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Tag words: Neisseria, gonococcus, meningococcus, meningococcal meningitis, gonorrhea, nonatal ophthalmia, urethritis

Neisseria gonorrhoeae

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Beta Proteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus: Neisseria
Species: N. gonohorrhoeae




Neisseria meningitidis

Kingdom: Bacteria
Phylum: Proteobacteria
Class: Beta Proteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus: Neisseria
Species: N. meningitidis


Common References: Neisseria, Neisseria meningitidis, Neisseria gonorrhoeae, N gonorrhoeae, N meningitidis, diplococcus, gonococcus, meningococcus, meningococcal meningitis, meningococcemia, meningitis, gonorrhea, nonatal ophthalmia, urethritis








Kenneth Todar currently teaches Microbiology 100 at the University of Wisconsin-Madison.  His main teaching interest include general microbiology, bacterial diversity, microbial ecology and pathogenic bacteriology.

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Pathogenic Neisseriae: Gonorrhea, Neonatal Ophthalmia and Meningococcal Meningitis (page 7)

(This chapter has 7 pages)

© Kenneth Todar, PhD

Host Defenses

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 integrity of the pharyngeal and respiratory epithelium appears to be important in protection from invasive disease. Chronic irritation of the mucosa due to dust or low humidity, or damage to the mucosa resulting from a concurrent  upper respiratory infection, may be predisposing factors for invasive disease.

The presence of serum bactericidal IgG and IgM is probably the most important host factor in preventing invasive disease. These antibodies are directed against both capsular and noncapsular surface antigens. The antibodies are produced in response to colonization with carrier strains of N. meningitidis, as well as N. lactamica, and other nonpathogenic Neisseria species that are normal inhabitants of the upper respiratory tract. Protective antibodies are also stimulated by cross-reacting antigens on other bacterial species such as Escherichia coli. 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.

Epidemiology

The meningococcus usually inhabits the human nasopharynx without causing detectable disease. This carrier state may last for a few days to months and is important because it not only provides a reservoir for meningococcal infection but also stimulates host immunity. Between 5 and 30% of normal individuals are carriers at any given time, yet few develop meningococcal disease. Carriage rates are highest in older children and young adults. Attack rates highest in infants 3 months to 1 year old. Meningococcal meningitis occurs both sporadically (mainly groups B and C meningococci) and in epidemics (mainly group A meningococci), with the highest incidence during late winter and early spring. Whenever group A strains become prevalent in the population, the incidence of meningitis increases markedly.

Treatment

Penicillin is the drug of choice to treat meningococcemia and meningococcal meningitis. Although penicillin does not penetrate the normal blood-brain barrier, it readily penetrates the blood-brain barrier when the meninges are acutely inflamed. Either chloramphenicol or a third-generation cephalosporin such as cefotaxime or ceftriaxone is used in persons allergic to penicillins.

Meningococcal disease is contracted through association with infected individuals, as evidenced by the 500- to 800-fold greater attack rate among household contacts than among the general population. Because such household members are at high risk, they require chemoprophylaxis. Sulfonamides were the chemoprophylactic agent of choice until the emergence of sulfonamide-resistant meningococci. At present, approximately 25 percent of clinical isolates of N. meningitidis in the United States are resistant to sulfonamides; nowadays, rifampin is the chemoprophylactic agent of choice.

Control

Groups A, C, AC, and ACYW135 capsular polysaccharide vaccines are available. However, the polysaccharide vaccines are ineffective in young children (in children under 1 year old, antibody levels decline rapidly after immunization) and the duration of protection is limited in children vaccinated at 1 to 4 years of age.  Routine vaccination is not currently recommended because the risk of infection is low. The group B capsular polysaccharide is a homopolymer of sialic acid and is not immunogenic in humans. A group B meningococcal vaccine consisting of outer membrane protein antigens has recently been developed, but is not licensed in the United States.

Tailpiece

Search for a universal vaccine for meningococcal meningitis

There is an obvious need for a universal vaccine for meningococcal meningitis,  but the development of an effective vaccine against all forms of N. meningitidis has been hampered by the high degree of variation in the proteins on the surface of the bacterium which leads to the occurrence of many different antigenic types.

More than 10% of the population may be carrying the bacterium at any one time on the mucosal surfaces of the nose and throat. The majority of these carriers will not have any symptoms of the disease, but this continual exposure to the immune system puts pressure on the bacterium to mutate its surface components in order to survive. Thus, natural selection is the driving force for the emergence of new antigenic variants.

Among the class 2 and 3 outer membrane proteins of N. meningitidis, Por A has been considered a primary target for a vaccine-induced antibody.  PorA is a major component of the outer membrane of N. meningitidis, and anti-PorA antibodies are thought to be a critical component in immunity. Interactions between antibodies and  PorA have been studied. Different strains of the bacterium have different PorA amino acid sequences within the region of the protein that specifically binds to antibody molecules. PorA  has several large amino acid "loop" regions that protrude from the surface, and it is these loops that are targets for antibody binding.

In the laboratory, the antigen-binding fragment (Fab) of anti-PorA antibodies can be crystallized and reacted with the antigenic loop regions of PorA  in order to determine the specificity of binding between antigen and antibody. Slight changes in PorA amino acid sequence have been shown to cause loss in the ability to bind to antibody molecules.  In nature, the bacterium mutates to insert new amino acid residues into the tip of the loop, which alters or eliminates many of the interactions with  antibody and allows the bacterium to bypass previous immune responses.


Figure 5. Image of the antibody (Fab) molecular surface, with the PorA antigen superimposed. The dark colored groove on the surface of the antibody matches precisely the shape of the PorA antigen; hence any changes in the sequence of PorA in this region can disrupt antibody binding. Jeremy Derrick, UMIST. SRS Annual Report.

Hence, by introducing changes into portions of the PorA protein that are exposed at the surface, the bacterium can evade the attention of the immune system. These alterations are apparently introduced without compromising the biological function of PorA, as a pore-forming protein. Designing vaccines that are able to take into account these changes is a huge challenge, but as more information of this type becomes known, it leads to a more rational approach to design of a universal vaccine for meningococcal meningitis.




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