Meningococcal which is categorized into 13 serogroups: A, B,

Meningococcal disease is an infection caused by a type of encapsulated gram negative bacteria called Neisseria meningitidis. It is commonly known as an aerobic meningococcus which is categorized into 13 serogroups: A, B, C, D, 29E, H, I, K, L, W-135, X, Y, and Z ( Rouphael and Stephans 2015). The serogroups prevalence is different based on geographic region, but in UK only five are commonly associated with disease: A, B, C, Y, and W-135, they causing more than 90% of the invasive disease across the world.

 

Figure 1. shows the Africa’s meningitis belt where many meningococcal disease occurs.

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Meningococcal disease will normally cause two serious illnesses : meningitis which is the inflammation of the protective layers that surround the brain and spinal cord and septicaemia which is blood poisoning, these can occur on their own or more commonly they can happen together (MacNeil and Meyer 2017). The disease is very contagious and can spread through droplets of respiratory or close contact such as kissing an infected person, smoking, sneezing, sharing eating utensils, toothbrush or cigarette or living in close quarters with an infected person (Mayo Clinic 2017; WHO 2015). This disease can affect all age groups, but the most cases are seen in infants under age of one year old and second peak occurs at adolescents or young adults.

 

N. meningitides will usually begin with host acquisition by nasopharyngeal colonization followed by systemic invasion and development of a high-grade bacteremia. MenC and Hib posses surface characteristics such as fimbriae or pili that will help enhance mucosal colonization by mediate adhesion of bacteria to nasopharyngeal epithelial cells of the host. They are transported within a phagocytic vacuole across the non-ciliated nasopharyngeal columnar epithelia cells. Natural antibodies such as IgA, found mainly in mucosal secretions, is stimulated by the colonization of bacteria , this may inhibit the adherence of microorganisms to mucosal surfaces. The presence of high concentrations of circulating IgA antibodies to N. meningitidis may paradoxically permit the development or worsen the progression of invasive disease by preferentially binding to the organism, thereby blocking the beneficial effects of IgG and IgM antibodies (Tunkel and Scheld 1993). MenC and Hib produce immunoglobulin A subclass 1 (IgAl) proteases that cleave IgA in the hinge region of IgA1, these enzymes may have a pathogenic role by promoting attachment of bacterial strains to mucosal surfaces through local destruction of IgA. Once the bacteria pass the mucosal barrier, bacteria can now access to the bloodstream and the bacteria have to overcome host defence mechanisms to survive and invade the central nervous system (CNS). Bacterial capsule is the most important virulence factor, the capsule can effectively inhibit neutrophil phagocytosis and resist the complement-mediated bactericidal activity, this may enhance bloodstream survival of the bacteria and aid intravascular replication. The bacteria travel to the subarachnoid space in CNS through the bloodstream and release virulence factors and stimulate the formation of inflammatory cytokines within the cerebrospinal fluid (CSF), increased permeability of blood-brain barrier will occur at the level of the choroid plexus epithelium, the cerebral microvascular endothelium, or both. This allow protein, leukocyte and neutrophils to penetrate the arachnoid membrane and move into subarachnoid space. As a result, brain inflammation and intracranial pressure will raise which then causes nerve damage (Agamanolis 2016).

 

Characteristics to differentiate cerebral capillaries from other capillaries in the body?

(i)             adjacent endothelial cells mix together by a tight junctions that prevent intercellular transport

(ii)           rare or absent pinocytotic vesicles

(iii)          abundant mitochondria.

 

The increased BBB permeability that occurs during bacterial meningitis at the level of the cerebral capillary endothelial cell may result from separation of intercellular tight junctions, from increased pinocytosis, from both alterations.

 

For the cases of septicaemia, meningococci release endotoxin to the bloodstream. The endotoxin is then bound to a circulating plasma protein called endotoxin binding protein. The interaction between them change the conformation of endotoxin to increase binding and activation of macrophages and other inflammatory cells. A soluble form of CD14 acts as the receptor for endotoxin on endothelial surfaces. Endotoxin will bind and triggers an inflammatory process. Macrophages undergo activation to produce a range of cytokines, including tumour necrosis factor ? (TNF?) and interleukin 1? (IL-1?), this may lead to septic shock. Increased production of interferon ? by T cells and natural killer occurs, and the interferon ? in turn increase release of TNF by the macrophage. A number of studies have documented high levels of cytokines including TNF?, IL-1?, IL-6, IL-8, GM-CSF, IL-10, and interferon ? in meningococcal sepsis. Neutrophils appear to be activated both through the effects of endotoxin and through complement mediated stimuli. Neutrophils undergo a respiratory burst with the production of reactive oxygen species, as well as undergoing degranulation and the release of a range of inflammatory proteins, proteases, and other enzymes, which can degrade tissues. Binding of neutrophils to the endothelial lining in sepsis enable proteolytic enzymes to be released, which damage the endothelial surface especially the vascular endothelium surface. They lost their function when entry of meningococci into bloodstream. The complex physiology of meningococcal sepsis is largely explained by four basic processes affecting the microvasculature:

1.     Increased vascular permeability

2.     Pathological vasoconstriction and vasodilatation

3.     Loss of thromboresistance and intravascular coagulation

4.     Profound myocardial dysfunction.