Pathogenic Neisseriae: Gonorrhea, Neonatal Ophthalmia and Meningococcal Meningitis (page 6)
(This chapter has 7 pages)
© Kenneth Todar, PhD
Clinical manifestations of N. meningitidis
The onset of meningococcal meningitis may be abrupt or insidious.
with meningococcal meningitis rarely display signs of meningeal
Irritability and refusal to take food are typical; vomiting occurs
in the disease and may lead to dehydration. Fever is typically absent
children younger than 2 months of age. Hypothermia is more common in
As the disease progresses, apnea, seizures, disturbances in motor tone,
and coma may develop.
In older children and adults, specific symptoms and signs are
present, with fever and altered mental status the most consistent
Headache is an early, prominent complaint and is usually very severe.
vomiting, and photophobia are also common symptoms.
Neurologic signs are common; approximately one-third of patients
convulsions or coma when first seen by a physician. Signs of meningeal
irritation such as spinal rigidity, hamstring spasms and exaggerated
Petechiae (minute hemorrhagic spots in the skin) or purpura
into the skin) occurs from the first to the third day of illness in 30
to 60% of patients with meningococcal disease, with or without
The lesions may be more prominent in areas of the skin subjected to
such as the axillary folds, the belt line, or the back.
Fulminant meningococcemia occurs in 5 to 15% of patients with
disease and has a high mortality rate. It begins abruptly with sudden
fever, chills, myalgias, weakness, nausea, vomiting, and headache.
restlessness, and delirium occur within the next few hours. Widespread
purpuric and ecchymotic skin lesions appear suddenly. Typically, no
of meningitis are present. Pulmonary insufficiency develops within a
hours, and many patients die within 24 hours of being hospitalized
appropriate antibiotic therapy and intensive care.
Figure 4. The characteristic
skin rash (purpura) of meningococcal septicemia, caused by Neisseria
For a time, the virulence of Neisseria meningitidis was
to the production of an "exotoxin" that could be recovered from culture
filtrates of the organism. But when studies revealed that antitoxin
equally well with washed cells as culture filtrate, it was realized
the bacteria underwent autolysis during growth and released parts of
cell walls in a soluble form. Hence, the major toxin of N.
is its lipooligosaccharide,LOS, and its mechanism is endotoxic.
The other important determinant of virulence of N. meningitidis
is its antiphagocytic polysaccharide capsule.
The human nasopharynx is the only known reservoir of N.
Meningococci are spread via respiratory droplets, and transmission
aspiration of infective particles. Meningococci attach to the
columnar epithelial cells of the nasopharynx. Attachment is mediated by
and possibly by other outer membrane components. Invasion of the
cells occurs by a mechanism similar to that observed with gonococci.
involved after bloodstream invasion are unclear and how the
enters the central nervous system is not known.
Purified meningococcal LOS is highly toxic and is as lethal for mice
as the LOS from E. coli or Salmonella typhimurium;
meningococcal LOS is 5 to 10 times more effective than enteric LPS in
a dermal Shwartzman phenomenon (a characteristic type of inflammatory
in rabbits. Meningococcal LOS has been shown to suppress leukotriene B4
synthesis in human polymorphonuclear leukocytes. The loss of
B4 deprives the leukocytes of a strong chemokinetic and chemotactic