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Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
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Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

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Autoimmune encephalitis after Japanese encephalitis in children: A prospective study.

Benke Liu1, Jie Liu1, Hong Sun2

  • 1Department of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China; Pediatric Research Institute, Children's Hospital of Chongqing Medical University, Chongqing, China; National Clinical Research Center for Child Health and Disorders, Chongqing, China; Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China; Chongqing Key Laboratory of Pediatrics, Chongqing, China.

Journal of the Neurological Sciences
|March 27, 2021
PubMed
Summary

Autoimmune encephalitis can develop after Japanese encephalitis (JE), triggered by various antibodies. Serum CXCL13 levels may predict this serious complication, indicating a poorer prognosis for affected patients.

Keywords:
Anti-neuronal surface antibodiesAutoimmune encephalitisCytokinesJapanese encephalitisOutcomes

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Area of Science:

  • Neuroimmunology
  • Infectious Diseases
  • Autoimmune Disorders

Background:

  • Japanese encephalitis (JE) is a significant cause of neurological morbidity.
  • Autoimmune encephalitis is an emerging complication following JE.
  • Identifying predictors and triggers of post-JE autoimmune encephalitis is crucial for patient outcomes.

Purpose of the Study:

  • To investigate anti-neuronal surface antibodies in JE patients.
  • To identify serum predictors of autoimmune encephalitis post-JE.
  • To correlate antibody presence with clinical outcomes.

Main Methods:

  • Prospective study of 31 JE patients.
  • Detection of anti-neuronal surface antibodies and cytokines in serum and CSF during acute and convalescent phases.
  • Analysis of JE virus RNA in CSF during relapse.
  • One-year follow-up for clinical outcomes.

Main Results:

  • No anti-neuronal surface antibodies detected at JE onset.
  • Five patients developed autoimmune encephalitis in the convalescent phase, with anti-N-methyl-D-aspartate receptor (NMDAR), anti-gamma-aminobutyric acid-B receptor (GABABR), or other antibodies.
  • Autoimmune encephalitis patients had poorer one-year outcomes (p=0.044).
  • Elevated serum CXCL13 and IL-6, and CSF CXCL13, BAFF, CXCL10, MMP-9 in the convalescent phase of autoimmune encephalitis patients.

Conclusions:

  • Anti-NMDAR and anti-GABABR antibodies, along with others against unknown antigens, can cause autoimmune encephalitis post-JE.
  • Autoimmune encephalitis following JE is associated with a worse prognosis.
  • Serum CXCL13 shows potential as a predictor for autoimmune encephalitis after JE.