Cases reported "Keratitis"

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1/15. extracellular matrix components in a case of retrocorneal membrane associated with syphilitic interstitial keratitis.

    PURPOSE: A web-like retrocorneal membrane (RCM) is an uncommon complication of chronic syphilitic interstitial keratitis. extracellular matrix components have not yet been defined in this structure, although previous histologic examinations have suggested the presence of collagen. We examined the presence and distribution of extracellular matrix components in a patient with an RCM. methods: A specimen of the opaque cornea affected by syphilitic interstitial keratitis with RCM formation was obtained during penetrating keratoplasty in a 62-year-old woman and was evaluated by histology, immunohistochemistry, and scanning electron microscopy (SEM). antibodies against collagen types I, III, and IV; fibronectin; vimentin; alpha-smooth muscle actin (alpha-SMA); heat shock protein 47 (Hsp 47); proliferating cell nuclear antigen (PCNA); and Ki67 were used. RESULTS: Histologic analysis detected multiple concentric, acellular layers positive for collagen types I, III, and IV. The corneal endothelial cells (CECs) were positive for vimentin, collagen I, fibronectin, and Hsp 47 but not for alpha-SMA. Furthermore, the CECs were negative for PCNA and Ki67, indicating that they were not proliferating. SEM revealed the RCM was covered by CECs with a fibroblastic appearance. CONCLUSION: RCM associated with syphilitic interstitial keratitis contained collagen types I, III, and IV and fibroblast-like CECs. These CECs may secrete the extracellular matrix components found in the RCM. Hsp 47 up-regulation in the CECs may play an important role in RCM formation. These findings provide further insights into the phenotypic modulation of CECs.
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2/15. Demonstration of biofilm in infectious crystalline keratopathy using ruthenium red and electron microscopy.

    OBJECTIVE: Bacterial biofilm formation has been implicated in the pathogenesis of infectious crystalline keratopathy. Biofilm cannot be visualized by electron microscopy without the addition of a fixative that stabilizes the polysaccharide-rich bacterial extracellular matrix that surrounds the bacterial colonies in a biofilm. We used ruthenium red as a fixative to evaluate corneal biopsy specimens for the presence of bacterial biofilm in three cases of infectious crystalline keratopathy (ICK) and five cases of chronic microbial keratitis without crystalline changes. DESIGN: Case series with clinicopathologic correlation. PARTICIPANTS: Eight patients underwent corneal biopsy or therapeutic keratoplasty as part of their management for chronic unresponsive microbial keratitis. methods: The corneal specimens removed were trisected for microbiology, pathology, and transmission electron microscopy (TEM). The TEM specimens were fixed in 2.5% glutaraldehyde in 0.1 M sodium cacodylate buffer with 0.05% ruthenium red. MAIN OUTCOME MEASURES: Demonstration of bacterial biofilm with TEM. RESULTS: TEM demonstrated organisms with a surrounding extracellular matrix consistent with a bacterial biofilm in the three cases of ICK but not in the five other cases of chronic microbial keratitis. CONCLUSIONS: The presence of biofilm in ICK can be demonstrated with TEM with appropriate fixation techniques that stabilize the bacterial extracellular matrix. Biofilm stains intensely with periodic acid-Schiff because of the polysaccharide-rich extracellular matrix and weakly with Gram stain because of the high proportion of nonviable organisms. Biofilm formation occurs in ICK but probably not in chronic bacterial keratitis without crystalline changes. Secretion of an extracellular matrix by bacteria to form a biofilm is a response to a nutrient-deprived environment in which growth and replication is depressed. The extracellular matrix of the biofilm may mask bacterial antigens, explaining the relative lack of inflammatory response in these infections. It may also be one of the mechanisms explaining the resistance to in vivo antimicrobial therapy when in vitro sensitivities have been proven.
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3/15. Dissecting folliculitis of the scalp with marginal keratitis.

    We describe a young man with dissecting folliculitis of the scalp, who subsequently developed marginal keratitis. We are unaware of any previous reports of this association. The aetiology of dissecting folliculitis is thought to relate to abnormal follicular occlusion with subsequent suppuration, although an infective process has never been established. Marginal keratitis is postulated, but not proven, to be caused by an enhanced immune response to staphylococcus aureus antigens. We suggest that a similar abnormal response to infection may be important in these two conditions. This case also highlights ocular complications which may occur in patients with dissecting folliculitis.
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4/15. Corneal autoimmunity in Cogan's syndrome? Report of two cases.

    Autoimmune reactivity against corneal antigens is described in two patients with Cogan's syndrome, a nonsyphilitic deep interstitial keratitis with vestibuloauditory symptoms. In both cases corneal antibodies were found at the beginning or during an exacerbation of the disease. After administration of high doses of corticosteroids the corneal antibodies diminished. Interstitial keratitis can generally be controlled by local or systemic corticosteroids. The effect of corticosteroid therapy on the audiovestibular symptoms is variable. The possibility of an autoimmune pathogenesis of Cogan's syndrome is discussed.
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5/15. Mooren's ulcer and evidence of stromal graft rejection after penetrating keratoplasty.

