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)

Acute ocular infection followed both intracerebral and intranasal inoculation of herpes simplex type I virus (HSVI) in mice. Eye infections were a terminal complication of fatal encephalitis. After intracerebral inoculation HSVI spread directly along the optic nerves to infect the retina provoking a necrotizing retinitis. In contrast after intranasal inoculation, HSVI spread via the fifth cranial nerve to the anterior chamber of the eye producing keratitis and uveitis. Necrotizing retinitis was also produced by intracerebral inoculation of mice with a drug-resistant mutant HSVI known to have relatively low neurovirulence. These animals developed only mild encephalitis but this was associated with florid retinitis. The mice survived cerebral infection with the mutant virus and several weeks after initial inoculation cataracts were observed. There was no evidence, at any time, of virus infection of lens epithelium and cataracts appeared to be a non-specific consequence of retinal injury. It is suggested that these examples of murine ocular infection provide animal models for herpetic eye lesions in man and thus may elucidate the pathogenesis of herpetic keratitis, retinitis and cataract.
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PMID:An animal model of ocular herpes. Keratitis, retinitis and cataract in the mouse. 633 86

A 70 year-old-man with recurrent herpetic keratitis had a meningo-encephalitis with transient left hemiplegia and disorders of consciousness. EEG disclosed periodic slow waves on the right temporal region. Isotope and CT scans showed focal abnormalities in the same region. Antibodies to herpes simplex virus were demonstrated by complement fixation in serum and specific antiherpes IgG and IgM by immunofluorescence assay in serum and CSF. A year later the patient had a status epilepticus. CT scan showed a large right temporal hypodense area. CSF was abnormal with pleiocytosis, increased protein and IgG levels. High titers of antiherpes IgG persisted in serum and CSF. Neuropsychological tests did not demonstrate any memory impairment. The occurrence of persistent inflammation after herpes simplex encephalitis is discussed. The unusual benign course without antiviral therapy, may be related to the reactivation of a latent infection with an efficient immunological response. The unilateral temporal necrosis may explain the absence of amnestic sequelae.
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PMID:[Acute necrotizing herpetic encephalitis with a spontaneously improving clinical course]. 669 26

Herpesvirus type 1 thymidine-kinase-negative mutants are readily selected for in tissue culture and in humans by acyclovir, a promising antiviral agent. We investigated the ocular pathogenicity of thymidine-kinase-negative mutants in the rabbit. The natural course of untreated keratitis induced by the herpesvirus type 1 thymidine-kinase-negative strain was characterized by superficial dendrites and geographic ulcers that healed spontaneously without loss of corneal clarity. We also studied the relationship between herpesvirus type 1 thymidine-kinase activity and virulence in the rabbit with three strains of herpesvirus type 1: NIH thymidine-kinase-positive (100% thymidine-kinase activity), NIH thymidine-kinase-intermediate (25% thymidine-kinase activity), and NIH thymidine-kinase-negative (0% thymidine-kinase activity). Despite comparable ocular titers, the NIH thymidine-kinase-positive strain proved to be the most virulent, causing significantly (P less than .002) more keratitis, encephalitis, and death than the other strains.
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PMID:The role of herpesvirus type 1 thymidine kinase in experimental ocular infections. 682 49

A 72-year-old man developed bullous skin lesions two months before he was discovered to have malignant lymphoma. Herpes zoster virus grew from the skin bullae. He developed encephalitis, keratitis in the left eye, and bilateral retinitis 18 months later. Herpes simplex virus type 1 grew from cultures of the eyelid vesicles and corneal scrapings from the left eye. The patient died two years after the diagnosis of malignant lymphoma. Virus particles believed to be herpes simplex virus were demonstrated on electron microscopy in the necrotic retinal cells.
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PMID:Herpes simplex type 1 retinitis in an adult with systemic herpes zoster. 727 Jun 36

Herpetic stromal keratitis (HSK) has an immune-mediated pathogenesis that involves T cells that have a type 1 cytokine profile. IFN-gamma is suspected to be the type 1 cytokine involved in ocular pathology, and to test this notion more directly the pathogenesis of HSK was compared in mice deficient in the IFN-gamma gene (gamma knockout or gko) and control mice (wild-type littermates or BALB/c mice). The clinical course of HSK in gko mice closely paralleled that in control mice, yet virus persisted in the corneas of gko mice for an extended period of time, severe periocular skin lesions developed, and gko mice were far more susceptible to encephalitis. Delayed-type hypersensitivity to viral Ag was present, though diminished, in knockout mice, and serum herpes simplex virus-specific IgG isotypes indicated a Th2 shift. No differences existed in proliferative responses to in vitro Ag stimulation in gko vs control mice nor in T cell or proinflammatory cytokine mRNA levels in the corneas of infected mice. However, up-regulation of Th2 cytokine mRNA did occur in in vitro Ag-stimulated gko immune splenocytes. Histopathologic lesions were not statistically different between any of the groups of mice analyzed. These observations indicate that although IFN-gamma plays an important role in the clearance of virus from the eye, the pathogenesis of HSK lesions most likely involves additional cytokines, inflammatory mechanisms, or immune responses to nonviral Ags.
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PMID:Characterization of herpes simplex virus type-1 infection and herpetic stromal keratitis development in IFN-gamma knockout mice. 756 Nov 4

