Detection Of Varicella-zoster Virus DNA Research Articles

Neurological complications of varicella zoster virus reactivation.

Varicella zoster virus (VZV) reactivation results in zoster, which may be complicated by postherpetic neuralgia, myelitis, meningoencephalitis, and VZV vasculopathy. This review highlights the clinical features, laboratory abnormalities, imaging changes, and optimal treatment of each of those conditions. Because all of these neurological disorders produced by VZV reactivation can occur in the absence of rash, the virological tests proving that VZV caused disease are discussed. After primary infection, VZV becomes latent in ganglionic neurons along the entire neuraxis. With a decline in VZV-specific cell-mediated immunity, VZV reactivates from ganglia and travels anterograde to the skin to cause zoster, which is often complicated by postherpetic neuralgia. VZV can also travel retrograde to produce meningoencephalitis, myelitis, and stroke. When these complications occur without rash, VZV-induced disease can be diagnosed by detection of VZV DNA or anti-VZV antibody in cerebrospinal fluid and treated with intravenous acyclovir. Awareness of the expanding spectrum of neurological complications caused by VZV reactivation with and without rash will improve diagnosis and treatment.

Association between viral load of varicella zoster virus in cerebrospinal fluid and the clinical course of central nervous system infection

Varicella zoster virus (VZV) like other alphaherpes viruses stays latent after its primary infection. During its reactivation, it can infect the central nervous system (CNS) causing a variety of clinical presentations. Using polymerase chain reaction (PCR) for detection of VZV DNA in cerebrospinal fluid (CSF), it is now recognized in some series as the most common causative agent of viral CNS infection. We aimed to investigate in our study the correlation between VZV viral load in the CSF and the clinical course of its infection, using quantitative real-time PCR. For this purpose, we examined 56 specimens of consecutive patients with positive CSF for VZV DNA in a qualitative test, with a clinical picture of meningitis or encephalitis collected over 10years in Rambam medical center. We found a significant correlation between VZV viral load and the severity and duration of neurological disease. We believe that using quantitative measurement of VZV DNA in the CSF, could serve as a prognostic marker which would influence treatment decisions.

A case of zoster sine herpete presenting with thoracic radicular pain diagnosed by polymerase chain reaction in skin exudate

Varicella zoster virus (VZV) can cause radicular pain in the absence of skin lesions; such cases are referred to as zoster sine herpete (ZSH) and are usually diagnosed by using serological assays or polymerase chain reaction (PCR). An effort is underway to detect VZV DNA in novel specimens rather than conventional samples (e.g., blood or cerebrospinal fluid) for PCR. There are two reports that PCR analysis in the exudate of the auricular skin can be a useful diagnostic tool for the diagnosis of ZSH in patients presenting with cranial nerve paralysis without herpetic eruptions. Here, we report a case of ZSH diagnosed by using PCR analysis of skin exudates in a patient who developed thoracic radicular pain. This is believed to be the first case of ZSH diagnosed using PCR analysis of skin exudate in a patient in whom the cranial nerve was not involved.

Search for varicella zoster virus DNA in saliva of healthy individuals aged 20–59 years

All neurological and ocular complications of varicella zoster virus (VZV) reactivation can occur without rash. Virological verification requires detection of VZV DNA or anti-VZV IgG antibody in cerebrospinal fluid (CSF), or anti-VZV IgM antibody in serum or CSF. If VZV were readily detected in other tissue in patients with neurological disease without rash and found to correlate with tests listed above, more invasive tests such as lumbar puncture might be obviated. Saliva is a potential source of VZV DNA. To study the potential diagnostic value of detecting VZV DNA in saliva from patients with neurological disease, saliva of healthy adults was searched for VZV DNA. A single saliva sample obtained by passive drool was centrifuged at 16,000g for 20 min. DNA was extracted from the supernatant and cell pellet and examined in triplicate for VZV DNA by real time PCR. A single random saliva sample from 80 healthy men and women aged 20-59 years revealed no VZV DNA (Table ), but was uniformly positive for cell (GAPdH) DNA. Because VZV DNA was not found in a random saliva sample from 80 individuals 20-59-year-old, a VZV-positive sample during neurologic disease may have potential significance. Further studies will determine whether VZV DNA in saliva correlates with VZV DNA or anti-VZV antibody in CSF in patients with neurological disease.

