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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 5)

(This chapter has 7 pages)

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Neisseria meningitidis

The bacterium Neisseria meningitidis, the meningococcus, is identical in its staining and morphological characteristics to Neisseria gonorrhoeae. However, at the ultrastructural level, N. meningitidis has a prominent antiphagocytic polysaccharide capsule. N. meningitidis strains are grouped on the basis of their capsular polysaccharides, into 12 serogroups, some of which are subdivided according to the presence of outer membrane protein and lipopolysaccharide antigens.

Neisseria meningitidis is usually cultivated in a peptone-blood base medium in a moist chamber containing 5-10% CO2. All media must be warmed to 37 degrees prior to inoculation as the organism is extremely susceptible to temperatures above or below 37 degrees. This trait is rather unique among bacteria. Also, the organism tends to undergo rapid autolysis after death, both in vitro and in vivo. This accounts for the dissemination of lipopolysaccharide (endotoxin) during septicemia and meningitis.

The organism tends to colonize the posterior nasopharynx of humans, and humans are the only known host. Individuals who are colonized are carriers of the pathogen who can transmit disease to nonimmune individuals. The bacterium also colonizes the posterior nasopharynx in the early stages of infection prior to invasion of the meninges. Most individuals in close contact with a case of meningococcal meningitis become carriers of the organism. This carrier rate can reach 20 percent of the contact group before the first case is recognized, and may reach as high as 80 percent at the height of an epidemic.

Structure and Classification

The only distinguishing structural feature between N. meningitidis and N. gonorrhoeae is the presence of a polysaccharide capsule in the former. The capsule is antiphagocytic and is an important virulence factor.

Meningococcal capsular polysaccharides provide the basis for grouping the organism. Twelve serogroups have been identified (A, B, C, H, I, K, L, X, Y, Z, 29E, and W135). The most important serogroups associated with disease in humans are A, B, C, Y, and W135. The chemical composition of these capsular polysaccharides is known. The prominent outer membrane proteins of N. meningitidis have been designated class 1 through class 5. The class 2 and 3 proteins function as porins and are analogous to gonococcal Por. The class 4 and 5 proteins are analogous to gonococcal Rmp and Opa, respectively. Serogroup B and C meningococci have been further subdivided on the basis of serotype determinants located on the class 2 and 3 proteins. A handful of serotypes are associated with most cases of meningococcal disease, whereas other serotypes within the same serogroup rarely cause disease. All known group A strains have the same protein serotype antigens in the outer membrane. Another serotyping system exists based on the antigenic diversity of meningococcal LOS.


The term meningitis refers to inflammation the meninges of the brain or spinaL cord. Meninges are any of the three membranes that envelope the brain and spinal cord. The disease meningitis is caused by a number of different bacteria and viruses. Bacterial causes include Haemophilus influenzae, Escherichia coli, Streptococcus pneumoniae,Streptococcus pyogenes, Staphylococcus aureus, and Neisseria meningitidis. Although a variety of cocci cause meningitis, the term meningococcus is reserved for the Gram-negative, bean-shaped diplococcus, Neisseria meningitidis. Like its relative N. gonorrhoeae, the organism tends to occur intracellularly in the cytoplasm of neutrophils which are attracted to the site of inflammation in the mininges, so this type of infection is called pyogenic (pus-forming).

Marchiafava and Celli were the first to report observing Gram-negative diplococci in cerebrospinal fluid of a fatal case of meningitis in 1884. In 1887, Weichselbaum isolated the bacterium from six cases of meningitis and established the isolates as a distinct species and proven to be the cause of meningitis.


Infection with N. meningitidis has two presentations, meningococcemia, characterized by skin lesions, and acute bacterial meningitis. The fulminant form of disease (with or without meningitis) is characterized by multisystem involvement and high mortality.

Infection is by aspiration of infective bacteria, which attach to epithelial cells of the nasopharyngeal and oropharyngeal mucosa, cross the mucosal barrier, and enter the bloodstream. If not clear whether blood-borne bacteria may enter the central nervous system and cause meningitis.

The mildest form of disease is a transient bacteremic illness characterized by a fever and malaise; symptoms resolve spontaneously in 1 to 2 days. The most serious form is the fulminant form of disease complicated by meningitis. The manifestations of meningococcal meningitis are similar to acute bacterial meningitis caused by other bacteria such as Streptococcus pneumoniae, Haemophilus influenzae, and E. coli. Chills, fever, malaise, and headache are the usual manifestations of infection.  Signs of meningeal inflammation are also present.

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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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