Operationalizing a Hub-and-Spoke Telemedicine Model for Mpox Surveillance in a High-Alert, Zero-Prevalence Setting: An Observational Study, Real-World Experience From Iran.

A 65-year-old right-handed woman with history of nonsmall-cell-lung cancer (NSCLC) metastatic to the brain presented to the emergency room with right facial weakness. She was diagnosed with lung cancer 3 months prior after a workup for persistent cough and dyspnea. Biopsy revealed poorly differentiated NSCLC. Staging brain magnetic resonance imaging (MRI) showed multiple enhancing lesions consistent with metastatic disease to the CNS. She received a cycle of Carboplatin and paclitaxel and whole brain irradiation. Two days prior to admission, she underwent stereotactic radiosurgery (SRS) for residual metastatic disease following administration of intravenous steroids. These lesions were cortically based and not in the typical location of the gray–white junction (Fig. 1). Significantly, none of these metastatic lesions (left medial parietal region, left parietal region, right frontal cystic lesion and right superior frontal region) was close to the brain stem or the right 7th cranial nerve. On admission, spinal fluid evaluation showed glucose of 80 mg/dl, protein of 108 mg/dl, 80 white blood cells (85% lymphocytes), and 15 red blood cells. Cytology (14 cc) evaluation was negative for malignant cells. The patient was treated empirically with Valacyclovir and two additional spinal fluid evaluations were obtained to rule out carcinomatous meningitis (12 and 10 cc, respectively). On the forth hospital day a vesicular rash was noted over the patient’s right ear (Fig. 2). Cerebrospinal Varicella Zoster virus (VZV) PCR returned positive. The patient was diagnosed with Ramsay Hunt syndrome and anti-viral treatment was continued for 2 weeks. This case emphasizes the importance of meticulous evaluation in a patient presenting with cranial neuropathy and metastatic cancer. If no other diagnosis was found, the patient would have met the criteria for presumed carcinomatous meningitis [1] and may have received chemotherapy. Unfortunately, not all patients with Ramsay Hunt syndrome develop a rash [2] and even though VZV PCR is highly specific, it is positive in only about 44% of the cases [3].

Case presentation: A 58-year-old woman with hypertension, type 2 diabetes, dyslipidemia, and childhood epilepsy, was brought to the hospital due to a 12-day history of confusion, inattention, spatial disorientation, and incoherent speech, with an insidious onset and progressive course. Two days before admission, she developed aggressive and hypersexualized behavior, nausea and emesis. Upon admission, she had stable vital signs, no skin lesions, was agitated, disoriented and aphasic. An initial cranial CT scan showed no abnormalities. Lumbar puncture revealed an opening pressure of 43 cmH2O, cerebrospinal fluid (CSF) analysis showed 355 cells/µL (83% lymphocytes), protein of 219 mg/dL and positive PCR for Varicella-zoster virus (VZV), with other microbiological tests negative. An EEG at admission showed lateralized rhythmic delta activity and bilateral frontotemporal epileptiform discharges. Cranial MR angiography revealed cerebral venous thrombosis in the left sigmoid sinus and internal jugular vein. She was treated with intravenous acyclovir for 14 days and enoxaparin 1mg/kg bid, showing clinical and electroencephalographic improvement, and was discharged without sequelae for outpatient follow-up on anticoagulation with direct oral anticoagulant (DOAC). Discussion: VZV is a neurotropic herpesvirus. It causes varicella (chicken pox) as a primary infection, after which the virus remains latent in different ganglionic neurons, capable of reactivating during immunosuppression or advanced age. CNS involvement by VZV is uncommon, particularly in immunocompetent population, occurring in both primary infection and reactivation, and can manifest as diffuse encephalitis, acute cerebellar ataxia, myelitis, stroke, polyneuropathy, and aseptic meningitis. Acute diffuse encephalitis more frequently affects adults, presenting with delirium, seizures, and focal neurological signs. The most accurate diagnostic method for viral encephalitis is VZV PCR in CSF. Current data suggest VZV as an emerging cause of encephalitis in young, immunocompetent patients. Although skin lesions are a hallmark of the disease, up to 50% of reported cases of VZV neurological complications occur without cutaneous manifestations. This case features two unusual characteristics of VZV CNS involvement: varicella encephalitis not preceded by a rash, in an immunocompetent patient younger than 60 years. Final comments: We describe an atypical case of an immunocompetent patient with acute varicella-zoster meningoencephalitis without preceding rash, complicated by a cerebral thrombotic event. This condition is classically described more frequently in immunosuppressed individuals. However, This case highlights the importance of considering VZV in the differential diagnosis of encephalitis presentations in immunocompetents.

