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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measurement of cerebrospinal fluid lactic acid by gas liquid chromatography and by an enzymatic Monotest lactate test was evaluated for the early detection of bacterial meningitis in 396 patients. Spinal fluid specimens from 62/62 patients with a bacterial or mycoplasma etiology yielded lactate levels greater than the upper limits of normal, whereas specimens from 334 patients with no bacterial involvement gave values within the normal range. The duration of elevated CSF lactate values coincided with the clinical response to therapy. When considered along with the history and physical examination of the patient, determination of lactic acid proved to be a rapid and reliable diagnostic test for the early detection of untreated as well as partially treated pyogenic meningitis.
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PMID:Cerebrospinal fluid lactic acid levels in meningitis. 89 5

Acid phosphatase staining is performed on cerebrospinal fluid cells of 365 samples from 105 patients with various types of meningitis. This enzyme activity is strongly positive in the early samples of bacterial meningitis, as far as the patients had not received a pretreatment with antibiotics for more than 24 h. It allows monitoring the response to therapy in subsequent samples. Acid phosphatase activity is positive in 2 cases of cryptococcus meningitis. It is negative in all cases of aseptic and Mycoplasma pneumoniae meningitis. The results in herpes encephalitis are variable, depending on the clinical state and the degree of brain destruction. Acid phosphatase staining is a useful and rapid cytological technique for determination of the nature of the meningitis and for monitoring the therapeutical response.
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PMID:Acid phosphatase activity of cerebrospinal fluid cells in bacterial and abacterial meningitis. 378 Jul 80

The presence of viral infection was evaluated in 160 children older than three months with bacterial meningitis who were admitted to Children's Medical Center or Parkland Memorial Hospital, Dallas, TX, between October 1979 and March 1982. Results were compared with a single serologic specimen in 138 children without meningitis. A recent history of upper respiratory infection was obtained from 60% of patients, including 10/13 with pneumococcal, 9/16 with meningococcal, and 77/131 with Haemophilus influenzae meningitis. Viral infection was documented by serologic response (23.8%) or viral isolation (13.2%) in 63/160 (40%) of patients with meningitis. There were 23 positive cultures (one patient with both adenovirus and respiratory syncytial virus). Picornaviruses, including two rhinoviruses, were isolated from six of the 24 subjects without meningitis who had viral cultures. There were 69 serologic conversions in meningitis patients, with 12 patients converting to two organisms and four patients converting to three organisms. Viral diagnoses included: adenovirus, 32 children; respiratory syncytial virus, 14; influenza A, 8; influenza B, 4; parainfluenza (1, 2, and 3), 12; picornaviruses, 9; herpes simplex virus, 1; and cytomegalovirus, 1. Additionally, 6/15 seroconverted to Mycoplasma pneumoniae. The acute geometric mean serum antibody titers of meningitis patients were lower than those of the comparison group for adenovirus (3.5 vs. 6.6, p less than or equal to 0.001) and influenza B (1.2 vs. 1.6, p less than or equal to 0.05). Twenty nine of 131 patients with H. influenzae had evidence of recent adenovirus infection. Primary infection with adenoviruses and possibly influenza B or mycoplasma precedes development of bacterial meningitis in some patients and may be a predisposing factor.
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PMID:Possible association of mycoplasma and viral respiratory infections with bacterial meningitis. 381 56

Antigen from purified Mycoplasma pneumoniae organisms treated with Tween-80-ether was used in a solid phase enzyme immunoassay and compared with the conventional lipid containing complement fixation antigen for measuring antibodies in sera from patients with aseptic or bacterial meningitis or with apparent M pneumoniae infection. In immunoblotting of the enzyme immunoassay antigen, enzyme immunoassay positive sera detected a polypeptide at Mr = 180.000-200.000, while enzyme immunoassay negative sera whether positive or negative in the complement fixation test did not. These results indicate that the enzyme immunoassay antigen containing the high molecular weight polypeptide can be used to measure M pneumoniae antibodies more specifically than the conventional lipid containing complement fixation antigen.
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PMID:Mycoplasma pneumoniae protein involved in the antibody response in human infection. 643 37

A fourfold or greater increase in titer of complement-fixing (CF) antibodies to Mycoplasma pneumoniae was found in 40.7% of paired sera from 54 patients with bacterial meningitis that had been proven by culture and in 10.3% of 39 patients with other bacteremic infections, but in none of eight patients with whooping cough or 40 patients with mumps meningitis. The CF antigen used was a crude lipid antigen, but comparable antibody increases were found by an enzyme-linked immunosorbent assay using a crude M. pneumoniae protein antigen. Increases were also frequently seen in nonspecific antibodies to the capsular polysaccharide of group A Neisseria meningitidis; these increases were significantly, but not completely, correlated to the nonspecific reactions to the mycoplasmal antigens. The data call for caution in interpreting serologic tests for M. pneumoniae when dealing with diseases not commonly associated with M. pneumoniae.
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PMID:Increase in titers of antibodies to Mycoplasma pneumoniae in patients with purulent meningitis. 680 46

