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)

Stromal keratitis and iritis developed in the left eye of a healthy 45-year-old man with no history of ocular disease, trauma, or contact lens wear. The clinical course over a 2-year period was characterized by progressive central disciform keratitis, recurrent anterior stromal patchy infiltration, and iritis which was partially controlled with topical corticosteroids and broad-spectrum antibiotics. Results of bacterial, viral, fungal, and chlamydial cultures were negative. Results of histopathologic examination of a corneal biopsy specimen and, later, a penetrating keratoplasty specimen showed many extracellular and intracellular spores in degenerating keratocytes. By electron microscopy there were encapsulated oval structures measuring approximately 3.5 to 4 microns in length x 1.5 microns in width. Mature spores had well-developed cell walls that contained two abutted nuclei (diplokaryon) and a redundant polar tubule with six coils. These structures are characteristic of a protozoa in the genus Nosema.
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PMID:Corneal microsporidiosis. A case report including ultrastructural observations. 238 10

Stromal keratitis is typically the consequence of infection with herpes simplex virus type 1 (HSV-1). The pathogenesis of this disease remains elusive, although it is generally believed that there is an important immunological component. It has been proposed that stromal keratitis is mediated by virus-specific T lymphocytes of the delayed hypersensitivity type. However, while virtually all individuals infected with HSV-1 develop delayed hypersensitivity, only a small fraction actually develop stromal keratitis. To explain this discrepancy, we reasoned as follows: epidermal Langerhans cells are believed to be crucial to the induction of delayed hypersensitivity; since the cornea normally contains few or no cells of this type, the presence of Langerhans cells in the central corneal epithelium at the time of virus infection might promote the development of stromal keratitis. To test this hypothesis, cautery wounds of central regions of mouse corneas were used to induce migration of Langerhans cells into the corneal epithelium. These mice were then infected with HSV-1 on the ipsilateral snout, an infection that results in zosteriform spread of virus via the trigeminal nerve into the anterior segment of the ipsilateral eye within 3-5 days after inoculation. We found that the eyes of cauterized mice displayed a very high incidence of severe stromal keratitis. By contrast, non-cauterized corneas of control, snout-infected mice displayed much less evidence of stromal disease. Moreover, the rapidity of onset of systemic delayed hypersensitivity to HSV-1 was accelerated in the mice with cauterized corneas, compared to the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunobiology of Langerhans cells on the ocular surface. II. Role of central corneal Langerhans cells in stromal keratitis following experimental HSV-1 infection in mice. 256 60

Corneal complications of herpes zoster ophthalmicus include pseudodendritic keratitis, late mucous adherent keratopathy, varied forms of stromal keratitis, and exposure/neurotrophic keratopathy. Prophylactic therapy of acute herpes zoster ophthalmicus with oral acyclovir is of proven benefit in reducing the incidence of early pseudodendritic keratopathy and stromal keratitis but has no evident effect on exposure/neurotrophic keratopathy. Although early pseudodendritic keratitis is due to virus infection of epithelial cells, it is self-limited and does not require topical antiviral therapy. Stromal keratitis and associated epithelial mucous adherent keratopathy are responsive to topical corticosteroids but chronic therapy is often required and may prolong the duration of keratitis and result in cataract or secondary glaucoma. Exposure and neurotrophic keratopathy may respond to topical lubricants and correction of lid abnormalities but severely affected corneas may require tarsorrhaphy or conjunctival flap to maintain corneal integrity.
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PMID:Corneal complications of herpes zoster ophthalmicus. Prevention and treatment. 325 20

Recurrent erosion of the cornea has been well documented in patients with nontraumatic anterior membrane dystrophies of various types. We examined five patients who, in addition to an erosion, developed stromal keratitis. Three of these patients were subjected to a complete microbiologic workup, but the lesions were all sterile. The lesions healed with conservative treatment of patching and, in some cases, a soft contact lens. Stromal keratitis should be recognized as a complication of the non-traumatic recurrent erosion syndrome, which in turn is frequently associated with anterior membrane dystrophy. The finding of such anterior membrane changes in either eye will lead to the correct diagnosis and treatment of the affected eye.
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PMID:Stromal keratitis complicating anterior membrane dystrophy. 387 50

We determined the therapeutic efficacy of iontophoretic application of acyclovir and vidarabine monophosphate (ara-AMP) for the treatment of herpes simplex virus (HSV) type 1-induced stromal keratitis in rabbits. The therapeutic efficacy of intravenous administration of acyclovir was assessed in the same model. Stromal keratitis was produced by intrastromal injection of 10 microliters purified HSV-1, McKrae strain. Treatment began the first day after intrastromal injection. Iontophoresis (0.5 mAmp for four minutes) of 3.4 percent (0.1 M) ara-AMP and 5.0 percent (0.22 M) acyclovir was performed once daily for five consecutive days in two treatment groups. Intravenous administration of 50 mg acyclovir/kg was performed twice daily for eight consecutive days. Intravenous administration of NaCl (0.14 M) and ocular iontophoresis of NaCl (0.14 M) were performed as controls in the two treatment groups. At least two scorers performed a single masked evaluation of the disease severity (lesion scoring) of the conjunctiva, corneal epithelium, stroma, and iris by still lamp examination. The eyes were scored daily for 12 consecutive days, and then every other day up to day 22. Iontophoresis of acyclovir or ara-AMP significantly reduced the course of the disease compared with iontophoresis of NaCl. Intravenous administration of acyclovir significantly reduced the disease compared with intravenous NaCl. This suggests that iontophoresis of acyclovir or ara-AMP either alone or in combination with intravenous administration of acyclovir may be of value in the treatment of HSV-1 stromal keratitis.
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PMID:Acyclovir and vidarabine monophosphate: comparison of iontophoretic and intravenous administration for the treatment of HSV-1 stromal keratitis. 617 15

