Cases reported "Eye Infections, Viral"

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11/86. Sight-threatening varicella zoster virus infection after fludarabine treatment.

    Varicella zoster virus (VZV) infection involving the posterior segment of the eye after fludarabine treatment has not previously been described. Two patients, who had completed fludarabine treatment 3 and 18 months previously, presented with visual loss that had been preceded by a recent history of cutaneous zoster. The use of the polymerase chain reaction (PCR) for VZV dna from ocular specimens allowed rapid confirmation of clinical diagnosis and treatment with a good outcome in one patient. With the increasing use of fludarabine and other purine analogues, an awareness of such complications is important because of their potentially sight-threatening consequences.
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12/86. ganciclovir for the treatment of anterior uveitis.

    BACKGROUND: ganciclovir, administered systemically or intraocularly, is effective in controlling cytomegalovirus (CMV) retinitis in immunocompromised patients. The efficacy of therapy with this antiviral substance was investigated in an immunocompetent patient with CMV uveitis causing secondary glaucoma. methods: To identify the presence of an intraocular viral infection, anterior chamber taps to detect the intraocular synthesis of IgG antibodies and PCR testing were carried out. Clinically, the degree of intraocular inflammation and the intraocular pressure (IOP) values were monitored. During this time, the patient was treated systemically with ganciclovir administered orally and intravenously. RESULTS: The intraocular synthesis of IgG antibodies specific for CMV was found in two samples of aqueous humor, but negative for other viruses. PCR testing was negative for HSV, VZV and CMV at each time. During this time, the patient was treated systemically with ganciclovir administered either intravenously or orally. As a response to therapy with ganciclovir, the elevated IOP values decreased to normal and the intraocular inflammation declined. After cessation of ganciclovir administration, the inflammation and secondary glaucoma recurred. CONCLUSION: In this case of anterior uveitis presumably caused by CMV inducing secondary glaucoma, treatment with ganciclovir led to a decrease of the inflammation and normalization of IOP. It appears that continuous administration may be required to control the infection in an immunocompetent patient.
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13/86. Latent intracellular Epstein-Barr Virus dna demonstrated in ocular posttransplant lymphoproliferative disorder mimicking granulomatous uveitis with iris nodules in a child.

    A case of intraocular posttransplant lymphoproliferative disorder (PTLD) is described in a 9-year-old female who underwent orthotopic liver transplantation at the age of 18 months. The prevalence of ophthalmic involvement in PTLD can be expected to rise with the increasing number of major organ transplantations, as well as improved survivorship. Children are particularly at risk for this posttransplant complication because they are usually seronegative for the Epstein-Barr virus (EBV) prior to transplant. Accurate diagnostic classification of PTLD to include confirmation of EBV infection carries significant therapeutic and prognostic implications.
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14/86. Coexistent adenoviral keratoconjunctivitis and acanthamoeba keratitis.

    A 17-year-old youth presented with bilateral follicular conjunctivitis and nummular subepithelial corneal infiltrates. Failure of this to settle in an outpatient setting led to corneal scraping with microscopy and culturing for bacteria, fungi, herpes simplex, adenovirus and Acanthamoeba as an inpatient. polymerase chain reaction analysis of corneal cells was positive for adenovirus, and culture on live escherichia coli-coated agar plates was positive for Acanthamoeba by phase contrast microscopy on day two. We conclude that Acanthomoeba infection can complicate adenoviral keratoconjunctivitis. This observation is in keeping with previously reported modes of infection by Acanthamoeba, whereby any epithelial breach seems to allow inoculation of the eye by this opportunistic organism.
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15/86. New corneal findings in human T-cell lymphotrophic virus type 1 infection.

