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Donald H. Gilden - One of the best experts on this subject based on the ideXlab platform.
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Varicella-Zoster Virus Infections of the Nervous System
2009Co-Authors: Bette K. Kleinschmidt-demasters, Donald H. GildenAbstract:Abstract Background.—Diseases that present with protean manifestations are the diseases most likely to pose diagnostic challenges for both clinicians and pathologists. Among the most diverse disorders caused by a single known toxic, metabolic, neoplastic, or infectious agent are the central and peripheral nervous system complications of Varicella-Zoster Virus (VZV). Methods.—The pathologic correlates of the neurologic complications of VZV infection, as well as current methods for detecting viral infections, are discussed and presented in pictorial format for the practicing pathologist. Results.—Varicella-Zoster Virus causes chickenpox (Varicella), usually in childhood; most children manifest only mild neurologic sequelae. After chickenpox resolves, the Virus becomes latent in neurons of cranial and spinal ganglia of nearly all individuals. In elderly and immunocompromised individuals, the Virus may reactivate to produce shingles (Zoster). After Zoster resolves, many elderly patients experience postherpeti...
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Multifocal Varicella-Zoster Virus vasculopathy without rash.
Archives of neurology, 2003Co-Authors: Andrew Russman, Richard J. Lederman, Leonard H. Calabrese, Peter J. Embi, Bagher Forghani, Donald H. GildenAbstract:51-year-oldwomanwithCRESTsyndrome(calcinosis,Raynaudphenomenon,esophageal dysmotility, sclerodactyly, and telangiectasia) developed stepwise progressive focal neurological deficits without Zoster rash. Multifocal ischemic infarcts were seen on magnetic resonance imaging, and cerebral angiography revealed focal stenosis of arteries affecting the intracranial circulation. A brain biopsy was nondiagnostic. Virological etiology of the disease was verified by the detection of Varicella-Zoster Virus antibody in cerebrospinal fluid and by reduced serum–cerebrospinal fluid Varicella-Zoster Virus IgG ratios (compared with normally high ratios of total IgG and albumin). Treatment with intravenous acyclovir stabilized but did not significantly improve her neurological deficits. Arch Neurol. 2003;60:1607-1609 The main central nervous system complication of Varicella-Zoster Virus (VZV) reactivation is vasculopathy. Both unifocal and multifocal vasculopathy usually developsdaystoweeksafterZosterrash.Multifocal VZV vasculopathy may also occur without rash, thus making diagnosis difficult. Herein, we describe a patient with multifocal central nervous system vasculopathy without rash that was confirmed virologicallytobecausedbyVZV.Thisreport illustrates the need for early antiviral treatment, and emphasizes the diagnostic value of VZV antibody detection in the serum and cerebrospinal fluid (CSF).
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Neurologic complications of the reactivation of Varicella-Zoster Virus.
The New England journal of medicine, 2000Co-Authors: Donald H. Gilden, Ravi Mahalingam, Bette K. Kleinschmidt-demasters, James J. Laguardia, Randall J. CohrsAbstract:Varicella–Zoster Virus is an exclusively human herpesVirus that causes chickenpox (Varicella), becomes latent in cranial-nerve and dorsal-root ganglia, and frequently reactivates decades later to produce shingles (Zoster) and postherpetic neuralgia. In immunocompetent elderly persons or immunocompromised patients, Varicella–Zoster Virus may produce disease of the central nervous system. Since the last major review of Varicella–Zoster Virus in the Journal, 1,2 advances in molecular biology have provided important new insights into the pathogenesis of infection with Varicella–Zoster Virus. The detection of Varicella–Zoster Virus in blood vessels and other tissues by methods based on the polymerase chain reaction (PCR) has widened the recognized . . .
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Fatal Varicella-Zoster Virus meningoradiculitis without skin involvement
Annals of neurology, 1991Co-Authors: Aud N. Dueland, Mary Devlin, John R. Martin, Ravi Mahalingam, Randall J. Cohrs, Herbert J. Manz, Irene K. Trombley, Donald H. GildenAbstract:A 77-year-old man with T-cell lymphoma developed an acute fatal meningoradiculitis of cranial nerve roots and cauda equina, pathologically and virologically confirmed to be caused by Varicella-Zoster Virus. This is the first report of fatal Varicella-Zoster Virus-induced neurological disease in the absence of skin lesions. Varicella-Zoster Virus should be included in the differential diagnosis of acute radiculoneuropathy in the immunocompromised patient, particularly because antiviral treatment for Varicella-Zoster Virus exists.