Thirty patients with bilateral herpetic keratitis were evaluated, 40% of whom were atopic. Stromal keratitis occurred in 40% of the eyes and recurrent ulceration in 68%. Four patients (5 eyes) developed secondary microbial keratitis. Visual acuity decreased to 6/60 or less because of corneal opacification in 17% of the eyes.
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PMID:Bilateral herpetic keratitis. 726 8

A series of 21 pediatric patients with ocular herpes simplex infections is reported. Two groups are presented: those with clinical primary herpes and those with documented recurrences. The corneal manifestations including clinical resistance to idoxuridine are presented. Stromal keratitis and visual loss were not marked in the primary group, but were difficult to prevent in those children with recurrences. The problems encountered in the overall management of children with herpetic keratitis are discussed.
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PMID:Herpetic ocular infections of childhood. 736 5

Inflammation of the corneal stroma (stromal keratitis) is a serious complication of infection with the nematode parasite Onchocerca volvulus. Because stromal keratitis is believed to be immunologically mediated in humans, we used a murine model to examine the role of T cells and T helper cell cytokines in the immunopathogenesis of these eye lesions. BALB/c mice immunized subcutaneously and injected intrastromally with soluble O. volvulus antigens (OvAg) developed pronounced corneal opacification and neovascularization. The corneal stroma was edematous and contained numerous eosinophils and mononuclear cells. Stromal keratitis in immunized mice was determined to be T cell dependent based on the following observations: (a) T cell-deficient nude mice immunized and injected intrastromally with OvAg fail to develop corneal pathology; and (b) adoptive transfer of spleen cells from OvAg-immunized BALB/c mice to naive nude mice before intrastromal injection of OvAg results in development of keratitis. OvAg-stimulated lymph node and spleen cell cytokine production was dependent on CD4 cells and included interleukin (IL)-4 and IL-5, but not interferon gamma, indicating a predominant T helper type 2 cell-like response. Inflamed corneas from immunized BALB/c mice and from reconstituted nude mice had greatly elevated CD4 and IL-4 gene expression compared with interferon gamma. Mice in which the IL-4 gene was disrupted failed to develop corneal disease, demonstrating that IL-4 is essential in the immunopathogenesis of O. volvulus-mediated stromal keratitis.
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PMID:Interleukin 4 and T helper type 2 cells are required for development of experimental onchocercal keratitis (river blindness). 756 96

Interleukin-8 (IL-8) is a proinflammatory cytokine released at sites of tissue damage by various cell types. One important function of IL-8 is to recruit neutrophils into sites of inflammation and to activate their biological activity. Stromal keratitis induced by herpes simplex virus type 1 (HSV-1) is characterized by an initial infiltration of neutrophils. This study was carried out to determine whether cells resident in the cornea synthesize IL-8 after virus infection. Pure cultures of epithelial cells and keratocytes established from human corneas were infected with HSV-1, and the medium overlying the cells was subsequently assayed for IL-8 by an enzyme-linked immunosorbent assay. Cytokine mRNA levels in cell lysates were monitored by Northern (RNA) blot analysis. It was found that virus infection of keratocyte cultures led to the synthesis of IL-8-specific mRNA with more than 30 ng of IL-8 made per 10(6) cells. Neither UV-inactivated virus nor virus-free filtrates collected from HSV-1-infected keratocytes could induce IL-8 protein or mRNA, suggesting that viral gene expression was needed for induction of IL-8 gene expression. Unlike keratocytes, HSV-1-infected epithelial cells failed to synthesize IL-8 protein or mRNA. However, these cells readily produced both molecules following tumor necrosis factor alpha stimulation. HSV-1 had similar titers in both cell types. Thus, the failure to induce IL-8 synthesis was not due to an inability of the virus to replicate in epithelial cells. The capacity of HSV-1-infected corneal keratocytes to synthesize IL-8 suggests that these cells can contribute to the induction of the acute inflammatory response seen in herpes stromal keratitis.
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PMID:Induction of interleukin-8 gene expression is associated with herpes simplex virus infection of human corneal keratocytes but not human corneal epithelial cells. 768 2

Stromal keratitis resulting from ocular infection with herpes simplex virus is a common cause of blindness. This report investigates the role of neovascularization in the pathogenesis of stromal keratitis by measuring the outcome of treatment with the potent anti-angiogenesis cytokine endothelial monocyte-activating polypeptide II (EMAP II). We show that systemic and topical administration of EMAP II from the outset of infection resulted in markedly diminished levels of herpes simplex virus-induced angiogenesis and significantly reduced the severity of stromal keratitis lesions. EMAP II treatment had no demonstrable pro-inflammatory or toxic effects and failed to express antiviral activity. The mechanism of action of EMAP II was shown to proceed by causing apoptosis in vascular endothelial cells. Our data document for the first time the essential role of angiogenesis in the pathogenesis of stromal keratitis and also indicate that the therapy of herpetic stromal keratitis could benefit by procedures that diminish angiogenesis.
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PMID:Control of stromal keratitis by inhibition of neovascularization. 1154 94


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