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Clin Infect Dis. 2015 Oct 1;61(7):1092-8. doi: 10.1093/cid/civ473. Epub 2015 Jun 17.

Neurological Complications of PCR-Proven M. pneumoniae Infections in Children: Prodromal Illness Duration May Reflect Pathogenetic Mechanism.

Author information

1
Department of Pediatrics and Neurology, Nationwide Children's Hospital and The Ohio State University Center for Gene Therapy, Research Institute at Nationwide Children's Hospital, Columbus, Ohio.
2
Division of Neurology.
3
Division of Paediatric Medicine, Department of Paediatrics.
4
Division of Microbiology, Department of Paediatric Laboratory Medicine.
5
Division of Infectious Diseases, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Canada.

Abstract

BACKGROUND:

The spectrum of neurologic disease attributable to Mycoplasma pneumoniae in children is incompletely understood in part because of limitations of microbiologic diagnostic methods. Our objective was to characterize the neurologic complications of M. pneumoniae in children using stringent diagnostic criteria.

METHODS:

All children admitted to the Hospital for Sick Children over a 16-year period with acute neurologic manifestations and polymerase chain reaction (PCR)-confirmed M. pneumoniae infection were eligible for inclusion. Cases were categorized as definite, probable, or possible according to strength of evidence implicating M. pneumoniae. Children with underlying noninfectious neurologic conditions or an alternative infectious cause were excluded.

RESULTS:

A total of 365 children had M. pneumoniae detected in the cerebrospinal fluid (CSF) or respiratory tract by PCR, 42 (11.5%) of whom had neurologic disease attributable to M. pneumoniae. The most common clinical syndromes were encephalitis (52%), acute disseminated encephalomyelitis (12%), transverse myelitis (12%), and cerebellar ataxia (10%). Two distinct disease patterns were observed, one with a prolonged prodrome (≥7 days), respiratory manifestations, an immunoglobulin M (IgM) response in peripheral blood, and detection of M. pneumoniae in the respiratory tract, but not the CSF, and one with a brief (<7 days) or no prodrome, less frequent respiratory manifestations and IgM response, and detection of M. pneumoniae in the CSF, but not the respiratory tract.

CONCLUSIONS:

Our findings support the hypothesis of two separate pathogenetic mechanisms for M. pneumoniae-associated neurologic disease, one related to direct infection of the central nervous system and one indirect, likely immunologically mediated.

KEYWORDS:

CSF; Mycoplasma pneumoniae; PCR; encephalitis; encephalopathy

PMID:
26084846
DOI:
10.1093/cid/civ473
[Indexed for MEDLINE]

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