Varicella Zoster Virus Meningoencephalitis Research Articles

A rare case of AIDS co-infected with COVID-19 presenting with disseminated Herpes zoster complicated with CMV and Varicella zoster virus meningoencephalitis.

During the COVID-19 pandemic, numerous co-infections have been reported, with some studies indicating that patients with HIV/AIDS have worse outcomes when co-infected with COVID-19. Here, we present the case of a young adult male who presented with disseminated Varicella and was simultaneously diagnosed with AIDS and COVID-19 virus with several infection-related complications. A 25-year-old African-American male presented to the Emergency Department with vesicular, blistering rashes in multiple dermatomes including his eyelids. The screening test in the ED was positive for COVID-19. Given his high-risk sexual history, he was tested for HIV which returned positive with a CD4 count of zero. He was started on IV antivirals for disseminated varicella with zoster ophthalmicus. The patient was intubated for worsening respiratory failure and required intensive care. During the hospital course, he developed worsening encephalopathy and CSF analysis was positive for CMV and VZV. The patient has a prolonged hospital stay and exhibited evidence of infectious CNS vasculitis and HIV myelopathy. Anti-retroviral therapy was started after the acute period and the patient showed slow but definite clinical improvement. To the best of our knowledge, this is the first case report of a patient with AIDS with COVID-19 and disseminated VZV and with multiple complex infection-related complications.

Abstract 13090: Not Your Simple Swimmer’s Ear: Ramsay Hunt Syndrome Complicated by Gradenigo Syndrome, Varicella Zoster Meningoencephalitis, and Superimposed Bacterial Necrotizing Otitis Externa in a Heart Transplant Patient on Chronic Immunosuppression

Introduction: Orthotopic heart transplantation (OHT) increases the risks of varicella-zoster reactivation, and severe complications may arise due to infection in the setting of active immunosuppression. Complications include meningitis, facial nerve palsy (known as Ramsay Hunt Syndrome), and bacterial superinfection. When severe bacterial ear infections spread to the petrous apex, facial pain accompanied by otitis media and abducens nerve palsy may also occur, classically known as Gradenigo Syndrome. Case Report: We present a case of a patient 15 months post OHT who came in with left-sided facial droop and pain, abducens palsy, crusting facial rash, and ear swelling. Imaging revealed necrotizing otitis externa, with associated otitis media, petrous apicitis, and signs suggestive of encephalitis. A viral panel resulted positive for zoster infection, with superimposed methicillin-resistant staphylococcus aureus infection. Despite treatment with antibiotics and antivirals, the patient's mentation declined, with subsequent lumbar puncture revealing zoster meningoencephalitis. The patient’s mycophenolate mofetil (MMF) immunosuppression was suspended, and he was continued solely on therapeutic tacrolimus. His antiviral was switched to intravenous acyclovir and he was continued on six weeks of antibiotic therapy. The patient demonstrated resolution of his acute infection, however he continues to have residual facial and abducens nerve palsies. On discharge, the patient was resumed on MMF without any cardiac complications. Conclusions: This is the first documented case of Ramsay Hunt Syndrome, complicated by Gradenigo Syndrome and varicella-zoster virus meningoencephalitis in an OHT recipient. Our patient's immunosuppression level was the most important factor leading to the concurrence of these novel complications. Physicians should consider and assess for symptoms of these potential sequelae in all transplant patients, and carefully manage immunosuppressive agents to allow for resolution of the infection, while avoiding rejection. While residual neurologic deficits may be challenging to manage, this case demonstrated successful treatment of these complications while avoiding significant cardiac sequelae.

