Disseminated Varicella Zoster Virus Research Articles

A survival case of visceral disseminated varicella zoster virus infection in a patient with systemic lupus erythematosus

BackgroundVisceral disseminated varicella zoster virus (VZV) infection is a rare but life-threatening complication in immunosuppressed patients. Herein, we report a survival case of visceral disseminated VZV infection in a patient with systemic lupus erythematosus (SLE).Case presentationA 37-year-old woman was diagnosed as SLE and initial induction therapy was started. Two months after starting the immunosuppressive therapy consisting of 40 mg of prednisolone (PSL) and 1500 mg of mycophenolate mofetil (MMF) daily, she suddenly developed strong abdominal pain, which was required opioid analgesics, followed by systemic skin blisters, which were diagnosed as varicella. Laboratory findings showed rapid exacerbation of severe liver failure, coagulation abnormalities and increased numbers of blood VZV deoxyribonucleic acid (DNA). Therefore, she was diagnosed as visceral disseminated VZV infection. Multidisciplinary treatment with acyclovir, immunoglobulin and antibiotics was started, the dose of PSL was reduced, and MMF was withdrawn. By their treatment, her symptoms were resolved and she finally discharged.ConclusionsOur case highlights the importance of a clinical suspicion of visceral disseminated VZV infections, and the necessity of immediate administration of acyclovir and reduced doses of immunosuppressant to save patients with SLE.

Disseminated Varicella-zoster Virus Infection in an Immunocompetent Host


 
 
 
 Disseminated varicella-zoster virus (VZV) infection has devastating impacts on patients’ quality of life, with increasing morbidity and mortality. Thus, it is imperative that a diagnosis be made early. This case description illustrates a unique and dramatic presentation of disseminated VZV infection with important clinical implications.
 
 
 

Rapidly Progressive Aneurysmal Disease Associated with Epstein Barr Virus-Positive Lymphoproliferative Disease in a CVID patient with NFKB-1 Mutation

IntroductionCommon variable immunodeficiency (CVID) is a genetically heterogeneous group characterized by hypogammaglobulinemia and poor immune response to vaccines. CVID patients are at higher risk for autoimmune diseases or malignancy. We demonstrate a rare case of a patient with CVID (NFKB-1 mutation) presenting with features of vasculitis and rapidly progressive aneurysmal disease secondary to an Epstein Barr Virus (EBV)-associated lymphoproliferative disorder. Case descriptionA 36-year-old man with CVID presented with hoarseness and left vocal cord paralysis. Imaging revealed an aortic arch and descending thoracic aorta abnormality concerning for a plaque, vasculitis or focal thrombosed dissection. He later devloped severe back pain and imaging studies demonstrated an abdominal aortic aneurysm, thickening of the common iliac arteries and a focal aneurysm of the right common iliac artery. PET CT scan showed uptake in the upper abdominal aorta extending to the right renal artery and the distal abdominal aorta near the bifurcation extending to the right common iliac artery, concerning for large vessel vasculitis. He was started on high-dose steroids for large vessel vasculitis. One month later, he was hospitalized for disseminated histoplasmosis and disseminated varicella zoster virus (VZV) and started on amphotericin B and acyclovir with steroid taper. Whole exome next-generation sequencing (NGS) revealed NFKB-1 mutation consistent with CVID-12 with autoimmunity. He later developed worsening back pain prompting repeat imaging which showed further progression of his aneurysmal disease. He was also found to have EBV viremia with a titer of 33,700 IU/mL. A left superior gluteal artery biopsy was performed which showed evidence of an EBV+ lymphoproliferative disorder with concern for an EBV-positive fibrin-associated diffuse lymphoproliferative B-cell lymphoma (DLBCL). DiscussionCVID-12 is an autosomal dominant disease resulting from a mutation in NFKB-1. This mutation leads to an impaired immune response associated with recurrent infections and approximately 20% of patients developing lymphomas at some point in their lifetime. However, there are few case reports of CVID associated large vessel aneurysms or vasculitis. Our patient with CVID demonstrated a rare presentation of an EBV-positive lymphoproliferative disorder driving progression of large vessel disease.