The objective of this study was to assess the impact of the Enhanced Recovery After Surgery (ERAS) programme implementation on treatment costs at a university-type centre, using the DRG scheme. Retrospective analysis of patients' data in a group of 604 individuals enroled in the study. We evaluated three groups of patients according to the ERAS clinical protocol (CP): (1) CP oncogynaecology, (2) CP simple hysterectomy, (3) CP laparoscopy. The study aimed to evaluate the impact on the length of stay (LOS), savings in bed-days, and the reduction in direct treatment costs. Three parameters-antibiotic consumption, blood derivative consumption and laboratory test costs-were chosen to compare direct treatment costs. The statistical significance of the difference in the observed parameters was tested by a two-sample unpaired t test with unequal variances at the 0.05 significance level. We analysed data from 604 patients. In all three groups, the length of stay (LOS) was significantly reduced. The most significant reduction was observed in the CP oncogynaecology group, where the LOS was reduced from 11.1 days to 6.8 days (2022) and 7.6 days (2023) compared to 2019 (p < 0.05). Furthermore, there was a notable reduction in inpatient bed-days, which resulted in the capacity being made available to admit additional patients. A statistically significant reduction in direct costs was observed in the group of CP hysterectomy (antibiotic use) and in the CP laparoscopy (laboratory test costs). The implementation of the ERAS principles resulted in a number of significant positive economic impacts-reduction in the LOS and a corresponding increase in bed capacity for new patients. Additionally, direct treatment costs, including those related to antibiotic use or laboratory testing were reduced. The Czech Republic's acute healthcare system, like the majority of European healthcare systems, is financed by the DRG system. This flat-rate payment per patient encourages hospital management to seek cost-reduction strategies. The results of our study indicate that fast-track protocols represent a potential viable approach to reducing the cost of treatment while simultaneously meeting the recommendations of evidence-based medicine.

Varicella zoster virus (VZV) causes infections of the central nervous system (CNS) manifesting as meningitis or encephalitis. It is not commonly tested in CNS infections when compared with enterovirus (EV) and herpes simplex virus 1 (HSV-1) and 2 (HSV-2). Cerebrospinal fluid (CSF) findings of viral CNS infections are thought to be comparable. To describe the manifestations of VZV CNS infections and ascertain if there is a predominant syndrome. To compare CSF parameters of VZV with EV, HSV-1 and HSV-2. Retrospective study at two hospitals in Brisbane, reviewing medical notes and laboratory information system for results between January 2001 and 2019. The following parameters were recorded - disease classification, presence of rash, duration of symptoms prior to hospitalisation, length of admission, duration of antiviral treatment and 30-day mortality. CSF biochemistry, cell count (differential), PCR for VZV, EV, HSV-1 and HSV-2 were recorded. Statistical analysis of CSF parameters included Student's t-test and linear regression. Incidence of meningitis was comparable to encephalitis (44 vs 39%) in 52 cases. CSF protein in VZV was significantly elevated compared with EV (median 1121 vs 569 mg/L; P < 0.001) as was CSF monocytosis (96% vs 61%; P < 0.001). CSF parameters between VZV, HSV-1 and HSV-2 were similar. VZV had a higher incidence than HSV-1 or 2, while it was tested one-third as often. VZV CNS infection cannot be predicted by syndrome. CSF findings are markedly different from EV but like HSV-1 and 2. VZV should be routinely tested with HSV-1 and 2 when viral CNS infection is suspected.

