Clinical characteristics and cerebrospinal fluid adenosine deaminase activity in patients with meningitis caused by Varicella-Zoster virus

2013 ◽  
Vol 333 ◽  
pp. e635
Author(s):  
H.G. Oh ◽  
E.J. Rhee
Keyword(s):  
Cerebrospinal Fluid ◽  
Varicella Zoster Virus ◽  
Adenosine Deaminase ◽  
Clinical Characteristics ◽  
Varicella Zoster ◽  
Adenosine Deaminase Activity

When infection mimics cauda equina syndrome: a cautionary tale

2021 ◽  
Vol 103 (6) ◽  
pp. e181-e183
Author(s):  
R Shah ◽  
N Jayakumar ◽  
S Athar ◽  
N Ashwood
Keyword(s):  
Magnetic Resonance Imaging ◽  
Cerebrospinal Fluid ◽  
Magnetic Resonance ◽  
Varicella Zoster Virus ◽  
Cauda Equina Syndrome ◽  
Cauda Equina ◽  
Lessons Learned ◽  
Resonance Imaging ◽  
Varicella Zoster ◽  
Elsberg Syndrome

A 63-year-old man presented to the emergency department with low back pain, perineal and genital numbness, together with bilateral lower limb paraesthesia and urinary retention. He was admitted under the orthopaedic service for investigation of suspected cauda equina syndrome. Magnetic resonance imaging of his spine did not reveal any evidence of cauda equina compression. Magnetic resonance imaging of his brain demonstrated nonspecific multiple hyperintensities in the right frontotemporal and left temporo-occipital regions. Computed tomography of his chest, abdomen, and pelvis did not identify any evidence of malignancy. Cerebrospinal fluid from a lumbar puncture showed a high leucocyte count (predominantly lymphocytes). Viral cerebrospinal fluid polymerase chain reaction was positive for varicella zoster virus. A diagnosis of varicella zoster virus myeloradiculitis (Elsberg syndrome) was established and the patient was treated with intravenous aciclovir. Unfortunately, the patient succumbed to a devastating intracerebral haemorrhage during his inpatient stay, probably due to vasculopathy from the underlying varicella zoster virus infection. This case describes a rare infectious mimic of cauda equina syndrome. Elsberg syndrome is an infectious syndrome characterised by bilateral lumbosacral myeloradiculitis, with varicella zoster virus being a well-recognised aetiological agent. We discuss the relevant literature in detail and identify the key, cautionary lessons learned from this case.

scholarly journals Amylin, Aβ42, and Amyloid in Varicella Zoster Virus Vasculopathy Cerebrospinal Fluid and Infected Vascular Cells

2020 ◽  
Author(s):  
Andrew N Bubak ◽  
Cheryl Beseler ◽  
Christina N Como ◽  
Christina M Coughlan ◽  
Noah R Johnson ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Varicella Zoster Virus ◽  
Amyloid Fibrils ◽  
Central Nervous System Infection ◽  
Amyloid Deposition ◽  
Amyloid Formation ◽  
Varicella Zoster ◽  
Arterial Inflammation ◽  
Amyloidogenic Peptides ◽  
Interfering Rna

Abstract Background Varicella zoster virus (VZV) vasculopathy is characterized by persistent arterial inflammation leading to stroke. Studies show that VZV induces amyloid formation that may aggravate vasculitis. Thus, we determined if VZV central nervous system infection produces amyloid. Methods Aβ peptides, amylin, and amyloid were measured in cerebrospinal fluid (CSF) from 16 VZV vasculopathy subjects and 36 stroke controls. To determine if infection induced amyloid deposition, mock- and VZV-infected quiescent primary human perineurial cells (qHPNCs), present in vasculature, were analyzed for intracellular amyloidogenic transcripts/proteins and amyloid. Supernatants were assayed for amyloidogenic peptides and ability to induce amyloid formation. To determine amylin’s function during infection, amylin was knocked down with small interfering RNA and viral complementary DNA (cDNA) was quantitated. Results Compared to controls, VZV vasculopathy CSF had increased amyloid that positively correlated with amylin and anti-VZV antibody levels; Aβ40 was reduced and Aβ42 unchanged. Intracellular amylin, Aβ42, and amyloid were seen only in VZV-infected qHPNCs. VZV-infected supernatant formed amyloid fibrils following addition of amyloidogenic peptides. Amylin knockdown decreased viral cDNA. Conclusions VZV infection increased levels of amyloidogenic peptides and amyloid in CSF and qHPNCs, indicating that VZV-induced amyloid deposition may contribute to persistent arterial inflammation in VZV vasculopathy. In addition, we identified a novel proviral function of amylin.

Adenosine deaminase activity in cerebrospinal fluid

2013 ◽  
Vol 115 (12) ◽  
pp. 2555
Author(s):  
Aurore Bousquet ◽  
Sarah Bugier ◽  
Franck Ceppa ◽  
Hervé Delacour
Keyword(s):  
Cerebrospinal Fluid ◽  
Adenosine Deaminase ◽  
Adenosine Deaminase Activity

scholarly journals Varicella Vaccine Meningitis as a Complication of Herpes Zoster in Twice-Immunized Immunocompetent Adolescents

2020 ◽  
Vol 35 (13) ◽  
pp. 889-895 ◽  
Author(s):  
Veena Ramachandran ◽  
Stephen C. Elliott ◽  
Kathie L. Rogers ◽  
Randall J. Cohrs ◽  
Miles Weinberger ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Herpes Zoster ◽  
Varicella Zoster Virus ◽  
Varicella Vaccine ◽  
The United States ◽  
Vaccine Virus ◽  
Virus Reactivation ◽  
Wild Type ◽  
Varicella Zoster ◽  
Intravenous Acyclovir

