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

Cortical visual impairment (CVI) following bacterial meningitis is a very uncommon complication. Two children with CVI following bacterial meningitis are reported. Bacterial agents were Haemophilus influenzae type B in one and meningococci in the other child. Both children showed only insufficient recovery from CVI, mental retardation and residual neurological symptoms. Flash visual evoked potentials (VEP) showed preserved cortical response at onset of CVI. Re-evaluations several months later showed significantly reduced amplitudes, but normal latencies for P100. Thus, flash VEP does not allow prediction of visual outcome. MRI results have not been reported before. MRI at onset of diagnosis showed occipital parenchymal irregularities with enlarged sulci and subarachnoid spaces. Follow up MRI 15 months after onset of CVI in one patient showed marked atrophy of the occipital cortex, hyperintensities of the cortical white matter and no visible optic radiation. The MRI findings indicate hypoxic-ischaemic lesions in the border zone between the distribution of the great cerebral arteries.
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PMID:Cortical visual impairment following bacterial meningitis: magnetic resonance imaging and visual evoked potentials findings in two cases. 142 3

Despite the availability of potent antibiotics, bacterial meningitis is still a major clinical problem. Mortality is high, and up to a third of survivors are left with neurologic sequelae that may range from mild behavioral disorders to mental retardation or deafness. New therapeutic approaches to meningeal inflammation, however, are reducing the neurologic risks.
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PMID:Mediators of meningitis: therapeutic implications. 189 48

All types of central nervous system (CNS) infections were investigated in a 1966 birth cohort of 12,000 children from Northern Finland followed up from birth to the age of 14. 174 CNS infections occurred in 167 children, 110 boys and 64 girls. The annual incidence of bacterial CNS infections was 36.3/100,000 and that of viral infections 688.0/100 000. It is concluded that bacterial CNS infections were recorded very fully but only 2/3 of the viral infections could be traced, even though the more severe cases were quite well documented. 8/55 children (14.5%) with bacterial meningitis died; the corresponding figure for viral encephalitis and meningitis (excluding mumps) was 3/67 (4.5%). 17/55 (30.9%) developed mental retardation, epilepsy, cerebral palsy or hearing defect or some combination of these after bacterial CNS infection, and 9 (8.1%) after viral infection. The difference with respect to the children who had not experienced CNS infection was statistically significant only for the bacterial infection cases. CNS infections explained 7.6% of all deaths from 28 days to 14 years, 3% of the handicapping cases of cerebral palsy, mental retardation and epilepsy or some combination of these, and 6.6% of the hearing defects.
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PMID:Incidence and prognosis of central nervous system infections in a birth cohort of 12,000 children. 376 48

In a group of 124 children with mental retardation, a study showed 21% of chromosomal abnormalities, 26% of perinatal causes and 33% of undetermined causes. Current preventive measures are well adapted. They might be usefully completed by mandatory ultrasonographic examinations during pregnancy and promotion of birth of at-risk children in well-equipped centers for perinatal medicine. In cases when in utero transfer is not possible, transfer by specialized pediatric emergency care services should be generalized. A better supervision of families where retarded children are living would be advisable. The detection of bacterial meningitis should be improved. Finally, an active research should be undertaken in order to better dissociate and understand the as yet unknown causes of mental retardation.
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PMID:[Etiology and prevention of severe mental handicaps]. 714 93

We abstracted the results of all English language reports of the outcomes of bacterial meningitis published after 1955. We used hierarchical Bayesian meta-analysis to determine the overall and organism-specific frequencies of death and persistent neurologic sequelae in children 2 months to 19 years of age. A total of 4920 children with acute bacterial meningitis were included in 45 reports that met the inclusion criteria. Children described in the 19 reports of prospectively enrolled cohorts from developed countries had lower mortality (4.8% vs. 8.1%) and were more likely to have no sequelae (82.5% vs. 73.9%). In these 19 studies 1602 children were evaluated for at least 1 sequela after hospital discharge. The mean probabilities of these sequelae were: deafness, 10.5%; bilateral severe or profound deafness, 5.1%; mental retardation, 4.2%; spasticity and/or paresis, 3.5%; seizure disorder, 4.2%; and no detectable sequelae, 83.6%. Mean probabilities of outcomes varied significantly by etiologic bacteria, e.g. mortality: Haemophilus influenzae, 3.8%; Neisseria meningitis, 7.5%; Streptococcus pneumoniae, 15.3%.
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PMID:Outcomes of bacterial meningitis in children: a meta-analysis. 832

