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

We have studied prospectively the C-reactive protein values in the cerebrospinal fluid of 54 patients with bacterial meningitis, tuberculous meningitis, and severe malarial infection and convulsions without infections of the central nervous system. CSF CRP above 1 mg/l was observed in 23 out of 28 patients with bacterial meningitis (sensitivity of 82%). The specificity was 73% at the 1 mg/l level. Five out of 19 patients with severe malarial infection had CSF CRP levels above 1 mg/l. Two patients with TB meningitis were also studied. Both of them had CSF CRP above 1 mg/l. Five patients with febrile convulsions or sepsis without meningitis had CSF CRP below 1 mg/l. It is concluded that CSF CRP would not be used as a useful discriminatory test in areas where malaria and TB meningitis are common.
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PMID:C-reactive protein and bacterial meningitis. 246 9

Specific aetiological diagnosis of bacterial meningitis (BM) in developing countries is often difficult. Frequently, differentiating BM from viral and TB meningitis is not easy. A study was carried out with the easily and quickly performed CSF morphological and biochemical changes as a diagnostic test against the gold standard of CSF culture and/or the latex agglutination test (LAT). Children between 2 months and 11 years of age, suspected to have acute meningitis, were prospectively recruited. CSF cell count and morphology, Gram stain, culture, and protein and sugar estimations were carried out as per standard procedures. The laboratory personnel were blind to the clinical details and the findings of each other. Diagnosis based on gold standard was possible in 55 out of 114 cases. With CSF polymorphs > 60 per cent and sugar < 50 per cent of blood level as constants, various levels of total cells and protein were considered for their diagnostic properties. The protein level was not useful. We found the best cut-off level of cell count for diagnosis of BM to be 300/mm3, based on the receiver operating characteristics curve, the point of maximum accuracy. These findings were validated by comparing the clinical features, CSF changes and outcome characteristics of non-confirmed cases with the above criteria with the confirmed cases; these were found to be the same except for age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of CSF variables as a diagnostic test for bacterial meningitis. 827 35

Mycobacterial infection has been recognized as a complication in patients with malignancy. Tuberculous (TB) meningitis has not been reported in patients with nasopharyngeal carcinoma (NPC); it may have been overlooked or confused with the underlying malignancy or meningitis caused by other microorganisms. We describe the occurrence of culture-proven TB meningitis in 2 NPC patients. The time lag between the diagnosis of NPC and the occurrence of TB meningitis was 4 years in 1 patient and 6 years in the other. In both patients, the diagnosis of TB meningitis was delayed; they were initially treated for bacterial meningitis. Subsequent antituberculous chemotherapy was successful in 1 patient but failed in the other. Recognition of the infection is important for early diagnosis and proper treatment of this potentially fatal condition in patients with NPC.
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PMID:Tuberculous meningitis in patients with nasopharyngeal carcinoma. 879 91

Tuberculous meningitis is characterized by cerebral tissue destruction. Monocytes, pivotal in immune responses to Mycobacterium tuberculosis, secrete matrix metalloproteinase-9 (MMP-9), which facilitates leukocyte migration across the blood-brain barrier, but may cause cerebral injury. In vitro, human monocytic (THP-1) cells infected by live, virulent M. tuberculosis secreted MMP-9 in a dose-dependent manner. At 24 h, MMP-9 concentrations increased 10-fold to 239 +/- 75 ng/ml (p = 0.001 vs controls). MMP-9 mRNA became detectable at 24--48 h. In contrast, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) gene expression and secretion were similar to constitutive levels from controls at 24 h and increased just 5-fold by 48 h. In vivo investigation revealed MMP-9 concentration per leukocyte in cerebrospinal fluid (CSF) from tuberculous meningitis patients (n = 23; median (range), 3.19 (0.19--31.00) ng/ml/cell) to be higher than that in bacterial (n = 12; 0.23 (0.01--18.37) ng/ml/cell) or viral meningitis (n = 20; 0.20 (0.04--31.00) ng/ml/cell; p < 0.01). TIMP-1, which was constitutively secreted into CSF, was not elevated in tuberculous compared with bacterial meningitis or controls. Thus, a phenotype in which MMP-9 activity is relatively unrestricted by TIMP-1 developed both in vitro and in vivo. This is functionally significant, since MMP-9 concentrations per CSF leukocyte (but not TIMP-1 concentrations) were elevated in fatal tuberculous meningitis and in patients with signs of cerebral tissue damage (unconsciousness, confusion, or neurological deficit; p < 0.05). However, MMP-9 activity was unrelated to the severity of systemic illness. In summary, M. tuberculosis-infected monocytic cells develop a matrix-degrading phenotype, which was observed in vivo and relates to clinical signs reflecting cerebral injury in tuberculous meningitis.
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PMID:Identification of a matrix-degrading phenotype in human tuberculosis in vitro and in vivo. 1123 75