Varicella-Zoster Virus Meningoencephalitis in a Lung Transplant Recipient

Introduction Solid organ transplant (SOT) recipients are susceptible to an array of infections and atypical clinical presentations. Varicella-zoster virus (VZV) becomes latent in dorsal root ganglia after the initial infection, and reinfection commonly presents with a painful rash. In SOT recipients, VZV can present as meningoencephalitis without an associated rash and is associated with high morbidity and mortality. We present a rare case of VZV meningoencephalitis in a lung transplant recipient. Case Report A 71-year-old woman with a history of bilateral lung transplant in 2014 and rheumatoid arthritis presented to an outside hospital with one week of fever and confusion. She was subsequently intubated after suffering a generalized tonic-clonic seizure. Upon transfer to our facility she had an unremarkable exam including skin exam. She was started on vancomycin, ceftriaxone, ampicillin, acyclovir, and fluconazole for presumed meningoencephalitis. Lumbar puncture revealed 100 WBC/mm3, with 93% lymphocytes. The cerebrospinal fluid (CSF) glucose was 125 mg/dL, protein was 233 mg/dL, cultures were negative but qualitative polymerase chain reaction (PCR) was positive for VZV. Electroencephalogram (EEG) revealed status epilepticus and magnetic resonance imaging (MRI) showed a T1 and T2 hypointensity in the right posterior periventricular white matter and scattered foci in bilateral cerebral white matter. Her status epilepticus was treated with antiepileptics and resolved by hospital day eight. She received 14 days of intravenous (IV) acyclovir 10mg/kg every 8 hours and was transitioned to oral valacyclovir for suppression for two months. On discharge her mental status had significantly improved but had not fully returned to her baseline. Summary Zoster is a common, benign disease caused by VZV and associated with painful cutaneous lesions. However, neurological manifestations without a rash are possible in SOT patients. Lumbar puncture and CSF analysis are crucial for diagnosis and typically shows lymphocytosis with viral culture, antibody, or PCR positive for VZV. Treatment of choice for VZV encephalitis is IV acyclovir for 7 days in the immunocompetent patient and 14 days in the immunosuppressed patient. This case demonstrates how prompt recognition and treatment of VZV meningoencephalitis can decrease mortality and neurologic disease in the immunocompromised patient. Solid organ transplant (SOT) recipients are susceptible to an array of infections and atypical clinical presentations. Varicella-zoster virus (VZV) becomes latent in dorsal root ganglia after the initial infection, and reinfection commonly presents with a painful rash. In SOT recipients, VZV can present as meningoencephalitis without an associated rash and is associated with high morbidity and mortality. We present a rare case of VZV meningoencephalitis in a lung transplant recipient. A 71-year-old woman with a history of bilateral lung transplant in 2014 and rheumatoid arthritis presented to an outside hospital with one week of fever and confusion. She was subsequently intubated after suffering a generalized tonic-clonic seizure. Upon transfer to our facility she had an unremarkable exam including skin exam. She was started on vancomycin, ceftriaxone, ampicillin, acyclovir, and fluconazole for presumed meningoencephalitis. Lumbar puncture revealed 100 WBC/mm3, with 93% lymphocytes. The cerebrospinal fluid (CSF) glucose was 125 mg/dL, protein was 233 mg/dL, cultures were negative but qualitative polymerase chain reaction (PCR) was positive for VZV. Electroencephalogram (EEG) revealed status epilepticus and magnetic resonance imaging (MRI) showed a T1 and T2 hypointensity in the right posterior periventricular white matter and scattered foci in bilateral cerebral white matter. Her status epilepticus was treated with antiepileptics and resolved by hospital day eight. She received 14 days of intravenous (IV) acyclovir 10mg/kg every 8 hours and was transitioned to oral valacyclovir for suppression for two months. On discharge her mental status had significantly improved but had not fully returned to her baseline. Zoster is a common, benign disease caused by VZV and associated with painful cutaneous lesions. However, neurological manifestations without a rash are possible in SOT patients. Lumbar puncture and CSF analysis are crucial for diagnosis and typically shows lymphocytosis with viral culture, antibody, or PCR positive for VZV. Treatment of choice for VZV encephalitis is IV acyclovir for 7 days in the immunocompetent patient and 14 days in the immunosuppressed patient. This case demonstrates how prompt recognition and treatment of VZV meningoencephalitis can decrease mortality and neurologic disease in the immunocompromised patient.

