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?
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What is encephalitis? Its signs and symptoms? Its causative agents?
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What is myelitis? Its signs and symptoms? Its causative agents?
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What does neurotoxin infection affect? Its signs and symptoms? Its causative agents?
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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:
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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)
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