Severe varicella-zoster virus meningoencephalomyelitis coexisting with visceral disseminated varicella-zoster virus infection in a patient with lupus nephritis: A case report

Meningoencephalomyelitis and visceral dissemination infection are rare but life-threatening complications of either the primary infection or reactivation of varicella-zoster virus (VZV) in immunocompromised patients. To date, few studies have reported the co-existence of VZV meningoencephalomyelitis and the visceral dissemination of VZV infection. A 23-year-old male was diagnosed with lupus nephritis class III and was being treated with oral prednisone and tacrolimus. The patient exhibited herpes zoster 21-day after the initiation of therapy and experienced unbearable abdominal pain and generalized seizures 11 days after the onset of a zoster rash. Magnetic resonance imaging showed progressive lesions in the cerebrum, brainstem, and cerebellum, as well as meningeal thickening and thoracic myelitis. Computed tomography showed pulmonary interstitial infiltration, partial intestinal dilatation, and effusion. Metagenomic next-generation sequencing revealed 198,269 and 152,222 VZV-specific reads in the cerebrospinal fluid and bronchoalveolar lavage fluid, respectively. Based on the clinical and genetic findings, this patient was finally diagnosed with VZV meningoencephalomyelitis and visceral disseminated VZV infection. The patient received intravenous acyclovir (0.5 g every 8 hours) combined with plasma exchange and intravenous immunoglobulin. Treatment against secondary bacterial and fungal infections, organ support therapy and rehabilitation training were given simultaneously. The patient's peripheral muscle strength did not improve and repeated metagenomic next-generation sequencing showed the persistence of VZV-specific reads in the cerebrospinal fluid. The patient finally abandoned therapy due to financial constraints at the 1-month follow-up. Patients with autoimmune diseases receiving immunosuppressive therapy should be warned about the possibility of developing serious neurological infections and visceral disseminated VZV infections as side effects. Early diagnosis and the early initiation of intravenous acyclovir therapy are important for such cases.

330 Safety of abrocitinib in 3582 patients with moderate-to-severe atopic dermatitis with over 900 patients exposed for almost 2 years

Abstract Abrocitinib is an oral Janus kinase 1 inhibitor with demonstrated efficacy in moderate-to-severe atopic dermatitis (AD). To evaluate the long-term safety profile of abrocitinib and provide relevant information for practitioners. Data from patients who received ≥1 dose of abrocitinib 200 mg or 100 mg in the JADE clinical program were pooled in two cohorts. The consistent-dose (CD) cohort comprised patients who received the same abrocitinib dose during the entire exposure time in parent phase 3 studies and/or the long-term extension study JADE EXTEND (NCT03422822). Parent studies were: JADE MONO-1 (NCT03349060), JADE MONO-2 (NCT03575871), JADE TEEN (NCT03796676), JADE COMPARE (NCT03720470), JADE DARE (NCT04345367; 200 mg only) and JADE REGIMEN (NCT03627767); in JADE REGIMEN only patients from the open-label run-in phase (200 mg only) who did not subsequently enter the randomized phase were included. Patients from the phase 2b study (NCT02780167) were also included in the CD cohort. The variable-dose (VD) cohort comprised patients who received different doses of abrocitinib (200 and 100 mg) throughout exposure time in the parent study JADE REGIMEN and in JADE EXTEND, if enrolled. Patients included in the VD cohort completed the open-label period of JADE REGIMEN (abrocitinib 200 mg only) and entered the randomized phase (abrocitinib 200 mg, abrocitinib 100 mg or placebo); some patients subsequently entered the JADE REGIMEN rescue phase (abrocitinib 200 mg) and/or JADE EXTEND (abrocitinib 200 or 100 mg). The data cutoff was 16 April 2021. A Cox regression analysis evaluated risk factors for specific events of interest. Data from 3582 patients (4313.4 patient-years) were analysed: 2784 patients in the CD cohort (abrocitinib 200 mg, n = 1761, abrocitinib 100 mg, n = 1023) and 798 patients in the VD cohort. Duration of exposure was ≥48 weeks in 43.6%, 66.9% and 86.1% and ≥96 weeks in 18.0%, 23.2% and 45.4% of patients in the CD 200 mg, 100 mg and VD cohorts, respectively. In the CD and VD cohorts, the median age was 30.0 and 29.0 years; 490 (17.6%) and 145 patients (18.2%) were adolescents, and 143 (5.1%) and 30 patients (3.8%) were aged ≥65 years at screening, respectively. Incidence rates (IRs; unique patients with events per 100 patient-years) of serious adverse events (SAEs), deaths, and treatment-emergent adverse events of special interest are shown in Table 1. IRs for SAEs were consistent across abrocitinib doses but were higher in patients aged ≥65 years vs. younger patients. Serious infections were the most frequent SAEs; frequency was not dose related. Herpes zoster (HZ), herpes simplex and pneumonia were the most frequent serious infections. From a Cox regression analysis, potential risk factors for treatment-emergent HZ included abrocitinib dose, baseline age, medical history of HZ, absolute lymphocyte count <1000 mm−3 prior to infection and region. Most (95%) adjudicated opportunistic HZ infections were cutaneous; 2 (5%) were extracutaneous (one serious disseminated varicella-zoster virus infection, one serious HZ meningitis). IRs for nonmelanoma skin cancer, malignancy (excluding nonmelanoma skin cancer), thrombocytopenia and lymphopenia were higher in patients aged ≥65 years vs. younger patients but were not dose related. Abrocitinib has an acceptable long-term safety profile in this large analysis of patients with moderate-to-severe AD. Risk of SAEs, HZ infection, malignancies and hematologic abnormalities increased with older age; HZ risk was also related to dose and prior HZ infection.