Editorial Commentary: Strokes and Infection With Varicella Zoster Virus

It was long assumed, before recent developments proved otherwise, that the presence of an infection with varicella zoster virus (VZV) was inevitably associated with a rash. We now know, due to the use of polymerase chain reaction (PCR) and other methods that have improved diagnosis, that patients can harbor infections with VZV even in the absence of cutaneous manifestations Such “occult” VZV infections often affect the nervous and gastrointestinal systems. Central nervous system (CNS) VZV infections without rash were initially identified at autopsy [1] and subsequently in patients with meningitis through the PCR detection of VZV DNA in cerebrospinal fluid (CSF) [2]. Although there appears to be a relationship between VZV infection and arterial ischemic stroke (AIS) [3], these patients also do not display a rash when they develop symptoms involving the CNS. In the current issue of Clinical Infectious Diseases, Thomas et al describe the connection between varicella and subsequent AIS in children. They used 4 large databases and a self-controlled case series, analyzing data from strokes in the varicella cases. Data were analyzed 0–6 months after an episode of varicella and again at a later time. This method avoids confounding factors and is efficient at relating a rare condition, such as stroke in childhood, to a common infection, varicella, although it does not provide information on the absolute risk of postvaricella stroke. Thomas et al’s study revealed that in the 6 months following varicella, the incidence of childhood stroke is increased by a factor of approximately 4. There was no significant increase in strokes in adults after varicella, nor was there any increase in strokes 7– 12 months after varicella in children. The pathogenesis of postvaricella stroke is not known, but VZV can infect cerebral arteries, which provokes inflammatory responses that damage the infected arteries and may lead to aneurysms [4–6]. Because the interval between an episode of varicella and a stroke can be as long as 6 months, reactivation of latent VZV acquired during varicella, rather than a smoldering persistent infection in arteries, seems more likely to cause AIS, although either possibility remains plausible. The VZV that infects arteries could be delivered from sensory neurons in which VZV reactivates or as a result of a viremia. It may well be that most strokes following varicella are, in reality, strokes following zoster without rash. When one such stroke develops, there may be recurrences [7]. Strokes may also follow classic zoster, particularly when the ophthalmic branch of the trigeminal nerve is involved. It is conceivable that AIS after varicella in children is a manifestation of a rare defect in innate immunity described in certain severe alpha herpesvirus infections [8–12]. One mystery is why VZV would be at increased risk for reactivation soon after varicella. This timing may reflect the putative immunologic predisposition. Clearly, additional knowledge of the state of VZV prior to infection of cerebral arteries, as well as the immunologic status of the host who has experienced a VZV-induced stroke, is needed. A relationship between zoster and stroke was appreciated before postvaricella stroke was recognized. At first termed giant cell arteritis, it now appears that this vasculitis syndrome is similar to what is termed VZV vasculopathy [13]. VZV vasculopathy may be a subset of giant cell arteritis. It was recognized historically that in the months following zoster, patients (usually adults) might manifest symptoms of stroke ipsilateral to the side of the body where zoster occurred. Because strokes in children are unusual or rare, this increase in CNS disease from varicella, albeit serious to individuals, is not a major public health problem. The morbidity (which may be long-lasting) Received 16 September 2013; accepted 18 September 2013; electronically published 2 October 2013. Correspondence: Anne A. Gershon, MD, Department of Pediatrics, Columbia University College of Physicians and Surgeons, 622 W 168th St, PH 19-110, New York, NY 10032 (aag1@columbia.edu). Clinical Infectious Diseases 2014;58(1):69–71 © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com. DOI: 10.1093/cid/cit663

Complications of varicella zoster virus reactivation.

Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), which can occur anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of pain usually takes 4-6 weeks. Zoster can be followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, meningoencephalitis, cerebellitis, myelopathy, multiple ocular disorders and vasculopathy that can mimic giant cell arteritis. All of the neurological and ocular disorders listed above may also develop without rash. Diagnosis of VZV-induced neurological disease may require examination of cerebrospinal fluid (CSF), serum and/ or ocular fluids. In the absence of rash in a patient with neurological disease potentially due to VZV, CSF should be examined for VZV DNA by PCR and for anti-VZV IgG and IgM. Detection of VZV IgG antibody in CSF is superior to detection of VZV DNA in CSF to diagnose vasculopathy, recurrent myelopathy, and brainstem encephalitis. Oral antiviral drugs speed healing of rash and shorten acute pain. Immunocompromised patients require intravenous acyclovir. First-line treatments for post-herpetic neuralgia include tricyclic antidepressants, gabapentin, pregabalin, and topical lidocaine patches. VZV vasculopathy, meningoencephalitis, and myelitis are all treated with intravenous acyclovir.

