Outcome Of Bacterial Meningitis Research Articles

Bacterial meningitis in Swaziland: an 18 month prospective study of its impact.

To describe the epidemiology, clinical features, and outcome of bacterial meningitis in Swaziland. Prospective study of patients diagnosed as having meningitis of nonviral aetiology during an 18 month period from February 1991 to July 1992. Four regional hospitals covering the population of the four districts in Swaziland. All patients with non-viral meningitis admitted to hospital within the study period. Altogether 85 patients were reported to have bacterial meningitis: 48.3% were aged under 1 year. Causative organisms were identified in 60% of cases, and Streptococcus pneumoniae was found to be the commonest (49% of cases). Overall, case fatality was 38.8% for all age groups, and 62.5% (15 of 25) for adults. Neurological sequelae occurred in 22.4%. Three of the adult cases were HIV seropositive. Seizures, but not duration of symptoms before admission, were associated with a poor prognosis. There was a significant rise in incidence related to a period of drought. Fifteen patients were reported with tuberculous meningitis, of whom five were known to be HIV seropositive; the case fatality was 73.3%. The aetiology and age distribution of cases of meningitis differs greatly from that in developed countries. Rising HIV infection may have an important impact on the future incidence of meningitis. The high case mortality found should encourage efforts towards earlier diagnosis and treatment, and strengthens the need to develop appropriate vaccines.

Duration of symptoms and outcome in bacterial meningitis: An analysis of causation and the implications of a delay in diagnosis: Radetsky M. Pediatr Infect Dis J 1992; 11:694–8

Duration of symptoms and outcome in bacterial meningitis: An analysis of causation and the implications of a delay in diagnosis: Radetsky M. Pediatr Infect Dis J 1992; 11:694–8

Duration of symptoms and outcome in bacterial meningitis

The prompt diagnosis and therapy of bacterial meningitis remain enduring clinical challenges, for no physician would knowingly delay appropriate therapy. However, whether a delay in the initiation of antimicrobials in fact causes a worse outcome is a separate and tangential question. In clinical medicine a treatment decision involves a bedside estimate of the risk and potential severity of illness balanced against the benefits and adverse effects of therapy. For severe infections, the inexorable damage of untreated disease is presumed, and antimicrobials properly are given without hesitation. In contrast the methodical weighing of evidence regarding the issue of causation is for the purpose of characterizing biologic phenomena. Although legal and medical implications may be contained in such an analysis, its relevance to any particular clinical case is only retrospective. To judge responsibly the strength of a causative link, all available scientific evidence must be analyzed by established criteria. Such as analysis suggests that any connection between a delay in the treatment of bacterial meningitis and outcome depends on the presenting clinical pattern. If the presentation is that of a nonspecific illness with general symptoms, then a short delay of < 3 to 5 days does not appear to alter the risk of sequelae or death. In the case of fulminant meningitis a delay in initiating therapy seems unconnected to outcome. Finally for patients with a history of clinically overt meningitis, an inappropriate delay in commencing therapy incrementally increases the risk of permanent injury.

Temperature-dependent modulation of lipopolysaccharide-induced interleukin-1 beta and tumor necrosis factor alpha expression in cultured human astroglial cells by dexamethasone and indomethacin.

In bacterial meningitis, LPS induces production in cerebrospinal fluid of the cytokines IL-1 beta and tumor necrosis factor alpha (TNF alpha), which are the principle mediators of meningeal inflammation. IL-1 beta and TNF alpha induce fever, and elevated temperature may affect cytokine expression. Dexamethasone treatment improves outcome in bacterial meningitis possibly by inhibiting IL-1 beta and TNF alpha. In this report, the effects of elevated temperature and dexamethasone on LPS-stimulated IL-1 beta and TNF alpha mRNA gene expression and protein synthesis were studied in human astrocytoma cell lines and primary cultures of human fetal astrocytes. Cells cultured at 40 degrees C exhibited smaller peaks of IL-1 beta and TNF alpha transcription and protein synthesis compared with cells cultured at 37 degrees C. The addition of dexamethasone before, during, or after exposure of the cells to LPS resulted in temperature-dependent inhibition of IL-1 beta transcription and protein synthesis. The most extensive inhibition occurred in pretreated cells cultured at 37 degrees C. Cotreatment with LPS and dexamethasone also inhibited TNF alpha mRNA transcription at both temperatures. The effects of another antiinflammatory agent, indomethacin, on LPS induction of IL-1 beta and TNF alpha mRNA were temperature and cell line dependent. These findings provide a possible explanation for the efficacy of dexamethasone treatment of bacterial meningitis and support the proposal that fever may be beneficial to the host in this disease.