Acyclovir-induced neurotoxicity with a positive cerebrospinal fluid varicella zoster PCR result creating a management dilemma: a case report

BackgroundVaricella zoster virus central nervous system infections can present as aseptic meningitis, encephalitis, myelitis, and vasculopathy. Diagnosis is based on identification of varicella zoster virus deoxyribonucleic acid (DNA) in the cerebrospinal fluid by polymerase chain reaction. Therapy for these infections is acyclovir or valacyclovir. However, acyclovir can have neurotoxic effects that can mimic the presentation of varicella zoster virus central nervous system disease. We present a rare presentation of a patient who had acyclovir-induced neurotoxicity who also had a false-positive cerebrospinal fluid varicella zoster virus polymerase chain reaction result, creating a management dilemma. We review the clinical characteristics of acyclovir-induced neurotoxicity. In addition, we present the diagnostic characteristics of the cerebrospinal fluid viral polymerase chain reaction and alternative methods to diagnose central nervous system varicella zoster virus disease.Case presentationA 68-year-old Hispanic man with end-stage renal disease was diagnosed with cutaneous zoster at an outside facility and was started on acyclovir 4 days prior to admission. His family noted worsening confusion, agitation, speech difficulty, and hallucinations, leading them to bring him to the emergency department. His cerebrospinal fluid varicella zoster virus polymerase chain reaction result was positive, indicating the presence of varicella zoster virus deoxyribonucleic acid in the cerebrospinal fluid; however, he did not have cerebrospinal fluid pleocytosis typical of varicella zoster virus meningoencephalitis. Pharmacy records from the outside hospital revealed supratherapeutic acyclovir dosing. This led to a diagnostic dilemma over whether this patient had varicella zoster virus encephalitis or acyclovir-induced neurotoxicity. Acyclovir was discontinued, and the patient underwent two sessions of hemodialysis to remove acyclovir, which led to a full neurologic recovery.ConclusionsVaricella zoster virus encephalitis and acyclovir-induced neurotoxicity can have similar presentations. Varicella zoster virus deoxyribonucleic acid can be present in the cerebrospinal fluid during active cutaneous zoster in the absence of central nervous system disease. If concern for central nervous system varicella zoster virus disease remains high, additional testing with cerebrospinal fluid serology can be performed. Compared with central nervous system varicella zoster virus disease, acyclovir-induced neurotoxicity has a more predictable clinical resolution once drug therapy is discontinued or the patient undergoes hemodialysis, which can aid in making the diagnosis. Clinicians should be aware of this rare and dangerous complication of acyclovir. In addition, clinicians should have an understanding of the diagnostic limitations of cerebrospinal fluid viral polymerase chain reaction and have alternative approaches available to diagnose central nervous system varicella zoster virus disease when it is suspected.

A Case of Varicella-Zoster Meningoencephalitis Presented by Ramsay Hunt Syndrome.

Varicella-zoster virus (VZV) reactivation can cause meningoencephalitis. Ramsay Hunt syndrome is the reactivation of VZV in facial nerve, consisting of ear pain, facial nerve paralysis, and auricular rash. We present a case of VZV meningoencephalitis presented with Ramsay Hunt syndrome. Early clinical suspicion was beneficial in starting aggressive treatment.

G1m1 predominance of intrathecal virus-specific antibodies in multiple sclerosis.

We have previously shown that plasmablasts of the G1m1 allotype of IgG1 are selectively enriched in the cerebrospinal fluid of G1m1/G1m3 heterozygous patients with multiple sclerosis, whereas both allotypes are equally used in neuroborreliosis. Here, we demonstrate a strong preference for the G1m1 allotype in the intrathecal humoral immune responses against measles, rubella, and varicella zoster virus in G1m1/G1m3 heterozygous multiple sclerosis patients. Conversely, intrathecally synthesized varicella zoster virus‐specific IgG1 in varicella zoster virus meningoencephalitis comprised both allotypes. This implies that G1m1 B cells are selected to the central nervous system of multiple sclerosis patients regardless of specificity and suggests that an antigen‐independent mechanism could drive the intrathecal humoral immune response.

Varicella meningitis : An atypical presentation in an immunocompetent individual with seizures managed with acyclovir

