Seropositive anti-MOG antibody-associated acute disseminated encephalomyelitis (ADEM): a sequelae of Mycoplasma pneumoniae infection.

Acute disseminated encephalomyelitis (ADEM) is a demyelinating, autoimmune disease of the central nervous system (CNS). It causes motor and sensory deficits, altered mental status and other neurological symptoms. Though rarely fatal, it has been associated with residual motor and neurocognitive deficits. Our case consisted of a 4-year-old girl who presented with fatigue and unsteady gait after a respiratory illness. During her hospital course, she became progressively weaker and experienced seizures. Imaging showed sections of demyelination in the CNS, and appropriate treatment was started. Additional labs resulted in positive Mycoplasma pneumoniae serum serology. Antimyelin oligodendrocyte glycoprotein (anti-MOG) antibodies were also found, which is a risk factor for relapsing, multiphasic ADEM. To our knowledge, this is the first case of anti-MOG antibody-associated ADEM due to M. pneumoniae infection. Our patient has made a complete recovery. The parents only report slightly increased fatigue and irritability.

Increased concentrations of soluble B7-H3 and interleukin 36 in bronchoalveolar lavage fluid of Children with Mycoplasma pneumoniae pneumonia.

BACKGROUND: The purpose of this study is to explore the correlations of interleukin 36 (IL-36) and Soluble B7-H3 (sB7-H3) levels in bronchoalveolar lavage fluid (BALF) with clinical characteristics and laboratory findings. METHODS: A total of 35 children with M. pneumnoiae pneumonia (MPP) and 15 control subjects were enrolled. BALF concentrations of sB7-H3 and IL-36 were detected using enzyme-linked immunosorbent assays and clinical profiles of children with MPP were obtained. RESULTS: Children with MPP had significantly higher levels of sB7-H3 and IL-36 compared to control subjects (both P < 0.05). Meanwhile, children with pleural effusion had significantly higher levels of sB7-H3 and IL-36 compared to children without pleural effusion (both P < 0.05). BALF concentration of sB7-H3 was strongly associated with concentration of IL-36 (r = 0.796, P < 0.0001) and sB7-H3 was correlated with duration of fever (r = 0.427, P = 0.11) and length of stay (r = 0.345, P = 0.043). Both concentrations of sB7-H3 and IL-36 were significantly decreased in convalescent phase after treatment (both P < 0.05). CONCLUSION: Both soluble B7-H3 and IL-36 may play an important role in pathogenesis of M. pneumoniae infection and sB7-H3 could be useful as a prognostic predictor or biomarker of MPP.

Yield of diagnostic studies in children presenting with complex febrile seizures.

OBJECTIVE: The objective of this study was to determine the yield of diagnostic workup in children presenting with complex febrile seizures. METHODS: We performed a retrospective review of charts of patients who presented to our pediatric emergency department with complex febrile seizures (focal, prolonged, or recurrent). Patients with known seizure disorder, congenital central nervous system malformations, or hydrocephalus were excluded. The charts were reviewed for diagnostic workup. RESULTS: There were 71 eligible encounters (mean age, 1.5 years); 59.2% were males. None of the 71 patients had positive blood or urine cultures; none had abnormal blood count or serum chemistries. Only 1 patient who had a very abnormal presentation in febrile status epilepticus had positive cerebrospinal fluid culture and abnormal brain computed tomography scan and magnetic resonance imaging. CONCLUSIONS: Most patients with complex febrile seizures do not require extensive diagnostic workup.

Fatal outcomes in family transmission of Mycoplasma pneumoniae.

