It is the causative organism of meningitis and meningococcemia.
Morphology
N.meningitidis are gram negative, kidney bean shaped , encapsulated diplococci typically seen intracellularly.
Classification:
Meningococci are serotyped into 13 groups based on their capsular polysaccharide.
Human Pathology
N.meningitidis is spread by close contact, especially in military recruits, college dorms etc. Incidence is high in the “meningitis belt” of sub- Saharan Africa. The bacteria colonize the nasopharynx and spread from there.
Meningitis presents classically as 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 getting 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 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 morphological features being gram negative diplococci which are non motile and oxidase positive. They are difficult to culture on blood agar. They can be cultured on chocolate agar which is made of blood heated to 80 degree C.
A rapid test on CSF to detect capsular polysaccharide antigen by latex agglutination test is available. N.meningitidis DNA can also be detected by PCR.
Meningococci can be differentiated from gonococci by maltose fermentation as meningococci ferment maltose while gonococci do not.
