Conclusion

Many aspects of the pathophysiology of bacterial meningitis have been clarified in recent years. It has become clear that neuronal damage is not caused by the initial bacterial infection but results from host reactions to the invading pathogen. Nevertheless, important issues still need to be addressed and await further exploration to approach pharmacological options that supplement antibiotic treatment.

Apart from ameliorations of therapeutic measures, broadening the focus on other blood-CNS barrier interfaces could offer new insights in pathophysiological events. In times where antibiotic resistance of microbial pathogens increases and new modalities in treating meningitis patients such as the application of dexamethasone drastically influence the plethora of cellular and molecular events, penetration of the blood-CNS barriers with suitable drugs might gain more attention.

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