Insulin-like growth factors (IGFs) have 6 types of binding proteins (IGFBPs), and IGFBP-3 is the major IGFBP in human sera. A proteolytic enzyme for IGFBP-3 has recently been reported to be present in human and animal pregnant sera. Although the physiological significance of a pregnancy-associated IGFBP-3 protease remains to be established, the proteolysis could result in lowering the affinity for IGFs, thereby enhancing their delivery to target tissues by increasing free IGFs in the circulation. The methods for detection of IGFBP-3 protease which have been widely used so far are a method reported by Lamson et al. which used affinity crosslinking or western ligand blotting. These methods need radioactive materials (iodinated IGFs and IGFBP-3) and it takes at least a few days to get the results. We have now developed a simple assay for the proteolysis of IGFBP-3. The method is western immunoblotting without radioactive materials. The results can be obtained in a day. With this method, we proved the absence of significant proteolytic activity in sera from rapidly growing children (early stage of puberty or precocious puberty), and sera from a severe type of growth hormone deficiency. Significant proteolytic activity, as in pregnant women, was detected in 6 out of 11 patients with acute disorders such as measles, Kawasaki disease, bacterial meningitis and mycoplasma pneumonia, some of whom were probably in a catabolic condition. These data suggests that the proteolysis of IGFBP-3 might also be important in modulating IGF action in some acute diseases during childhood. The increased bioavailability of IGFs by IGFBP-3 proteolysis may play a role in overcoming catabolic conditions.
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PMID:Proteolytic activity of IGFBP-3 in various clinical conditions during childhood studied by means of western immunoblotting. 855 66

The role of infectious and inflammatory causes of stroke is much more significant in children than in adults. Conversely, that of atherosclerotic disease, ischaemic heart disease and hypertensive haemorrhages has a lesser prominence in children. Bacterial meningitis caused by Streptococcus pneumoniae, Haemophilus influenzae, or Neiserria meningitidis has been known to cause stroke in children. The mechanism appears to be the spread of meningeal inflammation to involve the walls of intracranial vessels, resulting in arterial thrombosis with ischaemia or rupture with haemorrhage. Other infections caused by atypical bacterial agents such as Mycoplasma tuberculosis and viral agents such as varicella-zoster virus have also been well documented as causes of stroke. Non-infectious, inflammatory causes of stroke, such as collagen vascular disease and primary angiitis of the central nervous system, have been reported in children as well as adults. In this review, we will focus on recent advances in the field of childhood stroke caused by infectious and inflammatory disorders.
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PMID:Infectious and inflammatory disorders of the circulatory system and stroke in childhood. 1192 29

A 23-year-old woman with mild psychomotor retardation presented with fever, coughing, reduced consciousness and a stiff neck. A chest X-ray revealed an infiltrate in the left lower lobe; the cerebrospinal fluid was cloudy with a mild pleocytosis. Ceftriaxone was prescribed and the fever subsided. On the second day of admission she had a seizure, and a paraparesis emerged. Despite changes in the antibiotic regimen, her clinical condition hardly improved. On the fifth day, antibodies against Mycoplasma pneumoniae were found to be strongly positive and the diagnosis was M. pneumoniae infection. This accounted for the pneumonia together with meningoencephalitis and a transverse myelitis. The antibiotics were switched to doxycycline and the clinical condition improved dramatically. Six weeks after discharge, the patient had made a complete recovery. In patients suffering from meningitis with an atypical presentation, uncommon causes of infection should be considered. Together with a pneumonia, M. pneumoniae, Chlamydia pneumoniae, Legionella pneumophila and Listeria monocytogenes should be high on the list of potential causes for bacterial meningitis.
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PMID:[Clinical reasoning and decision-making in practice. A young woman with fever, shortness of breath, and reduced consciousness]. 1289 64

Acute cerebellar ataxia is a relatively common neurologic disorder among children. Our aim was to characterize the clinical picture, etiology, and prognosis of acute cerebellar ataxia. The medical records of all children with a diagnosis of acute cerebellar ataxia hospitalized in our center and Hasharon Medical Center from 1990 to 2001 were reviewed. The diagnosis of acute cerebellar ataxia was based on the following criteria: acute onset of ataxia with or without nystagmus; absence of known genetic predisposing factors, such as familial degenerative disorders; and absence of drug intoxication, bacterial meningitis, and metabolic disorders. Thirty-nine children were identified; 54% were male; mean age at presentation was 4.8 +/- 3.8 years. All patients were observed for at least 1 year. A prodromal febrile illness was noted in 74.4%: varicella, 31%; mumps, 20%; nonspecific viral infection, 15.4%; mycoplasma, 5%; Epstein Barr virus, 3%. Latency from the prodromal illness to the onset of ataxia was 8.8 +/- 7.4 days. The most common associated neurologic findings were nystagmus and dysmetria. Full gait recovery took less than 2 weeks on average, and the longest duration of neurologic signs was 24 days (mumps-related). Acute cerebellar ataxia in childhood is a self-limited disease. The recovery was faster than that reported in previous publications and was complete in all children without any neurologic sequelae. Imaging studies are needed only in atypical presentation or if there is no spontaneous improvement after 1 to 2 weeks.
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PMID:Post-infectious acute cerebellar ataxia in children. 1455 15

Thirteen children in whom electroencephalography revealed periodic lateralized epileptiform discharges in the acute phase of cerebral involvement were included in this study. Four were diagnosed as having influenza-associated encephalopathy, two nonherpetic limbic encephalitis, two theophylline-associated seizures, one Mycoplasma pneumoniae encephalitis, one acute encephalopathy, and one bacterial meningitis. All patients developed seizures; six developed hemiconvulsions. As to prognosis, two died, six had some neurologic sequelae, and five had no neurologic sequelae. Although periodic lateralized epileptiform discharges are not disease specific, the importance of these disorders had not been focused on as a cause of periodic lateralized epileptiform discharges.
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PMID:Periodic lateralized epileptiform discharges in children. 1469 11


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