Varicella-Zoster Virus Infection After Marrow Transplantation for Aplastic Anemia or Leukemia

The occurrence of varicella zoster virus (VZV) reactivation is increased after allogeneic transplantation, whereas limited data are available for herpes zoster (HZ) after autologous SCT (ASCT). We determined the incidence and the prognostic significance of HZ and its correlation with VZV serology in 191 consecutive myeloma patients undergoing high-dose melphalan chemotherapy with ASCT. We found that VZV reactivation occurred in 57 (30%) patients, in 8.5% during induction and in 21.5% after ASCT peaking at 8 months after ASCT. Disease burden due to HZ was assessed as high or rather high in 70% of the patients. By immune fluorescence and Serion Elisa VZV IgG assessment, 90.8% of all patients had specific anti-VZV antibodies at ASCT. Lower specific antibody titers at transplantation were observed in patients with HZ after ASCT than in those without reactivation (P = 0.009). Finally, OS was better in myeloma patients with HZ after ASCT compared with patients without HZ (P = 0.007). Our data indicate that VZV reactivation after ASCT is a frequent event carrying a significant disease burden and it is associated with improved survival. Low levels of specific VZV antibodies at ASCT suggest increased vulnerability for VZV reactivation.

Section: Discussionmentioning

confidence: 99%

“…HZ is common after allogeneic or autologous BM or peripheral blood hematopoietic SCT. [4][5][6][7][8][9][10][11][12][13][14][15][16] The incidence of HZ at 1 year following autologous SCT (ASCT) varies from 8 to 30%. 3,11,[14][15][16] However, little is known about the incidence of HZ specifically in myeloma patients undergoing ASCT.…”

Section: Introductionmentioning

confidence: 99%

Varicella zoster virus reactivation after autologous SCT is a frequent event and associated with favorable outcome in myeloma patients

Kamber

Zimmerli

Suter‐Riniker

et al. 2015

“…3 Recipients of haemopoietic stem cell transplants (HSCT) are therefore at significantly increased risk of VZV reactivation, with an incidence of zoster ranging from 17 to 52%, [4][5][6] with approximately 80% episodes occurring within the first year. 5,7 This compares to an annual incidence of 0.4% among an unselected adult population. 8 The majority of reactivations occur in a localised dermatomal distribution, although with new lesion formation persisting for longer than in the immunocompetent, and with increased rates of post-herpetic neuralgia (68 vs 9%) 4 and of bacterial superinfection.…”

mentioning

confidence: 99%

The effect of low-dose aciclovir on reactivation of varicella zoster virus after allogeneic haemopoietic stem cell transplantation

Thomson

Hart

Banerjee

et al. 2005

Summary:Patients undergoing haemopoietic stem cell transplants (HSCT) are at high risk of varicella zoster virus (VZV) reactivation, with a significant incidence of dissemination. This study reports a retrospective analysis of 247 allogeneic HSCT recipients receiving anti-viral prophylaxis with low-dose oral aciclovir 400 mg/day, administered until immunosuppression was discontinued and the CD4 þ cell count exceeded 200/mm 3 . Viral reactivation was successfully suppressed by aciclovir prophylaxis, with only one case of breakthrough infection. The cumulative incidence of zoster infection at 1 year post transplant was 2% and at 5 years 34%. In all, 64 patients discontinued prophylaxis. Zoster developed in 26 of these, giving a cumulative incidence of infection at 1 year after stopping aciclovir of 39% and at 3 years 44%. Infection occurred in a localised dermatomal distribution in 93% of cases. This supports previous findings that aciclovir prophylaxis prevents early VZV reactivation, although the long-term incidence is not affected as infection occurs once prophylaxis is discontinued. Such infection, however, is mild and localised. This study does not support the idea that use of such low-dose aciclovir regimens reduces the zoster incidence by permitting subclinical reactivation during prophylaxis, and therefore the re-establishment of protective anti-viral immunity. Varicella zoster virus (VZV), a human herpesvirus, causes chicken pox as a primary infection, following which it establishes latency within the dorsal root sensory ganglia. During reactivation, the virus travels via neuronal axons to skin innervated by the relevant ganglion, resulting in the classical dermatomal vesicular rash. 1As immune surveillance is required for the maintenance of latency, immunocompromised individuals are at increased risk of reactivation, with viral escape being associated with declining numbers of VZV-specific memory T cells. 2 In addition, in the immunocompromised host, reactivation can result in disseminated infection, with a generalised vesicular rash and/or other organ involvement, the proposed mechanism for this distant spread being the tropism of VZV for circulating mononuclear cells. 3 Recipients of haemopoietic stem cell transplants (HSCT) are therefore at significantly increased risk of VZV reactivation, with an incidence of zoster ranging from 17 to 52%, 4-6 with approximately 80% episodes occurring within the first year. 5,7 This compares to an annual incidence of 0.4% among an unselected adult population. 8 The majority of reactivations occur in a localised dermatomal distribution, although with new lesion formation persisting for longer than in the immunocompetent, and with increased rates of post-herpetic neuralgia (68 vs 9%) 4 and of bacterial superinfection.In a significant minority of patients, however, viral dissemination can occur, resulting either in a generalised cutaneous rash or in hepatic, pulmonary or central nervous system (CNS) involvement. One early series reported a VZV dissemination rate of 45% ...