Disseminated varicella zoster virus infection following live attenuated herpes zoster vaccine: descriptive analysis of reports to Australia’s spontaneous vaccine pharmacovigilance system, 2016–2020

ObjectivesTo examine the reported incidence and features of disseminated varicella zoster virus (VZV) infection following live attenuated herpes zoster vaccine live (ZVL: Zostavax, Merck) in immunocompromised people in Australia.Design and...

Visceral disseminated varicella zoster infection: a rare cause of acute abdomen in a patient with well-controlled diabetes mellitus\u2014a case report

BackgroundVisceral disseminated varicella zoster virus (VZV) infections frequently affect immunocompromised patients. Diabetes mellitus has been associated with VZV infection, and most cases of disseminated infection involve patients with poorly controlled blood glucose levels. It initially presents as severe abdominal pain, which is evaluated as an acute abdomen, however, the cause is typically unidentified due to unremarkable computed tomography (CT) findings. We report a case of visceral disseminated VZV infection in a patient with well-controlled diabetes mellitus with fat stranding around the celiac and superior mesenteric artery on CT.Case presentationA 61-year-old Japanese woman with well-controlled diabetes mellitus presented to the emergency department with severe abdominal pain that gradually worsened. She had stable vital signs and skin rashes, suggestive of varicella. Abdominal CT showed fat stranding around the celiac and superior mesenteric arteries. The patient tested positive for the VZV antigen and was diagnosed with a visceral disseminated VZV infection. Acyclovir was administered, and the patient was discharged on the 14th day.ConclusionsVisceral disseminated VZV infection may affect patients with well-controlled diabetes mellitus and causes acute abdomen. Periarterial fat stranding on CT is associated with abdominal pain due to visceral disseminated VZV infection.

