8/23/CNS Infections: Meningitis - Malhotra Flashcards
types of meningitis
- acute meningitis
- onset: hours-days
- duration: < 4wk
- bacterial (septic) vs. aseptic
- chronic meningitis
* greater than 4 weeks duration - recurrent meningitis
* multiple acrute episodes within sub-4wk period
acute meningitis
- infl fo meninges
- infection of subarachnoid space
- exudate over spinal cord and brain
- CSF with infl changes (pleocytosis)
ways that pathogens can enter cells
- paracellular passage
- transcellular transport (active or passive transcytosis)
- invasion within WBCs during diapedesis
etiology of acute bacterial meningitis
Streptococcus pneumoniae
- 25-35% penicillin resistant
- primary agent in adults, young children
Neisseria meningitidis
- most common in children/adolescents/young adults
Group B beta-hemolytic Streptococcus
- most common cause in neonates
Haemophilus influenzae type B (less common secondary to vaccine)
Gram-neg enterics
Listeria monocytogenes
Staphylococcus aureus
Bacillus anthracis
meningitis: epidemiology
seasonal
- S. pneumo - winter
- N. meningitidis - year round, winter/spring peak
age
- increased incidence rates of bacterial in kids, esp < 2yr
- 75% of cases in < 15yr
- median age: 42 yr
- higher incidence among AfAm
meningitis : predisposing factors
- altered immune status
- malnutrition, steroids, chemotherapy, malignancy, complement deficiency, HIV
- functional or congenital asplenia
- sickle cell disease
- chronic disease
- diabetes, alcoholism, HIV, liver disease
- bacteremia
- contiguous focus of infection
- sinus/middle ear inf
- head trauma
- csf leak
- neurosurgery/instrumentation
- household/daycare/military barracks/college dorms
meningitis: pathogenesis
most common : hematogenous spread
less common : direct spread or extension
- established neighboring infection
- postsurgical or cranial injury (skull fracture)
- secondary to congenital malformation
how do you get meningitis?
nasopharynx is portal of entry : mucosal epithelium provides local immunity but is also attachment site for bacteria
breach of host defenses
- N. meningitidis produce IgA protease and escape phagocytosis via capsular polysacch
- encapsulated organisms inhibit neutrophil phagocytosis and complement-mediated killing
from that point, organism replicates in subepithelial tissue → hematogenous spread to CNS
seeding of meninges by blood-borne organisms via choroid plexus → penetration of BBB → devpt of infl response
- brain edema and incr ICP
- brain ischemia
how does bacterial meningitis cause inflammatory response?
infection → production of cytokines (infl response mediators)
endothelial injury by cytokines and bacterial endotoxins → incr permeability of bbb
infl of meninges and brain → alteration of CSF dynamics
- brain edema
- incr ICP
- reduced cerebral blood flow
thrombosis and vasculitis of cerebral blood vessels
- brain ischemia and neuronal injury
types of brain edema
1. vasogenic edema
- disruption of bbb, leakage of cap vessels
2. cytotoxic edema
- incr ICF secondary to cell injury
3. interstitial edema
- purulent exudate in arachnoid space interferes with reabs of csf and obstructs flow
- movement of fluid from ventricular system to parenchyma
within vessels, within cells, within arachnoid space!
pathogenesis of meningitis
clinical characteristics of meningitis
bacterial meningitis
- life threatening emergency
- acute and fulminant presentation
- common findings: fever, neck stiffness, abnormal state of consciousness
other findings include:
- nausea/vomiting/anorexia, confusion/irritability, pain on neck flexion,
- Brudzinski (flex neck)
- Kernig (flex hip and knee)
- photophobia
- lethargy
clinical chars: bact meningitis
increased ICP
- infants : bulging fontanelle
- adults : worst headache of life
cerebral edema and ischemia, thromobsis of cerebral vessels, cortical necrosis
- coma, ataxia, seizures, focal neurological signs, cranial nerve palsies (deafness, ocular muscle weakness)
- papilledema is UNUSUAL early on (happens in hours/days, not immediately on pressure)
clinical characteristics
special features/clues
N. meningitidis?
- petechiae (1mm, non-blanching, red/flat skin lesions) and/or purpura
S. pneumoniae meningitis?
- resp infections (ear or sinus inf)
in neonates, might see following non-specific findings:
- poor feeding, incr sleeping, decr uring output, irritability, vomiting/diarrhea
lab diagnosis
CSF examination
- opening pressure
- appearance (check to see if clear/colorless)
- cell count (WBC, RBC)
- chemistries (glucose/protein)
- Gram staining, bacterial culture
bacterial meningitis : see lots of cells, low glu, high protein, high pressure, positive staining and culture
