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2A - Nervous System > Infections of the Nervous System > Flashcards

Infections of the Nervous System Flashcards

1
Q

What is inflammation of the meninges called?

A

Meningitis

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2
Q

What is inflammatio of the brain substance called?

A

Encephalitis

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3
Q

What is inflammation of the spinal cord called?

A

Myelitis

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4
Q

Do patients normally present with inflammation of only one part of the nervous system?

A

No, they present with a mixture of meningitis, encephalitis and myelitis

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5
Q

What are the clinical features of meningitis?

A
  • Classical triad
    • Fever, neck stiffness and altered mental status
  • Present with a short history of progressive headache associated with
    • Fever (>38 degrees)
    • And meningism (neck stiffness, photophobia, nausea and vomiting)
  • Cerebral dysfunction
    • Confusion, delirium, declining conscious level)
    • GCS <14 in 69%
  • Cranial nerve palsy (30%), seizures (30%), focal neurological deficits (10-20%)
  • Petechial skin rash (look for with Tumbler test)
    • Hallmark of meningococcal meningitis but can also occur in viral meningitis
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6
Q

What is the classical triad of clinical features for meningitis?

A
  • Fever, neck stiffness and altered mental status
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7
Q

What is meningism?

A

Clinical syndrome of headache, neck stiffness, and photophobia, often with nausea and vomiting

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8
Q

What cerebral dysfunction can patients with meningitis present with?

A

Confusion

Delirium

Declining conscious leve

GSC < 14

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9
Q

What is the differential diagnosis for meningitis?

A
  • Infective
    • Bacterial, viral, fungal
  • Inflammatory
    • Sarcoidosis
  • Drug induced
    • NSAIDs
    • IVIG
  • Malignant
    • Metastatic
    • Haematological
      • Such as leukaemia, lymphoma, myeloma
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10
Q

What are some bacterial causes of meningitis?

A
  • Neisseria meningitidis (meningococcus)
  • Streptococcus pneumoniae (pneumonococcus)
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11
Q

What is the most common viral cause of meningitis?

A

Enteroviruses

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12
Q

What are the clinical features of encephalitis?

A
  • Flu like prodrome (4 to 10 days)
  • Progressive headache associated with fever
    • With or without meningism
    • Progressive cerebral dysfunction
      • Confusion
      • Abnormal behaviour
      • Memory disturbance
      • Depressed conscious level
    • Seizures
    • Focal symptoms/signs
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13
Q

What progressive cerebral dysfunction can patients with encephalitis display?

A
  • Confusion
  • Abnormal behaviour
  • Memory disturbance
  • Depressed conscious level
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14
Q

Is the onset of viral encephalitis faster or slower than the onset of bacterial meningitis?

A

Slower

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15
Q

Is cerebral dyfunction worse with viral encephalitis or bacterial meningitis?

A

Viral encephalitis

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16
Q

What is the differential diagnosis for encephalitis?

A
  • Infective
    • Viral (most common is HSV)
  • Inflammatory
    • Limbic encephalitis (anti VGKC anti NMDA receptor)
    • ADEM
  • Metabolic
    • Hepatic
    • Uraemic
    • Hyperglycaemic
  • Malignant
    • Metastatic
    • Paraneoplastic
  • Migraine
  • Post ictal (after seizure)
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17
Q

What are 3 different kinds of encephalitis?

A

Viral encephalitis

Autoimmune encephalitis

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18
Q

What are 2 important antibodies associated with autoimmune encephalitis?

A
  • Anti-VGKC (voltage gated potassium channel)
    • Frequent seizures
    • Amnesia (not able to retain new memories)
    • Altered mental state
  • Anti-NMDA receptor
    • Flu like prodrome
    • Prominent psychiatric features
    • Altered mental state and seizures
    • Progressing to a movement disorder and coma
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19
Q

How does the clinical presentation differ between autoimmune encephalitis associated with anti-VGKC and anti-NMDA?

A
  • Anti-VGKC (voltage gated potassium channel)
    • Frequent seizures
    • Amnesia (not able to retain new memories)
    • Altered mental state
  • Anti-NMDA receptor
    • Flu like prodrome
    • Prominent psychiatric features
    • Altered mental state and seizures
    • Progressing to a movement disorder and coma
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20
Q

When dealing with someone who presents with meningitis/encephalitis like symptoms, what is the priority?

