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Teixeira et al. (2019), state that when the pathogen enters the bloodstream, it crosses the blood-brain barrier, causing inflammation which leads to increased intracranial pressure, impairing CSF circulation and dysfunction of neurons. The vascular system becomes permeable, which leads to ischemia, edema and the release of pro-inflammatory cytokines that exacerbate the condition. Seizures occur due to these neurological changes.
The bacteria in the CSF trigger an inflammatory response, at the cellular level, inducing an innate immune response. This results in microglial activation and, the release of pro-inflammatory cytokines (such as IL-1, and TNF-alpha). This increases the permeability of the blood-brain barrier, because of swelling of the brain tissue, and recruitment of the immune cells or white blood cells (neutrophils) (Zimmermann & Curtis, 2021). All these changes cause fever, headaches, altered consciousness, vomiting, edema, ischemia, and neuronal injury. Other clinical signs such as photophobia and irritability also prevail and all can contribute to seizure or neurological damage, and may lead to comma (Yekani & Memar, 2023) as observed in Jones's case.
Jones’s symptoms and clinical findings have suggested the possibility of Acute Bacterial Meningitis. Griffiths et al. (2020), the increased risk of ABM due to age, unvaccinated status and history of respiratory issues contributes to the possibility.
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