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

A focus on the pathogenesis, clinical manifestations and therapy. Contemporary ideas on viral infections of the anterior segment are examined.--The pathogenesis of lesions (viral activity, delayed hypersensitivity reaction), the clinical aspects of herpes infections of the anterior segment are the result of the relative importance of these two factors. Schematically--dendritic keratitis infiltrates and stromal necrosis and hypopion represent active viral infection. Disciform keratitis, oedematous keratitis, serous iridocyclitis represent delayed hypersensitivity reaction. Corticosteroids are contrindicated in the former cases and recommended in the latter.--Special features concerning zoster inflammations of the anterior segment are considered.--An important number of adenoviral anterior segment infections are also reported and their benign nature stressed.
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PMID:[Viral infections of the anterior segment (author's transl)]. 15 79

The inflammatory response to herpes simplex virus infection of the cornea was studied in athymic nude (nu/nu) and heterozygote (nu/+) BALB/c mice. Although athymic mice were highly susceptible to HSV infection and died 13 to 17 days after corneal inoculation, they failed to develop necrotizing keratitis of the cornea. Heterozygote mice survived the initial virual infection, but many of these mice developed necrotizing keratitis and permanent corneal scarring. Light and electron microscopy showed numerous inflammatory cells (polymorphonuclear leukocytes and lymphocytes) in the corneas of heterozygote mice, but not in the athymic mice. These studies suggest that the immune system plays a dual role in herpes simplex virus infection of the cornea: protection against dissemination of the virus and immunopathogenesis of necrotizing keratitis in the cornea.
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PMID:Herpetic keratitis in athymic (nude) mice. 16 Aug 87

Pretreatment of human fibroblast cultures with human leukocyte interferon (HIF, 1,000 IU/ml) resulted in a 24-h delay of virus replication after infection with vaccinia virus and herpes simplex virus type 1 and type 2. Additional HIF treatment 24 h after infection effectively lowered the maximum yield of viral infectivity. Equal results were obtained in simian cells with 3,000 IU of HIF per ml. The spread of two cell-bound herpesviruses, varicella zoster virus and Medical Lake macaque herpesvirus, was inhibited by 2,000 IU of HIF per ml in human fibroblasts and Vero cells, respectively. Varicella zoster virus infectivity was notably reduced by HIF, whereas the latter system showed a low sensitivity. To study the effect of HIF in the infected cornea, keratitis was induced experimentally in both eyes of 12 rhesus monkeys and 12 African green monkeys by inoculation with vaccinia virus and herpes simplex virus, respectively. In each monkey one eye served as a control for the full cycle of disease. In the other eye HIF treatment was initiated prophylactically 15 h before or simultaneously with the challenge virus infection or 6 to 20 h postinfectionally or therapeutically after onset of the disease, and the treatment was continued for 2 to 7 days. Prophylactic and simultaneous administration equally resulted in inhibition of both vaccinia and herpes keratitis. Postinfectional and therapeutic administration of interferon moderated the course of keratitis slightly and shortened the period of virus shedding.
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PMID:Effect of human leukocyte interferon on vaccinia-and herpes virus-infected cell cultures and monkey corneas. 16 24

A gereral, overall pattern of the temporal relationship and interaction between cell and antibody-mediated immune responses following herpes simplex virus infection of the rabbit cornea can be synthesized from our studies. Cell-mediated immunity (CMI) appears early following infection, at a time when mononuclear and lymphocytic cellular proliferation occur at the limbus. Interaction between specifically immune lymphocytes with virus antigens are detected by lymphocyte blastogenesis and migration inhabiting factor. During stromal keratitis, a second phase of CMI involves transient virus-specific cytotoxic lymphocytes, which destroy cells that display viral-induced antigens on their surface. Chemotatic factors generated by viral antigens alone or with antiviral antibody or by virus-sensitized lymphocytes play a role in attracting polymorphonuclear leukocytes to the cornea during stromal keratitis. Soluble mediators of CMI secreated by activated lymphocytes act both specifically and nonspecifically on virus-infected cells, allowing cell destruction and making intracellular virus available for neutralization by antiviral antibody. Cell-mediated immunity in the acute infection, diminishes with the appearance of significant antiviral antibody titers. The late phase of the corneal immune response results from a local antigen-antibody interaction and is characterized by cells predominantly of the plasmacytic type. The presence of complement-dependent cytotoxic antibodies capable of destroying virus-infected cells provide an additional factor in restriction of infection.
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PMID:Immunology of herpesvirus infection: immunity to herpes simplex virus in eye infections. 18 41

