CNS infections Flashcards
what are the 4 routes of entry of CNS infections
Haematogenous
Direct implantation - via instruments
Local extension - secondary to established infections
PNS into CNS - virus
signs and sx of meningitis
fever
headache
stiff neck
some disturbance of brain function
vomiting
light aversion
drowsy
joint pain
fitting
agents that cause meningitis
neisseria meningitidis
streptococcus pneumoniae
Haemophilus influenzae
TB
various viruses
cryptococcus neoformans
pathophysiology of meningitis
Neuro damage by:
- Direct bacterial toxicity - meningococcus in menignes -> infection
- Indirect inflammatory process and cytokine release and oedema
- Seizure, shock, and cerebral hypoperfusion
px of meningits
10% mortality
5% morbidity of survivors - neuro sequelae mainly sensineural deafness
signs and sx of encephalitis
disturbance of brain function
agents that cause encephalitis
rabies virus
arbovirus
trypanosoma species
prions
amoeba
signs and sx of myelities (affects spinal cord)
disturbance of nerve transmission
agent that causes myelitis
poliovirus
signs and sx of neurotoxin (affects CNS and PNS)
paralysis
rigid - tetanus
or flaccid - botulism
agents that cause neurotoxin
clostridium tetani
clostridium botulinum
what is meningitis
inflammatory process of
meninges and CSF
what is meningencephalitis
inflammation of meninges and
brain parenchyma
causes of acute meningitis in order of liklihood
Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae
Listeria monocytogenes - old, poor immune system
GBS - colonise vagina, can go through microabrasions in baby head -> meningitis
E coli - vaginas -> neonatal sepsis
summarise neisseria meningitides
Infectious cause of childhood death in all countries.
Transmission is person-to-person, from asymptomatic carriers.
non-blanching rash in 80%
stains - A B C Y W135 - vaccines for all
1/2 present just as meningits
1/2 have some degree of septicaemia
Pathogenic strains are found in only 1% of carriers.
Cause infections in less than 10 days.
how can we reduce N meningitidis transmission
stop travel and contact
why is it important to differentiate between meningitis and septicaemia
patients who present with shock are treated differently than patients who present primarily with increased intracranial pressure (ICP).
pathophysiology of septicaemia
capillary leak:
* albumin and other plasma proteins -> hypovolaemia
coagulopathy -> bleeding and thrombosis
* Endothelial injury results in platelet-release reactions
* The protein C pathway.
* Plasma anticoagulants.
* no LP - because will clot - important to look at bloods before LP!!
metabolic derangement - esp acidosis
myocardial failure - multiorgan failure
severe meningococcal disease and purpura fulminans
meningococcal septicaemia
Amputation or skin grafting due to digital or limb ischemia is required in 2-5% of survivors
features of chronic TB meningitis
indolent
Week long presentation
Not associated with rash
more common immunocomp
involves meninges and basal cisterns of brain and spinal cord
Can become TB abscess/granulomas or cerebritis in brain
epidemiology of aseptic meningitis
most common infection of CNS
mostly children less than 1yr
sx of aseptic meningitis
headache
stiff neck
photophobia
nonspecific rash