A

Exclude and treat infection

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21
Q

What investigations are done for meningitis?

A
  • Blood cultures (bacteraemia)
  • Lumbar puncture (CSF culture)
  • No need for imaging if no contraindications to lumbar puncture
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22
Q

What investigations are done for encephalitis?

A
  • Blood cultures
  • Imaging
    • CT scan with or without MRI
  • Lumbar puncture
  • EEG
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23
Q

What are indications for CT scan before lumbar puncture (contraindications to lumbar puncture)?

A
  • Focal neurological deficit, not including cranial nerve palsies
    • Suggests a focal brain mass
  • New-onset seizures
  • Papilloedema
  • Abnormal level of consciousness, interfering with proper neurological examination (GCS < 10)
    • Reduced conscious level suggests raised intracranial pressure
  • Severe immunocompromised state
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24
Q

How does the CSF differ between bacterial meningitis and viral meningitis/encephalitis in terms of:

  • opening pressure
  • cell count
  • glucose
  • protein
A
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25
Q

What is done to identify the bacteria responsible for bacterial meningitis?

A
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26
Q

What does HSV stand for?

A

Herpes simplex virus

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27
Q

What is required to diagnose HSV encephalitis?

A
  • Lab diagnosis by PCR of CSF for viral DNA
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28
Q

What is HSV encephalitis treated with?

A
  • Treat with aciclovir on clinical suspicion
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29
Q

What are the different herpes group of viruses?

A

VZV

EBV

CMV

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30
Q

What are the 2 different kinds of HSV?

A

Type 1

Type 2

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31
Q

What kind of sores are caused by HSV types 1 and 2?

A
  • Cold sores (type 1 more than 2)
  • Genital herpes (type 1 and 2)
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32
Q

Where does HSV remain latent after primary infection?

A

Virus remains latent in the trigeminal or sacral ganglion after primary infection:

  • As with all herpes viruses, once infected, always infected
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33
Q

Does type 1 or type 2 HSV more commonly cause encephalitis as a complication?

A

Type 1

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34
Q

What are enteroviruses?

A

Are a large family of RNA viruses

Human infections with no animal reservoir

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35
Q

By what route are enteroviruses spread?

A

Spread by the faecal-oral route

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36
Q

What are examples of enteroviruses?

A
  • Polioviruses
  • Coxsackieviruses
  • Echoviruses
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37
Q

What are some other, less common causes of encephalitis?

A

Arbovirus encephalitis

Brain abscess and empyema

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38
Q

How is arbovirus transmitted?

A
  • Transmitted to man by vector (mosquito or tick) from non-human host
  • Is arthropod borne
  • Relevant to travel
    • Travel history important
    • Some preventable by immunisation
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39
Q

What is a brain abscess?

A
  • Brain abscess is localised area of pus within the brain
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40
Q

What is subdural empyema?

A
  • Subdural empyema is a thin layer of pus between the dura and arachnoid membranes over the surface of the brain
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41
Q

What are clinical features of brain abscess and empyema?

A
  • Fever, headache
  • Focal symptoms/signs
    • Seizures dysphagia, hemiparesis
  • Signs of raised intracranial pressure
    • Papilloedema, false localising signs
    • Depressed conscious level
  • Meningism may be present, particularly with empyema
  • Features of underlying source
    • Such as dental, sinus or ear infection
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42
Q

What is the differential diagnosis for brain abscess and empyema?

A
  • Any focal lesion, but most commonly tumour
  • Subdural haematoma
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43
Q

What are some causes of brain abscess and empyema?

A
  • Penetrating head injury
  • Spread from adjacent infection
    • Dental, sinusitis, otitis media
  • Blood borne infection
    • Bacterial endocarditis

Neurosurgical procedure

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44
Q

How is a brain abscess and empyema diagnosed?

A
  • Imaging
    • CT or MRI
    • Investigate source
    • Blood cultures
    • Biopsy (drainage of pus)
45
Q

What organs are normally present in a brain abscess?

A

Often mixture of organisms present (polymicrobial) which depends on predisposing condition

Streptococci is present in 70% of cases, especially the penicillin-sensitive “strep milleri” goup:

  • Strep anginosus, Strep intermedius, Strep constellatus

Anaerobes in 40-100% of cases:

  • Bacteroides
  • Prevotella
46
Q

What organisms are most commonly present in a brain abscess?