Varicella zoster virus quantitation in blood from symptomatic and asymptomatic individuals

Primary infection with varicella zoster virus (VZV) occurs in immunocompromised and immunocompetent individuals. Clinical and asymptomatic reactivation with shedding of infectious virus and viremia may occur. The prevalence of VZV viremia is unknown. The aim of this study was to detect VZV viremia and quantify VZV DNA using quantitative polymerase chain reaction (qPCR) in blood from different populations. A qPCR-based method using EvaGreen® was used to quantify VZV DNA in 491 samples, including whole blood, plasma and buffy-coat, from patients hospitalized with varicella-associated disease (Group 1, n=10) and three groups with no VZV disease: individuals with a first clinical diagnosis of central nervous system demyelination (Group 2, n=213) with their age and sex-matched controls (Group 3, n=218); and HIV-infected individuals (Group 4, n=50). VZV-specific IgG antibody titres were measured in Group 3. The proportion positive for viremia and mean detectable VZV DNA load (copies/ml) were: Group 1: 100% (10/10) and 4.6 × 10(6) ± 1.4 × 10(7) ; Group 2: 4% (9/213) and 1.5 × 10(3) ± 1.8 × 10(4) ; Group 3: 8% (17/218) and 1.1 × 10(3) ± 7.8 × 10(3) ; Group 4: 12% (6/50) and 7.7 × 10(1) ± 2.8 × 10(2) . VZV DNA load and IgG titres were not significantly correlated (Group 3 only). VZV load in Group 1 was significantly elevated compared to Groups 2-4 (P<0.001); the latter were not significantly different from each other (P=0.05). VZV genotypes from clades 1-5 were identified in Group 1. VZV DNA was detected but at low frequency and viral load in both immunocompetent and immunocompromised individuals asymptomatic for VZV infection, compared to individuals with active VZV infection.

Sampling of herpes zoster skin lesion types and the impact on viral DNA detection

This was a multicenter, non-therapeutic study to determine the optimal type of lesion sample for quantitative PCR detection of varicella zoster virus (VZV) DNA in herpes zoster patients. Up to three crusts, three crust swabs, three vesicle swabs, and three papule swabs were collected from 41 adults with clinically diagnosed herpes zoster. 83% of subjects had at least one valid crust swab (detectable VZV or β-actin DNA), 78% had at least one valid crust, 78% had at least one valid vesicle swab, and 32% had at least one valid papule swab. Of valid samples, 97% of crusts, 94% of vesicle swabs, 90% of crust swabs, and 84% of papule swabs were VZV-DNA-positive (≥10 DNA copies/sample). 37 (90%) subjects had at least one VZV DNA-positive sample. VZV DNA copy numbers were highest for vesicle swabs and crusts. The probability of a false-negative result was 5% for crusts, 6% for vesicle swabs, 14% for papule swabs, and 24% for crust swabs. Overall, vesicle swabs and crusts were the most specific and sensitive samples for detecting VZV.

Chickenpox-related Pulmonary Granulomas in Immunocompetent Adults

Pulmonary granulomas represent a common inflammatory reaction to several lung infective or noninfective diseases. However, little is known about the histology and clinical presentation of chickenpox-related granulomas in immunocompetent subjects. We collected a series of 8 adult patients (mean age, 40 y; range, 33 to 53 y) with several bilateral pulmonary granulomas incidentally discovered after imaging studies. All patients were asymptomatic and had experienced a varicella-zoster virus (VZV) infection as adults but were clinically suspected to have a metastatic neoplasm of unknown origin. Chest computed tomography scan revealed numerous, tiny (few millimeters to 1 cm in size) nodules randomly dispersed through the lungs. Positron emission tomography scan performed in 4 patients was negative. All patients underwent video-assisted thoracoscopic surgical resection and were still alive and well. At histology, granulomas consisted of well-defined, rounded, small nodules centered by a deeply eosinophilic, acellular necrosis rimmed by lamellar dense collagen and a chronic inflammatory infiltrate with or without multinucleated giant cells. Chickenpox-related granulomas were included in the differential diagnosis along with several other granulomatous diseases. Polymerase chain reaction-based molecular analysis for VZV performed on paraffin sections detected VZV DNA in all 8 cases. By contrast, 85 cases of pulmonary granulomas of different etiologies were simultaneously studied by molecular analysis with negative results. Pathologists should be familiar with the peculiar morphologic appearance of chickenpox-related granulomas. A careful search for a history of VZV infection in adulthood and molecular studies may be very helpful in confirming the diagnosis.