BACKGROUND: Mycoplasma pneumoniae continues to be a significant cause of community-acquired pneumonia and, on rare occasions, manifests as fulminant disease that leads to mortality, even in healthy individuals. METHODS: We conducted a retrospective study on members of a family who were quarantined by the Centers for Disease Control and Prevention in 2002 for respiratory failure and death of a 15-year-old brother (sibling 1) and a 13-year-old sister (sibling 2). Collected airway, cerebrospinal fluid (CSF), and serum samples from both deceased siblings and serum samples from both parents and the remaining 3 ill siblings (sibling 3-5) were tested using a range of diagnostic assays. Autopsy lung tissue samples from sibling 2 were also assessed using immunohistochemical and immunoelectron microscopic methods. RESULTS: Autopsy evaluation of sibling 1 revealed cerebral edema consistent with hypoxic ischemic encepatholopathy and pulmonary findings of bronchiolitis obliterans with organizing pneumonia (BOOP). Postmortem lung examination of sibling 2 revealed lymphoplasmacytic bronchiolitis with intraluminal purulent exudate, BOOP, and pulmonary edema. Results of diagnostic assays implicated the household transmission of M. pneumoniae among all 5 siblings and both parents. Further analysis of lung tissue from sibling 2 demonstrated the presence of M. pneumoniae organisms and community-acquired respiratory distress syndrome toxin. M. pneumoniae was cultured directly from sibling 2 autopsy lung tissue. CONCLUSION: Evidence is provided that M. pneumoniae was readily transmitted to all members of the household and that the resulting infections led to a spectrum of individual responses with variation in disease progression, including lymphoplasmacytic bronchiolitis, BOOP, and death.

[Parainfectious polyneuropathy and miller-fisher-syndrome in combination with anemia in Mycoplasma pneumoniae infection]. / Parainfektiöse Polyneuropathie und Miller-Fisher-Syndrom in Kombination mit Anämie bei Mycoplasma-pneumoniae-Infektion.

Neurological complications are among the most common in Mycoplasma pneumoniae (M.p.) infection and appear in up to 4,8 % of M.p.-infected patients . Whereas direct intracerebral infection can occur and often puts patients into critical, intensive care-requiring conditions, different forms of parainfectious autoimmune Guillain-Barré-syndrome (GBS) and Miller-Fisher syndrome (MFS) make up the most frequent neurological complications. M.p.-associated alterations of the blood count are common, and sometimes can take a dramatical course. We here report a 64-year-old female and a 53-year-old male patient who both suffered from severe parainfectious autoimmune neurological syndromes in combination with different forms of anemia, in the case of the first patient to a transfusion-requiring degree. With this report we would like to stress the importance to include M.p. in the diagnostic procedures in the case of inflammatory neurological syndromes, especially when combined with alterations of the blood count.

[Optic neuritis attributable to Mycoplasma pneumoniae]. / Névrite optique à Mycoplasma pneumoniae.

Optic neuritis (ON) is an inflammatory disease whose etiology remains obscure. We report a case of ON attributable to Mycoplasma pneumoniae (MP). A 26-year-old man presented a sudden onset bilateral loss of visual acuity, without any history of pulmonary or ear-nose-throat infection. Diagnosis of optic neuritis was made on the basis of visual field loss, though optic disks and visual evoked potentials were normal. Color vision could not be assessed due to a congenital dyschromatopsia. The neurological examination was normal. On magnetic resonance imaging, there was no enhancement or enlargement of optic nerves, but a demyelinating lesion of the cervical spinal cord. Lumbar puncture revealed lymphocytic meningitis with 60 white blood cells, all of them being lymphocytes. Oligoclonal bands were presents in the CSF. With no evidence of any other infection or auto-immune disease, the diagnosis of Mycoplasma pneumoniae infection was established due to the presence of Mycoplasma pneumoniae specific IgM antibodies. Outcome was quite favorable within three months without treatment. Neurological symptoms--encephalitis, meningitis, polyradiculitis, or more rarely ON or cerebella ataxia--are the main extra pulmonary manifestations of Mycoplasma pneumoniae infection. Search for anti-Mycoplasma pneumoniae IgM antibodies should be performed routinely when On is diagnosed.

Reversible myeloradiculopathy due to Mycoplasma pneumoniae.