The meta-herpetic keratitis is clinically characterized by the occurrence of a parenchymatous keratitis due to iterative herpetic corneal wounds. The rupture of the Bowman membrane which makes such a deep wound possible is performed by an enzyme: collagenase. This parenchymatous keratitis is rarely due to an extension of the viral infection. Most often it has an immunologic origin. It is a disciform keratitis due to a viral allergy, or a polymorphic keratitis connected with a bacterial, often tubercular, origin. In this case, one always notices a characteristic sugar tongs like composite limbic vascularization. Recovery can only be obtained by a specific desensitization.
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PMID:[Considerations on the meta-herpetic keratitis (author's transl)]. 20 62

A high incidence of keratoconjunctivitis was observed in a closed colony of inbred Lewis/Wistar rats. Clinical signs including blinking, ocular discharge, circumcorneal flush, corneal opacity, ulceration, pannus, hypopyon, and hyphema were observed at about three weeks of age. Acute disease subsided by six weeks of age, but some lesions progressed to low-grade chronic keratitis. Six per cent of affected rats developed megaloglobus, which usually appeared by three weeks of age. Lesions included focal or diffuse interstitial keratitis, corneal ulceration, anterior synechia, and inflammatory exudate in the anterior chamber. A high incidence of lenticular and retinal degeneration was associated with megaloglobus. Most affected rats also had harderian dacryoadenitis. Sialodacryoadenitis virus (SDA) was recovered from nasal washes, but not from affected eyes. Serological evidence indicated that SDA virus infection was widespread in the colony.
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PMID:Keratoconjunctivitis associated with sialodacryoadenitis in rats. 93

The various surgical managements of herpes simplex keratitis are listed. Our management is "atraumatic" keratoplasty, if vision is reduced, if the disease is protracted, or if perforation occurs. Our preoperative care is aimed at the production of a quiet eye with no active virus infection, by the use of antiviral drops, steroids, antibiotics, and bandage contact lenses. Removal of all corneal disease is desirable, but not mandatory. Perforations are managed in the same manner, but the host window is started at the perforation. Postoperative management is characterized by the use of therapeutic modalities necessary to prevent or treat complications, including steroids and frequent observation to check for complications of treatment. Our understanding of herpes simplex virus infections as they relate to surgical management is presented. The results of treatment warrant continuation of our efforts--but lead to the conclusion that it would be most helpful if latent virus infection could be eradicated.
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PMID:Surgical management of herpes simplex keratitis. 101 11

Recurrences of herpetic stromal keratitis are believed to be initiated by reactivation of herpes simplex virus infection, probably in the trigeminal ganglion. Genetic features of the virus and the host as well as the immune status of the host influence the outcome of infection. Following infection on the snout with HSV-1, mice with normal corneas usually develop mild anterior segment disease. We studied the induction of herpetic infection in mice that had abnormal corneas, containing center due to trauma or a spontaneous dystrophy. The corneal abnormality led to more frequent herpetic stromal keratitis and more severe anterior chamber reaction. In addition, we found that snout-infected mice with dystrophic corneas had an increased risk of dying from viral infection. Our data suggest that not only the strain of virus and the genetic background of the mouse, but also the state of the cornea itself, can contribute to susceptibility to ocular herpes infection.
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PMID:Presence of Langerhans cells in the central cornea linked to the development of ocular herpes in mice. 132 20

The cumulative clinical and experimental data regarding the role of viral infection versus the immune response in the pathogenesis of herpes simplex stromal keratitis and central disciform endotheliitis are discussed. Ultrastructural and viral isolation studies have been performed in only a limited number of cases of human stromal keratitis and disciform endotheliitis. Virus has been isolated from the minority of corneas cultured, whereas viral particles have been demonstrated in selected cases of stromal keratitis, most of which had been treated with steroids at some point in time. The possibility of corneal latency in cases of quiescent herpetic stromal keratitis will require further systematic study. Review of the experimental and clinical findings suggests a dialectical role of the immune response in limiting viral infection, while contributing to corneal opacification and scar formation.
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PMID:Herpes simplex keratitis: role of viral infection versus immune response. 203 19

Individuals with atopic dermatitis are particularly susceptible to herpes simplex viral infection and may develop dissemination (eczema herpeticum). Additionally, they may develop severe and bilateral herpetic ocular disease. The keratitis is commonly complicated by stromal scarring and slow epithelial healing despite topical antiviral therapy. We treated three patients who had herpetic keratoconjunctivitis associated with eczema herpeticum. In all three cases the keratitis resolved promptly (48 to 72 hours) without residual scarring after treatment with systemic acyclovir and topical trifluridine. The combined use of systemic acyclovir and topical trifluridine may be of similar value in treating all cases of atopic herpetic keratitis.
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PMID:Treatment of ocular disease in eczema herpeticum. 211 23


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