Persistence of Varicella Zoster Virus DNA in Saliva After Herpes Zoster

Analysis of saliva samples from individuals aged ≥ 60 years who had a history of zoster (group 1), zoster and postherpetic neuralgia (PHN; group 2), or no history of zoster (group 3) revealed varicella zoster virus (VZV) DNA in saliva samples from 11 of 17 individuals in group 1, 10 of 15 individuals in group 2, and 2 of 17 individuals in group 3. The frequency of VZV DNA detection was significantly higher (P = .001) in saliva of subjects with a history of zoster, with or without PHN (21 [67%] of 32 subjects in groups 1 and 2), than in saliva of age-matched subjects with no zoster history (2 [12%] of 17 subjects in group 3). Thus, persistence of VZV DNA in saliva is the outcome of zoster, independent of PHN. Because VZV infection can produce neurological and ocular disease without zoster rash, future studies are needed to establish whether VZV DNA can be detected in the saliva of such patients.

Persistence of Varicella Zoster Virus DNA in Saliva After Herpes Zoster

Analysis of saliva samples from individuals aged ≥ 60 years who had a history of zoster (group 1), zoster and postherpetic neuralgia (PHN; group 2), or no history of zoster (group 3) revealed varicella zoster virus (VZV) DNA in saliva samples from 11 of 17 individuals in group 1, 10 of 15 individuals in group 2, and 2 of 17 individuals in group 3. The frequency of VZV DNA detection was significantly higher (P = .001) in saliva of subjects with a history of zoster, with or without PHN (21 [67%] of 32 subjects in groups 1 and 2), than in saliva of age-matched subjects with no zoster history (2 [12%] of 17 subjects in group 3). Thus, persistence of VZV DNA in saliva is the outcome of zoster, independent of PHN. Because VZV infection can produce neurological and ocular disease without zoster rash, future studies are needed to establish whether VZV DNA can be detected in the saliva of such patients.

The History and Mystery of VZV in Saliva

The History and Mystery of VZV in Saliva

Early detection of Varicella-Zoster Virus (VZV)-specific T-cells before seroconversion in primary varicella infection: case report

Here we report the case of a 54-year old, immunocompetent German patient with primary varicella whose Varicella-Zoster Virus (VZV)-specific T-cell responses could be detected early in infection and before the onset of seroconversion. This case demonstrates that the detection of VZV-specific T-cells may under certain circumstances support the diagnosis of a primary varicella infection, as for example in cases of atypical or subclinical varicella or in the absence of detectable VZV DNA in plasma.

Detection of varicella‐zoster virus DNA in 414 human trigeminal ganglia from cadavers by the polymerase chain reaction: A comparison of the detection rate of varicella‐zoster virus and herpes simplex virus type 1

Investigation of varicella-zoster virus (VZV) is important epidemiologically, and determination of its prevalence rate in human trigeminal ganglia is important to provide surveillance data. To date, studies on VZV detection in trigeminal ganglia have used specimens obtained from a relatively limited number of cadavers. This study attempted to detect VZV DNA as well as Herpes simplex virus type 1 (HSV-1) DNA by the polymerase chain reaction (PCR) from 414 samples of trigeminal ganglia obtained from 207 cadavers selected at random. The detection rate was examined to determine whether there were significant differences in the positive rate between the left and right trigeminal ganglia, males and females, and among age groups. A relationship was found between the positive rates for VZV and HSV-1. VZV DNA was detected in 391 of the trigeminal ganglia (94.4%) and 201 of the cadavers (97.1%) in 121/124 males and 80/83 females. HSV-1 DNA was detected in 251 of the samples (60.6%) and 134 of the cadavers (64.7%) in 72/124 males and 62/83 females. There was no significant difference for either virus in the detection rates between the left and right trigeminal ganglia and males and females. Age and positivity for HSV-1, but not VZV, showed a significant relationship. All 134 cadavers positive for HSV-1 were also positive for VZV. VZV and HSV-1 become latent in bilateral trigeminal ganglia, and are not affected by gender. The prevalence of HSV-1 was greater in advanced age, and the HSV-1-positive rate was correlated with the VZV-positive rate.

