MICRO: CNS infections and meningitis Flashcards
What are the 4 routes of pathogen entry into the CNS? What is the most common route of entry?
Routes of Pathogen Entry into the CNS – 4 routes of entry…
- Haematogenous (e.g. pneumococcus, meningococcus carriage may penetrate and seed) - MOST COMMON
- Direct implantation (e.g. trauma)
- Local extension (e.g. from the ear like swimmer’s ear)
- PNS into CNS (e.g. rabies after bite)
What is meningtitis? Its signs and symptoms? Its causative agents?
What is encephalitis? Its signs and symptoms? Its causative agents?
What is myelitis? Its signs and symptoms? Its causative agents?
What does neurotoxin infection affect? Its signs and symptoms? Its causative agents?
What is meningoencephalitis?
inflammation of the meninges and brain parenchyma
What is neurological damage caused by in meningitis? How common is it?
Neurological damage = 10% mortality, 5% neurological sequelae; sensorineural deafness)
Caused by:
- Direct bacterial toxicity
- Indirect inflammatory process and cytokine release and oedema (n.b. tight space, oedema = bad)
- Shock, seizures and cerebral hypoperfusion
How can you classify CNS infections?
- Classification:
- Acute (hours to days) - usually bacterial meningitis
- Chronic (days to weeks) - usually TB
- Aseptic (caused by viruses so there is no pus) - usually viral
In which group would you classify meningococcal meningitis?
Acute
What are the main 3 causes of acute meningitis?
- Neisseria meningitidis
- Streptococcus penumoniae
- Haemophilus influenzae
Also:
- Listeria
- GBS
- E.coli
Other causes below:
What are the other causes of meningitis in specific populations?
- Listeria monocytogenes - key cause of meningoencephalitis, old, pregnant,
- Group B Streptococcus - common in females, 1/3 of European women, can cause neonatal meningitis after birth
- Escherichia coli - biphasic in old people and neonates
What are the rash presentations in N. meningitidis?
- Non-blanching rash (80% of children)
- Maculopapular rash (13% of children)
- No rash (7% of children)
What are the other phenotypes of N. meninitidis? Why is it important to distinguish?
- 50% have meningitis,
- 7-10% have septicaemia,
- 40% have meningitis AND septicaemia
- Important to distinguish as treatment for shock and raised ICP is different *
What four processes govern the clinical presentation of septicaemia?
- Capillary Leak – albumin and other plasma proteins leads to hypovolaemia
- Coagulopathy – leads to bleeding and thrombosis (endothelial injury results in platelet release reactions, the protein C pathway and plasma anticoagulants are affected)
- Metabolic Derangement – particularly acidosis
- Myocardial failure – and multi-organ failure
How many serotypes of N meningitidis? How is it acquired?
- ≥12 serotypes (90% = A, B, C); A, B, C, W and Y are vaccinated against
- Transmitted from person-to-person, from asymptomatic carriers
- Pathogenic strains are only found in about 1% of carriers
Give an examples of chronic meningitis.
Tuberculous chornic meningitis
What are the complications of tuberculous chronic meningitis?
- Tuberculous granulomas
- Tuberculous abscesses (i.e. enhancing thick-walled abscesses) in the brain
- Cerebritis
Below: normal brain vs TB brain vs tuberculoma (leading to death)