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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 3)

(This chapter has 7 pages)

© Kenneth Todar, PhD

Virulence Factors

Like the other pyogenic bacteria, Neisseria gonorrhoeae has a wide range of virulence determinants, although it does not produce any exotoxins. The first stages of infection, involving adherence and invasion, are mediated by surface components of the gonococci. The bacterium first attaches to epithelial cells by means of its fimbriae, specifically N-methylphenylalanine (Type 4) pili, the main subunit of which is PilE. After initial attachment, the bacteria enter a second stage of binding mediated by the outer membrane protein P.II (also known as Opa) which is needed for tight binding and invasion of epithelial cells. Also, P.II from one bacterium will bind to LOS of an adjacent bacterium, which allows for the construction of a microcolony which may be functionally analogous to a biofilm. However, the invasion of a cell involves a single bacterium, not whole microcolonies. Neisseria gonorrhoeae also produces an IgA1 protease that probably play a role in the colonization stage.

The outer membrane porin of N. gonorrhoeae P.I (also known as Por) is equivalent to the ompC and ompF porins of E. coli that are involved in the passage of solutes through the outer membrane. However, P.I apparently has a role in virulence that allows the gonococci to survive inside of phagocytes. Purified P.I has been shown to inhibit the ability of phagocytes to kill ingested bacteria.

The lipooligosaccharide (LOS) of the outer membrane is thought to be responsible for most of the symptoms of gonorrhea. Gonococcal LOS triggers an intense inflammatory response. Subsequent activation of complement, attraction and feeding by phagocytes, and the lysis of the phagocytes themselves, contributes to the purulent discharge. The local production of TNF, elicited by LOS, is thought to be the main cause of damage to the fallopian tubes. In addition, in strains that cause systemic infection, LOS binds sialic acid from the serum forming a microcapsule of sialylated LOS, which allows the gonococci to resist the host immune response and serum bactericidal reaction.

Nonsialyated LOS and P.I (Por) on the bacterial surface are known to be effective targets for bactericidal antibodies. However, if antibodies produced against P.III (also known as Rmp) react with their antigenic site on the gonococcal surface, the effect is to block bactericidal antibodies against LOS and P.I and to protect the bacterium from complement-mediated lysis.

Finally, Neisseria gonorrhoeae has a well-developed iron acquisition system that permits it to obtain iron from its host during growth that is necessary to support bacterial invasion. Under low-iron conditions the bacterium expresses two transferrin receptors (Tbp1 and Tbp2) and one lactoferrin receptor (Lbp) in its outer membrane, which are able to directly extract iron from transferrin and lactoferrin, respectively. The proteins can also extract iron from heme and hemoglobin.

Table 1. Surface components of N. gonorrhoeae that may play a role in virulence
Designation Location Contribution
PilE major fimbrial protein initial binding to epithelial cells
P.II (Opa) outer membrane protein contributes to invasion
P.I (Por) outer membrane porin may prevent phagolysosome formation in neutrophils and/or reduce oxidative burst
LOS outer membrane lipooligosaccharide  elicits inflammatory response, triggers release of TNF
P.III (Rmp) outer membrane protein elicits formation of ineffective antibodies that block that block bactercidal antibodies against P.I and LOS
Tbp1 and Tbp2 outer membrane receptors for transferrin iron acquisition for growth
Lbp outer membrane receptor for lactoferrin iron acquisition for growth

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Kenneth Todar has taught microbiology to undergraduate students at The University of Texas, University of Alaska and University of Wisconsin since 1969.

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