Varicella-zoster virus vaccination is recommended for virtually all young children in the United States, Canada, and several other countries. Varicella vaccine is a live attenuated virus that retains some of its neurotropic properties. Herpes zoster caused by vaccine virus still occurs in immunized children, although the rate is much lower than in children who had wild-type varicella. It was commonly thought that 2 varicella vaccinations would protect children against the most serious complication of meningitis following herpes zoster; however, 2 meningitis cases have already been published. We now report a third case of varicella vaccine meningitis and define risk factors shared by all 3 immunized adolescents. The diagnosis in cerebrospinal fluid in this third case was verified by amplifying and sequencing portions of the viral genome, to document fixed alleles found only in the vaccine strain. Viral antibody was also detected in the cerebrospinal fluid by confocal microscopy. When compared with the other 2 cases, remarkably all 3 were 14 years old when meningitis occurred. All 3 were treated with intravenous acyclovir, with complete recovery. The adolescent in our case report also had recurrent asthma, which was treated with both prednisone tablets and beclomethasone inhaler before onset of meningitis. When the 3 cases were considered together, they suggested that immunity to varicella-zoster virus may be waning sufficiently in some twice-immunized adolescents to make them vulnerable to varicella vaccine virus reactivation and subsequent meningitis. This complication rarely happens in children after wild-type varicella.

scholarly journals Role of cerebrospinal fluid adenosine deaminase activity in the diagnosis of tuberculous meningitis in children

2017 ◽  
Vol 4 (2) ◽  
pp. 411
Author(s):  
T. Hima Bindu ◽  
R. Maheshwara Reddy
Keyword(s):  
Cerebrospinal Fluid ◽  
Adenosine Deaminase ◽  
Tuberculous Meningitis ◽  
Mean Value ◽  
Successful Outcome ◽  
Correct Treatment ◽  
Cross Sectional ◽  
Adenosine Deaminase Activity ◽  
The Mean ◽  
Meningitis In Children

Background: Early and correct treatment is essential for successful outcome in patients of tuberculous men-ingitis. Adenosine deaminase activity in the cerebrospinal fluid has been found to be a simple and useful investigation in the diagnosis of tuberculous meningitis in children.Methods: It is a cross sectional observational hospital based study conducted at the Department of Paediatrics, Deccan College of Medical Sciences, Kanchanbagh, Hyderabad, India. Children aged 2 months to 12 years were included in the study during April 2016 to October 2016.Results: The mean value of adenosine deaminase activity in the cerebrospinal fluid of tuberculous meningitis cases was 13.3±14.49. The mean cerebrospinal fluid adenosine deaminase levels in tuberculous meningitis patients was significantly higher than non-tuberculous meningitis patients with P <0.01.Conclusions: The mean cerebrospinal fluid adenosine deaminase level was significantly raised in tuberculous meningitis patients.

scholarly journals Analysis of Cerebrospinal Fluid (CSF) – Adenosine Deaminase (ADA) in Meningitis

2021 ◽  
Vol 10 (16) ◽  
pp. 1102-1105
Author(s):  
Akkamahadevi V. Nipanal ◽  
Madhukumar M.H ◽  
Nagappa H
Keyword(s):  
Cerebrospinal Fluid ◽  
Early Diagnosis ◽  
Adenosine Deaminase ◽  
Viral Meningitis ◽  
Tubercular Meningitis ◽  
Acid Fast Bacilli ◽  
Group I ◽  
Adenosine Deaminase Activity ◽  
Function Test ◽  
The Mean

BACKGROUND Acute infections of the nervous system are generally widespread and cause significant problems in the field medicine and therefore early detection, right decision making, and early initiation of therapy can be lifesaving. Meningitis is the inflammation of the membranes that cover the brain and spinal cord. It is a general clinical problem during infancy and childhood. Delay in differentiating between bacterial, tubercular & viral meningitis and institution of its treatment may have irreparable consequences that lead to significant morbidity & mortality. The present study was conducted to find out the utility of cerebrospinal fluid-adenosine deaminase (CSF-ADA) for the early diagnosis & differentiation of tubercular & viral meningitis in adults. METHODS 50 meningitis patients who met the inclusion criteria were selected. Investigations including complete haemogram, liver function test (LFT), renal function test (RFT), random blood sugar (RBS), serum electrolytes, human immunodeficiency virus (HIV) test, chest x-ray and computed tomography (CT) brain (plain) were done. CSF cytology, biochemistry, gram stain, acid-fast bacteria (AFB) stain & culture were done. These cases were further divided in to two groups based on clinical and CSF laboratory findings as group I: tubercular meningitis, group II: viral meningitis. An estimation of CSF-ADA was done in all patients. RESULTS The mean age of the 50 patients studied was 37.76 + 15.58 years, with the maximum number of patients suffering from tubercular meningitis. The incidence of meningitis was more in males. CSF-adenosine deaminase activity was found to be higher in tubercular meningitis, the mean value was 17.67 ± 8.13 IU / L. CONCLUSIONS Assessment of CSF-ADA will be helpful for early diagnosis and differentiation of tubercular and viral meningitis. This is needed when gold standard investigations for meningitis like smear and / or culture for acid fast bacilli are not available or negative or are time consuming. KEY WORDS CSF-Cerebrospinal Fluid, ADA-Adenosine Deaminase, AFB-Acid Fast Bacilli.

Sign in / Sign up

Export Citation Format

Share Document