Acute Disseminated Encephalomyelitis (ADEM) Due to Mycoplasma pneumoniae Infection in an Adolescent

Riedel, K. G.; Kempf, Volkhard A. J.; Bechtold, A.; Klimmer, M.

doi:10.1007/s15010-001-1173-z

Cited by 42 publications

(40 citation statements)

References 7 publications

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“…M. pneumoniae RNA can be detected in brain tissue by nucleic acid hybridization (8), and the presence of the organism was demonstrated in cerebrospinal fl uid by PCR (1,(9)(10)(11)(12) and by culture (3,12). As shown in our case, the microbial antigens can be immunohistochemically detected in histopathologically involved areas of the CNS, both in brain biopsy specimens and at autopsy.…”

supporting

confidence: 52%

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Stamm

Moschopulos

Hungerbuehler

et al. 2008

Emerg. Infect. Dis.

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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...

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supporting

confidence: 52%

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Stamm

Moschopulos

Hungerbuehler

et al. 2008

Emerg. Infect. Dis.

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“…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.…”

Section: Acute Disseminated Encephalomyelitismentioning

confidence: 99%

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

Narita¹

2011

Advances in the Etiology, Pathogenesis and Pathology of Vasculitis

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“…14 However, to our knowledge only two other case reports have described ADEM due to bacterial meningitis, and none was associated with Hib. 14,19 Here we have shown, for the first time, to our knowledge, that ADEM can occur in association with acute Hib meningitis. In the setting of an acute bacterial meningitis, complicated with depression of consciousness and focal neurological deficits, the hypothesis of ADEM must be considered and should prompt further neurological investigation.…”

Section: Discussionmentioning

confidence: 56%

Probable acute disseminated encephalomyelitis due to Haemophilus influenzae meningitis

Beleza

Ribeiro

Pereira

et al. 2008

Develop Med Child Neuro

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We report the case of a 17-year-old male on long-term steroid therapy for minimal lesion glomerulopathy who, after an upper respiratory infection, presented with Haemophilus influenzae type b meningitis. Twenty-four hours later he developed depression of consciousness which progressed to coma and left hemiparesis. Brain magnetic resonance imaging (MRI) revealed multiple lesions (hyperintense on T2 and slightly hypointense on T1) involving mainly white matter suggestive of inflammation. MRI features were compatible with acute disseminated encephalomyelitis (ADEM), although a differential diagnosis included cerebritis or vasculitis, secondary to bacterial meningitis. The patient was treated with high-dose steroids which resulted in a gradual improvement followed by complete clinical recovery. We propose a diagnosis of ADEM was the best diagnosis because of the radiological features and response to steroids. The occurrence of ADEM associated with acute meningitis, however rare, represents an important diagnostic challenge for the clinician.Neurological complications of bacterial meningitis presenting with brain lesions include venous sinus thrombosis, arterial stroke, subdural empyema, vasculitis, abscesses, and acute disseminated encephalomyelitis (ADEM). 1 We report a case illustrating the difficulty in establishing a differential diagnosis between ADEM and cerebritis or vasculitis on the basis of the current, nonspecific neuroradiological criteria of ADEM. The association of ADEM with meningitis is rare; however, a high level of awareness is needed to reach a timely diagnosis and initiate appropriate treatment. Case reportA 17-year-old male was admitted to the Emergency Department of the São Marcos Hospital, Braga, Portugal with a dull occipital progressive headache of rapid onset that began 6 hours earlier. This clinical picture occurred in the setting of an upper respiratory infection which had lasted for 1 week, and had been treated with acetaminophen. His medical history was remarkable for minimal lesion glomerulopathy, at that time in remission with prednisolone (10mg administered daily). The patient had been vaccinated against Haemophilus influenzae type b (Hib) at 2, 4, 6, and 18 months, in accordance with the national immunization programme. On examination in the emergency department he was found to have neck rigidity and hyperthermia (38.5˚C). Blood tests showed leukocytosis (17.6×10 9 /L), neutrophilia (0.85), and increased reactive C protein (75.52mg/L). Chest X-ray and brain computed tomography (CT) were normal. Cerebrospinal fluid (CSF) revealed 1120 cells/μL (78% neutrophils, 15% monocytes, 7% lymphocytes), 1.44g/L proteins, and 41mmol/L glucose; Hib was disclosed with a latex particle agglutination antigen test, but no bacteria were detected with Gram's stain. Case reportSee end of paper for list of abbreviations. Case Report 389We were, therefore, facing acute bacterial meningitis, probably caused by Hib, in an immunocompromised young male. Antibiotic therapy against Hib was initiated with cefot...

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Acute Disseminated Encephalomyelitis (ADEM) Due to Mycoplasma pneumoniae Infection in an Adolescent

Cited by 42 publications

References 7 publications

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Mycoplasma pneumoniae as an Under- Recognized Agent of Vasculitic Disorders

Probable acute disseminated encephalomyelitis due to Haemophilus influenzae meningitis

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