Post Varicella-Zoster virus transverse myelitis: Diagnostic and therapeutic challenges – A case report and literature review

Zoster in childhood is an unusual occurrence and probably even less common after varicella-zoster virus (VZV) immunization.1-5 We report a normal child with no history of varicella who developed uncomplicated zoster caused by natural VZV 12 days after VZV immunization. The rates of zoster in children and the possible role of varicella immunization in the stimulation of natural VZV occurrence are reviewed. Case report. HV is a 6-year-old boy with no personal or family history of varicella. It is not known whether his mother had varicella during her pregnancy with him. The child had had no serious prior infections, HIV risk factors or other evidence of immunodeficiency. Because of the negative chickenpox history, he received one dose of the varicella vaccine (Varivax; Merck and Co., West Point, PA) in the right arm. He experienced intermittent fevers for 8 days, as high as 40.0°C. with no other physical findings. No other laboratory evaluations were done during this time. Twelve days after the immunization he had onset of a pruritic rash beginning on his back and extending to the posterior portion of his left arm. When seen 3 days later, 15 days after the immunization, he was afebrile, complained of nausea and vomiting for 3 days and had a vesicular rash in a left second thoracic dermatome pattern on his back and extending to the posterior aspect of his left arm. Viral cultures were obtained as were specimens for VZV PCR; prochlorperazine was prescribed for nausea and ibuprofen for mild pain. Nine days later there was complete crusting of all lesions, resolution of pain and no further complaints. The viral cultures were negative for herpes simplex virus and VZV. VZV sample preparation and PCR amplification were performed as previously described.6, 7 Briefly 2 sets of primer pairs were used to amplify a 222-base pair (bp) fragment in gene 54 and a 350-bp fragment in gene 38 of the VZV genome. The 222-bp product contains an asymmetrically placed BglI restriction site present in the Oka vaccine strain and in ∼15 to 20% of American wild-type strains. The 350-bp product contains an asymmetrically placed PstI restriction site present in all known wild-type strains but is absent in the vaccine strain. Ethidium bromide-stained amplified product (8 μl) was then visualized under ultraviolet light after electrophoresis in a 1.8% agarose gel. If the expected bands were seen, then 60 μl of remaining amplified product were divided into two aliquots which were digested with the restriction endonucleases, BglI and PstI. The products of digestion were then separated by electrophoresis in a 4% agarose gel. The pattern of the bands produced by the two digestions were compared with those of wild-type and vaccine strains. VZV-negative controls are included in every assay. If no VZV DNA was amplified, the presence of amplifiable DNA was assessed by subjecting these specimens to a second amplification using a primer pair that amplifies a 268-bp fragment of the human beta-globin gene. Analysis of the patient's sample demonstrated a pattern consistent with wild-type varicella-zoster virus. Discussion. Zoster in a normal child is an unusual occurrence. In several population-based studies the rate of zoster in children ages 0 to 19 years was from 0.63 to 1.6/1000 person years.1-3 The rate in children age 6 years ranged from 0.3 to 1.5/1000 person years.1-3 It is generally agreed that varicella occurring in the first year of life is associated with a higher risk of zoster,1, 4 although this finding is not uniform.3 It is not clear when the child in the present case was first infected with VZV because the disease was either asymptomatic or so mild as to be inapparent to the child and his family. There are few data regarding the risk of zoster after VZV immunization. The risk of zoster in 9454 healthy children after immunization was 0.18/1000 person year (8 cases in 44 994 person years followed). The one positive culture recovered was of natural VZV. The time from immunization ranged from 1.2 to 5.8 years.5, 8 Review of the world's literature on PCR or culture-confirmed zoster in VZV-immunized healthy9-11 and leukemic12 children and the 1 adult case13 revealed 12 published cases. Six were wild type. None of the 12 cases occurred before 32 days postimmunization. In immunocompromised children, the risk of zoster after immunization is considerably lower than that after natural varicella infection.14-17 Indeed receipt of a booster dose of vaccine or a household exposure to varicella further decreased the risk of zoster in immunized leukemic children.12 A population-based study has provided evidence that a high intensity of varicella transmission suppresses viral reactivation.18 The risk of zoster has been associated with lower cell-mediated immunity to VZV in infants and in children with leukemia after immunization.16, 19 VZV immunization has been shown to increase cell-mediated immunity in older individuals.20 A large long term placebo-controlled VZV immunization trial is ongoing to determine whether VZV immunization can decrease the rate of zoster in the elderly, a group with particularly high rates of zoster (M Oxman, personal communication, 1998). It is against this background that we report a child with the onset of zoster caused by natural VZV shortly after receiving VZV immunization. The probability of a normal 6-year-old having zoster in a given 2-week period are 1 to 5/100 000 person years.1-3 It would be even lower for a child with a negative history for chickenpox, as in the present case. While this case may be an extraordinary coincidence, it mandates a careful review of all cases of zoster occurring after VZV immunization and their time from immunization that have been reported in postmarketing surveys. A statistical analysis by investigators at Merck using the adverse vaccine reports database is ongoing to determine whether cases of zoster caused by natural VZV are closely related to VZV immunization. Induction of natural zoster by immunization could result from cytokine stimulation of viral emergence from latency or from transient viral-induced immunosuppression. Zoster induced by VZV immunization could have special implications for the use of immunization to prevent zoster in the elderly, a population with almost uniform VZV latent virus and higher risks for zoster. Steve Kohl, M.D. Jonathan Rapp, M.D. Phillip La Russa, M.D. Anne A. Gershon, M.D. Sharon P. Steinberg, B.S. Departments of Pediatrics and Family and Community Medicine; University of California, San Francisco; San Francisco General Hospital; San Francisco, CA (SK, JR) Department of Pediatrics; Columbia University College of Physicians and Surgeons; New York, NY (PLR, AAG, SPS)

