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

Apoptosis and necrosis in brain account for neurological sequelae in survivors of bacterial meningitis. In meningitis, several mechanisms may trigger death pathways leading to activation of transcription factors regulating caspases mRNA synthesis. Therefore, we used a multiprobe RNA protection assay (RPA) to examine the expression of 9 caspase-mRNA in the course of experimental Streptococcus pneumoniae meningitis in mouse brain. Caspase-6, -7 and -11 mRNA were elevated 6 hours after infection. 12 hours after infection caspases-1, -2, -8 and -12 mRNA rose. Caspase-14 mRNA was elevated 18 h and caspase-3 mRNA 24 h after infection. In situ hybridization detected caspases-3, -8, -11 and -12 mRNA in neurons of the hippocampal formation and neocortex. Development of sepsis was paralleled by increased transcription of caspases mRNA in the spleen. In TNFalpha-deficient mice all caspases examined were less upregulated, in TNF-receptor 1/2 knockout mice caspases-1, -2, -7, -11 and -14 mRNA were increased compared to infected control animals. In caspase-1 deficient mice, caspases-11, and -12 mRNA levels did not rise in meningitis indicating the necessity of caspase-1 activating these caspases. Hippocampal formations of newborn mice incubated with heat-inactivated S. pneumoniae R6 showed upregulation of caspase-1, -3, -11 and -12 mRNA. These observations suggest a tightly regulated caspases network at the transcriptional level in addition to the known cascade at the protein level.
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PMID:Transcriptional regulation of caspases in experimental pneumococcal meningitis. 1141 71

A 42-year-old man was admitted due to recurrent bacterial meningitis, as he had been treated here for bacterial meningitis three years prior to the current event. He had a remote history of head injury that he had almost forgotten, and his laboratory data showed no immunodeficiency state. 111In-DTPA cisternography showed an abnormal radioactive accumulation in the frontal lobe adjacent to the left frontal sinus at 23 hours after intrathecal injection, and MPR CT images revealed the left frontal sinus bone fracture. These findings indicated that he had a head injury by which a delayed CSF fistula has been formed. He was surgically treated for a CSF leakage. Although a combination therapy of ABPC and CTRX was efficacious for this patient, this regimen may not be ideal, as meningitis by PRSP has been increasing in incidence. Pneumococcal meningitis, once not a difficult infection to treat, could be a difficult one, as resistant strains to ABPC and CTRX have been more common.
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PMID:[A case of recurrent bacterial meningitis by delayed cerebrospinal fluid (CSF) leakage due to a head trauma]. 1242 68

Neuronal damage in the hippocampal formation is a common feature in animal models of bacterial meningitis and human disease. In mouse and rabbit models of Streptococcus pneumoniae meningitis, proliferation of neural progenitor cells quantified by bromodeoxyuridine (BrdU) incorporation was enhanced in the subgranular layer of the dentate gyrus. In mice, the density of BrdU-labeled cells was maximal on Day 2 after infection. Approximately 60% of the cells labeled by BrdU between Days 7 and 10 after infection that remained present 28 days later had migrated into deeper layers of the dentate gyrus and differentiated into neurons, as evidenced by immunohistochemical staining for TUC-4, MAP-2 and beta-tubulin. This suggests that endogenous repair mechanisms may limit consequences of neuronal destruction after meningitis.
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PMID:Increased neurogenesis after experimental Streptococcus pneumoniae meningitis. 1289 28

