Varicella zoster virus infection in neurological patients in Bulgaria

Shikova, Evelina; Kumanova, Аntoniya; Tournev, Ivailo; Zhelyazkova, Sashka; Vassileva, Evgenia; Ivanov, Ivan; Pishmisheva, Maria

doi:10.1007/s13365-021-00952-6

Cited by 3 publications

(8 citation statements)

References 34 publications

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“…Thus, combined with the characteristics of CSF changes, the diagnosis of myelitis was established. VZV induced acute transverse myelitis (ATM) has been reported to rarely occur in the event of VZV reactivation [ 7 , 13 ]. Myelitis has been reported to be caused by the direct viral invasion based on post-mortem findings about the diagnosis of Cowdry type A intranuclear inclusions in spinal root ganglia and positive immunostaining of VZV antigens [ 13 – 15 ].…”

Section: Discussionmentioning

confidence: 99%

“…To avoid the possibility of infection spread caused by pulse steroid therapy, a small dose of steroid (5 mg/d dexamethasone) was initially applied in this case. VZV has been found to be a causative factor for a broad spectrum of neurological diseases [ 3 , 7 ]. However, most of the previously reported cases were observed to be either multiple cranial neuritis or myelitis.…”

Section: Discussionmentioning

confidence: 99%

“…PHN is considered to be the most common complication of VZV, which can occur in ~ 15% of cases, and diagnosed in 40% of the patients over 60 years of age [ 3 , 4 ]. VZV is still recognized as the most or second common infectious etiology of meningitis and encephalitis in adults, contributing 4.4–24% and 12–27.5% cases, respectively [ 5 – 7 ]. VZV infection can account for 8–28% of Bell’s palsy (BP) cases and 15.2% of cranial neuritis cases.…”

Section: Introductionmentioning

confidence: 99%

“…VZV infection can account for 8–28% of Bell’s palsy (BP) cases and 15.2% of cranial neuritis cases. VZV infection may trigger GBS, accounting for 11.1% of cases [ 7 , 8 ]. However, exact epidemiological data related to VZV vasculopathy and myelopathy are still unknown, and generally they are considered to be less than 10% [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…VZV infection may trigger GBS, accounting for 11.1% of cases [ 7 , 8 ]. However, exact epidemiological data related to VZV vasculopathy and myelopathy are still unknown, and generally they are considered to be less than 10% [ 7 ]. VZV myelopathy can present itself as a self-limiting or sometimes fatal myelitis, and mostly occurs in immunocompromised individuals [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

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Acute myelitis with multicranial neuritis caused by Varicella zoster virus: a case report

Liu

Zhou

2022

BMC Neurol

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Background Varicella zoster virus (VZV) can remain lifelong in the latent state in ganglionic neurons and adrenal glands after the initial infection. However, it can be reactivated anytime and can trigger several severe neurological manifestations such as encephalitis, meningitis, Ramsay-Hunt syndrome, cerebellitis, myelitis, and stroke. In addition, due to the diversity of clinical manifestations, clinical diagnosis of VZV can be difficult, especially in the absence of varicella. Here, we describe the case of a 52-year-old male who presented with symptoms of acute myelitis as well as polycranial neuritis, and was finally diagnosed with VZV infection through metagenomic next-generation sequencing (mNGS). Case presentation A 52-year-old male came to our hospital with complaint of headache, fever, weakness of right lower limb, abdominal distension, and hearing loss. T2-weighted MRI revealed a hyperintense lesion in the spinal cord extending from T8 to T11. In addition, enhanced MRI showed small patches and strips hyperintensities in both the spinal cord and meninges. Plain abdominal radiographs and abdominal computed tomography (CT) scan displayed air-fluid levels and incomplete bowel obstruction. Moreover, electrophysiological evaluation of the peripheral neuropathy in the extremities was found to be normal. Finally, by using metagenomic next-generation sequencing (mNGS) we found that the copy number of VZV DNA in cerebrospinal fluid (CSF) was significantly increased and IgG antibody against VZV in CSF was also noted to be positive. Hence, VZV infection was identified in patient’s central neuron system. Finally, after a few days of low dose steroid treatment, the patient's symptoms were found to be significantly improved. Conclusions The findings indicate that we should pay proper attention to the various symptoms caused by VZV infection due to the clinical heterogeneity, especially in the absence of cutaneous lesions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acute myelitis with multicranial neuritis caused by Varicella zoster virus: a case report

Liu

Zhou

2022

BMC Neurol

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Varicella‐zoster virus‐related neurological complications: From infection to immunomodulatory therapies

