Pathogenic Neisseriae: Gonorrhea, Neonatal Ophthalmia and Meningococcal Meningitis (page 5)
(This chapter has 7 pages)
© Kenneth Todar, PhD
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.
Meningitis
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.
Pathogenesis
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.