Led astray by serology

A 27-year-old man of South Asian ethnicity presented with abdominal pain, nausea and constipation. Eight months earlier he had undergone myeloablative, haplo-identical, allogeneic stem cell transplantation (SCT) for acute lymphoblastic leukaemia. Immunosuppression had been stopped 4 months before presentation; he had continued prophylactic aciclovir, co-trimoxazole and phenoxymethylpenicillin. He was febrile and abdominal imaging revealed oedematous pancreatitis and non-obstructive cholecystitis. Despite fluids and antibiotics (co-amoxiclav, gentamicin), he deteriorated and two days later, a painless, non-pruritic rash emerged, spreading from the face to trunk and limbs. He also developed profuse diarrhoea, melaena and anaemia. His abdomen was soft with generalised tenderness and active bowel sounds. A diffuse rash affected face, trunk and limbs, sparing palms and soles. Lesions were dark, 1–4 mm haemorrhagic vesicles over an erythematous base. Pigmented, ulcerating lesions were noted over the hard palate. An endoscopy showed multiple gastric ulcers. Methylprednisolone was commenced for possible acute Graft-versus-Host Disease, and disseminated infection was treated empirically with piperacillin-tazobactam, ivermectin and aciclovir. Disseminated varicella zoster virus (VZV) infection was confirmed by identifying VZV viraemia and positive VZV PCR from lesion swabs. Pre- and post-SCT VZV IgG titres were > 150mIU/ml. There was CD4 + lymphopenia (56 x106/L). As no additional cause was identified, the pancreatitis and small bowel inflammation was felt most likely to be due to visceral reactivation of VZV. Take-home messages: 1. VZV reactivation may still occur despite aciclovir prophylaxis. 2. Immune reconstitution post-SCT is highly variable. 3. Seemingly adequate VZV IgG titres do not necessarily prevent infection if there is immunosuppression. Abstract without diagnosis A 27-year-old man of South Asian ethnicity presented with abdominal pain, nausea and constipation. Eight months earlier he had undergone myeloablative, haplo-identical, allogeneic stem cell transplantation (SCT) for acute lymphoblastic leukaemia. Immunosuppression had been stopped 4 months before presentation; he had continued prophylactic aciclovir, co-trimoxazole and phenoxymethylpenicillin.

Disseminated varicella-zoster virus infection during FOLFIRINOX therapy in a patient with pancreatic cancer with local recurrence and distant metastases

Disseminated varicella-zoster virus infection during FOLFIRINOX therapy in a patient with pancreatic cancer with local recurrence and distant metastases

Occupational Exposure to Varicella Zoster in a Tertiary-Care Healthcare Setting

Background: Disseminated varicella zoster virus (dVZV) infection is a feared complication of varicella zoster virus (VZV) reactivation in immunocompromised patients. The CDC recommends contact and airborne precautions for localized VZV in immunocompromised patients until dissemination has been ruled out. Pre-emptive isolation can be problematic for medical centers without access to negative-pressure rooms. When we identify a case of dVZV at our facility, we perform an investigation to identify occupational exposures. Methods: We conducted a retrospective, descriptive review of occupational exposure investigations related to dVZV from January 2016 to December 2018. We collected baseline characteristics of the dVZV patient, and we evaluated whether the exposure occurred due to a delay in diagnosis or a progression from “localized” to disseminated VZV disease. Results: We identified 21 immunosuppressed patients with dVZV whose infection resulted in an occupational exposure during the specified study period. Average age was 58.6 years, with 10 males and 12 females. The immunocompromised patients included 11 with hematologic malignancy, 5 with solid-organ malignancy, 3 with rheumatologic disease on immunosuppressive therapy, and 2 with a solid-organ transplant. Most of the exposures (72.7%) occurred in an inpatient setting. The exposures resulted from either delayed recognition of dVZV or delayed initiation of appropriate precautions for all of the immunosuppressed patients. Two additional exposures occurred as a result of a change from “localized” to “disseminated” VZV. These patients whose diagnosis changed from localized to dVZV were considered previously immunocompetent, and dissemination took place 2 days after seeking healthcare evaluation. Conclusions: Most occupational exposures to varicella zoster are the result of delayed initiation of appropriate isolation precautions due to delayed diagnosis of dVZV infection or failure to recognize the need for instituting precautions in disseminated disease. Instituting preemptive airborne precautions for immunocompromised patients with localized varicella zoster would be unlikely to reduce occupational exposures.Funding: NoneDisclosures: Consulting fee- Merck Priya Sampathkumar

Unusual presentation of fatal disseminated varicella zoster virus infection in a patient with lupus nephritis: a case report

