Bacterial meningitis in Africa

Abstract

Bacterial meningitis differs globally, and the incidence and case fatality rates vary by region, country, pathogen, and age group; being a life-threatening disease with a high case fatality rate and long-term complications in low-income countries. Africa has the most significant prevalence of bacterial meningitis illness, and the outbreaks typically vary with the season and the geographic location, with a high incidence in the meningitis belt of the sub-Saharan area from Senegal to Ethiopia. Streptococcus pneumoniae (pneumococcus) and Neisseria meningitidis (meningococcus) are the main etiological agents of bacterial meningitis in adults and children above the age of one. Streptococcus agalactiae (group B Streptococcus), Escherichia coli, and Staphylococcus aureus are neonatal meningitis's most common causal agents. Despite efforts to vaccinate against the most common causes of bacterial neuro-infections, bacterial meningitis remains a significant cause of mortality and morbidity in Africa, with children below 5 years bearing the heaviest disease burden. The factors attributed to this continued high disease burden include poor infrastructure, continued war, instability, and difficulty in diagnosis of bacterial neuro-infections leading to delay in treatment and hence high morbidity. Despite having the highest disease burden, there is a paucity of African data on bacterial meningitis. In this article, we discuss the common etiologies of bacterial neuroinfectious diseases, diagnosis and the interplay between microorganisms and the immune system, and the value of neuroimmune changes in diagnostics and therapeutics.

Keywords: Africa; bacterial; diagnosis; management; meningitis; pathophysiology.

Figure 1

Bacterial mechanisms cross the blood-brain barrier (BBB). S. pneumoniae (pneumococcus) uses the pilus-1 and PspC (CbpA) to bind to PECAM-1 and pIgR expressed on the plasma membrane of brain endothelial cells; The PAF receptor plays also a role in pneumococcal adhesion to the BBB endothelium, although whether bacteria directly to it is still unclear; The laminin receptor (LR) mediates the passage of pneumococci from the basement membrane of the BBB endothelium promoting bacterial translocation into the brain. E. coli crosses the BBB via transcellular traversal or paracellular traversal. E. coli also binds with CD48 on brain microvascular endothelial cells via a type 1 fimbrial adhesion (FimH), outer-membrane protein A (OmpA) via N-acetylglucosamine (GlcNAc) or glucose-regulated protein-96 (Gp96), and cytotoxic-necrotizing factor 1 (CNF1) via the laminin receptor (LR). L. monocytogenes disrupts the phagosome membrane, releasing the phospholipases phosphatidylinositol-specific phospholipase C (Pic)-A and PIcB, as well as the toxin listeriolysin O. Internalin (Inl)-A and Inl-B bind to endothelial cells' receptors for the globular head of the complement component C1q (gC1qR) or VE-cadherin to cross the BBB. Mycobacterium tuberculosis infects brain tissue free or inside of macrophage, trojan-horse mechanism. The second mechanism is an active process that depends on an intact ESX-1, also known as type VII secretion systems, that induces phagosomal rupture in host phagocytes during transcellular migration. N. meningitidis uses Type IV pili and Opa, Opc binding proteins to adhere onto the mucocutaneous cells and uses Factor H to inhibit the alternative, complementary pathway.