The authors tested the protective efficacy of, and the immune response to, immunisation with a synthetic peptide of glycoprotein D (gD) of HSV-1 in a murine model of herpes stromal keratitis (HSK). HSV-1 susceptible A/J mice were immunised subcutaneously with a peptide corresponding to the N-terminal epitope gD(5-23) prior to corneal HSV-1 challenge. Divergent immunisation protocols were compared for their protective potency, their ability to prevent the establishment of latency in the trigeminal ganglion, and their effect on the immune system. Low dosages (31 micrograms) of gD(5-23) protected against encephalitis and HSK. Protective efficacy was higher when gD(5-23) was coupled to the carrier protein keyhole limpet haemocyanin (KLH) and was emulsified with adjuvant. Latent infection was found in all control mice but in only 50-75% of immunised mice. The most potent protection was correlated with anti-HSV-1 neutralising antibodies of IgG1 and IgG2a isotypes, but free gD(5-23) protected in the absence of anti-HSV-1 antibodies. Our results suggest that immunisation with gD(5-23) stimulates both humoral and cellular immune mechanisms which protect against HSV-1 keratitis.
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PMID:Immunisation against HSV-1 keratitis with a synthetic gD peptide. 771 56

It has been previously shown that the strain of virus, immune competence of the host, and innate resistance of the host have an effect on the severity of ocular disease induced by topical infection with herpes simplex virus type 1 (HSV-1). This study has expanded on earlier work by examining the effect of virus inoculum and host age on mortality, incidence of ocular disease, and severity of ocular disease. BALB/c mice were infected with inocula ranging from 2 x 10(3) to 1 x 10(6) pfu of HSV-1 strain CJ394. The most significant effect of variation in the inoculum was on the percent of mice developing disease. Increasing the inoculum resulted in significantly increased disease incidence, but at 5 x 10(3) pfu/mouse or higher, there was little difference in disease severity in those animals exhibiting symptoms. Decreasing host age also resulted in a significant increase in the incidence of ocular disease, but the dependence of disease severity on host age varied with the symptom being scored. In animals exhibiting disease, the peak severity of stromal keratitis and vascularization of the cornea were unaffected by host age. However, the severity of blepharitis was significantly reduced in older mice. Increasing host age also resulted in increased resistance to encephalitis. Three to four-week old mice were very susceptible to encephalitis (100% mortality), while only 20% of 4-5 week old mice died by day 15 post-infection. Mice older than 5 weeks were completely resistant to lethal encephalitis after corneal infection.
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PMID:The effect of viral inoculum level and host age on disease incidence, disease severity, and mortality in a murine model of ocular HSV-1 infection. 776 6

Infections of the cornea with herpes simplex virus type 1 cause inflammatory lesions which frequently lead to blindness. The disease is suspected to be immunopathological in nature. To establish this point and to study possible mechanisms involved, corneal infections in C.B-17 scid/scid and cell-reconstituted scid mice were investigated. Whereas unreconstituted scid mice failed to develop herpetic stromal keratitis (HSK) and died of encephalitis, mice reconstituted with T lymphocytes generated severe lesions. T cells of the CD4+ subset were found to be essential mediators of the HSK lesion, while T cells of the CD8+ subset protected mice from lethality. The results confirm that HSK is an immunopathological disease and that scid mice provide a convenient model that should prove valuable in establishing the biochemical mechanisms by which HSK is mediated.
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PMID:Herpetic stromal keratitis in the reconstituted scid mouse model. 809 78

Replication-defective mutants of herpes simplex virus type 1 (HSV-1) were used as a new means to immunize mice against HSV-1-mediated ocular infection and disease. The effects of the induced immune responses on pathogenesis of acute and latent infection by challenge virus were investigated after corneal inoculation of immunized mice with virulent HSV-1. A single subcutaneous injection of replication-defective mutant virus protected mice against development of encephalitis and keratitis. Replication of the challenge virus at the initial site of infection was lower in mice immunized with attenuated, wild-type parental virus (KOS1.1) or replication-defective mutant virus than in mice immunized with uninfected cell extract or UV-inactivated wild-type virus. Significantly, latent infection in the trigeminal ganglia was reduced in mice given one immunization with replication-defective mutant virus and was completely prevented by two immunizations. Acute replication in the trigeminal ganglia was also prevented in mice immunized twice with wild-type or mutant virus. The level of protection against infection and disease generated by immunization with replication-defective mutant viruses was comparable to that of infectious wild-type virus in all cases. In addition, T-cell proliferative and neutralizing antibody responses following immunization and corneal challenge were of similar strength in mice immunized with replication-defective mutant viruses or with wild-type virus. Thus, protein expression by forms of HSV-1 capable of only partially completing the replication cycle can induce an immune response in mice that efficiently decreases primary replication of virulent challenge virus, interferes with acute and latent infection of the nervous system, and inhibits the development of both keratitis and systemic neurologic disease.
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PMID:Immunization with replication-defective mutants of herpes simplex virus type 1: sites of immune intervention in pathogenesis of challenge virus infection. 828 72

Acanthamoeba, a free-living ameba of soil and water, produces the rare infections of granulomatous amebic encephalitis and amebic keratitis. We report a 38-year-old white man with the acquired immunodeficiency syndrome (AIDS) who experienced Acanthamoeba infection that presented as multiple skin nodules without associated encephalitis. Histologic examination revealed necrotizing granulomatous inflammation with numerous amebic organisms that were cultured and identified as Acanthamoeba group 2, probably Acanthamoeba castellani by monoclonal antibodies. Results of in vitro susceptibility testing demonstrated resistance to all six tested drugs. A partial clinical response, however, was obtained with multidrug therapy.
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PMID:Cutaneous Acanthamoeba infection in the acquired immunodeficiency syndrome: response to multidrug therapy. 856 15


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