    A Mooren's ulcer developed in a 6-year-old girl after a penetrating keratoplasty for Peters' anomaly. A destructive, circumferential, and centripetal stromal ulceration recurred despite conjunctival resection, corneal gluing, topical and systemic administration of corticosteroids, and repeat graftings. Results of a systemic and a rheumatologic examination were unremarkable. Histopathologic evaluations of donor grafts consistently disclosed a lymphocytic and a plasma cell infiltrate. Indirect immunofluorescent staining using a normal donor cornea substrate was positive at the level of Bowman's membrane and stroma. The patient's lymphocytes were stimulated by a partially purified bovine corneal antigen and a positive antibody titer was found in the patient's sera to the same corneal antigen. These results suggest humoral and cell-mediated immune mechanisms can be involved in the initiation and perpetuation of a stromal rejection process after penetrating keratoplasty.
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keywords = antigen
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6/15. Rapid streptococcal antigen detection in experimental keratitis.

    We assessed the role of commercially available immunodiagnostic procedures in comparison to Gram stain and culture in experimental bacterial keratitis. Rabbit corneas were inoculated with streptococcus pneumoniae, S. pyogenes, S. faecalis, or haemophilus influenzae. Corneal scrapings were processed before and during antibacterial therapy using a coagglutination assay to detect pneumococcal capsular antigen (Phadebact Pneumococcus test) and an enzyme immunoassay to detect group A streptococcal cell-wall antigen (TestPack Strep A test). In untreated infected eyes, both immunoassays were highly specific and as sensitive as Gram stain for detection of the respective microorganisms. For S. pneumoniae keratitis, the sensitivity of coagglutination was 82% and Gram stain, 73%. For S. pyogenes keratitis, the sensitivity of enzyme immunoassay was 100% and Gram stain, 62%. Immunoassays and Gram stain were less sensitive than culture during antibacterial therapy. Successful clinical application of the coagglutination assay in a patient with pneumococcal keratitis permitted early use of specific cephalosporin treatment.
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7/15. Atypical Cogan's syndrome: an autoimmune disease?

    A 22-year-old woman is described with gastrointestinal complaints, sclerokeratitis, and a bilateral progressive hearing loss. The clinical picture, the outcome of lymphocyte stimulation tests against S antigen (retina soluble antigen), outer rod segment, and scleroprotein, and the successful administration of corticosteroids after a partial spontaneous hearing improvement, are suggestive of an autoimmune disease.
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keywords = antigen
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8/15. Varicella dendritic keratitis.

    A 7-year-old boy and a 3-year-old girl suffered from unilateral disciform keratitis and iritis associated with varicella. While they were treated with topical corticosteroid, idoxuridine, and atropine drops, dendritic lesions typical of herpes zoster appeared four months after the onset of eruptive skin lesions. Using the direct immunofluorescent method, we showed varicella-zoster virus antigen in the epithelial cells scraped from the dendritic lesion.
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keywords = antigen
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9/15. acanthamoeba keratitis successfully treated with penetrating keratoplasty: suggested immunogenic mechanisms of action.

    A patient with a corneal ulcer caused by Acanthamoeba polyphaga has been successfully treated with a penetrating keratoplasty. The pathologic specimen showed no inflammatory infiltrate surrounding the intact amoeba, whereas necrotic organisms were surrounded by an intense cellular reaction. Indirect immunochemical studies showed that the trophozoite stained profusely, but the cyst form exhibited the antigenic site on the cyst wall.
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10/15. Autoimmune reactivity in Cogan's syndrome: a preliminary report.

    Autoimmune inner ear disease was first described by McCabe in 1979. The diagnosis is supported by cell-mediated immune responses to inner ear membrane antigen stimulation. Cogan's syndrome consists of vestibuloauditory dysfunction, ocular inflammation, and nonreactive serologic tests for syphilis. The ocular disease can be controlled by steroids; unfortunately, some patients ultimately become totally deaf. An autoimmune etiology has long been suspected but only recently confirmed by McCabe. In our study two patients with Cogan's syndrome were studied for autoimmune inner ear disease with the use of both cellular and humoral immune tests. Results were compared to normal control subjects. On the basis of test results, preliminary conclusions were that (1) the vestibuloauditory symptoms of Cogan's syndrome are autoimmune in origin; (2) the autoimmune process is mediated through cellular rather than humoral (antibody) pathways; (3) systemic steroids may suppress positive test results; and (4) test results are more likely to be positive when symptoms are acute. Therapeutic implications are significant: the addition of cytotoxic drugs to steroids in selected cases may help prevent total deafness that otherwise might be inevitable.
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