A

Streptococci is present in 70% of cases, especially the penicillin-sensitive “strep milleri” goup:

  • Strep anginosus, Strep intermedius, Strep constellatus

Anaerobes in 40-100% of cases:

  • Bacteroides
  • Prevotella
47
Q

What is the management of a brain abscess?

A
  • Surgical drainage if possible
  • Penicillin or ceftriaxone to cover streps
  • Metronidazole for anaerobes
  • High doses required for penetration
  • Culture and sensitivity tests on aspirate provide useful guide
  • High mortality without appropriate treatment
48
Q

What are examples of HIV indicator illnesses in the brain?

A
  • Cerebral toxoplasmosis
  • Aseptic meningitis/encephalitis
  • Primary cerebral lymphoma
  • Cerebral abscess
  • Cryptococcal meningitis
  • Space occupying lesion of unknown cause
  • Dementia
  • Leukoencephalopathy
49
Q

What is done to diagnose HIV indicator brain illnesses?

A
  • Cryptococcal antigen
  • Toxoplasmosis serology
  • CMV PCR
  • HIV PCR
50
Q

What are examples of spirochaetes in the CNS?

A
  • Lyme disease
    • Borrelia burgdorferi
  • Syphillis
    • Trepomena pallidum
  • Leptospirosis
    • Leptospira interrogans
51
Q

What bacteria causes lyme disease?

A
  • Borrelia burgdorferi
52
Q

What bacteria causes syphillis?

A
  • Trepomena pallidum
53
Q

What bacteria causes leptospirosis?

A
  • Leptospira interrogans
54
Q

How is lyme disease transmitted?

A
  • Vector borne
    • Tick (wooded areas)
55
Q

What are the stages of lyme disease?

A
  • Stage 1
    • Early localised infection (1-30 days)
    • Characteristic expanding rash at the site of the tick bite (erythema migrans)
    • 50% flu like symptoms (days to 1 week)
      • Fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness)
  • Stage 2
    • Early disseminated infection (weeks to months)
    • One or more organ system becomes involved
      • Haematologic or lymphatic spread
    • Musculoskeletal and neurological involvement are most common
    • Neurological involvement occurs in 10-15% of untreated patients
      • Mononeuropathy
      • Mononeuritis multiplex
      • Painful radiculoneuropathy
      • Cranial neuropathy
      • Myelitis
      • Meningo-encephalitis
      • PNS > CNS
  • Stage 3
    • Chronic infection
      • Months to years
      • Occurring after a period of latency
    • Musculoskeletal and neurologic involvement most common
    • Neurologic involvement
      • As described for stage 2
      • Subacute encephalopathy
      • Encephalomyelitis
    • Does not cause a chronic fatigue syndrome
56
Q

What is stage 1 on lyme disease?

A
  • Early localised infection (1-30 days)
57
Q

What is the clinical presentation of stage 1 lyme disease?

A
  • Characteristic expanding rash at the site of the tick bite (erythema migrans)
  • 50% flu like symptoms (days to 1 week)
    • Fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness)
58
Q

What is stage 2 lyme disease?

A
  • Early disseminated infection (weeks to months)
  • One or more organ system becomes involved
    • Haematologic or lymphatic spread
59
Q

What is the clinical presentation of stage 2 lyme disease?

A
  • Early disseminated infection (weeks to months)
  • One or more organ system becomes involved
    • Haematologic or lymphatic spread
  • Musculoskeletal and neurological involvement are most common
  • Neurological involvement occurs in 10-15% of untreated patients
    • Mononeuropathy
    • Mononeuritis multiplex
    • Painful radiculoneuropathy
    • Cranial neuropathy
    • Myelitis
    • Meningo-encephalitis
    • PNS > CNS
60
Q

What is stage 3 lyme disease?

A
  • Chronic infection
    • Months to years
    • Occurring after a period of latency
61
Q

What is the clinical presentation of stage 3 lyme disease?

A
  • Musculoskeletal and neurologic involvement most common
  • Neurologic involvement
    • As described for stage 2
    • Subacute encephalopathy
    • Encephalomyelitis
  • Does not cause a chronic fatigue syndrome
62
Q

How is lyme disease a multi-system disease?

