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Pathogen Page

Neisseria meningitidis

General Information
Vaccine Related Pathogen Genes
1. ExbB
2. GNA1030
3. GNA1162
4. GNA1220
5. GNA1870
6. GNA1946
7. GNA2001
8. GNA2091
9. GNA2132
10. GNA33
11. GNA992 (hsf)
12. gp120
13. lctP
14. lpdA
15. metH
16. NadA
17. NspA from N. meningitidis MC58
18. P1
19. rfaF
20. siaD
21. tbp2
22. tbpA
Vaccine Information
References

I. General Information

1. NCBI Taxonomy ID:

487

2. Disease:

Meningitis

3. Introduction

Neisseria meningitidis, also simply known as meningococcus, is a Gram-negative β-proteobacterium and member of the bacterial family Neisseriaceaeis. There are 13 serogroups based on different capsular polysaccharide structures. Among them, six serogroups (A, B, C, W-135, X, and Y) cause most life-threatening disease (Stephens et al., 2007).

4. Microbial Pathogenesis

Meningococcus is spread through the exchange of saliva and other respiratory secretions during activities like coughing, kissing, and chewing on toys. Those with impaired immunity may be easier to get meningococcus. Meningococcal virulence is related to both capsule expression, expression of other surface structures, and underlying genotype. N meningitidis pathogenesis is related to its ability to express and modify capsule with serogroups A, B, C, W-135, X, and Y. Capsules of N meningitidis facilitate transmission and colonisation, and protect the meningococcus from desiccation, phagocytic killing, opsonisation, and complement-mediated bactericidal killing. Outer membrane proteins (e.g., PorB, PorA , Opa and Opc) contribute to meningococcal virulence. Outer membrane porins are involved in host-cell interactions and as targets for bactericidal antibodies. Endotoxin, or lipo-oligosaccharide, a major component of the outer membrane, differs in structure from enteric endotoxins and is crucial in inflammatory signalling via Toll-like receptor 4 (TLR4) (Stephens et al., 2007).

5. Host Ranges and Animal Models

It only infects humans; there is no animal reservoir.

6. Host Protective Immunity

N. mengingitidis establishes systemic infections only in individuals who lack serum bacterial antibodies directed against the capsular or noncapsular (cell wall) antigens of the invading strain, or in patients deficient in the late-acting complement components. The presence of serum bactericidal IgG and IgM is probably the most important host factor in preventing invasive disease. The role of bactericidal antibodies in prevention of invasive disease explains why high attack rates are seen in infants from 6 to 9 months old, the time at which maternal antibodies are being lost. Individuals with complement deficiencies (C5, C6, C7, or C8) may develop meningococcemia despite protective antibody. This emphasizes the importance of the complement system in defense against meningococcal disease (Textbook of Bacteriology).

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