It is the causative organism of meningitis and meningococcemia.

Morphology

N. meningitidis are gram-negative, kidney bean-shaped, encapsulated diplococci that are typically seen intracellularly.

Classification:

Meningococci are serotyped into 13 groups based on their capsular polysaccharide.

Human pathology

N. meningitidis spreads through close contact, especially in settings such as military recruit camps and college dorms. Incidence is high in the “meningitis belt” of sub-Saharan Africa. The bacteria colonize the nasopharynx and can spread from there.

Meningitis classically presents with fever, headache, photophobia, and neck stiffness. Meningococcemia may manifest as a rapidly fatal endotoxic shock. The endotoxin is the same as that seen in gram-negative bacilli.

Antibodies to the capsular polysaccharide provide resistance to disease. People with terminal complement deficiency (C6 to C9) are prone to meningococcal infections. Survivors of invasive meningococcal disease may develop sequelae such as hearing loss and neuropsychological defects.

Waterhouse Friderichsen Syndrome: Severe meningococcal endotoxic shock with widespread purplish skin rashes, DIC, thrombocytopenia, and bilateral adrenal hemorrhages. It can cause death within a few hours of the first onset of symptoms.

Laboratory diagnosis of meningococcal infections

Gram stain and culture can be done on CSF and blood for diagnosis before starting antibiotics. Meningococci are identified by their characteristic morphology as gram-negative diplococci that are non-motile and oxidase-positive. They are difficult to culture on blood agar. They can be cultured on chocolate agar, which is made by heating blood to 80°C.

A rapid test on CSF to detect capsular polysaccharide antigen by latex agglutination is available. N. meningitidis DNA can also be detected by PCR.

Meningococci can be differentiated from gonococci by maltose fermentation: meningococci ferment maltose, while gonococci do not.