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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine corneal specimens were obtained after penetrating keratoplasty for ultrastructural analysis. All the corneas had earlier suffered from herpetic infections and scarring. Six corneas presented vascularized interstitial keratitis and three corneas showed chronic keratitis. Five specimens with interstitial keratitis presented stromal herpes virus-like particles. All the corneas containing virus particles showed stromal lymphocytic infiltration, and in four, macrophages were present. In two cases, lymphocytes were in close contact with affected keratocytes, suggesting that cell-mediated immunity plays a role in herpetic interstitial keratitis. The corneas with disciform keratitis were free of virus particles and leukocytic infiltration. The observed ultrastructural findings suggest that retrocorneal ridges, a form of posterior corneal scarring, has its origin in a granulomatous reaction between the stroma and Descemet's membrane.
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PMID:Virus particles and leukocytes in herpes simplex keratitis. 608 18

We evaluated the ocular manifestations of Cogan's syndrome in 13 consecutive patients. The most frequent and earliest ocular finding was bilateral peripheral subepithelial keratitis consisting of faint, nummular lesions. The subepithelial keratitis was responsive to topical administration of corticosteroids. Peripheral subepithelial keratitis was seen in four patients and strongly suspected on review of history in three additional patients. Deep stromal keratitis was seen in two patients, while only one patient developed classic findings of Cogan's syndrome, ie. interstitial keratitis with vascularization. Additionally, five patients presented with noncorneal ocular inflammatory disease and deafness (atypical Cogan's syndrome). Early subepithelial keratitis in Cogan's syndrome may be mistakenly diagnosed as trival ocular inflammatory disease, and suppressed by topical corticosteroids, resulting in delayed diagnosis of Cogan's syndrome in the absence of classic corneal findings. Early diagnosis of Cogan's syndrome is important inasmuch as prompt treatment of cochlear symptoms with systemic corticosteroids may prevent or ameliorate deafness.
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PMID:Early corneal findings in Cogan's syndrome. 649 98

Corneal edema occurring in the congenital rubella syndrome can result from coexistent glaucoma or develop in the absence of an elevated intraocular pressure. We examined a 36-week-old female infant with documented congenital rubella syndrome who had bilateral corneal stromal edema without attendant congenital glaucoma. Histopathologic examination of the cornea revealed absent Descemet's membrane, deep interstitial keratitis, stromal corneal swelling, and deranged, focally absent endothelial cells. A viral infiltration of endothelium is postulated as the mechanism of the corneal edema and keratitis.
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PMID:Persistent corneal edema in the congenital rubella syndrome. 668 49

The retrocorneal linear ridges in corneas from one case of syphilitic and two cases of herpetic interstitial keratitis were examined by electron microscopy. The hyaline ridge in syphilitic keratitis showed duplicated Descemet's membrane with focal excrescences of basement membrane-like substances. The hyaline ridge in herpetic keratitis showed a triangular area of increased fibrous tissues in the deeper stroma adjacent to Descemet's membrane with no focal excrescences of Descemet's membrane.
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PMID:The retrocorneal ridge in syphilitic and herpetic interstitial keratitis: an electron-microscopic study. 704 92

A 33-year-old man developed Herpesvirus hominis type 2 (HVH-2) eye disease following a herpetic lesion of the penis. The sequence of ocular involvement suggested that the virus had been transmitted endogenously from the genital lesion: granulomatous iritis was followed by interstitial keratitis and then by dendritic keratitis. Recurrent bacterial ulcers ultimately required a conjunctival flap. The course of this man's ocular disease as well as those of other reported cases of HVH-2 adult eye infections appeared to be more severe and prolonged than that of the average patient with ocular herpes type 1 infection.
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PMID:Endogenous dissemination of genital Herpesvirus hominis type 2 to the eye. 742 49

Sclerosing keratitis is the major cause of blindness due to onchocerciasis; its pathogenesis is poorly understood. We have previously reported an immune-mediated model of experimental interstitial keratitis in guinea pigs following intrastromal challenge with soluble antigens from Onchocerca volvulus. This model system is ideal for evaluation of pathogenicity of multiple purified antigen preparations; however, reagents necessary for detailed immunologic analysis of the inflammatory cellular infiltrate are not yet available for guinea pigs. Because of the ready availability of these reagents for mice, a mouse model has been developed. The inflammatory response observed in this model was analogous to that seen in human onchocercal sclerosing keratitis as well as in the guinea pig model of onchocercal sclerosing keratitis. Granulocytes were present in the acute inflammatory response, whereas the chronic response showed lymphocytes, plasma cells, and histiocytes. Neovascularization and scarring of the corneal stroma was also observed. This model will be helpful in examining the mechanisms of immunopathogenesis and the contribution of the host genetic background to the disease.
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PMID:Immune-mediated Onchocerca volvulus sclerosing keratitis in the mouse. 769 31