Varicella Zoster Virus (VZV) in Solid Organ Transplant Recipients

-herpesvirus family. VZV is presentworldwide and is highly infectious. Primary infection leadsto acute varicella or ‘chickenpox,’ usually from exposureeither through direct contact with a skin lesion or throughairborne spread from respiratory droplets (1,2). After initialinfection, VZV establishes lifelong latency in cranial nerveanddorsalrootganglia,andcanreactivateyearstodecadeslater as herpes zoster (HZ) or ‘shingles’ (3). More than90% of adults in the United States acquired the disease inchildhood, while the majority of children and young adultshave been vaccinated with the live virus vaccine (2,4).Primary varicella typically presents with fever, constitu-tional symptoms and a vesicular, pruritic, widely dissem-inated rash that primarily involves the trunk and face (5).Thesymptomsusuallyresolvewithin7–10days,butinrarecases primary varicella leads to more severe disease andvisceral invasion. Complications, such as hepatitis, pancre-atitis, pneumonitis and encephalitis are infrequent but canbelife-threatening;adultsandveryyoungchildrenaremorelikely to develop such complications from primary infection(6,7). Rates of hospitalization and mortality due to varicellahave dropped with the institution of routine childhood vari-cella vaccination (8,9).Nearly all patients with HZ develop an exanthem of vesic-ular lesions in a dermatomal distribution. The annual inci-dence of HZ in the general population is 1.5–3.0 cases per1000 persons (2), and is estimated to occur in up to 20%of individuals during their lifetime (10). Secondary compli-cations such as bacterial superinfection and postherpeticneuralgia (PHN), or chronic neuropathic pain at the site ofHZ, lead to increased morbidity (11).Over 90% of adult solid organ transplant (SOT) recipientswill be seropositive for VZV. Rates are lower in pediatrictransplants(12,13),butimmunitywillincreaseasuptakeofvaricella vaccine improves. Varicella is rare in adult SOT re-cipients,butcanbedevastating,withvisceralinvolvement,severe skin disease, and disseminated intravascular coag-ulation (14–19). HZ is a frequent infectious complication inSOT recipients with an incidence of approximately 8–11%during the first 4 years posttransplant (20–22). Invasive dis-ease and dissemination similar to that seen in primary VZVinfection are uncommon but have been reported in SOTand other immunocompromised populations, and level ofimmunosuppression may alter the risk of developing thesecomplications (17,23,24). Rates of PHN in SOT recipi-ents may also be higher than in immunocompetent popu-lations (22).

Viremia in Acute Herpes Zoster

A phase 2 trial was conducted to evaluate the efficacy of a topical antiviral, sorivudine, as an adjuvant to valacyclovir for the treatment of acute herpes zoster. In this randomized, placebo-controlled, double-blind trial, 25 patients were treated with either sorivudine or placebo cream. All patients began 7 days of valacyclovir treatment on day 3. Zoster lesion swab samples and samples of peripheral blood mononuclear cells were collected periodically throughout the study and were analyzed for varicella-zoster virus (VZV) DNA by use of both qualitative and real-time polymerase chain reaction. Serum samples collected periodically throughout the study were analyzed for VZV DNA by use of real-time polymerase chain reaction. VZV DNA was detected in all 3 sample types, and the number of viral copies correlated with the progression of herpes zoster. No statistically significant differences were seen between the placebo- and sorivudine-treated groups with respect to clinical characteristics or laboratory test results. The detection of VZV DNA in the serum and peripheral blood mononuclear cells of all 25 zoster patients documents that viremia is a common manifestation of herpes zoster. Sorivudine cream appears to be a safe and well-tolerated adjuvant therapy; however, further phase 2 studies are needed to determine its clinical efficacy for the treatment of herpes zoster. Trials registration. ClinicalTrials.gov identifier: NCT00652184.

