What is the Group A Meningococcal?
The bacteria Neisseria meningitidis, more commonly known as meningococcus, is responsible for the invasive disease meningococcal meningitis. Group A Meningococcal is a subset of this causal agent. Although several variants or serogroups of the bacteria exist, Group A has historically posed the most serious public health concern, particularly in sub-Saharan Africa’s ‘meningitis belt'.
Medical literature about meningitis dates back as far as the 16th century, although the causal link to the Neisseria meningitidis bacteria was not made until much later. This breakthrough discovery was made by an Austrian bacteriologist named Anton Weichselbaum in 1982, who identified the meningococcus bacteria and classified it under Diplococcus intracellularis meningitidis.
Structurally, Neisseria meningitidis are Gram-negative oval-shaped diplococci (pairs of cocci). They have a cell wall made up of silicates and lipopolysaccharides that distinguishes them from most other bacteria. In particular, the Group A Meningococcal have a unique polysaccharide capsule that enables them to evade the immune system.
Symptoms of Group A Meningococcal
Group A Meningococcal leads to a range of severe symptoms including high fever, severe headache, neck stiffness, rash, and an altered mental state. In severe cases, it can lead to life-threatening sepsis and meningitis. If left untreated, the disease can be lethal within hours.
Proteins and Potential Antigens
The Group A Meningococcal contains several proteins. Some found in the outer membrane, like PorA, PorB, RmpM, Opa, Opc, FetA, NspA, and GNA2132, have potential to serve as antigens. These proteins can be recognized by the immune system and can elicit an immune response. The most common target for vaccine development has been the protein PorA.
Group A Meningococcal Antigen-related Signaling Pathways
The functional properties of these antigens are linked with many important signaling pathways. For instance, the PorB protein of Group A Meningococcal has been found to interact with TLR2 (Toll-like receptor 2), triggering a signaling cascade that includes the activation of the transcription factor NF-kB. This leads to the release of inflammatory cytokines, fostering an inflammatory response. However, certain proteins like Opc and PorB can also manipulate immune responses and cause immune evasion, contributing to the bacteria's virulence.
Another key signaling pathway is the complement system, which is part of the innate immune system. Meningococcal bacteria can evade this through their polysaccharide capsules, highlighting the complexity of the pathogen-host interaction.