BackgroundThe risk of life-threatening complications, such as visceral disseminated varicella zoster virus (VZV) infection, is greater in immunosuppressed individuals, such as systemic lupus erythematosus (SLE) patients.Case presentationHere, a case is reported of a Caucasian woman diagnosed with lupus nephritis and anti-phospholipid syndrome, who was subjected to mycophenolate mofetil and high-dose steroid remission-induction therapy. Two months later she developed abdominal pain followed by a fatal rapid multi-organ failure. As no typical skin rashes were evident, death was initially attributed to catastrophic anti-phospholipid syndrome. However, autopsy and virological examinations on archival material revealed a disseminated VZV infection.ConclusionsOverall, this case highlights the importance of having a high clinical suspicion of fatal VZV infections in heavily immunosuppressed SLE patients even when typical signs and symptoms are lacking.

Disseminated herpes zoster with cauda equina symptoms

Herpes zoster is a common infection resulting from the reactivation of dormant varicella zoster virus in a posterior dorsal root ganglion. The typical dermatomal involvement includes the thoracic region, followed by the face and the cervical and lumbosacral regions, with 1% having disseminated disease. We present a rare case of an immunocompetent 85-year-old man presenting with herpes zoster at the L3-S2 dermatomes, that evolved to disseminated varicella zoster virus (dVZV), with radiologically and laboratory-confirmed lumbosacral plexopathy manifesting with cauda equina syndrome. Here we also discuss the diagnosis and complications of dVZV as well as treatment strategy. By maintaining a high degree of clinical suspicion and initiating early treatment, high-quality patient care and good outcomes are able to be achieved in cases like this.

Fever, Rash, and Abdominal Pain

Question: A 35-year-old woman presented with a 1-week history of fevers, right upper quadrant and epigastric pain, and a non-pruritic, non-painful rash. Her past medical history was significant for a diagnosis of human immunodeficiency virus (HIV) 5 years prior, not currently on treatment, and hypertension, on Lisinopril. She had received highly active antiretroviral therapy (HAART) for one year after diagnosis but was subsequently lost to follow-up. Her last known CD4 count was 410 cells/mcL four years prior to presentation. Upon presentation, vital signs were within normal limits except for a fever of 38.8°C. Physical examination was notable for multiple crusted erosions and papules present on her face, abdomen, back, and extremities (Figures A–C). Laboratory evaluation demonstrated the following: alanine aminotransferase level 291 U/L, aspartate aminotransferase level 260 U/L, alkaline phosphatase level 135 U/L, total bilirubin 0.4 mg/dL, hemoglobin 12.9 g/dL, 2% blasts on peripheral smear, leukocytes 8 x 109/L, and platelet count 132 x 109/L. CD4 count was 118 cells/mcL and HIV-1 RNA 4,120,000 copies/mL. Chest x-ray demonstrated slight nodular peribronchovascular densities in both lungs and a right upper quadrant ultrasound demonstrated non-specific gallbladder wall edema. Computed tomography abdomen/pelvis was notable for diffuse heterogeneity of the hepatic parenchyma and innumerable small hypodensities in the liver and spleen, some with subtle peripheral enhancement. Which of the following is the most appropriate initial treatment for this patient’s condition?A.Supportive careB.Intramuscular penicillin G benzathineC.Intravenous acyclovirD.Highly active anti-retroviral therapy (HAART) Look on page 493 for the answer and see the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image(s) to Practical Teaching Cases. The correct answer is C. Intravenous acyclovir for disseminated varicella zoster virus infection in an immunocompromised host The differential for fever and widespread rash in an immunocompromised individual is broad, and includes disseminated herpes simplex virus, varicella zoster virus (VZV), secondary syphilis, bacillary angiomatosis, disseminated gonococcal infection, parvovirus, acute hepatitis B, cryptococcosis, histoplasmosis, blastomycosis, and others. Our patient underwent liver biopsy and pathology demonstrated hepatic parenchyma with portal and lobular inflammation but no necrosis (Figures D, E). VZV polymerase chain reaction (PCR) from the liver returned positive. Moreover, swab of facial lesion was performed with positive VZV PCR. A diagnosis of disseminated varicella zoster infection was made based on the biopsy results along with multi-organ involvement including pulmonary and hepatic manifestations. Notably, her VZV IgM and IgG were negative, indicating the need for a high degree of suspicion if the clinical scenario is consistent with VZV. While uncomplicated VZV can be treated with supportive care or oral antivirals, such as acyclovir, valacyclovir, or famciclovir, an immunocompromised host with disseminated VZV should typically be admitted to the hospital for intravenous acyclovir.1Ahmed A.M. Brantley J.S. Madkan V. et al.Managing herpes zoster in immunocompromised patients.Herpes. 2007; 14: 32-36PubMed Google Scholar Answer B would be appropriate if secondary syphilis was suspected. In this case, initiation of HAART (answer D) before treatment of VZV could increase the risk of immune reconstitution inflammatory syndrome and exacerbate her pneumonitis and hepatitis. Complications of VZV infection include post herpetic neuralgia, herpes zoster ophthalmicus or oticus, acute retinal necrosis, meningitis, and encephalitis. In immunocompromised hosts, VZV can present with cutaneous dissemination and visceral organ involvement with pneumonia and hepatitis. Biopsy proven VZV hepatitis is rare and is associated with a high mortality.2Anderson D.R. Schwartz J. Hunter N.J. et al.Varicella hepatitis: a fatal case in a previously healthy, immunocompetent adult. Report of a case, autopsy, and review of the literature.Arch Intern Med. 1994; 154: 2101-2106Crossref PubMed Google Scholar,3Sherman R.A. Silva Jr., J. Gandour-Edwards R. Fatal varicella in an adult: case report and review of the gastrointestinal complications of chickenpox.Rev Infect Dis. 1991; 13: 424-427Crossref PubMed Scopus (22) Google Scholar Fortunately, our patient did not develop fulminant hepatic failure. She was treated with 4 days of IV acyclovir with improvement in her fevers and transaminitis and then transitioned to oral valacyclovir. HAART was also initiated two days after the start of IV acyclovir. At a follow-up visit one week later, she continued to improve and had no recurrence of symptoms. We would like to thank Dr Taofic Mounajjed for his contribution of pathology photos and interpretation to this case.