A 22-year-old man presented with flaccid paraparesis and a thoracic sensory level in the context of a recent respiratory illness. Investigations established cerebrospinal pleocytosis with elevated protein, and subsequent serological testing confirmed raised antibody titres to Mycoplasma pneumoniae. Nerve conduction studies established that H-reflexes were prolonged and somatosensory evoked responses were delayed from the lower limbs bilaterally. Although imaging of the spinal cord revealed no abnormality, clinical and neurophysiological findings were consistent with a myeloradiculopathy. The patient was treated with pulse intravenous methylprednisone and underwent complete recovery over a 4-week period.

[Mycoplasma pneumoniae meningoencephalitis in a young adult]. / Meningoencefalitis por Mycoplasma pneumoniae en un adulto joven.

Mycoplasma pneumoniae infections have extrapulmonary complications that involve the nervous system. The neurologic manifestations are diverse. Although the prognosis is usually favorable, the patients can undergo severe permanent sequelae. We present a young female adult with acute meningoencephalitis as a complication of a lower respiratory infection, which followed a benign course without neurologic sequelae.

Mycoplasma pneumoniae encephalitis in childhood.

Mycoplasma pneumoniae is an important etiologic agent of acute childhood encephalitis. We retrospectively reviewed 17 cases of M. pneumoniae encephalitis at the Pediatric Department of the National Taiwan University Hospital from April 1997 through March 2000. These cases were diagnosed as having positive immunoglobulin M antibodies (94%), a minimum 4-fold change of complement-fixation antibody titers (47%), or nested polymerase chain reaction. The ages of these patients ranged from 1.5 to 10.9 years (mean, 5.3 years) with a male-to-female ratio of 8:9. The clinical manifestations included fever (94%), altered consciousness (65%), seizure (41%), personality or behavior changes (29%), meningeal sign (24%), visual hallucination (24%), ataxia (12%), Guillain-Barré syndrome (6%), blurred vision (6%), and aphasia (6%). Respiratory symptoms and signs were found in 76% of the patients. Abnormal electroencephalogram and neuroimage were observed in all cases, while abnormal cerebrospinal fluid examination was noted in about one-third of the patients. Five (29%) patients required intensive care because of intractable seizure or respiratory failure. Fourteen (82%) patients recovered completely, but 3 (18%) had sequelae including epilepsy, hydrocephalus, and global neurologic deficits with brain stem dysfunction. In Taiwan, M. pneumoniae should be considered an etiologic pathogen of acute childhood encephalitis if fever and respiratory symptoms and signs are observed with or without abnormal cerebrospinal fluid findings. Supportive treatment is the basis of management.

Neurological symptoms in patients whose cerebrospinal fluid is culture- and/or polymerase chain reaction-positive for Mycoplasma pneumoniae.

We describe 13 patients with neurological signs and symptoms associated with Mycoplasma pneumoniae infection. M. pneumoniae was isolated from the cerebrospinal fluid (CSF) of 9 patients: 5 with meningoencephalitis, 2 with meningitis, and 1 with cerebrovascular infarction. One patient had headache and difficulties with concentration and thinking for 1 month after the acute infection. M. pneumoniae was detected, by means of PCR, in the CSF of 4 patients with negative culture results. Two had epileptic seizures, 1 had blurred vision as a consequence of edema of the optic disk, and 1 had peripheral nerve neuropathy.

Mycoplasma pneumoniae: a cause of coma in the absence of meningoencephalitis.

Mycoplasma pneumoniae encephalitis is a recognized cause of reversible coma in children. As an etiology of infectious encephalitis, it yields a relatively poorer prognosis than most other causes of infectious encephalopathies. Encephalitis is generally diagnosed by a constellation of clinical symptoms and confirmed by a cerebrospinal fluid (CSF) examination revealing cell pleocytosis and elevated protein. That Mycoplasma pneumoniae encephalopathy can occur in the presence of a normal CSF examination is less well appreciated. The authors report two children who presented with coma and normal CSF findings in whom a diagnosis of acute Mycoplasma pneumoniae infection was made. The two children both had rapid and complete recovery over several days. These cases exemplify that coma can result from acute infection with Mycoplasma pneumoniae in the absence of an inflammatory CSF response and that a normal CSF may herald a more favorable prognosis.