Varicella-zoster virus (VZV) infection may trigger the inflammatory cascade that characterizes giant cell arteritis (GCA). Formalin-fixed, paraffin-embedded GCA-positive temporal artery (TA) biopsies (50 sections/TA) including adjacent skeletal muscle and normal TAs obtained postmortem from subjects >50 years of age were examined by immunohistochemistry for presence and distribution of VZV antigen and by ultrastructural examination for virions. Adjacent regions were examined by hematoxylin & eosin staining. VZV antigen-positive slides were analyzed by PCR for VZV DNA. VZV antigen was found in 61/82 (74%) GCA-positive TAs compared with 1/13 (8%) normal TAs (p < 0.0001, relative risk 9.67, 95% confidence interval 1.46, 63.69). Most GCA-positive TAs contained viral antigen in skip areas. VZV antigen was present mostly in adventitia, followed by media and intima. VZV antigen was found in 12/32 (38%) skeletal muscles adjacent to VZV antigen-positive TAs. Despite formalin fixation, VZV DNA was detected in 18/45 (40%) GCA-positive VZV antigen-positive TAs, in 6/10 (60%) VZV antigen-positive skeletal muscles, and in one VZV antigen-positive normal TA. Varicella-zoster virions were found in a GCA-positive TA. In sections adjacent to those containing VZV, GCA pathology was seen in 89% of GCA-positive TAs but in none of 18 adjacent sections from normal TAs. Most GCA-positive TAs contained VZV in skip areas that correlated with adjacent GCA pathology, supporting the hypothesis that VZV triggers GCA immunopathology. Antiviral treatment may confer additional benefit to patients with GCA treated with corticosteroids, although the optimal antiviral regimen remains to be determined.

