Neisseria meningitides

Categorization
Cell Wall: Gram Negative	Shape: Cocci, Diplococci
Metabolism: Obligate Aerobe

Culture and Detection

Culture: All Neisseria can be selectively grown on the Thayer-Martin chocolate agar selective media supplemented with the antibiotics Vancomycin, Colistin, and Amphotericin
Detection: Detection of intracellular gram negative diplococci
Biochemistry: G. meningitides is positive for Maltose fermentation which can distinguish it from G. gonorrhea

Virulence Factors

Capsule: Meningococcus possseses an antiphagocytic polysaccharide capsule. Multiple serotypes do exist; however, antibodies to the capsule are protective.
IgA Protease: Reduces mucosal immunity
Outermembrane Blebs: Meningococcus sheds blebs of its bacterial outer membrane (See: Bacterial Cell Wall) which contains the highly inflammatory lipopolysaccharide. It is thought that the rapid inflammatory response to Meningococcal infection may be due to systemic shedding of these outermembrane blebs.

Clinical Consequences

Meningococcus is part of the nasopharyngeal flora in a small fraction of the population and causes no symptoms. In some individuals, bacteria spread systemically and can cause the following complications.

Meningococcemia refers to a sepsis caused by meningococcus and is characterized by a unique purpuric and petechial skin rash along with high fevers.

When Meningococcemia becomes fulminant it is characterized by septic shock and DIC. Frequently there is acute hemorrhage into the adrenal cortex resulting in acute adrenocortical insufficiency.

Meningitis is the most common manifestation of pathological infection and often occurs in the absence of clinical meningococcemia.

Immunity and Incidence

Infections occur both sporadically and in epidemic waves. Epidemics occurs in those living in close quarters such as college dormitories or army barracks. Infants tend to be infected during the antibody window between 6mo - 2 yrs.

Vaccination

Treatment

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