To determine incidence of invasive Haemophilus influenzae type b (Hib) disease in a defined population of Jeonbuk Province, Korea, children <5 years were evaluated in prospective, population-based surveillance of invasive bacterial diseases using standardized methods for patient referral, clinical evaluation and laboratory testing (optimized culture, latex agglutination, polymerase chain reaction). Vaccine utilization was assessed with vaccination histories of patients in surveillance, monthly data on Hib vaccine distribution and a coverage survey of clinic patients in study population. From September 1999 to December 2001, 2176 children were evaluated for possible meningitis, 1541 had no cerebrospinal fluid (CSF) findings of meningitis, 605 had CSF abnormalities (suspected bacterial meningitis) but no pathogen identified; six patients had probable Hib meningitis and eight had confirmed Hib meningitis. The annual suspected bacterial meningitis incidence was 258.4/100,000 <5 years and the probable/confirmed Hib meningitis incidence was 6.0/100,000 <5 years. Pneumococcal meningitis incidence was 2.1/100,000 <5 years and Group B streptococcal meningitis incidence was 0.17/1000 live births. A total of 69,589 Hib vaccine doses were distributed during the study. Hib vaccine coverage was negligible initially but increased to 16% (complete Hib immunization) and 27% (partial immunization) in final months of study. Suspected bacterial meningitis incidence was high but proven invasive Hib meningitis incidence was low. Hib was leading cause of bacterial meningitis yet bacterial pathogens were identified in only 4% of abnormal CSF. These findings may reflect truly low incidence, presumptive antibiotic treatment, partial Hib immunization, or incomplete clinical evaluations. Given the apparent Hib meningitis burden in Jeonbuk Province, additional studies to describe other invasive Hib syndromes, Hib-associated mortality and disability, and economic impact of Hib disease will be useful to guide public health decisions regarding routine Hib vaccine introduction.
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PMID:Incidence of Haemophilus influenzae type b and other invasive diseases in South Korean children. 1536 44

We report a male with spinal cord infarction and tetraplegia after Streptococcus pneumoniae meningitis. He was subsequently found to have both a Chiari I malformation and factor V Leiden mutation. A literature search was conducted to identify previously reported cases of pediatric spinal cord infarction associated with acute bacterial meningitis, anatomic brain anomalies, and hypercoagulability disorders. This article is the first report of spinal cord infarction in a child with hypercoagulability disorder and structural brain anomaly in the setting of acute bacterial meningitis. The confluence of infection, inflammation, localized pressure, and predisposition to hypercoagulability produced unique conditions resulting in infarction of the cervical spine. This report emphasizes the polygenic nature of the expression of spinal cord infarction.
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PMID:Spinal cord infarction in meningitis: polygenic risk factors. 1566 74

The diagnosis of bacterial meningitis is rarely a difficult diagnostic dilemma when a patient presents with fever, headache, neck stiffness, and altered mental status. Unfortunately for the practicing clinician, patients are rarely that straightforward. Patients who are elderly, very young, or immuno-compromised often present with subtle findings, making the correct diagnosis a challenge. In addition, patients being treated with antibiotics may be misleading in their clinical presentation, leading to a missed diagnosis of meningitis. Only when one considers the diagnosis or obtains a sample of cerebrospinal fluid is the correct diagnosis made. Although the clinical scenario may suggest meningitis, it is the cerebrospinal fluid white blood cell count that establishes the definitive diagnosis. Despite the advent of systemic antibiotics over 50 years ago, bacterial meningitis continues to cause considerable morbidity and mortality worldwide. The following case report details a woman diagnosed with Streptococcus pneumoniae meningitis with an extremely high cerebrospinal white blood cell count. Although this is typically thought to be caused by abscesses or malignancy, meningitis alone may cause such an elevation. In addition, a brief review of the current epidemiology and treatment regimens for meningitis is discussed.
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PMID:Marked elevation of cerebrospinal fluid white blood cell count: an unusual case of Streptococcus pneumoniae meningitis, differential diagnosis, and a brief review of current epidemiology and treatment recommendations. 1596 Oct 5

A Substantial ratio of bacterial meningitis survivors suffers mild or serious intellectual and neuropsychological handicaps. We organized eighty subjects into three groups: 1) Pneumococcal meningitis (PM) who did not receive dexamethasone, 2) PM who received dexamethasone, 3) Other bacterial meningitis with different etiology. All subjects underwent Bender Visual Motor Gestalt test and age-appropriate Intelligence quotient (IQ) tests. The mean full-scale IQ scoring fell within normal range (90+/-17) in the post-meningitic cohort. There was no statistical difference between two pneumococcal groups regarding full scale IQ testing (88+/-16 and 91+/-18) and Bender-Gestalt scoring (4.0+/-3.3 and 3.8+/-2.6), respectively. However, the subjects with full scale IQ score <85 (below the average) were statistically less in the group with steroid therapy. PM patients who received dexamethasone therapy had statistically better academic performance. As a result, adjuvant steroid therapy has no significant impact on overall intellectual tests in PM subjects. However, dexamethasone seems to diminish development of below the average IQ scoring in PM cases. In addition, PM subjects who received steroids showed better academic achievement. These findings may support the idea of dexamethasone administration prior to first antibiotic dose in PM subjects.
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PMID:Long-term beneficial effects of dexamethasone on intellectual and neuropsychological outcome of children with pneumococcal meningitis. 1644