Successful management of visceral disseminated varicella zoster virus infection during treatment of membranous nephropathy: a case report

BackgroundVisceral disseminated varicella zoster virus (VDVZV) infection is a rare disease with a high mortality rate (55%) in immunocompromised patients, but it is not yet widely recognized in the field of nephrology. We report a case of VDVZV contracted during immunosuppressive therapy for membranous nephropathy.Case presentationA 36-year-old woman was diagnosed with membranous nephropathy and was being treated with immunosuppressive therapy consisting of 60 mg/day prednisolone, 150 mg/day mizoribine, and 150 mg/day cyclosporine. Nephrosis eased; therefore, the prednisolone dosage was reduced. However, 50 days after starting immunosuppressive therapy, the patient suddenly developed strong and spontaneous abdominal pain, predominantly in the epigastric area, without muscular guarding or rebound tenderness. Blood data indicated neutrophil-dominant elevated white blood cell count, reduced platelet count, elevated transaminase and lactate dehydrogenase, slightly increased C-reactive protein, and enhanced coagulability. Abdominal computed tomography revealed a mildly increased enhancement around the root of the superior mesenteric artery with no perforation, intestinal obstruction, or thrombosis. The cause of the abdominal pain was unknown, so the patient was carefully monitored and antibiotic agents and opioid analgesics administered. The following day, blisters appeared on the patient’s skin, which were diagnosed as varicella. There was a marked increase in the blood concentration of VZV-DNA; therefore, the cause of the abdominal pain was diagnosed as VDVZV. Treatment with acyclovir and immunoglobulin was immediately started, and the immunosuppressive therapy dose reduced. The abdominal pain resolved rapidly, and the patient was discharged 1 week after symptom onset.Discussions and conclusionsThis patient was VZV-IgG positive, but developed VDVZV due to reinfection. Abdominal pain due to VDVZV precedes the skin rash, which makes it difficult to diagnose before the appearance of the rash, but measuring the VZV-DNA concentration in the blood may be effective. Saving the patient’s life requires urgent administration of sufficient doses of acyclovir and reduced immunosuppressive therapy.