Viral meningitis, also known as aseptic meningitis, is the most common cause of meningitis and is responsible for between 26,000 and 42,000 hospitalizations yearly in the United States. Bacterial meningitis affects about 4,000 people each year, while viral meningitis affects about 10 people in every 100,000. The most commonly identified pathogens are enterovirus, herpes simplex virus and human immunodeficiency virus. Varicella, rabies and influenza are other viruses that are rarely responsible for viral meningitis. Varicella Zoster is a relatively common disorder in immunocompromised patients characterized by radicular pain and grouped vesicular eruptions. The typical findings in reported cases of VZV meningitis involve skin manifestations and classical signs of meningitis such as neck stiffness. However, only a few cases of meningitis caused by Varicella Zoster Virus (VZV) have been reported. The incidence of VZV meningitis in immunocompetent patients has been reported to be as low as 0.5%. We report an atypical presentation of VZV meningitis in an immunocompetent patient with headache, dizziness, sequalae of seizures without fever and skin manifestations.Our patient is a 59‐year‐ old African American male who presented with worsening dizziness, confusion, ataxia, lethargy and left‐sided frontal headache. Magnetic resonance imaging revealed mild to moderate burden of white matter abnormality, nonspecific but most likely due to chronic microvascular ischemic disease. No acute stroke. The next day sedation was weaned off and patient remained seizure free on continuous EEG and was extubated 3 days later the CSF came back positive for an elevated Varicella PCR of 42016. Patient was seen by infectious diseases consultant and was advised a course of acyclovir 10mg/kg intravenous every 8 hours for 14 days. All other antibiotics were stopped. Upon discharge, the patient had fully recovered from his symptoms with no neurologic sequalae.This unique case illustrates an atypical presentation of VZV meningoencephalitis in an immunocompetent patient that lacks many of the obvious features that usually distinguish the disease. Our patient lacked the vesicular rash, as well as other typical features of aseptic meningitis including nuchal rigidity, headache, photophobia, etc. Additionally, the patient's course was complicated by seizure, another relatively uncommon feature of VZV meningoencephalitis. VZV infection or reactivation is, rightfully, most commonly associated with the vesicular rash and prodromal pain that usually accompanies it.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Haemorrhagic conversion of infectious myelitis in an immunocompromised patient

A 28-year-old man recently diagnosed with HIV (CD4 19 cells/mm3, viral load 3.6 million copies/mL, not on highly active antiretroviral therapy on initial diagnosis at outside hospital), disseminated histoplasmosis, shingles...

Valacyclovir and Acyclovir Neurotoxicity With Status Epilepticus

We present the case of a 52-year-old man with hypertension, diastolic congestive heart failure, end-stage renal disease on hemodialysis 3 times a week and a remote history of a hemorrhagic stroke who presented to the emergency department with a vesicular rash on his left arm. The rash was observed to be in a dermatomal distribution, and a diagnosis of herpes zoster was made. The patient was discharged home on valacyclovir 1 g 3 times a day for a duration of 7 days. The patient took 2 doses of valacyclovir before presenting to the hospital again with irritability and hallucinations. Over the next several days, the patient's neurologic status declined and he became disoriented and increasingly somnolent. Because of a concern for varicella zoster virus (VZV) or herpes simplex virus (HSV) meningoencephalitis, acyclovir was initiated intravenously at 600 mg (10 mg/kg) for every 12 hours. Computed tomography and magnetic resonance imaging of the brain failed to reveal an acute process. Electroencephalogram was interpreted as seizure activity versus metabolic encephalopathy. Lumbar puncture was not suggestive for meningitis, subarachnoid hemorrhage, or HSV/VZV infection. The patient subsequently had a witnessed seizure during dialysis and was felt to have status epilepticus due to acyclovir and valacyclovir neurotoxicity. The patient underwent daily hemodialysis for removal of the drug and eventually made a full neurologic recovery. Our case highlights that acyclovir neurotoxicity can result in status epilepticus, hallucinations, and altered consciousness. Differentiating acyclovir neurotoxicity from HSV or VZV meningoencephalitis is of crucial importance because the symptoms are similar but the management is vastly different.

Neurological Sequale of Varicella Zoster Virus Infection

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.

Incidence and clinical features of herpes simplex viruses (1 and 2) and varicella‐zoster virus infections in an adult Korean population with aseptic meningitis or encephalitis

