Neisseria meningitidis
From DrugPedia: A Wikipedia for Drug discovery
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==Surface Characteristics== | ==Surface Characteristics== | ||
Bacterial surface contains of a homopolymer of α(2-->8)-linked sialic acid residues | Bacterial surface contains of a homopolymer of α(2-->8)-linked sialic acid residues | ||
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==Transmission== | ==Transmission== | ||
Revision as of 11:38, 9 July 2010
Neisseria meningitidis
It is a heterotrophic gram-negative diplococcal bacterium best known for its role in meningitis and other forms of meningococcal disease such as meningococcemia. N. meningitidis is a major cause of morbidity and mortality during childhood in industrialized countries and is responsible for epidemics in Africa and in Asia.
| Kingdom | Bacteria |
|---|---|
| Phylum | Proteobacteria |
| Class | Beta Proteobacteria |
| Order | Neisseriales |
| Family | Neisseriaceae |
| Genus | Neisseria |
| Species | N. meningitidis |
| Binomial | Neisseria meningitidis |
Contents |
Surface Characteristics
Bacterial surface contains of a homopolymer of α(2-->8)-linked sialic acid residues
Transmission
Meningococcus is spread through the exchange of saliva and other respiratory secretions during activities like coughing, kissing, and chewing on toys. N. meningitidis exploits host cell signaling pathways to promote its uptake by host cells. N.meningitidis does not have a type III secretion system nor a type IV secretion system. The signaling leading to bacterial internalization is induced by the type IV pili, which are the main means of meningococcal adhesion onto host cells. The signaling induced following Type IV pilus-mediated adhesion is responsible for the formation of microvilli-like structures at the site of the bacterial-cell interaction. These microvilli trigger the internalization of the bacteria into host cells. A major consequence of these signaling events is a reorganization of the actin cytoskeleton, which leads to the formation of membrane protrusions, engulfing bacterial pathogens into intracellular vacuoles. Efficient internalization of N. meningitidis also requires the activation of an alternative signaling pathway coupled with the activation of the tyrosine kinase receptor ErbB2. Beside Type IV pili, other outer membrane proteins may be involved in other mechanism of bacteria internalization into cells.
Pathogenic Activity
Septicaemia caused by Neisseria meningitidis has received much less public attention than meningococcal meningitis even though septicaemia has been linked to infant deaths. Meningococcal septicaemia typically causes a purpuric rash that does not lose its color when pressed with a glass ("non-blanching") and does not cause the classical symptoms of meningitis. This means the condition may be ignored by those not aware of the significance of the rash. Septicaemia carries an approximate 50% mortality rate over a few hours from initial onset. Many health organizations advise anyone with a non-blanching rash to go to a hospital emergency room as soon as possible.[citation needed] Note that not all cases of a purpura-like rash are due to meningococcal septicaemia; however, other possible causes need prompt investigation as well (e.g. ITP a platelet disorder or Henoch-Schönlein purpura). Some other severe complications include Waterhouse-Friderichsen syndrome (a massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia), adrenal insufficiency, and disseminated intravascular coagulation
Virulence
Lipooligosaccharide (LOS) is a component of the outer membrane of N. meningitidis which acts as an endotoxin which is responsible for fever, septic shock, hemorrhage due to the destructions of red blood cells. Other virulence factors include a polysaccharide capsule which prevents host phagocytosis and aids in evasion of the host immune response; and fimbriae which mediate attachment of the bacterium to the epithelial cells of the nasopharynx.