Sclerosing keratitis is the predominant cause of blindness due to onchocerciasis which is a major human parasitic disease caused by the filarial parasite Onchocerca volvulus. In the present investigation, native pathogenic antigens of O. volvulus which are particularly potent in causing interstitial keratitis were characterized utilizing a guinea pig model. Following demonstration of the protein nature of these antigens using pronase digestion, the crude O. volvulus antigen extract was subjected to stepwise procedures of protein purification. At each stage of purification, pooled antigen fractions were injected into one cornea of presensitized guinea pigs followed by clinical evaluation of stromal inflammation and vascularization at different intervals of time after intrastromal challenge. Initial purification of the pathogenic antigens was carried out in the following order: molecular sieve chromatography on Bio-gel A-5m. anion exchange chromatography on Mono Q followed by DEAE-Sepharose CL-6B and cation exchange chromatography on Mono S. Two out of six different pools from the Mono S column (pool a eluted unbound at 10 mM-NaCl and pool e eluted between 130 mM and 475 mM-NaCl) were found to be most pathogenic. Further purification of Mono S pool a and pool e separately by gel filtration chromatography using Superose 12 demonstrated that the fractions which were most potent in inducing interstitial keratitis contained proteins with approximate molecular masses between 100 and 200 kDa. These results show that minor subfractions of total crude antigens of O. volvulus are largely responsible for induction of experimental interstitial keratitis. We have demonstrated the presence of these antigens in O. volvulus microfilariae by their cross-reactivities with anti-microfilarial antibodies, and hence the relevance of the purified antigens to ocular onchocerciasis in man since sclerosing keratitis is associated with invasion of the cornea by O. volvulus microfilariae. Isolation of these two pathogenic antigen pools represents the practical limits of purification and subsequent animal experiments possible with the available amounts of native parasite material obtained from infected human individuals in the absence of a suitable non-human host or of an in vitro culture system for O. volvulus.
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PMID:Characterization of native pathogenic antigens of Onchocerca volvulus: identification of high molecular mass protein antigens eliciting interstitial keratitis in a guinea pig model. 778 15

We report a retrospective analysis of the clinical indications for 3555 penetrating keratoplasties performed at our department between 1971 and 1990. The cases were distributed among 12 diagnostic categories. Regrafting was the most common indication overall, accounting for 1452 cases (40.8%). Other major indications were, in order of decreasing frequency, keratoconus (17%), scarring secondary to herpes simplex keratitis (11.7%), aphakic bullous keratopathy (5.9%) and interstitial keratitis (5%). Further analysis of the relative percentages in each category within each 5-year interval of the study period was carried out to identify any changes in incidence. Viral disease as an indication for penetrating keratoplasty has shown a gradual decrease in frequency, accounting for only 6.4% of the cases during the last 5-year period (1986-90) compared with 19.6% during the first 5 years (1971-75). This finding is consistent with the marked improvement in the recognition and medical treatment of herpes simplex keratitis. The increase in incidence of grafting for pseudophakic bullous keratopathy in 1986-90 (6.7%) compared with 1981-85 (1.1%) correlates well with the dramatic increase in the number of cataract extractions with intraocular lens implantations performed during that period.
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PMID:Changing indications for penetrating keratoplasty, 1971-1990. 825 25

Sclerosing keratitis is the major cause of blindness due to onchocerciasis which results from chronic infection with the filarial parasite Onchocerca volvulus. Using a murine model of onchocercal sclerosing keratitis, we have demonstrated previously that predominantly (> 85%) CD3 + /CD4+ T-cells as well as the IL-2 receptor bearing cells infiltrate into the cornea in vivo during development and progress of the disease. The identification of CD4+ subsets TH1 and TH2 based on the cytokine secretion patterns of murine T-lymphocytes has been useful for understanding the immune basis of resistance and pathogenesis in murine models of several parasitic diseases. The present investigation was carried out to demonstrate whether the local immune response at the corneal lesion due to onchocercal interstitial keratitis correlated with such distinct patterns of cytokine production. For that purpose, mRNA was extracted separately from corneas obtained from the diseased eyes and the normal eyes of A/J mice with onchocercal interstitial keratitis, reverse transcribed and amplified by the polymerase chain reaction with four different cytokine specific primers. In corneas obtained from the eyes affected with onchocercal interstitial keratitis, mRNAs coding for IL-4 and IL-5 were up-regulated compared to the normal eyes having no lesions from the same animals. However, the levels of mRNAs for IL-2 and IFN gamma were found to be the same in the diseased and normal eyes. Taken together, these data suggest that IL-4 and IL-5 producing TH2-lymphocytes are active at the corneal lesion due to onchocercal interstitial keratitis.
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PMID:In vivo molecular analysis of cytokines in a murine model of ocular onchocerciasis. I. Up-regulation of IL-4 and IL-5 mRNAs and not IL-2 and IFN gamma mRNAs in the cornea due to experimental interstitial keratitis. 903 Sep 83

Onchocerciasis is a major cause of blindness. Although the World Health Organization has been successful in reducing onchocerciasis as a public health problem in parts of West Africa, there remain an estimated 17 million people infected with Onchocerca volvulus, the parasite that causes this disease. Ocular pathology can be manifested in any part of the eye, although disease manifestations are frequently characterized as either posterior or anterior eye disease. This review focuses on onchocerca-mediated keratitis that results from an inflammatory response in the anterior portion of the eye and summarizes what is currently known about human disease. This review also describes studies with experimental models that have been established to determine the immunological mechanisms underlying interstitial keratitis. The pathogenesis of keratitis is thought to be due to the host inflammatory response to degenerating parasites in the eye; therefore, the primary clinical symptoms of onchocercal keratitis (corneal opacification and neovascularization) are induced after injection of soluble O. volvulus antigens into the corneal stroma. Experimental approaches have demonstrated an essential role for sensitized T helper cells and shown that cytokines can regulate the severity of keratitis by controlling recruitment of inflammatory cells into the cornea. Chemokines are also important in inflammatory cell recruitment to the cornea, and their role in onchocerciasis is being examined. Further understanding of the molecular basis of the development of onchocercal keratitis may lead to novel approaches to immunologically based intervention.
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PMID:Pathogenesis of onchocercal keratitis (River blindness). 1039 75


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