Varicella zoster meningoencephalitis following treatment for dermatomal zoster in an alloBMT patient. (1/20)

Herpes zoster infections are frequently observed after allogeneic bone marrow transplantation (alloBMT). In the majority of cases, the infection is restricted to specific dermatomes and responds to oral acyclovir, without visceral dissemination. We report the case of a 40-year-old male who developed dermatomal herpetic infection 8 months post alloBMT. The herpetic rash responded well to treatment with high-dose oral acyclovir. However, within a week of cessation of therapy, the patient re-presented with dermatomal zoster and meningoencephalitis. Although the cutaneous lesions resolved with intravenous acyclovir, clinical features of meningoencephalitis persisted, along with evidence of varicella zoster virus (VZV) DNA in cerebrospinal fluid (CSF). A satisfactory response to treatment was observed only after the addition of intravenous foscarnet to acyclovir. Based on our experience with this patient, we suggest that in a subset of alloBMT recipients, late dermatomal herpes zoster infections may respond only partially to treatment with standard oral acyclovir. The use of oral acyclovir preparations with higher bioavailability (valacyclovir) or intravenous acyclovir early on may prevent the considerable morbidity associated with disseminated zoster infection. Bone Marrow Transplantation (2000) 26, 795-796.  (+info)

Varicella-zoster virus encephalitis in an AIDS patient. (2/20)

A 37-year-old man with a three-year history of Acquired Immunodeficiency Syndrome was admitted with impaired consciousness, seizures and fever. He was on highly active antiretroviral therapy and on neurotoxoplasmosis secondary prophylaxis. Laboratory exams from two months before showed a CD4 cell count of 37/microL and a viral load of 230,000 copies/mL. Three months before admission he developed herpetic skin rash in the right trunk and acyclovir was added to his treatment regimen. On physical exam he was drowsy and had motor and sensory aphasia. The patient had elevated protein levels and normal pressure in the cerebrospinal fluid (CSF). Contrast enhanced computed tomography scan of the brain showed a hypodense lesion in the left parietal lobe, with poorly defined margins and no contrast enhancement. The magnetic resonance scan (MRI) showed multiple hyperintensities in T2-weighted image in white and grey matters and hypointense products of hemorrhage in both hemispheres and in the cerebellum. He was empirically treated with intravenous acyclovir and prednisone. Viral DNA of Varicella-zoster virus (VZV) was detected in the CSF by means of polymerase chain reaction (PCR) analysis. Acyclovir was continued for 10 days and the patient became well, with improvement of aphasia. We present a case of VZV encephalitis, confirmed by nested PCR, in a patient with suggestive MRI findings, who succeeded with treatment. VZV encephalitis is a rare opportunistic infection, occurring in 0.1 to 4% of AIDS patients with neurological disease; it is related to severe immunodeficiency and has a high mortality.  (+info)

Varicella zoster virus meningitis complicating sodium stibogluconate treatment for cutaneous leishmaniasis. (3/20)

Sodium stibogluconate (Pentostam(R); GlaxoSmithKline) is a pentavalent antimonial compound used in the treatment of leishmaniasis, which has an association with reactivation of varicella zoster virus (VZV). We report the first known case of an immunocompetent adult who developed VZV aseptic meningitis and dermatomal herpes zoster during treatment with sodium stibogluconate.  (+info)

Absence or overexpression of the Varicella-Zoster Virus (VZV) ORF29 latency-associated protein impairs late gene expression and reduces VZV latency in a rodent model. (4/20)

Varicella-zoster virus (VZV) ORF29 encodes the viral single-stranded DNA binding protein and is expressed during latency in human ganglia. We constructed an ORF29 deletion mutant virus and showed that the virus could replicate only in cells expressing ORF29. An ORF29-repaired virus, in which ORF29 was driven by a cytomegalovirus promoter, grew to peak titers similar to those seen with the parental virus. The level of ORF29 protein in cells infected with the repaired virus was greater than that seen with parental virus. Infection of cells with either the ORF29 deletion or repaired virus resulted in similar levels of VZV immediate-early proteins but reduced levels of glycoprotein E compared to those observed with parental virus. Cotton rats infected with the ORF29 deletion mutant had a markedly reduced frequency of latent infection in dorsal root ganglia compared with those infected with parental virus (P < 0.00001). In contrast, infection of animals with the ORF29 deletion mutant resulted in a frequency of ganglionic infection at 3 days similar to that seen with the parental virus. Animals infected with the ORF29-repaired virus, which overexpresses ORF29, also had a reduced frequency of latent infection compared with those infected with parental virus (P = 0.0044). These studies indicate that regulation of ORF29 at appropriate levels is critical for VZV latency in a rodent model.  (+info)

Herpes zoster-associated encephalitis in a patient undergoing CAPD: case report and literature review. (5/20)

Neurological complications of varicella zoster virus (VZV) reactivation have rarely been described in dialysis patients. We report a case of a continuous ambulatory peritoneal dialysis (CAPD) patient who developed herpes zoster encephalitis. The patient was treated with acyclovir and steroids and had a slow but complete return to her prior cognitive status. The available literature is reviewed and the differential diagnosis with acyclovir toxicity is discussed.  (+info)

SUNCT and trigeminal neuralgia attributed to meningoencephalitis. (6/20)

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Varicella zoster virus meningo-encephalo-myelitis in an immunocompetent patient. (7/20)

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Recurrent varicella zoster virus myelopathy. (8/20)

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