Live zoster vaccination in an immunocompromised patient leading to death secondary to disseminated varicella zoster virus infection

In 2016, the live attenuated zoster vaccine (Zostavax, Merck and Co, USA) was introduced into the Australian National Immunisation Program for people aged 70 years who are not significantly immunocompromised. We report the administration of Zostavax in an immunocompromised patient with chronic lymphocytic leukaemia and no evidence of primary varicella zoster virus (VZV) infection. The patient presented with a bilateral vesicular facial rash 22 days after receiving Zostavax and was initially managed as an outpatient with oral acyclovir. He re-presented three days later and was diagnosed with disseminated VZV infection complicated by meningoencephalitis. The patient died following cardiac arrest on day 10 of hospitalisation. This unfortunate case highlights the challenge of safely implementing a high titre live vaccine in a population where contraindications are prevalent. The non-live recombinant herpes zoster subunit vaccine (Shingrix, GSK) may provide a safe and effective option to protect immunocompromised patients from shingles and post-herpetic neuralgia.

Non-dermatomal varicella-zoster skin infection: disseminated cutaneous herpes zoster without dermatome in an immunosuppressed woman

Disseminated herpes zoster is defined as the presence of more than 20 lesions outside the dermatome. This unusual presentation is more common in immunosuppressed patients. Complications such as hepatitis, encephalitis, and pneumonitis are more likely in individuals with disseminated varicella zoster virus infection.A 63-year-old woman being treated for breast cancer developed multiple pustules and vesicles days after starting doxorubicin and cyclophosphamide chemotherapy. Ten individual lesions appeared on her chest, abdomen, back, and leg. Non-dermatomal disseminated herpes zoster was suspected. She was treated with oral antiviral therapy, as well as with oral and topical antibiotics. Varicella zoster virus infection was confirmed by direct fluorescent antibody staining. After one month, her skin lesions had resolved and she resumed chemotherapy.In a setting of immunosuppression, the rare presentation of disseminated herpes zoster without dermatome should be considered. Appropriate antiviral therapy should be administered while waiting for confirmation of the diagnosis, so as to reduce the risk of visceral dissemination of the varicella zoster virus infection.

Disseminated herpes zoster infection initially presenting with abdominal pain in patients with lymphoma undergoing conventional chemotherapy: A report of three cases.

Visceral disseminated varicella zoster virus (VZV) disease has a high mortality rate, and occurs in immunocompromised hosts, mostly subsequent to allogeneic stem cell transplantation. Only a few cases of this disease that onset during conventional chemotherapy in patients with lymphoma have been reported. The present study reports the cases of 3 patients with disseminated and visceral VZV infection undergoing treatment for follicular lymphoma, diffuse large B-cell lymphoma and peripheral T-cell lymphoma, not otherwise specified. All 3 patients presented with initial symptoms of abdominal pain, and 2 patients demonstrated syndrome of inappropriate antidiuretic hormone and hepatitis. All patients developed widespread cutaneous dissemination, and all had a low cluster of differentiation 4 cell count or lymphocyte count at the time of VZV diagnosis and at least 4 month prior. With intravenous systemic acyclovir therapy (Cases 1 and 3, 1500 mg/day; Case 2, 750 mg/day), the patients achieved complete recovery by day 14 of therapy. Visceral disseminated VZV infection is not limited to patients undergoing stem cell transplantation, and may present with abdominal pain with or without skin eruption. Visceral infection may take a poor clinical course, therefore, in patients with prolonged duration of low lymphocyte count and/or long-term use of steroids, the prophylactic use of acyclovir may be considered.

HSV-2-related hemophagocytic lymphohistiocytosis in a fingolimod-treated patient with MS.