Background: Varicella-zoster virus meningoencephalitis is an uncommon complication in immunocompetent adults. Typically, most patients present with neurological symptoms within 7-10 days of onset of rash . Also neurological symptoms preceding the rash or in the absence of the rash are rare. Methods: A 50 year-old female experienced urinary and bowel retention and numbness of heel for three days. She had a painful rash on her right thigh eight weeks earlier. MRI was normal. VZV PCR was positive in the CSF. Her neurological symptoms resolved with Acyclovir. A 23 year-old woman experienced left lower extremity weakness and numbness of right leg and abdomen and urinary retention for one week. She had decreased pin prick in right leg up to T8 level. Serum Hepatitis B and Varicella Zoster virus antibodies were positive. MRI showed restricted diffusion and T2/FLAIR hyperintensity in the pons, mid brain and medial temporal lobe. She was treated with steroids and IVIG. After one month she developed fever, blurry vision and vesicular rash on left forearm. Skin biopsy was positive for Varicella zoster virus antibody. Retinal necrosis was found to be consistent with Varicella zoster virus infection. Patient improved neurologically on Valtrex 1 gm TID. An 84-year-old male had symptoms of severe radicular thoracic pain, urinary and bowel incontinence for one week. MRI of the Thoracolumbar spine showed an intradural, intramedullary enhancing lesion at the T7-T8 level with extensive edema. Autopsy revealed viral encephalomyelitis involving the medulla and multiple foci within the spinal cord with inflammation, necrosis, along with Cowdry viral inclusions consistent with Varicella-zoster virus. Conclusion: The above mentioned cases high light atypical presentation of varicella zoster virus infection.The possibility of varicella zoster virus infection should be considered in patients presenting with un explained myelopathy and restricted diffusion changes, mass lesion or un usual CNS symptoms. Importance: Multiple neurologic complications may follow the reactivation of varicella-zoster virus (VZV), including herpes zoster, vasculopathies, myelitis, retinitis, and zoster sine herpete (pain without rash). Myelitis is one of the rarest neurological complications of vzv infection. Observations: We report three cases of VZV myelitis, two of them were immunocompetent and in two myelitis was associated with concomitant cerebral and brain stem strokes. Conclusions and Relevance: In immunocompetent patient VZV myelitis can manifest in the absence of a rash. Diffusion weighted images on MRI can be normal in the setting of acute myelitis due to VZV infection requiring CSF VZV PCR analysis to make prompt diagnosis and appropriate early treatment can lead to full recovery. Oral treatment for VZV rash does not preclude development of myelitis and may require intravenous antiviral medications to treat the infection subsequently. VZV infection can present as mass lesion of the spinal cord. Concomitant cerebral hemisphere and brain stem ischemic lesions and myelitis can occur due to vzv infection.

PurposeDespite being an extremely successful procedure, recurrent disc herniation is one of the most common post-discectomy complications in the lumbar spine and contributes significant health care and socioeconomic costs. Patients with large annular defects are at a high risk for reherniation, but an annular closure device (ACD) has been designed to reduce reherniation risk in this population and may, in turn, help control direct health care costs after discectomy.Patients and methodsThis analysis examined the 90-day post-discectomy cost estimates among ACD-treated (n=272) and control (discectomy alone; n=278) patients in a randomized controlled trial (RCT). Direct medical costs were estimated based on 2017 Humana and Medicare claims. Index discectomies were assumed to occur in an outpatient (OP) setting, whereas repeat discectomies were assumed to be 60% in OP and 40% in inpatient (IP). A sensitivity analysis was performed on this assumption. The device cost was not included in the analysis in order to focus on costs in the 90-day post-operative period.ResultsWithin 90 days of follow-up, post-operative complications occurred in 3.3% of the ACD patients and 8.6% of the control patients (P=0.01). The average 90-day cost to treat an ACD patient was $10,257 compared to $11,299 per control patient for a 80:20 distribution of Commercial:Medicare coverage ($1,042 difference). This difference varied from $687 with 100% Medicare to $1,132 with 100% Commercial coverage. Varying the IP vs OP distribution resulted in a cost difference range of $968 to $1,156 with the ACD.ConclusionAugmenting discectomy with an ACD in high-risk patients with a large annular defect reduced reherniation and reoperation rates, which translated to a reduction of direct health care costs between $687 and $1,156 per patient during the 90-day post-operative period. Large annular defect patients are an easily identifiable high-risk population. Operative strategies that reduce complication risks in these patients, such as the ACD, could be advantageous from both patient care and economic perspectives.

