English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Before the introduction of antibiotic therapy, acute bacterial meningitis was invariably fatal. Even with the development of new and highly bactericidal antibiotics, the disease continues to carry a significant morbidity and mortality. Recent research suggests a key role for the inflammatory response in the pathogenesis of acute bacterial meningitis, implying that the addition of inflammation-modifying agents to the antibiotic treatment may help to achieve a significantly better outcome [1]. However, present results should be carefully evaluated before such a recommendation can be made. A correlation between the intensity of inflammation in the subarachnoid space and the outcome of acute bacterial meningitis was noted long ago [2]. The defence systems within the cerebrospinal fluid (CSF) are quite limited and the inflammatory response is largely recruited from the serum through disruption of the blood-brain barrier [3]. Cells within the central nervous system, including astrocytes, microglia, vascular endothelium, and macrophages, may also contribute to this response [4]. This cellular inflammatory response is not necessarily dependent on the presence of live bacteria in the subarachnoid space. Conversely, inflammation may increase following induction of massive bacterial lysis by a /S-lactam or other antibiotic, due to the release of Gram-positive cell wall constituents or Gram-negative endotoxin [5]. The major mediators of inflammation in the CSF are cytokines, whose production is induced by bacterial components. Tumour necrosis factor-a and interleukin-1 are particularly important, and interact to create synergistic and self-potentiating inflammatory cascades resulting in CSF pleocytosis and brain oedema [S, 6]. Elevated levels of these cytokines in plasma and CSF are correlated with seizures, severity of disease and even survival [7, 8].

Should We Add Corticosteroids to the Treatment of Acute Bacterial Meningitis?