A Kijlstra - One of the best experts on this subject based on the ideXlab platform.
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longitudinal analysis of Varicella Zoster Virus dna on the ocular surface associated with herpes Zoster ophthalmicus
American Journal of Ophthalmology, 2001Co-Authors: Michel J W Zaal, Hennie J Volkerdieben, M Wienesen, J Damaro, A KijlstraAbstract:Abstract PURPOSE: Longitudinal analysis of Varicella-Zoster Virus DNA on the ocular surface of patients with herpes Zoster ophthalmicus. METHODS: Clinical specimens were obtained from the bulbar conjunctival surface with a cotton-tipped swab at weekly intervals for 6 consecutive weeks from 21 patients with acute ophthalmic Zoster with a skin rash duration of less than 7 days. All patients received oral valacyclovir 1000 mg three times daily for 10 days without additional corticosteroids. The swabs were analyzed by means of polymerase chain reaction for the presence of Varicella-Zoster Virus and herpes simplex Virus type 1 DNA. Conjunctival swabs were also obtained from a control group of 20 patients with cataract. RESULTS: On inclusion, Varicella-Zoster Virus DNA was present on the ocular surface of 19 of the 21 patients. Six Varicella-Zoster Virus DNA–positive patients had no signs of ocular inflammation. All control swabs were negative for both Varicella-Zoster Virus and herpes simplex Virus DNA. The duration of Varicella-Zoster Virus DNA detection from rash onset varied from 2 to 34 days. The number of days between the onset of herpes Zoster skin rash and the latest positive Varicella-Zoster Virus DNA test was significantly longer in patients whose age was equal to or above the median age of 66 years than in the younger patients (Mann-Whitney test: P = .0004). At 6-week follow-up, all conjunctival swabs were negative for Varicella-Zoster Virus DNA. However, at that time, the eyes of seven patients were still inflamed. CONCLUSION: The duration of Varicella-Zoster Virus DNA shedding in herpes Zoster ophthalmicus is highly variable and age dependent, and is probably related to the host immune response.
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Longitudinal analysis of Varicella-Zoster Virus DNA on the ocular surface associated with herpes Zoster ophthalmicus
American journal of ophthalmology, 2001Co-Authors: Michel J W Zaal, M Wienesen, Hennie J. Völker-dieben, J. D'amaro, A KijlstraAbstract:Abstract PURPOSE: Longitudinal analysis of Varicella-Zoster Virus DNA on the ocular surface of patients with herpes Zoster ophthalmicus. METHODS: Clinical specimens were obtained from the bulbar conjunctival surface with a cotton-tipped swab at weekly intervals for 6 consecutive weeks from 21 patients with acute ophthalmic Zoster with a skin rash duration of less than 7 days. All patients received oral valacyclovir 1000 mg three times daily for 10 days without additional corticosteroids. The swabs were analyzed by means of polymerase chain reaction for the presence of Varicella-Zoster Virus and herpes simplex Virus type 1 DNA. Conjunctival swabs were also obtained from a control group of 20 patients with cataract. RESULTS: On inclusion, Varicella-Zoster Virus DNA was present on the ocular surface of 19 of the 21 patients. Six Varicella-Zoster Virus DNA–positive patients had no signs of ocular inflammation. All control swabs were negative for both Varicella-Zoster Virus and herpes simplex Virus DNA. The duration of Varicella-Zoster Virus DNA detection from rash onset varied from 2 to 34 days. The number of days between the onset of herpes Zoster skin rash and the latest positive Varicella-Zoster Virus DNA test was significantly longer in patients whose age was equal to or above the median age of 66 years than in the younger patients (Mann-Whitney test: P = .0004). At 6-week follow-up, all conjunctival swabs were negative for Varicella-Zoster Virus DNA. However, at that time, the eyes of seven patients were still inflamed. CONCLUSION: The duration of Varicella-Zoster Virus DNA shedding in herpes Zoster ophthalmicus is highly variable and age dependent, and is probably related to the host immune response.
Randall J. Cohrs - One of the best experts on this subject based on the ideXlab platform.