The varicella zoster virus vasculopathies: Clinical, CSF, imaging, and virologic features

Background: Varicella zoster virus (VZV) vasculopathy produces stroke secondary to viral infection of cerebral arteries. Not all patients have rash before cerebral ischemia or stroke. Furthermore, other vasculitides produce similar clinical features and comparable imaging, angiographic, and CSF abnormalities. Methods: We review our 23 published cases and 7 unpublished cases of VZV vasculopathy. All CSFs were tested for VZV DNA by PCR and anti-VZV IgG antibody and were positive for either or both. Results: Among 30 patients, rash occurred in 19 (63%), CSF pleocytosis in 20 (67%), and imaging abnormalities in 29 (97%). Angiography in 23 patients revealed abnormalities in 16 (70%). Large and small arteries were involved in 15 (50%), small arteries in 11 (37%), and large arteries in only 4 (13%) of 30 patients. Average time from rash to neurologic symptoms and signs was 4.1 months, and from neurologic symptoms and signs to CSF virologic analysis was 4.2 months. CSF of 9 (30%) patients contained VZV DNA while 28 (93%) had anti-VZV IgG antibody in CSF; in each of these patients, reduced serum/CSF ratio of VZV IgG confirmed intrathecal synthesis. Conclusions: Rash or CSF pleocytosis is not required to diagnose varicella zoster virus (VZV) vasculopathy, whereas MRI/CT abnormalities are seen in almost all patients. Most patients had mixed large and small artery involvement. Detection of anti-VZV IgG antibody in CSF was a more sensitive indicator of VZV vasculopathy than detection of VZV DNA ( p GLOSSARY: EIA = enzyme immunoabsorbent assay; VZV = varicella zoster virus.

A case of acute aseptic meningitis associated with herpes zoster

=Abstract= Herpes zoster is caused by the varicella-zoster virus (VZV), which affects nerve ganglions. VZV infection may be associated with neurologic complications, which are usually observed after vesicular exanthem. Acute aseptic meningitis is a rare compli- cation of VZV reactivation. We report the case of a previously healthy 14-year-old boy who suffered from aseptic meningitis that was attributed to reactivated VZV infection with exanthem; the patient had undergone vaccination against varicella. This condition can be confirmed by the detection of VZV DNA in the cerebrospinal fluid. The patient was treated with acyclovir and recovered fully. (Korean J Pediatr 2009;52:705-709)

The varicella zoster virus vasculopathies

Varicella zoster virus (VZV) vasculopathy produces stroke secondary to viral infection of cerebral arteries. Not all patients have rash before cerebral ischemia or stroke. Furthermore, other vasculitides produce similar clinical features and comparable imaging, angiographic, and CSF abnormalities. We review our 23 published cases and 7 unpublished cases of VZV vasculopathy. All CSFs were tested for VZV DNA by PCR and anti-VZV IgG antibody and were positive for either or both. Among 30 patients, rash occurred in 19 (63%), CSF pleocytosis in 20 (67%), and imaging abnormalities in 29 (97%). Angiography in 23 patients revealed abnormalities in 16 (70%). Large and small arteries were involved in 15 (50%), small arteries in 11 (37%), and large arteries in only 4 (13%) of 30 patients. Average time from rash to neurologic symptoms and signs was 4.1 months, and from neurologic symptoms and signs to CSF virologic analysis was 4.2 months. CSF of 9 (30%) patients contained VZV DNA while 28 (93%) had anti-VZV IgG antibody in CSF; in each of these patients, reduced serum/CSF ratio of VZV IgG confirmed intrathecal synthesis. Rash or CSF pleocytosis is not required to diagnose varicella zoster virus (VZV) vasculopathy, whereas MRI/CT abnormalities are seen in almost all patients. Most patients had mixed large and small artery involvement. Detection of anti-VZV IgG antibody in CSF was a more sensitive indicator of VZV vasculopathy than detection of VZV DNA (p < 0.001). Determination of optimal antiviral treatment and benefit of concurrent steroid therapy awaits studies with larger case numbers.

Triad of Severe Abdominal Pain, Inappropriate Antidiuretic Hormone Secretion, and Disseminated Varicella-Zoster Virus Infection Preceding Cutaneous Manifestations After Hematopoietic Stem Cell Transplantation

A hematopoietic stem cell transplant recipient developed abdominal pain, pneumatosis intestinalis, hepatitis, pancreatitis, and inappropriate antidiuretic hormone secretion. Blood for varicella-zoster virus (VZV) DNA polymerase chain reaction was positive. She was treated with acyclovir and subsequently developed VZV antigen-positive zoster. Detection of VZV DNA in blood may be useful for early diagnosis in immunocompromised hosts who present with zoster without skin lesions.