Myelin oligodendrocyte glycoprotein (MOG) antibody-associated encephalitis induced by Mycoplasma pneumoniae

Yan-Ru Liu1, Xiang-Dong Zeng2, Ying Xiong3

  • 1Department of Pediatric Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

PubMed
Abstract

Insights

Mycoplasma pneumoniae infections can trigger Myelin oligodendrocyte glycoprotein antibody-associated encephalitis in children. Early immunotherapy combined with antibiotics offers a promising treatment approach for this condition.

Area of Science:

  • Neurology
  • Infectious Diseases
  • Immunology

Background:

  • Mycoplasma pneumoniae infections are common, but their association with neurological disorders is increasingly recognized.
  • Myelin oligodendrocyte glycoprotein antibody-associated encephalitis (MOG-IgG-AE) is an inflammatory demyelinating disease of the central nervous system.
  • The link between M. pneumoniae and MOG-IgG-AE requires further investigation to understand the underlying mechanisms.

Purpose of the Study:

  • To report a series of pediatric cases of MOG-IgG-AE triggered by M. pneumoniae infection.
  • To highlight the clinical features and diagnostic challenges of this specific encephalitis.
  • To emphasize the potential therapeutic benefits of combined early immunotherapy and anti-M. pneumoniae treatment.

Main Methods:

  • Retrospective analysis of three pediatric patients diagnosed with MOG-IgG-AE and M. pneumoniae infection between September and November 2023.
  • Detailed investigation of patient demographics, clinical presentations, cerebrospinal fluid analysis, and neuroimaging findings (MRI).
  • Evaluation of treatment protocols, including immunotherapy and antimicrobial therapy, and patient outcomes.

Main Results:

  • Three children presented with neurological symptoms including headaches and seizures, accompanied by elevated cerebrospinal fluid mononuclear cells and intracranial lesions on MRI.
  • All patients tested positive for MOG-IgG in serum and were diagnosed with M. pneumoniae-associated MOG-IgG-AE within 10-14 days of infection onset.
  • Treatment with intravenous immunoglobulin, glucocorticoids, and erythromycin resulted in complete recovery for all three patients.

Conclusions:

  • M. pneumoniae infection can serve as a trigger for MOG-IgG-AE in pediatric patients.
  • Prompt diagnosis and combined treatment of early immunotherapy and anti-M. pneumoniae therapy are crucial for favorable outcomes.
  • This study underscores the importance of considering M. pneumoniae as a potential causative agent in MOG-IgG-AE and advocates for integrated therapeutic strategies.