Since there are limited data on the incidence and clinical findings of central nervous system (CNS) infection by three α-herpesviruses including human herpes simplex virus 1 (HSV-1), HSV-2 and varicella-zoster virus (VZV) in Korea, a retrospective analysis of clinical data and polymerase chain reaction (PCR) results was performed in patients who presented with suspicion of acute viral meningitis and/or encephalitis at the emergency department of a tertiary referral hospital in Seoul, Korea. During the 3-year study period, a total of 224 cerebrospinal fluid (CSF) samples from 224 patients were examined. Among the 224 patients, 135 (60.3%) patients were identified as having aseptic meningitis (n = 70, 51.9%), encephalitis (n = 41, 30.4%) or meningoencephalitis (n = 24, 17.8%) at discharge. Twenty-four (17.8%) patients were identified as having VZV meningitis (n = 16, 11.9%), VZV meningoencephalitis (n = 2, 1.5%), HSV-2 meningitis (n = 4, 3.0%), or HSV-1 encephalitis (n = 2, 1.5%). Of the 24 patients infected with the three herpesviruses, immunocompromised patients accounted for 33.3% (n = 8). Skin rashes were observed in half (n = 9) of the patients with VZV, and none with HSV-1 or HSV-2. One patient with VZV meningitis and four patients with brain parenchymal involvement had neurologic sequelae. In conclusion, three herpesviruses are important causative agents of CNS infectious disease with significant morbidity in adults, regardless of the immunologic status. Therefore, CSF should be examined for HSV-1, HSV-2, and VZV using sensitive diagnostic methods in all cases of adult patients with clinical manifestations of CNS disease in order to identify the correct etiology and to determine appropriate therapy.

Varicella-zoster meningoencephalitis — Case report

Introduction: Encephalitis is defined as inflammation of the brain parenchyma and meningoencephalitis when there is meningeal involvement. A viral etiology is the most common and the diagnostic method of choice is the polymerase chain reaction (PCR) of viral nucleic acids in cerebrospinal fluid (CSF). Herpes simplex virus is the leading cause of encephalitis and varicella-zoster virus (VZV) a less common cause, particularly in immunocompetent individuals. Case report: Woman, 67 years old, retired nurse, brought to the emergency room by disorientation. Physical examination: slowed, disoriented, incoherent and repetitive speech; subfebrile (T-37, 2 °C); no meningeal signs or skin lesions were identified. Laboratory tests revealed leukocytosis (10.5 × 10 ^9/L) with neutrophilia (86.9%). Computed tomography and magnetic resonance imaging (MRI) of the brain were performed and there were no lesions on brain parenchyma. Lumbar puncture (LP): 5 leukocytes/mm3; erythrocytes 2327/mm3; glucose: 80 mg/dl, and protein 26.7 mg/dl. Blood, cerebrospinal fluid cultures and capsular antigens were collected. The patient had clinical worsening at 48 h with fever (T-38, 7 °C), agitation, seizures, left hemiparesis and meningeal signs. LP was repeated: leukocytes 40/mm (98% of polymorphonuclear cells), glucose: 113 mg/dl, and protein: 30.4 mg/dl. CSF cultures were repeated and viral PCR in cerebrospinal fluid was requested. Human immunodeficiency virus testing was negative. Empirically ceftriaxone, ampicillin and acyclovir 10 mg/Kg ev, 8/8 h was established. Electroencephalography revealed severe cortical structural damage in the left hemisphere. MRI of the brain was repeated and showed no lesions. Microbiological study was negative and VZV PCR in CSF was positive. She completed 21 days of acyclovir. The patient had a good clinical and neurologic outcome with resolution of all the symptoms. Conclusion: VZV meningoencephalitis. The case stands out for infection of the central nervous system by VZV in an immunocompetent patient, along with the importance of a high clinical suspicion of viral encephalitis even in the presence of pleocytosis with a predominance of polymorphonuclear cells in the early phase of infection. The suspicion of encephalitis is critical in the decision of early antiviral therapy to prevent neurological sequelae.

Complications of varicella zoster virus reactivation.

Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), which can occur anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of pain usually takes 4-6 weeks. Zoster can be followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, meningoencephalitis, cerebellitis, myelopathy, multiple ocular disorders and vasculopathy that can mimic giant cell arteritis. All of the neurological and ocular disorders listed above may also develop without rash. Diagnosis of VZV-induced neurological disease may require examination of cerebrospinal fluid (CSF), serum and/ or ocular fluids. In the absence of rash in a patient with neurological disease potentially due to VZV, CSF should be examined for VZV DNA by PCR and for anti-VZV IgG and IgM. Detection of VZV IgG antibody in CSF is superior to detection of VZV DNA in CSF to diagnose vasculopathy, recurrent myelopathy, and brainstem encephalitis. Oral antiviral drugs speed healing of rash and shorten acute pain. Immunocompromised patients require intravenous acyclovir. First-line treatments for post-herpetic neuralgia include tricyclic antidepressants, gabapentin, pregabalin, and topical lidocaine patches. VZV vasculopathy, meningoencephalitis, and myelitis are all treated with intravenous acyclovir.