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Varicella Zoster Virus infection
Nature Reviews Disease Primers, 2015Co-Authors: Anne A. Gershon, Randall J. Cohrs, Judith Breuer, Jeffrey I. Cohen, Charles Grose, Michael D. Gershon, Don Gilden, Sophie Hambleton, Peter G. E. Kennedy, Michael N. OxmanAbstract:Infection with Varicella Zoster Virus (VZV) causes Varicella (chickenpox), which can be severe in immunocompromised individuals, infants and adults. Primary infection is followed by latency in ganglionic neurons. During this period, no Virus particles are produced and no obvious neuronal damage occurs. Reactivation of the Virus leads to Virus replication, which causes Zoster (shingles) in tissues innervated by the involved neurons, inflammation and cell death — a process that can lead to persistent radicular pain (postherpetic neuralgia). The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other Zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke (vasculopathy), retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is the only human herpesVirus for which highly effective vaccines are available. After Varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to Varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent Varicella and one to prevent Zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases. For an illustrated summary of this Primer, visit: http://go.nature.com/14xVI1 Varicella Zoster Virus (VZV) causes Varicella (chickenpox) and, upon reactivation following latency, Zoster (shingles). In this Primer, the authors discuss VZV pathogenesis, diagnosis, treatment and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases.
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Neurologic complications of the reactivation of Varicella-Zoster Virus.
The New England journal of medicine, 2000Co-Authors: Donald H. Gilden, Ravi Mahalingam, Bette K. Kleinschmidt-demasters, James J. Laguardia, Randall J. CohrsAbstract:Varicella–Zoster Virus is an exclusively human herpesVirus that causes chickenpox (Varicella), becomes latent in cranial-nerve and dorsal-root ganglia, and frequently reactivates decades later to produce shingles (Zoster) and postherpetic neuralgia. In immunocompetent elderly persons or immunocompromised patients, Varicella–Zoster Virus may produce disease of the central nervous system. Since the last major review of Varicella–Zoster Virus in the Journal, 1,2 advances in molecular biology have provided important new insights into the pathogenesis of infection with Varicella–Zoster Virus. The detection of Varicella–Zoster Virus in blood vessels and other tissues by methods based on the polymerase chain reaction (PCR) has widened the recognized . . .
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Fatal Varicella-Zoster Virus meningoradiculitis without skin involvement
Annals of neurology, 1991Co-Authors: Aud N. Dueland, Mary Devlin, John R. Martin, Ravi Mahalingam, Randall J. Cohrs, Herbert J. Manz, Irene K. Trombley, Donald H. GildenAbstract:A 77-year-old man with T-cell lymphoma developed an acute fatal meningoradiculitis of cranial nerve roots and cauda equina, pathologically and virologically confirmed to be caused by Varicella-Zoster Virus. This is the first report of fatal Varicella-Zoster Virus-induced neurological disease in the absence of skin lesions. Varicella-Zoster Virus should be included in the differential diagnosis of acute radiculoneuropathy in the immunocompromised patient, particularly because antiviral treatment for Varicella-Zoster Virus exists.
Stephen E. Straus - One of the best experts on this subject based on the ideXlab platform.
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Varicella-Zoster Virus Infections
Annals of Internal Medicine, 2020Co-Authors: Stephen E. Straus, Jeffrey M. Ostrove, Genevieve Inchauspe, James M. Felser, Alison G. Freifeld, Kenneth D. Croen, Mark H. SawyerAbstract:Abstract During the last 10 years, there have been major advances in the understanding of Varicella-Zoster Virus and the diseases it causes. The molecular biology of the Virus is being unraveled wi...
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Recent Advances in Varicella-Zoster Virus Infection
Annals of internal medicine, 1999Co-Authors: Jeffrey I. Cohen, Stephen E. Straus, Philip Alfred Brunell, Philip R. KrauseAbstract:This conference paper focuses on recent developments in the biology, clinical presentation, treatment, and prevention of Varicella-Zoster Virus infections.
