Cases reported "Keratitis, Dendritic"

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1/8. Allergic contact dermatitis caused by idoxuridine. Patterns of cross reactivity with other pyrimidine analogues.

    idoxuridine has been used for many years in the treatment of herpex simplex infections of the eye. Use of the drug for herpes simplex infection of the skin is increasing. Ophthalmologists have noted occasional conjunctival and corneal irritant reactions, but no true delayed cutaneous hypersensitivity has been verified. We report four cases of allergic contact dermatitis from idoxuridine, sensitized by both eye and skin applications. Cross reactivity to brominated and chlorinated, but not fluorinated, pyrimidine analogues is noted. Extensive patch testing indicates the general relationship between the structure of pyrimidine compounds and their antigenic cross reactivity.
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2/8. Recurrent herpes simplex keratitis with concurrent epithelial and stromal involvement. Immunohistochemical and ultrastructural observations.

    A 65-year-old man with recurrent herpetic keratitis underwent corneal transplantation for persistent nonimmunologic graft failure. Histopathologic examination of the corneal button revealed an epithelial dendrite containing Cowdry type A inclusion bodies, moderate stromal edema, and a retrocorneal fibrous membrane. Immunohistochemical studies demonstrated herpes simplex virus antigens in epithelial cells bordering the dendritic defect and in stromal keratocytes. The mean width of corneal epithelium displaying herpes simplex virus-positive epithelial cells on either side of the dendritic defect measured 200 /- 46 microns. By electron microscopy, herpesvirus particles were identified in epithelial cells lining the dendrite as well as in stromal keratocytes. Infected keratocytes were scattered throughout the stroma but were not observed subjacent to the epithelial dendrite. This study demonstrates that a recurrent epithelial dendrite can be associated with subclinical stromal infection of the graft.
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3/8. Immune cells in a case of postherpetic marginal trophic ulcer.

    The corneal surface was examined by means of replica histology, and the excised limbic conjunctiva was examined by routine histological and immunohistochemical methods with monoclonal antibodies directed against major histocompatibility class II antigens, lymphocyte subsets, langerhans cells (HLA-DR, OKT4-Leu3a, OKT8, BA1, B1, and OKT6) and immunoglobulins A, G, M, and D. The findings were compared with those found in normal conjunctiva. No inflammatory cells were present in the replica of the corneal surface. An inflammatory infiltrate composed of B lymphocytes and null cells, in addition to T lymphocytes, langerhans cells, and polymorphs, was present in the epithelium as well as in the stroma of the limbic conjunctiva. The composition of the infiltrate points towards the involvement of cell mediated immunity as well as humoral immunity. No immunoglobulins were bound to the conjunctival epithelium.
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4/8. Concurrent herpes simplex and cytomegalovirus retinitis and encephalitis in the acquired immune deficiency syndrome (AIDS).

    We present a case of bilateral herpes simplex and cytomegalovirus retinitis and concurrent encephalitis following acyclovir therapy in a homosexual male with the acquired immune deficiency syndrome (AIDS). At autopsy, herpes simplex virus antigens were readily detected in all retinal layers, retinal pigment epithelium, and choriocapillaris, using an immunoperoxidase technique, whereas herpes simplex antigens in the brain were localized in restricted foci of vascular and subependymal parenchymal cells. Cytomegalovirus antigens were identified in cells in all layers of retina, in retinal pigment epithelium, and in subependymal parenchymal cells in the brain. No cytomegalovirus antigens were detected in any vascular endothelium, in choroid, or anterior to the ora serrata. The widespread expression of herpes simplex virus antigens in this patient's retinas is in marked contrast to the restricted foci of herpes simplex antigens limited to the subependymal region of the brain, and is similar to that seen in murine models of herpes simplex retinitis produced by acyclovir-resistant viral mutants.
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5/8. A new rapid immunoperoxidase diagnostic staining of herpes simplex virus 1 indolent corneal ulcer.

    A tear film aspirate, from the lower fornix of a 64-year-old man with the clinical diagnosis of a herpes simplex indolent corneal ulcer, was examined via a new, rapid immunoperoxidase staining technique. This 4-hour modified immunoperoxidase stain is both sensitive and specific for herpes simplex virus type 1. The corneal epithelial cells shed in the tear film from the indolent ulcer were strongly positive for herpes simplex type 1 viral antigen using this new technique. This case report supports the theory that the pathogenesis of indolent herpetic corneal ulcers involves both a hypersensitivity response to viral antigen and an active viral infection.
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6/8. 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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7/8. Viral antigens in the immune ring of herpes simplex stromal keratitis.

    Corneal tissue obtained during superficial keratectomy from a patient with herpesvirus disciform keratitis was studied by immunoelectron microscopy. Clinically, this cornea had a dense central infiltrate with a circumferential opaque ring histologically resembling the immune ring described by Wessely. Histologically, along the line of altered keratocytes and ground substance, an infiltration of inflammatory cells was found. Herpesvirus particles were seen by electron microscopy in the corneal stroma, but these virus particles had abnormal, noninfective forms such as empty capsids and incomplete virions. By immunoelectron microscopy with a peroxidase-labeled antiherpesvirus antibody reagent, herpes-virus antigens were localized inthe corneal keratocytes and in the corneal stroma. The major localization of the virus antigens was in association with the herpes virions and surrounding vacuoles in the keratocyte nucleus and in the corneal stroma in the area of degenerating keratocytes. These findings support the view of a hypersensitivity mechanism in the pathogenesis of herpes simplex virus disciform keratitis.
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8/8. herpes simplex eye infections: clinical manifestations, pathogenesis and management.

    Herpes infection of the eye may be acquired as the patient's first exposure to the virus (primary infection) or as involvement of a new anatomical site (the eye) in a patient with previous HSV infection. In either case, patients with herpetic eye infection risk recurrent eye disease throughout their lives. The infective lesions of the corneal epithelium (dendritic and geographic ulcers) occasionally develop into noninfective indolent or trophic ulcers, particularly under the influence of cauterizing chemicals or corticosteroids. inflammation of the corneal stroma may accompany herpetic epithelial lesions or occur independently. Stromal keratitis probably represents the host's immune response to viral antigens filtering down from epithelial lesions or from viral replication in stromal cells. The clinical manifestations of ocular HSV infection are reviewed, pathogenesis and possible pathways of the infection are analyzed, and some practical guidelines for management and prevention are presented.
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