[A case of encephalitis due to Mycoplasma pneumoniae: detection of specific DNA from cerebrospinal fluid and elevation of interleukin-6].

A 9-year-old female was admitted to our hospital due to a generalized seizure and consciousness disturbance. The patient had a fever and rash four days before admission, but she had no respiratory symptoms. The seizure and consciousness disturbance was prolonged and intractable. We diagnosed the patient as having encephalitis because of the increase in the cell count in the cerebrospinal fluid (CSF) and a diffuse slow EEG wave. The computed tomography of the head was normal. The causative agent was identified as Mycoplasma pneumoniae because of the increase of antibodies, and the detection of a specific DNA with a polymerase chain reaction. The interleukin (IL)-6 level of CSF was high (384 pg/ml). In spite of intensive treatment she had severe neurological sequelae. The invasion of Mycoplasma pneumoniae to the central nervous system appeared to have a role in the development of encephalitis in the patient. We speculated that there is a possible relationship between the IL-6 levels of CSF and clinical severity of encephalitis.

Isolation of Mycoplasma pneumoniae from pleural fluid and/or cerebrospinal fluid: report of four cases.

Mycoplasma pneumoniae was isolated from pleural exudates of 2 children with pleuropneumonia. The organism was also isolated from cerebrospinal fluid of a child with meningeal manifestations and from the cerebrospinal fluid as well as pleural exudate of another child who died 21 days after onset of disease. More extensive attempts to cultivate M. pneumoniae from nonpulmonary sites are recommended.

Cerebrospinal fluid findings in mycoplasma pneumoniae infections with neurological complications.

The cerebrospinal fluid (CSF) findings of 16 patients with mycoplasma pneumoniae infections and different neurologic complications are presented. In acute meningitis there was predominantly a mononuclear cell reaction remitting in accordance with the improvement of the clinical symptoms. An early switch from IgM to IgG was observed. In cranial nerve neuritis and radiculitis in the beginning complement factors were decreased. Far beyond the clinical remission IgM and cell count were elevated. In Guillain-Barré-syndrome no IgM but increased IgG levels were detectable. In all patients both CSF IgM and IgG markedly exceeded the corresponding serum values. The possibility that different pathogenetic mechanisms are underlying these phenomena depending on the actual state of the hosts' immunity is discussed.

Neurological disease associated with Mycoplasma pneumoniae pneumonitis: demonstration of viable Mycoplasma pneumoniae in cerebrospinal fluid and blood by radioisotopic and immunofluorescent tissue culture techniques.

Several neurologic syndromes (including Guillain-Barré) complicated Mycoplasma pneumoniae pneumonitis in a young man. At onset of neurologic disease, buffy coat and cerebrospinal fluid cultures on inert media were negative for M. pneumoniae. However, metabolically active mycoplasma were identified in both body fluids by enhanced uptake of 14C-uracil versus 3H-uridine, with marked reduction in normal uridine-to-uracil uptake ratios (> 1000:1) in tissue culture. Uridine-to-uracil ratios were 8.5:1 and 15:1 for buffy coat and cerebrospinal fluid, respectively. Indirect fluorescent antibody (FA) studies confirmed the species as M. pneumoniae. In convalescence, uridine-to-uracil ratios and FA studies of buffy coat normalized, indicating clearance of M. pneumoniae from blood. Cell lines inoculated with "convalescent" cerebrospinal fluid showed slightly increased uracil uptake, slightly decreased uptake ratios, and persistent FA staining of approximately 5% of cells, indicating incomplete clearance of M. pneumoniae. Immune complexes were undetectable in either buffy coat or spinal fluid. This indicates that certain M. pneumoniae-associated neurologic disorders may be related to direct neural infection and not immunologically mediated as has been suggested.