Visceral Varicella Research Articles

Visceral Varicella in a Patient With Chronic Lymphocytic Leukemia Treated With Fludarabine: A Case Report

Introduction Opportunistic infections are a common cause of morbidity and mortality in patients with CLL. Dermatomal reactivation of the varicella zoster virus is seen in nearly half of patients undergoing treatment with fludarabine. Visceral involvement of varicella, however, is rare and likely marks severely dysfunctional cellular immunity. Visceral varicella has been reported in patients receiving high dose chemotherapy, cyclophosphamide, and rituximab. Here we report the first case of visceral varicella in a patient with CLL during fludarabine therapy. Immunosuppression associated with malignancy and its treatment can lead to infectious complications. Prompt diagnosis in the immunosuppressed patient requires recognition that common illnesses can have uncommon presentations. Opportunistic infections are often seen in patients receiving high dose chemotherapy but are less fre-

Visceral Varicella Zoster Virus (VZV) After Allogeneic Hematopoietic Stem Cell Transplant (HSCT) in Pediatric Patients With Chronic Graft-Versus-Host Disease (cGVHD)

Reactivation of latent varicella zoster virus is one infectious complication associated with the extensive immunosuppression necessary for hematopoietic stem cell transplant. Most cases are limited to skin and mortality is low. Isolated visceral zoster is rare, presenting with ileus/abdominal pain, hepatitis, and/or hyponatremia. We present 2 cases of visceral varicella zoster virus in adolescents with chronic graft-versus-host disease after hematopoietic stem cell transplant. Both presented with elevated liver enzymes, severe abdominal pain, and hyponatremia but lacked cutaneous involvement. Both received high-dose acyclovir and showed improvement, but eventually expired from hepatic failure. The diagnosis of visceral zoster can be difficult especially without cutaneous manifestations. Vigilance is necessary in patients with chronic graft-versus-host disease, abdominal pain, and/or hepatitis and antiviral therapy should be initiated promptly.

Visceral varicella zoster virus (VZV) after allogeneic hematopoietic stem cell transplant (HSCT) in pediatric patients with chronic GVHD

18027 Reactivation of latent VZV, a common infection caused by the extensive immunosuppression associated with HSCT, can lead to significant morbidity and mortality. The reported incidence of reactivation ranges from 23–67%. Most patients reactivate with cutaneous disease; mortality in pediatric patients is low in this setting. Isolated visceral zoster is rare and can be difficult to diagnose, presenting with ileus/abdominal pain, hepatitis and/or hyponatremia. We present 2 cases of visceral VZV in adolescents with cGVHD following unrelated donor HSCT. A 20 y.o, 11 months post-HSCT for Ph+ ALL was diagnosed with skin and hepatic cGVHD and began on prednisone 4 weeks before developing severe abdominal pain and constipation. A CT scan raised the possibility of intestinal obstruction. Concurrently, her Na+ dropped and transaminases markedly increased. Exploratory laporotomy revealed no obstruction but hepatic nodules were noted and biopsied. Acyclovir was begun before pathology returned positive for VZV. The patient developed fulminant hepatitis and died 3 days later, 9 days after first symptoms. The 2nd patient was a 19 y.o, 7 months post-HSCT for induction failure AML. Off immunosuppression, she developed hepatic cGVHD and was placed on prednisone with clinical improvement. The following week she developed abdominal pain and constipation. 2 days later she presented with a generalized seizure, hyponatremia, and elevated liver enzymes. She was begun on acyclovir and initially improved. Subsequent blood and CSF PCRs were positive for VZV. She died of hepatic failure 53 days after her initial symptoms. Given VZV in the spinal fluid, we postulate that the previously unexplained associated hyponatremia represents direct CNS viral toxicity. The diagnosis of visceral zoster can be difficult. A high level of suspicion for VZV is necessary in patients with cGVHD who have abdominal pain and/or hepatitis and antiviral therapy should be started promptly. Patient Summary Time post HSCT at VZV diagnosis: Day +386 Day +255 Conditioning: Cyclophosphamide Cyclophosphamide Total Body Irradiation Total Body Irradiation GVHD Prophylaxis: Tacrolimus Cyclosporine Rapamycin Methotrexate Steroids GVHD Involvement: Skin, liver, oral Liver Immunosuppression: Prednisone (1mg/kg) Prednisone (1.5mg/kg) Cyclosporine Lowest Na+: 117 (mmol/L) 112 (mmol/L) Highest LFT: AST:14920 AST:2506 ALT:7060 ALT:3631 Time from symptoms to acyclovir Initiation: 7 days 5 days Outcome: Death from hepatic failure 9 days after first presenting Death from hepatic failure 53 days after first presenting No significant financial relationships to disclose.

Abdominal pain and syndrome of inappropriate antidiuretic hormone secretion as a manifestation of visceral varicella zoster virus infection in a patient with non‐Hodgkin's lymphoma

Abdominal pain and syndrome of inappropriate antidiuretic hormone secretion as a manifestation of visceral varicella zoster virus infection in a patient with non‐Hodgkin's lymphoma

Concomitant Candida Epiglottitis and Disseminated Varicella zoster Virus Infection Associated With Acute Lymphoblastic Leukemia

Acute epiglottitis by nonbacterial pathogens is an uncommon but life-threatening clinical entity. Herein, we report the concomitant occurrence of Candida epiglottitis and mucosal and visceral Varicella zoster virus infection in a child with acute lymphoblastic leukemia. Both infections were atypical in their presentation, occurred in a severely immunocompromised host, and required invasive procedures for diagnosis.

Visceral varicella zoster virus infection after stem cell transplantation: a possible cause of severe abdominal pain

Reactivation of varicella zoster virus (VZV) is a common event after stem cell transplantation (SCT). When activated in the abdominal cavity, the infection may be life threatening. Visceral presentation with VZV infection is uncommon, although probably an under-diagnosed event in post-SCT patients. The interval from onset of abdominal pain to the development of skin eruptions may delay the initiation of specific antiviral therapy and symptoms may be incorrectly diagnosed as surgical disease or graft-versus-host disease. We describe the case of a 53-year-old man who had undergone stem cell autograft for multiple myeloma and developed visceral VZV infection with hepatitis, melaena and subileus 7 months later.