Neisseria meningitides
Meningitis
Human source either a carrier or the one with active disease (Nasopharynx)
Morphology
Gram negative diplococci with flattened sides "kidney bean shaped", polysaccharide capsule present, not readily seen, but serves as the basis for serotyping.
Endotoxic lipopolysaccharide complexed with protein in outer membrane
Capsules and pili
Cultural characteristics
Fastidious species require enriched media (chocolate agar)
Meningococcus grows as a transparent, non-pigmented, non-hemolytic colony under conditions of moisture and 5-10% C02. Mediums include blood agar, trypticase soy agar, supplemented chocolate agar, and Mueller Hinton agar.
Growth enhanced in CO2
Oxidase positive
Structural characteristics
Antigenic structure
Polysaccharide capsule
9 serogroups. A,B,C,Y,W-135 most important
immunogenic except Group B
Outer membrane proteins
Lipopolysaccaharide
Sporadic cases or local outbreaks in young adults
Access to humansNasopharynx (of a carrier or the one with disease) is a common source
Respiratory droplets requiring close contact and susceptibility (lack of antibody).
The majority of persons exposed do not contract the disease, likely due to the limited time exposure. The virulence of the strain, host defense and their interactions determine whether the disease is going to follow.
Attachment (respiratory colonization)
pilus mediated attachment- microvilli of nonciliated nasopharyngeal cells
Transverse cell in vesicle to submucosa
Damage ciliated cells
Blood stream survival enhanced by antiphagocytic polysaccharide capsule
Meningeal seeding follows bacteremia.
Bacterial cell wall components initiate a cascade of complement and cytokine mediated events.
CNS inflammation generated by cell wall peptidoglycan
LPS, other bacterial products and its mediated by IL-1 and TNF (host response)
Once in CSF, the paucity of antibodies, complement components, and white blood cells allow the bacterial infection to flourish.
Endotoxin mediated activation of complement leading to shock and hemorrhage
Human defencesPolysaccharide capsule resists neutrophil phagocytosis as well as complement mediated bactericidal activity.
Clinical pictureUntreated the patient will die either from systemic complications or from diffuse CNS ischemic injury.
Meningitis:
This invasion of meninges by this organism results in
Exudates extends throughout the CSF, particularly to basal cisterns
Damaging cranial nerves
Obliterating CSF pathways (obstructive hydrocephalus)
Impair cerebral blood flow: Change of mental status and decreasing alertness.
Intracranial pressure increases
Brain edema progresses
Endotoxin mediated events:
Fulminant meningococcal disease, manifested by endotoxin from the N. meningitides cell wall.
DIC (disseminated intravascular coagulation)
Shock
Bilateral hemorrhagic destruction of the adrenal glands (Waterhouse-Friderichsen syndrome) may occur.
This patient was started on intravenous penicillin, but over the next six hours he developed large purpuric skin lesions, refractory hypotension and died. He died of Waterhouse-Friderichsen syndrome
Symptoms from N. meningitis
Physical findings of N. meningitis
Meningeal irritation
Papiledema: Raised intracranial tension
Isolated cranial nerve abnormalities
Arthritis
Petechiae and cutaneous hemorrhage
Endotoxic shock
Altered mental status
DiagnosisSpinal tap: CSF
CBC with differential
Blood culture
Therapeutic strategy