Neisseria meningitidis is a leading cause of bacterial meningitis and sepsis in the US, Europe and in many other parts of the world, including parts of sub-Saharan Africa (known as the African 'meningitis belt'). There are > 500000 cases of meningococcal disease annually with an estimated death toll of 135000 worldwide. Approximately 10 - 15 % of survivors experience significant morbidity in the form of neurological sequelae, including hearing loss, speech disorders, loss of limbs, mental retardation and paralysis. Disease is usually caused by N. meningitidis serogroups A, B, C, Y or W-135. Prevention of meningococcal disease includes isolation, chemoprophylaxis and vaccination with available polysaccharide vaccines. However, the polysaccharide meningococcal vaccines (i.e., A and C; A, C and W-135; or A, C, Y and W-135) initially developed in the 1970s are generally poorly immunogenic in children or require repeated doses and do not produce long-lasting immunity. Conjugate vaccine technology has been very successfully used in childhood vaccines for the prevention of other bacterial meningitis pathogens, including vaccines against Haemophilus influenzae serotype b (Hib) and more recently, the seven- and nine-valent conjugate pneumococcal vaccines. Newly released meningococcal conjugate vaccines against N. meningitidis serogroup C have been highly efficacious in young children and adolescents, with minimal side effects. Conjugate vaccines targeting other important meningococcal serogroups (e.g., N. meningitidis serogroup A, responsible for the large pandemic outbreaks and the majority of disease in sub-Saharan Africa and serogroups Y and W-135) are under development and together with the serogroup C conjugates, have the potential to significantly impact worldwide sporadic and epidemic meningococcal disease. The search for an effective serogroup B meningococcal vaccine remains elusive. This manuscript reviews the conjugate meningococcal vaccines and their potential for meningococcal disease prevention.
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PMID:Meningococcal conjugate vaccines. 1510 68

Streptococcus pneumoniae is the most common cause of bacterial meningitis of high mortality and morbidity. Neurological sequelae include paralysis, mental retardation, and learning disorders. In humans, neurons of the hippocampus undergo apoptosis as a result of meningitis. Phosphatidylcholine (PtdCho) is an essential component of mammalian cell membranes and PtdCho deficiency, either due to chemicals or altered nutrition, leads to apoptosis, especially in hippocampal neurons. We show that apoptosis of a variety of brain cells after pneumococcal infection arises from inhibition of PtdCho biosynthesis, the first such activity described for a bacterium. Apoptosis inhibitors did not prevent the bacterial-dependent inhibition of PtdCho biosynthesis. Supplementation with exogenous lyso-phosphatidylcholine prevents cell death and treatment of mice with cytidine diphosphocholine attenuates hippocampal damage during meningitis, even after the onset of infection. We conclude that bacterial inhibition of PtdCho biosynthesis activates an apoptotic cascade that is a causative event in pathogenesis and amenable to therapeutic intervention.
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PMID:Bacterial inhibition of phosphatidylcholine synthesis triggers apoptosis in the brain. 1523 9

Bacterial meningitis remains a major cause of death and neurological and hearing sequels. In adults, the death rate ranges from 16 to 37% in meningitis due to Pneumococcus pneumoniae and neurological sequels occur in 30 to 52% of survivors. In childhood, the prognosis is better, with a death rate ranging from 2 to 15%, higher for Pneumococcus pneumoniae. Seventy-five percent of children survive without any sequel, 15% with hearing disorders (up to 30% with Pneumococcus), and rarely (3-4%) present with mental retardation, motor deficit, or epilepsy. In addition to the type of germ, the risk of sequels is six times higher in case of Pneumococcus, several factors of poor prognosis are described on admission: degree of coma, neurological deficit, cranial nerve palsy, high protein level, high erythrocytes count and low leukocytes count in CSF (less than 600 or 1000 leukocytes per microliter). Any neurological complication such as epilepsy, stroke, brain edema, hydrocephalus, or hemodynamic failure will be correlated to a poor outcome. Hearing must be tested within 15 days, followed by audiologic consultation and MRI focused on labyrinths to detect early onset cochlear ossification. One year after meningitis, behavior and cognitive skills must be assessed, including IQ, memory, attention and executive functions, adaptive abilities, to set up specific educative and teaching strategies.
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PMID:[Long-term follow-up of bacterial meningitis - sequels in children and adults: incidence, type, and assessment issues]. 1939 75