Hakami,

Khan,

Abdulaziz

et al. 2024

Reviews in Medical Virology

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The Varicella‐zoster virus (VZV), classified as a neurotropic member of the Herpesviridae family, exhibits a characteristic pathogenicity, predominantly inducing varicella, commonly known as chickenpox, during the initial infectious phase, and triggering the reactivation of herpes zoster, more commonly recognized as shingles, following its emergence from a latent state. The pathogenesis of VZV‐associated neuroinflammation involves a complex interplay between viral replication within sensory ganglia and immune‐mediated responses that contribute to tissue damage and dysfunction. Upon primary infection, VZV gains access to sensory ganglia, establishing latent infection within neurons. During reactivation, the virus can spread along sensory nerves, triggering a cascade of inflammatory mediators, chemokines, and immune cell infiltration in the affected neural tissues. The role of both adaptive and innate immune reactions, including the contributions of T and B cells, macrophages, and dendritic cells, in orchestrating the immune‐mediated damage in the central nervous system is elucidated. Furthermore, the aberrant activation of the natural defence mechanism, characterised by the dysregulated production of immunomodulatory proteins and chemokines, has been implicated in the pathogenesis of VZV‐induced neurological disorders, such as encephalitis, myelitis, and vasculopathy. The intricate balance between protective and detrimental immune responses in the context of VZV infection emphasises the necessity for an exhaustive comprehension of the immunopathogenic mechanisms propelling neuroinflammatory processes. Despite the availability of vaccines and antiviral therapies, VZV‐related neurological complications remain a significant concern, particularly in immunocompromised individuals and the elderly. Elucidating these mechanisms might facilitate the emergence of innovative immunomodulatory strategies and targeted therapies aimed at mitigating VZV‐induced neuroinflammatory damage and improving clinical outcomes. This comprehensive understanding enhances our grasp of viral pathogenesis and holds promise for pioneering therapeutic strategies designed to mitigate the neurological ramifications of VZV infections.

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Hippocampal Metabolic Alterations and Cognitive Dysfunction in Varicella Zoster Virus Meningitis: A Single-Center Case Series Study

et al. 2023

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The work was supported by grants from the Key Projects of Hangzhou Health Science and Technology Plan (ZD20210010), Guidance Project of Hangzhou Science Plan (agriculture and social development) (20211231Y034), and Construction Fund of Medical Key Disciplines of Hangzhou (2020-2024) Conflict of interest:None declared Background:Meningitis has been found to be associated with dementia. Different pathogens of meningitis lead to different cognitive impairments. However, the change of cognitive function and cellular metabolism in the hippocampus in varicella zoster virus (VZV) meningitis has received little attention. We aimed to explore the cognitive function and changes of cellular metabolism in bilateral hippocampal regions in VZV meningitis. Material/Methods:We used magnetic resonance spectroscopy to check the cellular metabolism in the bilateral hippocampal region in 23 VZV meningitis patients and 19 controls in our hospital from June 2020 to November 2022. Also, cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) scale, and the correlation between MoCA scores and cellular metabolism in the bilateral hippocampal region was analyzed. Results:Six (26.1%) of the 23 patients with VZV meningitis had cognitive decline. Compared with that of the control group, the MoCA scores of VZV meningitis patients was much impaired (25.88±2.31 vs 27.74±1.94, P<0.05), visual-spatial executive function and delayed recall were significantly decreased (P<0.05), and N-acetylaspartate (NAA)/creatine (Cr) ratios in the bilateral hippocampus of patients with VZV meningitis were significantly lower (P<0.05). NAA/Cr ratios in the left and right hippocampus were positively correlated with MoCA scores (r=0.4158, P=0.0385; r=0.5274, P=0.0010, respectively), and negatively correlated with white blood cell count (P<0.01) and protein content in cerebrospinal fluid (P<0.05). Conclusions:Patients with VZV meningitis had cognitive dysfunction and altered cellular metabolism of bilateral hippocampal regions. The main cognitive abnormalities were visual-spatial executive function and delayed recall.

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Varicella zoster virus infection in neurological patients in Bulgaria

Cited by 3 publications

References 34 publications

Acute myelitis with multicranial neuritis caused by Varicella zoster virus: a case report

Acute myelitis with multicranial neuritis caused by Varicella zoster virus: a case report

Varicella‐zoster virus‐related neurological complications: From infection to immunomodulatory therapies

Hippocampal Metabolic Alterations and Cognitive Dysfunction in Varicella Zoster Virus Meningitis: A Single-Center Case Series Study

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