“…Keywords: herpes zoster ophthalmicus; bone marrow transplantation; varicella zoster; keratitis; uveitis; scleritis Varicella zoster virus (VZV) infection is a relatively frequent complication following autologous and allogeneic BMT. [1][2][3][4][5][6] The clinical course of zoster in these immunosuppressed patients tends to be more severe and prolonged due to the profound impairment in cellular immunity following transplantation. VZV infection may develop as a primary infection or more commonly, reactivation of latent infection typically producing dermatomal zoster.…”

mentioning

confidence: 99%

Herpes zoster ophthalmicus following bone marrow transplantation in children

Walton

Reed

1999

Summary:Varicella zoster virus (VZV) infection is a frequent complication following bone marrow transplantation (BMT). Involvement of the ophthalmic division of the trigeminal nerve, herpes zoster ophthalmicus (HZO), can result in significant and potentially vision-threatening ocular complications. We report the frequency and characteristics of HZO following BMT, including the timing of infection, treatment, ocular complications, and visual outcome. Between 1983 and 1997, 572 patients underwent BMT and seven children developed HZO at a median of 150 days following transplantation. All but one of the children had undergone allogeneic BMT. All of the children were treated with acyclovir after onset of the rash but none had received prophylactic therapy. All seven children developed ocular complications within the first 4 weeks following the onset of the dermatomal rash but none reported any symptoms during this period. Complications included keratitis in six, anterior uveitis in three and scleritis in one. Keratitis was an early complication developing within the first 4 weeks, while anterior uveitis and scleritis occurred later in the course of the disease. The high frequency of ocular complications and lack of symptoms in children with HZO following BMT suggests that early ophthalmologic evaluation is warranted in this group of patients. Prompt diagnosis and treatment of ocular complications is essential in the prevention of acute and long-term ocular sequelae in these children. Keywords: herpes zoster ophthalmicus; bone marrow transplantation; varicella zoster; keratitis; uveitis; scleritis Varicella zoster virus (VZV) infection is a relatively frequent complication following autologous and allogeneic BMT. [1][2][3][4][5][6] The clinical course of zoster in these immunosuppressed patients tends to be more severe and prolonged due to the profound impairment in cellular immunity following transplantation. VZV infection may develop as a primary infection or more commonly, reactivation of latent infection typically producing dermatomal zoster. 6 In most series, the risk for infection appears to be highest during the 6-9 months following transplantation and up to 30% of patients who develop VZV following BMT will develop complications. [3][4][5][6] Involvement of the ophthalmic division of the trigeminal nerve -herpes zoster ophthalmicus -can result in serious and potentially vision-threatening ocular complications. 7 In adults, up to 72% of patients will develop ocular complications. 8 However, because HZO is uncommon in the pediatric population there is little information on the nature of the disease in children. 9 The purpose of this study was to describe the frequency and characteristics of HZO in children following BMT. Patients and methodsTo identify all children developing HZO following BMT, a computerized search of the BMT database at St Jude Children's Research Hospital in Memphis, TN was performed. All patients with a diagnosis of varicella zoster involving the ophthalmic division of the trigeminal nerve f...