CTLA4Ig appeared more directly on the HSV-specific Th1 response, correlating with the known role of such cells in HSK. Delay of treatment until the time of disease onset (day 8) had marginal or negligible effects. The results indicate that blockade of coreceptor interaction between T cells and antigen-presenting cells during the induction phase of immune response significantly impairs onset and severity of herpetic stromal keratitis.
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PMID:Control of herpetic stromal keratitis using CTLA4Ig fusion protein. 943

In patients with herpes virus dendritic epithelial keratitis, the pathologic morphogenesis of the dendritic lesion was investigated by means of impression cytology. Impression specimens were taken from the lesions of 24 consecutive patients assessed with a slit lamp biomicroscope. After a Millipore membrane impression was stained with hematoxylin-eosin and examined by light microscope, cellular patterns were analyzed. The results of these examinations showed that most cells were epithelial cells; there were also occasional multinucleated syncytial giant cells, inclusion bodies and inflammatory cells. Basal epithelial cells were most prominent at the actively infected lesion, whereas superficial epithelial cells were shown at the margin of the active lesion and terminal bulb. These findings suggest that in dendritic keratitis, viral spread and replication in the dendritic keratitis may progress through basal epithelial cells along the nerve within the basal epithelium-stromal interface.
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PMID:Infectivity of basal epithelial cells in herpetic dendritic epithelial keratitis. 951 Jun 49


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