Mycoplasma pneumoniae Intrathecal Antibody Responses in Bickerstaff Brain Stem Encephalitis Patrick M. Meyer Sauteur1,6 Christa Relly1,6 Annette Hackenberg2,6 Nikolai Stahr3,6 Christoph Berger1,6 Guido V. Bloemberg4 Enno Jacobs5 David Nadal1,6 1 Division of Infectious Diseases and Hospital Epidemiology, University
Children’s Hospital of Zurich, Zurich, Switzerland 2 Division of Neurology, University Children’s Hospital of Zurich, Zurich, Switzerland 3 Division of Radiology, University Children’s Hospital of Zurich, Zurich, Switzerland 4 Institute of Medical Microbiology, University of Zurich, Zurich, Switzerland 5 Institute of Medical Microbiology and Hygiene, Medical Faculty Carl Gustav Carus, Dresden University of Technology, Dresden, Germany 6 Children’s Research Center (CRC), University Children’s Hospital of Zurich, Zurich, Switzerland
Address for correspondence Dr. Patrick M. Meyer Sauteur, MD, Division of Infectious Diseases and Hospital Epidemiology, University Children’s Hospital of Zurich, Steinwiesstrasse 75, CH-8032 Zurich, Switzerland (e-mail: [email protected]
► Mycoplasma pneumoniae ► encephalitis ► Bickerstaff brain stem encephalitis ► cerebrospinal ﬂuid ► intrathecal antibody synthesis
The pathogenesis of Mycoplasma pneumoniae encephalitis is not established. We report, for the ﬁrst time, the case of a patient with severe Bickerstaff brain stem encephalitis in whom we detected intrathecal production of M. pneumoniae–speciﬁc antibodies, contrasting the ﬁndings in another patient with less severe encephalitis in whom we detected intrathecal M. pneumoniae DNA but no speciﬁc antibodies. Our observations suggest that intrathecal M. pneumoniae–speciﬁc antibody responses may contribute to a more severe course of M. pneumoniae encephalitis.
Introduction Mycoplasma pneumoniae is a leading cause of encephalitis in children.1 The paucity of reports on M. pneumoniae isolation from or detection in the central nervous system (CNS) favors the hypothesis that M. pneumoniae encephalitis (MPE) is caused by an immune-mediated inﬂammation.2 The inﬂammation may be induced by molecular mimicry between M. pneumoniae and neuronal cell components.3 We recently reported on the case of a 15-year-old girl with self-limiting MPE showing microbial CNS invasion but no intrathecal-speciﬁc antibody responses (►Table 1, Case 1). Therefore, we speculated that intrathecal antibody responses
received February 16, 2013 accepted after revision April 20, 2013 published online June 20, 2013
might be present in more severe MPE.4 Here, we report on a contrasting case of a patient with MPE with neurologic sequelae who indeed showed detectable intrathecal-speciﬁc antibody responses.
Case Presentation A 9-year-old boy was admitted in November 2012 to our hospital with a 3-week history of respiratory symptoms followed by headache and drowsiness (►Table 1, Case 2). He manifested meningism, ataxia, ophthalmoplegia, left-sided hemiplegia, and eventually coma within 24 hours. The analysis of cerebrospinal ﬂuid (CSF) revealed 11 white blood cells/μL,
© 2014 Georg Thieme Verlag KG Stuttgart · New York
DOI http://dx.doi.org/ 10.1055/s-0033-1348150. ISSN 0174-304X.
Intrathecal Antibody Responses in Mycoplasma pneumoniae Encephalitis
Meyer Sauteur et al.
Table 1 Microbiological and clinical data for two patients with conﬁrmed Mycoplasma pneumoniae encephalitis Diagnosis
Case 1: 15-year-old girl4 Meningoencephalitis
Case 2: 9-year-old boy Bickerstaff brain stem encephalitis
Prodromal respiratory symptoms (duration)
Cough and fever (2 weeks)
Cough and runny nose (3 weeks)
Pulmonary inﬁltrate (chest radiograph)
White blood cell count (4.5–13.5 109/L)
11.7 109/L (neutrophils 79%)
6.8 109/L (neutrophils 70%)
C-reactive protein (