Varicella vaccination in a child with acute lymphoblastic leukaemia

This case describes a 4-year-old female with a history of ataxia telangiectasia (AT) with compound heterozygous variants (ATM; c.1339C&amp;gt;T (p.Arg447*) and c.829G&amp;gt;T (p.Glu277*)) who received measles, mumps, rubella (MMR) live vaccine and varicella zoster virus (VZV) vaccination in error in the setting of moving and change of pediatrician. After receiving live vaccines, she was referred to the immunology clinic. She had no concerning symptoms and was started on IgG replacement for low IgG level (474 mg/dL). One month later, the patient developed an itchy rash and fever, diagnosed as a coxsackie infection. Four months following vaccination, the patient presented to her hematologist for scheduled evaluation and was noted to have facial palsy and sent to the emergency room for evaluation. Over the preceding few weeks, her parents had started to notice some slurring of words and her walking had become unstable with frequent falls and increasingly difficult time ambulating. Emergency room evaluation was significant for tachycardia without fever, right-sided facial droop with conjunctival injection, diffuse weakness, and healing skin lesions. Lab findings at the time showed stable lymphopenia. A lumbar puncture was performed with positive VZV PCR. Peripheral blood was also positive for VZV PCR. MRI brain was performed which showed nonspecific global inflammation which was consistent with VZV encephalitis given infectious studies. While inpatient, she was treated with intravenous acyclovir, and intravenous immunoglobulin (IVIG) replacement was started under the direction of neurology, infectious diseases, and immunology services. Her neurologic condition improved with antiviral treatment. With infectious workup, Epstein Barr virus (EBV) PCR was also positive in the blood. She was discharged and received 6 months of high-dose acyclovir therapy. 6 months following her admission for VZV encephalitis, the patient was diagnosed with EBV-associated lymphoma and is currently undergoing treatment. This case prompted reflection in terms of the prevention of accidental/contraindicated vaccinations and a discussion on the management of live vaccination administration to a patient with ataxia telangiectasia. The recommendation following vaccination is to monitor clinically for the development of infectious sequelae. For this particular patient, the lesions diagnosed as coxsackie viral infection were more likely acute disseminated VZV infection.

The polymerase chain reaction method (PCR) was used to investigate events in the pathogenesis of varicella-zoster virus (VZV) infection in strain 2, Hartley, and euthymic hairless guinea pigs. VZV was detected in peripheral blood mononuclear cells (PBMC) obtained 2-5 days after infection in 8 (50%) of 16 strain 2, 4 (40%) of 10 hairless, and 10 (34%) of 29 Hartley guinea pigs. The frequency of VZV-infected PBMC was estimated to be at least 1/200,000, which is comparable to that observed in human infection. When VZV PCR was used to test ganglia from hairless guinea pigs, samples from 6 of 8 animals were positive. Of 45 VZV-infected guinea pigs that were tested for cellular immunity by VZV T lymphocyte proliferation assay, 44 developed a stimulation index > 2.0. Control animals had no detectable virus by PCR and did not develop cellular immunity to VZV. These experiments showed that viremia was detectable by PCR during primary VZV infection of guinea pigs in about half of the animals regardless of the strain of guinea pig. Acquisition of cellular immunity provided a consistent marker of infection in all guinea pig strains. PCR was also useful for demonstrating VZV in guinea pig ganglia tissue, with VZV gene sequences being detectable for at least 80 days after infection. With the combination of PCR and immunologic assays, various guinea pig strains should be useful for studies of VZV pathogenesis and for the evaluation of antiviral agents and vaccine strategies.