Varicella zoster virus meningoencephalitis after allogeneic hematopoietic stem cell transplantation

Although the reactivation of varicella zoster virus (VZV) is a common complication after allogeneic hematopoietic stem cell transplantation (HSCT), VZV meningoencephalitis is a rare life-threatening infectious disease after HSCT. We describe here a patient who developed VZV meningoencephalitis 2 years after human leukocyte antigen-matched unrelated HSCT for acute myeloblastic leukemia. She developed chronic graft-versus-host disease, and cyclosporine (CSA) was continued until 17 months after HSCT. Low-dose acyclovir (ACV) at 200 mg/day was administered to prevent the reactivation of VZV from day -7 to the termination of CSA. At 22 months, she suddenly developed fever, loss of consciousness, and seizure, with generalized skin rash. A high level of VZV DNA was detected in her cerebrospinal fluid (CSF). She was diagnosed to have VZV meningoencephalitis. Intravenous ACV at 30 mg/kg/day was given for 2 months. Although loss of consciousness was quickly resolved, some neurologic symptoms persisted. She did not have any known risk factors for VZV reactivation. Therefore, we should keep in mind that any HSCT recipient may develop VZV meningoencephalitis, and examination of CSF for VZV infection with an empiric administration of ACV may be recommended for HSCT recipients with central nervous system symptoms, even in the absence of skin manifestations.

Varicella zoster vs. herpes simplex meningoencephalitis in the PCR era. A single center study

BackgroundThe introduction of polymerase chain reaction (PCR) for the diagnosis of herpesvirus central nervous system infections is reshaping our understanding of these illnesses. Varicella-zoster virus (VZV) is increasingly recognized as an important etiology of sporadic viral meningoencephalitis (ME). Furthermore, mild cases of herpes simplex virus (HSV) ME, traditionally considered a devastating infection, are frequently reported. MethodsWe compared the demographic and clinical features of patients with VZV (20) and HSV (17) ME diagnosed by Real-Time PCR of cerebrospinal samples in a single center during the years 2002–2010. ResultsVZV and HSV patients were comparable with respect to age, sex, underlying diseases, immune suppression, and the rates of fever, headache and altered mental status on presentation. Seizures, focal neurological signs, systemic complications and in-hospital death were noted only in the HSV group. ConclusionsOur study confirms the prevalence of VZV as a cause of sporadic ME over the last decade. While patients with HSV ME had more manifestations of severe disease, there also was a significant overlap with clinical and laboratory parameters of VZV ME. In the absence of dermatomal rash, differentiation between VZV and HSV ME on clinical grounds alone may represent a true challenge.

Varicella zoster virus meningoencephalitis accompanied by rhabdomyolysis without skin eruption

We report a case of a 38-year-old man with a Varicella zoster virus (VZV) reactivation who manifested meningoencephalitis accompanied by rhabdomyolysis without a skin eruption. During the acute phase, VZV DNA was detected in serum and cerebrospinal fluid (CSF) by the polymerase chain reaction (PCR). After 16 days, all symptoms and signs resolved, and follow-up PCR studies revealed negative conversion of VZV in the serum and CSF. We discuss the possible underlying mechanism of VZV reactivation in our patient. This is the first case report of VZV reactivation meningoencephalitis accompanied by rhabdomyolysis without skin eruption demonstrated by viral DNA in the serum and CSF.