    PURPOSE: Human T-cell lymphotrophic virus type 1 is a rna retrovirus that primarily affects CD4 T-cells. Human T-cell lymphotrophic virus type 1 infection is the established cause of adult T-cell leukemia/lymphoma, an aggressive malignancy of CD4 T-cells, and two nonneoplastic conditions: human T-cell lymphotrophic virus type 1-associated myelopathy/tropical spastic paraparesis and human T-cell lymphotrophic virus type 1 uveitis. Other reported ophthalmic manifestations of human T-cell lymphotrophic virus type 1 infection include lymphomatous and leukemic infiltrates in the eye and ocular adnexa in patients with adult T-cell leukemia/lymphoma, retinal pigmentary degeneration, and neuro-ophthalmic disorders in patients with human T-cell lymphotrophic virus type 1-associated myelopathy/tropical spastic paraparesis and keratoconjunctivitis sicca, episcleritis, and sclerouveitis in asymptomatic human T-cell lymphotrophic virus type 1 carriers. This report describes the ocular findings in three Jamaican patients with human T-cell lymphotrophic virus type 1 infection and adult T-cell leukemia/lymphoma. methods: The clinical records of three patients with human T-cell lymphotrophic virus type 1 infection and adult T-cell leukemia/lymphoma examined at the National eye Institute were reviewed. Each patient had one or more complete ophthalmic evaluations. RESULTS: All three patients had corneal abnormalities, including corneal haze and central opacities with thinning; bilateral immunoprotein keratopathy; and peripheral corneal thinning, scarring, and neovascularization. All three patients had elevated serum immunoglobulin levels. CONCLUSIONS: We believe that the novel corneal findings in these patients are most likely a consequence of the hypergammaglobulinemia induced by the human T-cell lymphotrophic virus type 1 infection or the T-cell malignancy.
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ranking = 1.8
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16/86. herpes simplex virus type 1 corneal infection results in periocular disease by zosteriform spread.

    In humans and animal models of herpes simplex virus infection, zosteriform skin lesions have been described which result from anterograde spread of the virus following invasion of the nervous system. Such routes of viral spread have not been fully examined following corneal infection, and the possible pathologic consequences of such spread are unknown. To investigate this, recombinant viruses expressing reporter genes were generated to quantify and correlate gene expression with replication in eyes, trigeminal ganglia, and periocular tissue. Reporter activity peaked in eyes 24 h postinfection and rapidly fell to background levels by 48 h despite the continued presence of viral titers. Reporter activity rose in the trigeminal ganglia at 60 h and peaked at 72 h, concomitant with the appearance and persistence of infectious virus. Virus was present in the periocular skin from 24 h despite the lack of significant reporter activity until 84 h postinfection. This detection of reporter activity was followed by the onset of periocular disease on day 4. Corneal infection with a thymidine kinase-deleted reporter virus displayed a similar profile of reporter activity and viral titer in the eyes, but little or no detectable activity was observed in trigeminal ganglia or periocular tissue. In addition, no periocular disease symptoms were observed. These findings demonstrate that viral infection of periocular tissue and subsequent disease development occurs by zosteriform spread from the cornea to the periocular tissue via the trigeminal ganglion rather than by direct spread from cornea to the periocular skin. Furthermore, clinical evidence is discussed suggesting that a similar mode of spreading and disease occurs in humans following primary ocular infection.
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ranking = 2.2
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17/86. Acute retinal necrosis in children caused by herpes simplex virus.

    PURPOSE: To report the diagnosis, management, and outcome of acute retinal necrosis syndrome in children. METHOD: Case series of three consecutive children aged 11 years and younger who were diagnosed with acute retinal necrosis. In addition to full ocular and systemic examinations, the children underwent vitreous biopsy (patients 1 and 2) or aqueous tap (Patient 3) for polymerase chain reaction analysis. RESULTS: All patients had unilateral retinitis that was associated with preexisting chorioretinal scars, and two patients (patients 1 and 3) had concurrent extraocular central nervous system abnormalities. Intraocular herpes simplex virus was detected in all three children: Type 1 in Patient 1 and Type 2 in patients 2 and 3. In addition, all three children had a history of extraocular herpes simplex virus infection. CONCLUSIONS: retinitis associated with preexisting chorioretinal scars and detectable intraocular herpes simplex virus on polymerase chain reaction was common to all three children with acute retinal necrosis.
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18/86. cytomegalovirus as a cause of anterior uveitis with sectoral iris atrophy.