Acute bacterial meningitis is a potentially life-threatening infection of the cranial and spinal leptomeninges. Recurrent episodes of meningitis are rarely seen, but when they occur, an extensive investigation has to be made to find out responsible factors. A single episode of acute meningitis may result from bacteriemia, but when followed by recurrent meningitis in pediatric patients, other possible routes of the bacteria invasion to the cerebrospinal fluid (CSF) should be considered. Patients with head injury have the highest risk of acquiring recurrent bacterial meningitis, followed by patients with a congenital anatomic lesion of the skull or duramater, such as meningomyelocele. The underlying cause is a transdural communication between the meningeal space and paranasal sinuses or skin. The first attack of meningitis may occur several weeks to 12 years after the head injury. In addition, recurrent bacterial meningitis may be due to disorders of the immune system, such as complement deficiency. We report a 14-year-old boy, who suffered from recurrent Streptococcus pneumoniae meningitis due to a well-defined defect at the ethmoid roof after a head trauma.
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PMID:Recurrent Streptococcus pneumoniae meningitis in a child with traumatic anterior cranial base defect. 1853 65

In bacterial meningitis, chemokines lead to recruitment of polymorphonuclear leucocytes (PMN) into the CNS. At the site of infection in the subarachnoid space, PMN release reactive oxygen species, reactive nitrogen intermediates (RNI) and interleukin-1beta (IL-1beta). Although these immune factors assist in clearance of bacteria, they also result in neuronal injury associated with meningitis. Transforming growth factor beta (TGFbeta) is a potent deactivator of PMN and macrophages since TGFbeta suppresses the production of ROI, RNI and IL-1. Here, we report that the deletion of the TGFbeta receptor II gene in PMN enhances PMN recruitment into the CNS of mice with Streptococcus pneumoniae meningitis. This was associated with more efficient clearance of bacteria, and almost complete prevention of intracerebral necrotizing vasculitis. Differences in PMN in the CNS of infected control mice and mice lacking TGFbeta receptor II were not explained by altered expression of chemokines acting on PMN. Instead, TGFbeta was found to impair the expression of L (leucocyte)-selectin on PMN from control mice but not from mice lacking TGFbeta receptor II. L-selectin is known to be essential for PMN recruitment in bacterial meningitis. We conclude that defective TGFbeta signalling in PMN is beneficial in bacterial meningitis by ameliorating migration of PMN and bacterial clearance.
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PMID:TGFbeta receptor II gene deletion in leucocytes prevents cerebral vasculitis in bacterial meningitis. 1689 35

Neuronal injury is frequent in bacterial meningitis, resulting in a high rate of death and neurological sequelae. In a search of potential neuroprotective strategies for treatment of bacterial meningitis, the antioxidant melatonin was neuroprotective in cell culture experiments and in a rabbit Streptococcus pneumoniae meningitis model, when treatment was started at the time of infection. In the present study, adjunctive melatonin treatment applied from the beginning of antibiotic therapy 12 hr after infection at a dose of 1.67 mg/kg/hr resulted in plasma concentrations of 451 +/- 198 ng/ml, cerebrospinal fluid (CSF) concentrations of 154 +/- 57 ng/ml and a CSF-to-plasma ratio of 0.38 +/- 0.19 (mean +/- SD). Melatonin therapy had antiinflammatory effects but did not reduce neuronal injury in either a rabbit model of gram-positive Streptococcus pneumoniae or gram-negative Escherichia coli meningitis.
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PMID:Antiinflammatory but no neuroprotective effects of melatonin under clinical treatment conditions in rabbit models of bacterial meningitis. 1699 17


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