BackgroundUnbiased metagenomic next-generation sequencing (mNGS) detects pathogens in a target-independent manner. It is not well-understood whether mNGS has comparable sensitivity to target-dependent nucleic acid test for pathogen identification.MethodsThis study included 31 patients with chickenpox and neurological symptoms for screening of possible varicella-zoster virus (VZV) central nervous system (CNS) infection. Microbiological diagnosing of VZV cerebrospinal fluid (CSF) infection was performed on stored CSF samples using mNGS, quantitative and qualitative VZV-specific PCR assays, and VZV IgM antibodies test.ResultsThe median age was 30.0 [interquartile range (IQR), 24.3–33.3] years. 51.6% of the patients were men. About 80.6% of the patients had normal CSF white blood cell counts (≤ 5 × 106/L). VZV IgM antibodies presented in 16.1% of the CSF samples, and nucleic acids were detectable in 16.1 and 9.7% using two different VZV-specific real-time PCR protocols. Intriguingly, maximal identification of VZV elements was achieved by CSF mNGS (p = 0.001 and p = 007; compared with qualitative PCR and VZV IgM antibody test, respectively), with sequence reads of VZV being reported in 51.6% (16/31) of the CSF samples. All VZV PCR positive samples were positive when analyzed by mNGS. Of note, human betaherpesvirus 6A with clinical significance was unexpectedly detected in one CSF sample.ConclusionsOur study suggests that CSF mNGS may have higher sensitivity for VZV detection than CSF VZV PCR and antibody tests, and has the advantage of identifying unexpected pathogens.

Monkeypox: Cutaneous clues to clinical diagnosis

Purpose: This study was performed to describe the clinical manifestations of hospitalized children due to varicella-zoster virus (VZV) infection Methods: This study included 40 children who were hospitalized for varicella or herpes zoster at Seoul National University Children’s Hospital, 2009-2012. Diagnosis of VZV infection was confirmed by VZV PCR or culture from vesicular fluid. Medicalrecords were reviewed to collect clinical features and outcome, antiviral treatment, history of varicella vaccination, and underlying diseases.Results: Sixteen patients with varicella and 24 patients with herpes zoster were included. Their median age was 10.5 years (16 days-19 years). Thirty-five (87.5%) patients had underlying diseases. Among 24 patients with herpes zoster, 11 patientshad previous history of varicella and 1 had herpes zoster. Twenty patients (50%) had a history of varicella vaccination, and 19 immunocompromised patients had VZV infection despite of vaccination. Most (95%) patients were treated by intra-venous or oral acyclovir, and no treatment failure of intravenous acyclovir was found. The median duration of fever was 4.4 days (1-10 days), and that of antiviral treatment was 12 days (7-23 days) in immunocompromised patients. Immuno-compromised patients received longer duration of antiviral treatment than imunocompetent patients (P=0.014). Eleven (27.5%) immunocompromised patients had postherpetic neuralgia, 2 (5%) had proven co-infection by Streptococcus pyogenesand Klebsiella oxytoca, and 1 (2.5%) complicated with pneumonia. Conclusion: Immunocompromised children require longer duration of treatment and are at risk of severe complication asso-ciated with VZV infection. Early initiation of antiviral therapy and close monitoring are necessary for those in immunocpom-promised conditions. (Korean J Pediatr Infect Dis 2013;20:161-167)KeyWords: Varicella-zoster virus, hospitalized, immunocompromised, children