    OBJECTIVE: To report two cases of recurrent anterior uveitis with sectoral iris atrophy and ocular hypertension during attacks caused by cytomegalovirus (CMV). DESIGN: Two observational case reports. PARTICIPANTS: Two immunocompetent patients with a history of recurrent unilateral hypertensive anterior uveitis with sectoral iris atrophy were referred to us with the presumptive diagnosis of herpetic uveitis. MAIN OUTCOME MEASURES: Comprehensive ophthalmic examination, aqueous humor polymerase chain reaction (PCR), and peripheral blood serologic studies were performed on both patients. RESULTS: Examination of aqueous humor by PCR was positive for CMV and negative for herpesvirus. serum IgG/IgM titers disclosed past CMV infection. Both patients responded well to antiviral therapy with ganciclovir. The final visual acuity level was 20/20 in both eyes of both patients. CONCLUSIONS: CMV infection can produce recurrent attacks of anterior uveitis with clinical characteristics indistinguishable from those previously considered highly suggestive or even pathognomonic for herpetic infection. This observation has implications for the therapeutic management of such patients.
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ranking = 0.6
keywords = infection
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19/86. optic disk vasculitis associated with chronic active Epstein-Barr virus infection.

    PURPOSE: To report two cases of optic disk vasculitis associated with chronic active Epstein-Barr virus infection (CAEBV). METHOD: We examined the eyes of two patients with CAEBV. RESULTS: In the first case, a 6-year-old boy, visual acuity was 20/20 in both eyes. Papillary and peripapillary exudates were observed in the right eye. fluorescein angiography showed hyperfluorescence of the optic disk and a leakage from the peripapillary retinal vessels in the right eye. Two months later, the exudates increased and preretinal hemorrhages appeared in the right eye. visual acuity decreased to 20/60. He was treated with systemic administration of corticosteroid, globulin and acyclovir. visual acuity returned to 20/20, but peripapillary exudates remained in the right eye. In the second case, a 16-year-old girl, visual acuity was 20/20 in both eyes. The right eye showed optic disk swelling and dilated retinal veins. fluorescein angiography showed hyperfluorescence of the optic disk but no leakage from the retinal vessels. Visual field examination revealed an enlarged blind spot in the right eye in both cases. These ocular manifestations are compatible with those of optic disk vasculitis, which shows swelling of the optic disk and dye leakage on and around the optic disk in fluorescein angiography, with an almost normal visual acuity and an enlargement of the blind spot. CONCLUSION: Persistent Epstein-Barr virus infection may cause optic disk vasculitis.
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ranking = 1.2
keywords = infection
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20/86. Human T-cell lymphotropic virus type-1 associated t-cell leukemia/lymphoma masquerading as necrotizing retinal vasculitis.

    OBJECTIVE: To report a case of adult T-cell leukemia/lymphoma (ATL) presenting as a bilateral retinal vasculitis and diagnosed by molecular detection of a rearrangement in the T-cell receptor (TCR) and the presence of the human T-cell lymphotropic virus type 1 (HTLV-1) pol gene in the malignant lymphoid cells. DESIGN: Case report. methods: Routine histologic and immunohistochemical analyses were performed on the retinal biopsy specimen before referral to the National eye Institute. Lymphoid cells associated with granulomatous inflammation infiltrating the retina and surrounding retinal blood vessels were microdissected from the paraffin sections of the retinal biopsy specimen. The polymerase chain reaction (PCR) was performed using primers for the TCR gene and HTLV-1 pol and gag genes. RESULTS: Microscopic examination showed a necrotizing granulomatous retinal vasculitis with a predominant T-cell infiltrate detected by immunohistochemistry. Molecular analysis demonstrated a clonal rearrangement of the TCR and the presence of the HTLV-1 pol gene in the microdissected lymphoid cells diagnostic of ATL. CONCLUSIONS: Necrotizing retinitis and retinal vasculitis are rare manifestations of ATL. Human T-cell lymphotropic virus type 1 infection should be considered in the differential diagnosis of patients from endemic areas who have retinal vasculitis at presentation. This case further demonstrates the usefulness of microdissection and PCR for the diagnosis of ocular disease, including HTLV-1 infection.
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ranking = 0.4
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