Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Abstract

We report the autopsy fi ndings for a 45-year-old man with polyradiculoneuropathy and fatal acute disseminated encephalomyelitis after having Mycoplasma pneumoniae pneumonia. M. pneumoniae antigens were demonstrated by immunohistochemical analysis of brain tissue, indicating neuroinvasion as an additional pathogenetic mechanism in central neurologic complications of M. pneumoniae infection.A 45-year-old, previously healthy man had fever, pain in the extremities, nasal discharge, and cough with nonpurulent sputum. He sought clinical care 1 week after onset of illness because of his deteriorating general state, including a headache and paresthesias in both hands. Bilateral basal pneumonia was diagnosed and treated with clarithromycin. During the ensuing 4 days, a rapidly ascending polyradiculoneuropathy resulted in tetraparesis, followed by facial palsy, ophthalmoplegia, and then paralysis of all cranial nerves. The initially fully alert patient became comatose, and assisted respiration was necessary.On day 9 of the patient's illness, an ELISA (Genzyme Diagnostics Virotech, Rüsselsheim, Germany) was performed on serum samples and showed a Mycoplasma pneumoniae immunoglobulin (Ig) G antibody titer of 28.2 Virotech-units/mL (VE) (cut-off 9.0-11.0) and an IgM antibody titer of 20.9 VE (cut-off 9.0-11.0). A PCR for M. pneumoniae was positive in tracheobronchial secretions on day 12, and complement fi xation test (antigen purchased from Virion CH-8803 Rüschlikon, Zürich, Switzerland) showed M. pneumoniae antibody titers of 1,280 (serum) and 4 (cerebrospinal fl uid) on day 16.Serologic tests for cytomegalovirus, Epstein-Barr virus, HIV, measles virus, mumps virus, spring-summer encephalitis virus, Borrelia burgdorferi, Brucella spp., Legionella spp., Treponema pallidum, and Toxoplasma gondii were negative. No herpes simplex virus 1 or 2 was detected by PCR in cerebrospinal fl uid, and PCR results were also negative for Chlamydia pneumoniae in tracheobronchial secretions.On day 8, cerebrospinal fl uid examinations showed a total cell count of 43/mm 3 (89% granulocytes and 11% mononuclear cells), total protein 1.3 g/L, and glucose 4.3 mmol/L. On day 15, when the patient was comatose, a total cell count of 794/mm 3 (84% granulocytes and 16% mononuclear cells), total protein 4.6 g/L, and glucose 1.5 mmol/L. Blood values showed leucocytosis with neutrophilia and mild thrombocytosis of 480 g/L.A computed tomographic scan on day 15 showed brain edema and multiple infl ammatory/demyelination lesions in the subcortical white matter of both hemispheres and within the brain thalami, capsulae internae, midbrain, and pons. Electroneurographic and myographic results showed a severe form of a peripheral axonal neuropathy. No antigangliosid (GM) 1 or anti-GM2 antibodies were found in the patient's serum on day 12. We did not look for GQ1b antibodies.The clinical diagnosis was polyradiculoneuropathy (atypical Guillain-Barré syndrome) and acute encephalitis as complications of bilateral pneumonia caused by M. pneumoniae. In addition to c...

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

“…Because of its diverse distribution of affected areas, an indirect mechanism has been postulated, namely, immune complexmediated vasculopathy [Behan et al, 1986;Guleria et al, 2005;Gupta et al, 2009]. On the other hand, recent studies on patients with acute disseminated encephalomyelitis have demonstrated the presence of M. pneumoniae genome in the cerebrospinal fluid [Matsumoto et al, 2009;Riedel et al, 2001;Yiş et al, 2008], or the presence of M. pneumoniae antigens inside the macrophages in the brain tissue [Stamm et al, 2008]. Thus it is highly possible that a direct mechanism, namely, vasculitis as a consequence of cytokine activation by M. pneumoniae, is responsible for some instances of acute disseminated encephalomyelitis.…”

Mycoplasmal panencephalitis: a neuropathologic documentation

“…Some of the perivascular macrophages revealed ''M. pneumoniae antigens inside macrophages present in the inflammatory infiltrate…'' [13]. The authors interpreted the latter finding as evidence of ''neuroinvasion'', which would confirm the hypothesis that direct infection may be the most probable pathomechanism for acute encephalitis in mycoplasmal infections.…”

“…The fourth was that of a 45-year-old male with the onset of neurological symptoms 7 days after the onset of fever, and death 10 days after the onset of neurologic symptoms. Postmortem examination revealed cerebral edema, ADEM, and hemorrhagic foci consisting of fibrinoid necrosis of small veins, perivascular necrosis and a mixed neutrophil-macrophage infiltrate [13]. These latter findings are most consistent with acute hemorrhagic leukoencephalitis of Hurst, considered by most to be a hyperacute form of ADEM [12].…”

“…Nevertheless, M. pneumoniae is suspected to be responsible for approximately 10% of cases of acute childhood encephalitis [13]. Significant respiratory symptoms are unusual in these patients (reviewed in Ref.…”

Infección por Mycoplasma neumoniae: microangeitis cerebral, síndrome de Bickerstaff y anemia hemolítica autoinmune

“…Más excepcional es el ataque directo al tejido nervioso, especialmente en niños, en quienes produce meningoencefalitis bacterianas, aunque algunas sean defi nidas como meningitis asépticas 5 . Sin embargo, lo clásico, sigue siendo que tanto el compromiso neurológico, vascular o hematológico, tengan un patomecanismo inmunomimético a partir de los glicolípidos y lipoproteínas, de la cobertura plasmática y del citoplasma bacteriano, capaces de activar respuestas autoinmunes contra lipoestructuras homólogas 4 .…”