The laboratory diagnosis of CNS infection is essential for optimal therapy. Acute infection requires rapid turn-around testing with high predictive values, that is, the ability of a test to accurately identify those patients who do or do not have disease caused by a specific etiology. The Gram's stain, fungal stains of direct smears, antigen testing for C. neoformans, and culture of bacteria, fungi, mycobacteria, and some viruses are important tests for the diagnosis of acute infection. The laboratory diagnosis of chronic infection necessitates discussion between the clinician and laboratory technician to allow triaging of testing. Antigen tests for bacteria, fungi, and viruses; antibody tests for multiple microorganisms; and PCR testing for bacteria, M. tuberculosis, and many viruses are all important in limited clinical situations. All testing for acute or chronic disease depends on sufficient specimen that is transported to the laboratory in a manner that will not compromise viability or chemical integrity. Sterile containers that maintain moisture content, exclude oxygen for anaerobic requests, and are stored at proper temperatures (22 degrees C room, 4 degrees C refrigeration, or -20 degrees C freezer depending on pathogen and test) are mandatory. Many laboratory issues addressing the diagnosis of CNS infection are changing or evolving. Most important is the recognition that bacterial antigen testing for the diagnosis of acute bacterial meningitis rarely impacts patient management and is not routinely needed, CSF shunt infections differ from usual meningeal infections and require rapid diagnosis, and TB meningitis remains a difficult disease to diagnosis but may be confirmed first by PCR testing of CSF. In addition, Whipple's disease of the CNS can be confirmed using PCR with CSF; CJD has a marker protein, referred to as 14-3-3 antigen, that can be detected in CSF, and the diagnosis of fungal CNS disease requires careful interpretation of direct smears, antigen and antibody testing, and culture. Most difficult to diagnose among the CNS infections are viral meningitis and encephalitis. The appearance of new etiologies, such as West Nile virus, and the common use of PCR for the herpes viruses and enteroviruses represent important advances. Evolving methods for the laboratory diagnosis of CNS infection represent significant improvements over previous testing; however, the array of tests available demands more attention for appropriate selection, is significantly more expensive, and requires new skills for performance and interpretation. The responsibility for proper use of laboratory testing lies both with the clinician and laboratory technician.
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PMID:Laboratory diagnosis of central nervous system infections. 1178 Feb 67

This review focuses on recent advances of topical interest regarding the diagnosis and treatment of common causes of bacterial meningitis occurring in children beyond the neonatal period. Tuberculous meningitis is beyond the scope of this review.
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PMID:Diagnosis and treatment of bacterial meningitis. 1281 10

Treatment of meningitis is no longer a question of the administration of antimeningococcal serum and awaiting results. Today there is at hand an ever expanding armamentarium of drugs effective on various bacteria, rickettsia and some of the larger viruses. The skillful use of these singly or in combination offers an excellent prognosis in most forms of bacterial meningitis. Tuberculous meningitis continues to present a poor outlook, but this has been improved with more intensive therapy. More effective agents are needed in the treatment of this disease."Shotgun" therapy may be indicated in critically ill patients prior to accurate bacteriological diagnosis; it is more important that therapy should include an effective agent or combination of agents than to attempt to determine in advance the most potent form of specific therapy. Partially treated purulent meningitis may be confused with aseptic meningitis. There is at present no effective therapeutic agent for the viral meningitides, but the prognosis is favorable in most of these diseases without specific therapy.
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PMID:The diagnosis and treatment of meningitis. 1477 56

Tuberculous meningitis (TBM) remains a common serious neurological emergency especially in the developing world. Elevated intracranial pressure (ICP) is often a feature of severe TBM and is associated with high morbidity and mortality. The pathology associated with TBM, such as cerebral edema, hydrocephalus, tuberculoma(s), and infarcts related to arthritis, contribute to increase in intracranial volume and, therefore, elevated ICP. The three types of edema (vasogenic, cytotoxic, and interstitial) may contribute to cerebral edema. The molecular mechanisms underlying the events that ultimately lead to brain damage and cerebral edema during infection are complex. Similarly to bacterial meningitis, cerebral blood flow autoregulation is probably impaired in TBM, and the mechanisms are unclear. Although no universal guidelines are available to institute ICP monitoring in patients with severe TBM, it is be prudent to monitor patients at risk for increases in ICP. Such an approach helps to detect the secondary brain insults, allowing for a more informed approach to treatment. Treatment of elevated ICP involves a multipronged approach. The first step should be to identify focal brain lesions and hydrocephalus (which require surgical intervention) by brain imaging. Cerebral edema is treated with hyperosmolar agents. Mannitol is currently the most commonly used agent. It appears that use of hypertonic saline as an osmotic agent in infection-related cerebral edema has certain advantages. However, this needs to be established by well-designed trials. Use of steroids reduces not only cerebral edema but also the production of cytokines and other chemicals involved in the immunopathogenesis of TBM. Fever associated with TBM should be aggressively treated, because fever can worsen the impact of elevated ICP. Hyponatremia may complicate TBM and requires appropriate correction because it can aggravate cerebral edema.
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PMID:Management of intracranial pressure in tuberculous meningitis. 1615 82

Tuberculous meningitis (TBM) is still a major cause of serious illness in many parts of the world. The newer diagnostic tests and neuroimaging methods are unlikely to be available in many developing countries. We attempt to identify simple parameters for early diagnosis. A retrospective study was performed to compare the clinical and laboratory features of cultured-confirmed, TBM (134) and other bacterial meningitis (709). Features independently predictive of TBM were studied by multivariate logistic regression to develop a diagnostic rule. Six features were found predictive: length of clinical history >5 days, headache, total cerebrospinal fluid (CSF) white blood cell count of <1000/mm3, clear appearance of CSF, lymphocyte proportion of >30%, and protein content of >100 mg/dL. Application of 3 or more parameters revealed 93% sensitivity and 77% specificity. Applying this diagnostic rule can help in the early diagnosis of TBM, in both children and adults.
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PMID:Differentiation of tuberculous meningitis from acute bacterial meningitis using simple clinical and laboratory parameters. 1662 6

Review of 497 cases of neuroinfections in 7 tropical clinics in Ethiopia, Uganda, Burundi, Kenya, Sudan within 2000-2007 was performed. 97.5% of all cases was cerebral malaria (40.1%) and bacterial meningitis (56.4%). TB meningitis, cerebral cryptococcosis and sleeping sickness were very rare.
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PMID:Ten years experience with 497 cases of neuroinfections in tropic: in limited laboratory infrastructure initially treat both, cerebral malaria and meningitis. 1755 83


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