Fingolimod is an oral, disease-modifying therapy used to treat multiple sclerosis (MS).1 However, severe viral infections, including disseminated varicella-zoster virus infection,1 herpes simplex encephalitis,1,2 varicella-zoster virus encephalitis and vasculopathy,3 or progressive multifocal leukoencephalopathy,4 have been reported during fingolimod therapy. Hemophagocytic lymphohistiocytosis (HLH), often triggered by certain viral infections, is a fatal disease characterized by fever, pancytopenia, elevated liver enzymes, hyperferritinemia, hepatosplenomegaly, and hemophagocytosis.5 A triggering infection causes persistent activation of lymphocytes and histiocytes, resulting in exaggerated immune responses and hemophagocytosis. We describe an autopsied case of disseminated herpes simplex virus type 2 (HSV-2) infection presenting with HLH, following 0.5 mg fingolimod and corticosteroid therapies. Acknowledgment: The authors thank the patient and his family for their cooperation regarding this report. This case report was approved by the ethical committee of Anjo Kosei Hospital. The authors obtained written informed consent from the patient's family for this publication.

Risk of Herpes Zoster and Disseminated Varicella Zoster in Patients Taking Immunosuppressant Drugs at the Time of Zoster Vaccination

ObjectiveTo determine the risks associated with zoster vaccine when administered to patients taking immunosuppressant medications. Patients and MethodsPatients enrolled in 1 of 7 managed care organizations affiliated with the Vaccine Safety Datalink between January 1, 2006, and December 31, 2009, were eligible. The exposure of interest was zoster vaccination in patients with current or remote immunosuppressant drug use. The primary outcomes were disseminated varicella zoster virus (VZV) and herpes zoster in the 42 days after vaccination. Automated data were collected on immunosuppressant drugs and baseline medical conditions. A logistic regression model using inverse probability treatment weights was used to estimate the odds of developing VZV or herpes zoster. ResultsA total of 14,554 individuals had an immunosuppressant medication dispensed around the time of vaccination, including 4826 with current use and 9728 with remote use. Most patients were taking low-dose corticosteroids. No cases of disseminated VZV were found in the current or remote users. The risk of herpes zoster was elevated in the 42 days after vaccination in current vs remote users (adjusted odds ratio, 2.99; 95% CI, 1.58-5.70). ConclusionWe found that patients taking immunosuppressant medications at the time of vaccination had a modest increased risk of herpes zoster in the 42 days after vaccination. The development of herpes zoster within 42 days after vaccination suggests that this is more likely due to reactivation of latent zoster virus than dissemination of the vaccine-derived varicella virus. These findings support the current zoster vaccination guidelines.

Prevalence and outcome of herpes zoster infection in renal transplant recipients.

Varicella zoster virus (VZV) is an important pathogen after renal transplant. The aim of this study is to assess the outcome of disseminated Varicella zoster virus infection in renal transplant recipients and to determine potential risk factors for mortality. From January 2001 to January 2014, we performed 1614 renal transplants at our institution. Varicella zoster virus infection was diagnosed in 41 patients (2.5%). Median time of diagnosis of Varicella zoster virus was 5 years after transplant (range, 3 mo to 13 y). Thirty-seven patients (90%) had dermatomal distribution of Varicella zoster virus, 4 patients (10%) had disseminated Varicella zoster virus infection. After diagnosis of Varicella zoster virus immunsuppressive therapy was reduced and patients received acyclovir. Cutaneous lesions were healed with a scar in 7 cases (17%). Two patients (5%) developed postherpetic neuralgia. Seventy percent of cases were diagnosed within 5 years, and 92% were diagnosed within 10 years after transplant. Mortality due to Varicella zoster virus was 2% (n = 1). Visceral involvement found to be a risk factor for mortality. Profilactic acyclovir or gancyclovir therapy following transplantation reduced Varicella zoster virus infection. However, Varicella zoster virus seropositivity did not influence fatal outcome. Early initiation of antiviral therapy may prevent development of complication and visceral dissemination of disease. Active immunization should be applied for all seronegative patients before organ transplant.