Acute lymphoblastic leukemia complicated with varicella zoster virus meningoencephalitis and visceral dissemination after related bone marrow transplantation

Acute lymphoblastic leukemia complicated with varicella zoster virus meningoencephalitis and visceral dissemination after related bone marrow transplantation

Facial herpes zoster complicated by varicella zoster virus (VZV) encephalitis: The diagnostic significance of atypical lymphocytes in cerebrospinal fluid (CSF)

Background In general, viral infections of the central nervous system (CNS) manifest as encephalitis and, less commonly, as meningoencephalitis or aseptic meningitis. Varicella zoster virus (VZV) is an uncommon cause of encephalitis. Methods Herpes zoster (shingles) is a cutaneous reactivation of previous chickenpox infection due to VZV. Herpes zoster may be dermatomal (ie, <3 dermatomes) or disseminated (ie, >3 dermatomes). Decreased cell-mediated immunity from stress, steroids, or immunosuppressive drugs often precede dermatomal/disseminated herpes zoster. With herpes zoster, the closer the dermatomal involvement is to the CNS (ie, head/neck shingles), the more likely a patient will have symptomatic CNS involvement (eg, encephalitis). Except for the association of the herpes zoster rash and the simultaneous/subsequent encephalitis, there are few clinical features that distinguish VZV encephalitis from that due to other viruses. The cerebrospinal fluid (CSF) profile of VZV encephalitis is usually clinically indistinguishable from that due to of other causes of viral encephalitis. In VZV meningoencephalitis or encephalitis, the CSF typically shows a modest lymphocytic pleocytosis with normal CSF glucose levels, variably elevated CSF protein levels, and normal CSF lactic acid levels. Atypical lymphocytes are rare in the CSF with VZV encephalitis. Results We present the case of a 75-year-old woman who developed VZV encephalitis after having herpes zoster on her forehead. Except for facial herpes zoster, there were no clinically distinguishing features to determine the cause of her encephalitis. Her CSF had 800 white blood cells/high power field with 26% lymphocytes (17% atypical lymphocytes). The patient’s CSF glucose and CSF lactate dehydrogenase levels were normal, and her CSF protein was elevated. The CSF lactic acid was minimally elevated secondary to red blood cells in the CSF. Electroencephalogram showed general background slowing bilaterally, typical of viral encephalitis. The absence of unilateral focal frontotemporal/parietal lobe focus on electroencephalogram argued against the diagnosis of herpes simplex encephalitis. CSF atypical lymphocytes provided the key clue to the etiology of her encephalitis. CSF atypical lymphocytes are not uncommon in Epstein–Barr virus or cytomegalovirus encephalitis. Less commonly, atypical lymphocytes may be present in the CSF with enteroviruses, West Nile encephalitis, and Japanese encephalitis. VZV is a rare cause of atypical lymphocytes in the CSF but was the clue to the diagnosis before CSF polymerase chain reaction results for VZV were available. Her CSF polymerase chain reaction was negative for Mycobacterium tuberculosis, herpes simplex virus, human herpesvirus-6, cytomegalovirus, enteroviruses, and West Nile virus, but was positive for VZV. She made an uneventful recovery with acyclovir. Conclusion CSF atypical lymphocytes, if present, are an important diagnostic clue in some causes of viral encephalitis. The most common cause of nonseasonal viral encephalitis is herpes simplex virus, which is not associated with CSF atypical lymphocytes. Patients with Epstein–Barr virus, cytomegalovirus, West Nile encephalitis, and enteroviruses usually have extra-CNS signs and symptoms which should suggest the cause of the patient’s encephalitis. CSF atypical lymphocytes limit the differential diagnostic possibilities in patients with viral encephalitis and may be the key clue to the diagnosis, as in the case presented.

Lethal varicella-zoster virus reactivation without skin lesions following renal transplantation

Patients after solid organ transplantation are at increased risk of developing herpes zoster and are more likely to develop major complications such as cutaneous dissemination, post-herpetic neuralgia and visceral organ involvement. We report on a 68-year-old woman being varicella-zoster virus (VZV)-seropositive prior to transplantation, who developed fatal VZV meningoencephalitis after renal transplantation presenting with non-specific neurologic symptoms. The case illustrates that VZV reactivation may occur in renal transplant recipients in the absence of skin lesions. Approaches towards risk assessment pre-transplantation and prophylactic regimens for the prevention of VZV recurrence are needed.

Varicella-zoster virus meningoencephalitis in an immunocompetent patient without a rash

Varicella-zoster virus (VZV) is an unusual cause of meningoencephalitis in the immunocompetent patient. Most cases of VZV-associated aseptic meningitis or encephalitis are associated with the skin rash of primary varicella, localized herpes zoster, or disseminated zoster. We report a case of VZV meningoencephalitis without a rash occurring in a normal host.