CNS infections Flashcards

1
Q

What is encephalitis?

A

Inflammation of the brain

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2
Q

If a patient presents with odd behaviour, decreased consciousness, focal neurology or seizure preceded by an infectious prodrome, what should you suspect?

A

Encephalitis.

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3
Q

What is usually the cause of encephalitis?

A

Viral infection

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4
Q

What viral infections can cause encephalitis?

A
HSV 1&2
Arboviruses
CMV
EBZ
VZV
Measles, mumps, rabies, west nile virus, tick-borne encephalitis
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5
Q

What are some non-viral causes of encephalitis?

A
Any bacterial meningitis
TB
Malaria
Listeria
Lyme disease
Legionella
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6
Q

Signs and symptoms of encephalitis?

A
Preceding flu-like illness
Bizarre behaviour
Confusion
Reduced GCS
Fever
Headache
Focal neurological signs
Seizures
History of travel or animal bite
Meningism is usually absent.
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7
Q

What things can we do to diagnose encephalitis?

A

Contrast enhanced CT scan done before LP
Lumbar puncture - moderately increased CSF protein and lymphocytes and low glucose
EEG showing diffuse abnormalities can help confirm diagnosis

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8
Q

How do we manage encephalitis?

A

Aciclovir for HSV and ZVZ within 30m of patient arriving for 14 days
Ganciclovir for CMV
Repeat LP to ensure successful treatment
Phenytoin for seizures if needed

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9
Q

What is the mortality of untreated viral encephalitis?

A

70%

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10
Q

What are the signs of a cerebral abscess?

A
Seizures
Fever
Localised signs or symptoms of raised ICP
Coma
Signs of sepsis elsewhere
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11
Q

Investigations for cerebral abscess?

A

CT/MRI

Increased WCC, increased ESR

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12
Q

What is meningitis?

A

Inflammation of the meninges (lining of brain and spinal cord)

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13
Q

What is meningococcal septicaemia?

A

Refers to the meningococcus bacterial infection in the bloodstream. It is the cause of the classic ‘non-blanching rash’

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14
Q

Infective and non-infective causes of meningitis?

A

Infective

  • Bacterial
  • Viral
  • Fungal
  • Parasitic

Non-infective

  • Paraneoplastic
  • Drug side effects
  • Autoimmune (SLE/vasculitis)
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15
Q

What are the 3 ways infection can enter the meninges?

A
  1. Direct contiguous spread - nasal carriage, otitis media, sinusitis
  2. Neurosurgical complications - post op or infected shunts, trauma
  3. Via blood stream - bacteraemic (most common)
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16
Q

Describe the pathophysiology of infective meningitis

A
  • Brain is normally protected by the BBB and prevents immune system from attacking brain tissue
  • In meningitis when pathogens have found their way into the brain, they can multiply and are evaded from the immune system
  • Blood vessels become leaky allowing, WBCs and cytokines to enter the meninges and accounts for the changes we see in the CSF (increased WCC etc)
  • Depending on the severity, infection might remain confined to the subarachnoid space but in severe forms, the brain parenchyma can become infected and cause permanent damage without treatment
17
Q

Clinical presentation of meningitis?

A

Classic

  • Fever
  • Headache
  • Neck stiffness

Others

  • nausea and vomiting
  • photophobia
  • irritability
  • confusion, sleepiness, coma in severe infection
18
Q

Treatment of meningitis at first presentation?

A
  • Bacterial meningitis is a medical emergency
  • 5% mortality when treated & 20% permanent effects
  • IM benzylpenicillin immediately and admit to hospital
19
Q

Management of meningitis at hospital?

A
  1. Assess GCS
  2. Blood cultures
  3. Broad spectrum IV antibiotics - ceftriaxone or cefotaxime
    • Special considerations - penicillin allergy, immunocompromised (listeria meningitis so add amoxicillin) and recent travel (penicillin resistance, add vancomycin)
  4. Steroids - dexamethasone to reduce morbidity, tissue inflammation and neuronal damage
  5. Lumbar puncture - definitive diagnosis for meningitis
    • Inserted in L3-L4 intervertebral space
    • CSF sent to microbiology to assess cell count
    • biochemistry to check glucose and protein concentration
    • microbiology for gram stain and culture
    • viral PCR
    • No absolute contraindication but some relative:
      • abnormal clotting, anticoagulation treatment, petechial rash, raised intracranial pressure
20
Q

When would we consider doing a CT head before a LP in meningitis?

A

Exclude a mass lesion or increased ICP as these can lead to brain herniation when removing CSF:

  • Aged >60
  • Immunocompromised state
  • History of CNS disease, previous stroke.
  • Seizures <1 week of presentation
  • GCS <14
  • Focal neurological signs
  • Papilloedema
  • Atypical history
21
Q

What type of bacteria is Neisseria meningitidis?

What percentage of adult and teenage populations are carriers?

A

Gram neg cocci

  • 5-11% adult carriers
  • 25% teenage carriers
22
Q

Describe how the infective organisms for meningitis differ depending on age (neonate, children, adult, elderly)

A

Neonate: listeria, group B strep, e coli

Children: N meningitidis, strep pneumoniae, Haemophilus influenzae type b

Adults: N meningitidis, strep pneumoniae

Elderly: N meningitidis, strep pneumoniae, Listeria

23
Q

How to tell the difference between viral and bacterial depending on analysis of CSF (appearance of CSF, microscopy, protein, glucose)

A

Appearance, microscopy, staining, protein, glucose of CSF bacterial

  • cloudy
  • polymorphs (neutrophils) on microscopy
  • staining: organisms can be seen on gram film
  • protein: high
  • glucose: low

Appearance, microscopy, staining, protein, glucose of CSF viral

  • Clear
  • lymphocytes on microscopy
  • no organisms seen on staining
  • protein high
  • glucose normal

Appearance, microscopy, staining, protein, glucose of CSF TB

  • fibrin web
  • lymphocytes on microscopy
  • protein high
  • glucose low

Appearance, microscopy, staining, protein, glucose of CSF in cryptococcal

  • appearance fibrin web
  • microscopy lymphocytes
  • protein high
  • glucose low
24
Q

what do we do for contacts of those with N meningitidis?

A

Identify close contacts and antibiotic prophylaxis (ciprofloxacin or rifampicin) to reduce the risk and prevent onward transmission

25
Q

Where are clostridium tetani spores found globally?

A

In soil

26
Q

Who is at higher risk of getting tetanus

A
  • those who are not vaccinated and IVDU
27
Q

What toxins are produced by tetanus

A
  • tetanolysin (tissue destruction)

- tetanospasmin (clinical tetanus)

28
Q

What is the difference between generalised tetanus and localised tetanus?

A

Generalised tetanus:

  • Spread through lymphatics or blood to multiple nerve terminals
  • Locked jaw → sardonic smile
  • Opisthotonos - spasm of back muscles
  • HTN, tachycardia, arrhythmia and fever if toxin affects the autonomic nervous system

Localised tetanus:
- Develops when only the nerve supplying the affected skin are involved causing painful contraction at the site of injury

29
Q

Can rabies be treated? How is it managed

A

No, invariably fatal 99%

Managed with sedatives.