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In utero diagnosis of congenital Varicella Zoster Virus infection by chorionic villus sampling and polymerase chain reaction
American Journal of Obstetrics and Gynecology, 1991Co-Authors: N B Isada, D P Paar, M P Johnson, M I Evans, W Holzgreve, F Qureshi, Stephen E. StrausAbstract:Abstract Varicella Zoster Virus infection acquired in pregnancy is reported to cause fetal damage in 5% to 10% of cases. We used polymerase chain reaction to attempt molecular diagnosis of fetoplacental Varicella Zoster Virus infection in two patients. Tissue obtained by chorionic villus sampling in the second trimester was analyzed by polymerase chain reaction with a Varicella Zoster Virus-specific primer, ORF-63, and was found to be positive in both patients. Viral cultures were negative. One patient elected pregnancy termination at 23 weeks. Southern blot hybridization of neonatal brain tissue for Varicella Zoster Virus was negative. The second patient carried the pregnancy to term and was delivered of a normal infant. Varicella Zoster Virus immunoglobulin M and viral cultures were negative. The presence of viral deoxyribonucleic acid sequences in placental tissue does not correlate with fetal disease. (AM J OBSTET GYNECOL 1991;165:1727-30.)
Todd P. Margolis - One of the best experts on this subject based on the ideXlab platform.
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A Polymerase Chain Reaction-based Assay for Diagnosing Varicella-Zoster Virus Retinitis in Patients With Acquired Immunodeficiency Syndrome
American journal of ophthalmology, 1997Co-Authors: Graham A. Short, Todd P. Margolis, Alexander R. Irvine, Baruch D. Kuppermann, Daniel F. Martin, Diane ChandlerAbstract:Purpose To develop a rapid, sensitive, and specific laboratory assay based on the polymerase chain reaction for the diagnosis of Varicella-Zoster Virus retinitis in patients with acquired immunodeficiency syndrome (AIDS). Methods We developed and tested a polymerase chain reaction-based assay for the detection of Varicella-Zoster Virus DNA in vitreous samples. We attempted to detect Varicella-Zoster Virus DNA in 14 vitreous samples from patients with AIDS and a clinical diagnosis of progressive outer retinal necrosis syndrome. For controls, we also attempted to detect Varicella-Zoster Virus DNA in vitreous samples from 75 immunocompetent patients with vitreoretinal disease and 88 patients with AIDS and vitreoretinal inflammatory disease not related to progressive outer retinal necrosis syndrome. Results Varicella-Zoster Virus DNA was detected in 11 of 14 vitreous samples from AIDS patients with progressive outer retinal necrosis syndrome. All three samples that scored negative for Varicella-Zoster Virus DNA came from eyes that had been treated aggressively with antiviral drugs and had clinically inactive disease at the time of vitreous biopsy. Varicella-Zoster Virus DNA was detected in only two of 75 control vitreous samples from immunocompetent patients with vitreoretinal disease and two of 88 control vitreous samples from patients with AIDS and vitreoretinal inflammatory disease not related to progressive outer retinal necrosis syndrome. Conclusion We have developed a rapid, sensitive, and specific polymerase chain reaction-based diagnostic assay for Varicella-Zoster Virus DNA that will assist in the diagnosis of Varicella-Zoster Virus retinitis in patients with AIDS.
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Varicella-Zoster Virus Retinitis in Patients With the Acquired Immunodeficiency Syndrome
American journal of ophthalmology, 1991Co-Authors: Todd P. Margolis, Careen Y. Lowder, Gary N. Holland, Richard F. Spaide, Andrew G. Logan, Scott S. Weissman, Alexander R. Irvine, Robert G Josephberg, David M. Meisler, James J. O'donnellAbstract:We examined five patients infected with the human immunodeficiency Virus who developed a rapidly progressive necrotizing retinitis characterized by early patchy choroidal and deep retinal lesions and late diffuse thickening of the retina. In all but one case, the retinitis began in the posterior pole with little or no clinical evidence of vasculitis. All five patients had relentless progression of disease and were left with atrophic and necrotic retinae, pale optic-nerve heads, and narrowed vasculature. None of the patients developed aqueous or vitreal inflammation or retinal detachment. Clinical and laboratory evidence suggested that Varicella-Zoster Virus was the causal agent in all five cases. First, the onset of retinitis in four cases either succeeded or was coincident with an eruption of dermatomal Zoster. Second, Varicella-Zoster Virus was cultured from the two chorioretinal specimens and Varicella-Zoster Virus antigen was detected in the vitreal aspirate from one case. Third, by means of immunocytochemistry, Varicella-Zoster Virus antigen was found in the outer retinae of both enucleation specimens. Fourth, viral capsids with the size and shape of herpesviridae were found in the outer retinae of both enucleation specimens. The clinical features observed in this study are distinct from those described for the acute retinal necrosis syndrome and appear to constitute a new and highly characteristic pattern of Varicella-Zoster Virus-induced disease.
