Post‐infectious central and peripheral nervous system diseases complicating <i>Mycoplasma pneumoniae</i> infection Report of three cases and review of the literature

Pfausler, Bettina; Engelhardt, K.; Kampfl, A.; Spiss, H.; Taferner, E.; Schmutzhard, Erich

doi:10.1046/j.1468-1331.2002.00350.x

Cited by 76 publications

(73 citation statements)

References 13 publications

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“…The occasional demonstration of circulating antibodies against neural tissue supports this hypothesis. Necrosis of the spinal cord found at autopsy in our patient was probably due to secondary ischemia caused by edema and vascular thrombosis, and a similar process may be responsible for the permanent paraplegia of other reported patients with transverse myelitis after M. pneumoniae infection (5,6).…”

supporting

confidence: 63%

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: 63%

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Stamm

Moschopulos

Hungerbuehler

et al. 2008

Emerg. Infect. Dis.

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“…The lack of clear evidence that mycoplasmas were actually present in neurological tissues led to theories that damage to brain tissue occurred as a result of cross-reacting or autoimmune antibodies (129, 142) and even to concern that neurological (312). Postinfectious leukoencephalopathy due to M. pneumoniae also suggests a role for autoimmunity in some cases (325). Proof that viable organisms or M. pneumoniae DNA can be detected directly in neural tissues and CSF provides convincing evidence that this organism does indeed disseminate from the respiratory tract in some instances (3,105,198,251,307,401,403,415).…”

Section: Extrapulmonary Manifestationsmentioning

confidence: 99%

“…A trial of intravenous immunoglobulin in a critically ill patient with encephalitis and M. pneumoniae pneumonia was associated with neurological improvement within 48 h of treatment (361). A patient with M. pneumoniae infection suffering from bilateral optic neuritis as well as acute Guillain-Barré syndrome recovered after plasmapheresis (325). A survey of commercial intravenous immunoglobulin therapy preparations found that most preparations had significant activity against M. pneumoniae (246).…”

Section: Treatment Of Infections Due To M Pneumoniaementioning

confidence: 99%

Mycoplasma pneumoniaeand Its Role as a Human Pathogen

2004

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Mycoplasma pneumoniae is a unique bacterium that does not always receive the attention it merits considering the number of illnesses it causes and the degree of morbidity associated with it in both children and adults. Serious infections requiring hospitalization, while rare, occur in both adults and children and may involve multiple organ systems. The severity of disease appears to be related to the degree to which the host immune response reacts to the infection. Extrapulmonary complications involving all of the major organ systems can occur in association with M. pneumoniae infection as a result of direct invasion and/or autoimmune response. The extrapulmonary manifestations are sometimes of greater severity and clinical importance than the primary respiratory infection. Evidence for this organism's contributory role in chronic lung conditions such as asthma is accumulating. Effective management of M. pneumoniae infections can usually be achieved with macrolides, tetracyclines, or fluoroquinolones. As more is learned about the pathogenesis and immune response elicited by M. pneumoniae, improvement in methods for diagnosis and prevention of disease due to this organism may occur

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“…Es existieren Beschreibungen von Fäl-len, in denen nach einem pulmonalen Infekt durch Mycoplasma pneumoniae sowohl Affektionen des peripheren und zentralen Nervensystems als auch eine passagere Proteinurie beobachtet wurden [4,12,15]. Die neurologischen Symptome reichen von Leukenzephalitis, z. T. hämorrhagisch, GBS bzw.…”

Section: Guillain-barré Syndrome · Myelitisunclassified

Koinzidenz von Guillain-Barré-Syndrom und Myelitis

Beerhorst¹,

Klein²,

Oelerich

et al. 2007

Nervenarzt

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A 28-year-old male patient developed Guillain-Barré syndrome after a pulmonary infection with typical CSF findings. Five days after the onset, pyramidal signs and spastic increase of muscle tonus in the legs were found. The MRI showed increased signals in the whole spinal cord which were identified as myelitis after review of clinical and neurophysiologic findings. There was a remarkable difference between the dramatic pathologic signals on MRI and the mild clinical symptoms. Four months after onset the patient had no more complaints and presented basically recovered in the clinical examination. The existence of Guillain-Barré syndrome together with myelitis is very rare. A patient with such a good outcome in spite of an extended myelitis is extraordinary.

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Post‐infectious central and peripheral nervous system diseases complicating Mycoplasma pneumoniae infection Report of three cases and review of the literature

Cited by 76 publications

References 13 publications

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Neuroinvasion byMycoplasma pneumoniaein Acute Disseminated Encephalomyelitis

Mycoplasma pneumoniaeand Its Role as a Human Pathogen

Koinzidenz von Guillain-Barré-Syndrom und Myelitis

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