A
  • Skin, rheumatological, neurological, cardiac and ophthalmological involvement

Untreated 80% will develop multi-system disseminated disease

63
Q

What investigations are done for lyme disease?

A
  • Complex range of serological tests
  • CSF lymphocytosis
  • MRI brain/spine (if CNS involvement)
  • Nerve conduction studies/EMG (if PNS involvement)
64
Q

What is the treatment for lyme disease?

A
  • Prolonged antibiotic treatment
    • Intravenous ceftriaxone
    • Oral doxycycline
65
Q

What is neurosyphillis caused by?

A

Caused by Treponema pallidum

66
Q

What is the 3 stage presentation of neurosyphillis?

A
  • Primary
  • Secondary
  • Latent
67
Q

What investigations are done for neurosyphillis?

A
  • Treponema specific and non-treponemal specific antibody tests
  • CSF lymphocytes increased
  • Evidence of intrathecal antibody production
68
Q

What is the treatment for neurosyphillis?

A

Treatment is high dose penicillin

69
Q

What are some examples of important vaccines?

A
  • Poliomyelitis
  • Rabies
  • Tetanus
  • Botulism
70
Q

What is poliomyelitis caused by?

A
  • Caused by poliovirus types 1, 2 or 3:
    • All enteroviruses
71
Q

Where does poliovirus infect to cause poliomyelitis?

A
  • Infects anterior horn cells of lower motor neurons
72
Q

What is the clinical presentation of poliomyelitis?

A
  • Asymmetric, flaccid paralysis, especially legs
  • No sensory features
73
Q

What is rabies?

A

Acute infectious disease of CNS affecting almost all mammals

74
Q

How is rabies transmitted?

A

Transmitted to human by bite or salivary contamination of open lesion

75
Q

What is the pathogenesis of rabies?

A

Neurotropic meaning virus enters peripheral nerves and migrates to CNS

76
Q

What is the clinical presentation of rabies?

A

Paraesthesia at the site of original lesion

Ascending paralysis and encephalitis

77
Q

How is rabies encephalitis diagnosed?

A
  • Diagnosis is by PCR and serology
78
Q

What are the possible outcomes of rabies encephalitis?

A
  • Possibilities are sedation, intensive care or death
79
Q

Who is the rabies vaccine given to in the UK?

A
  • Bat handers
  • Regular handlers of important animals
  • Selected travellers to enzootic zones
80
Q

What is some rabies post-exposure treatment?

A
  • Wash wound
  • Give active rabies immunisation
  • Give human rabies immunoglobin (passive immunisation) if high risk
81
Q

What are important sources of rabies infection?

A
  • Dogs in Africa/Asia
  • Bats in developed world
82
Q

What infection causes tetanus?

A
  • Infection with Clostridium tetani
  • Anaerobic gram positive bacillus, spore forming
83
Q

Where do the toxins that cause tetanus act?

A
  • Toxins act at neuro-muscular junction
  • Blocks inhibition of motor neurons
84
Q

What is the clinical presentation of tetanus?

A
  • Rigidity and spasm (risus sarconicus)
85
Q

What can be done to prevent tetanus?

A
  • Immunisation (toxoid)
  • Given combined with other antigens (DTaP)
  • Penicillin and immunoglobin for high risk wounds/patients
86
Q

What kind of vaccine is used for rabies?

A

Killed vaccine

87
Q

What kind of vaccine is used for tetanus?

88
Q

What is botulism caused by?

A

Caused by Clostridium botulinum:

  • Anaerobic spore producing gram positive bacillus
  • Neurotoxin
    • Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junction
    • Toxin binding blocks acetylcholine release
    • Recovery is by sprouting new axons

Naturally present in soil, dust and aquatic environments

89
Q

How does the botulism toxin act?

A
  • Neurotoxin
    • Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junction
    • Toxin binding blocks acetylcholine release
    • Recovery is by sprouting new axons
90
Q

Where is clostridium botulinium naturally found?

A
  • Naturally present in soil, dust and aquatic environments
91
Q

What are the 3 modes of infection of clastridium botulinium?

A
  • Infantile (intestinal colonisation)
  • Food-borne (outbreaks)
  • Wound
    • Almost exclusively by injecting drug users
92
Q

What is the clinical presentation of botulism?

A
  • Incubation period 4-14 days
  • Descending symmetrical flaccid paralysis
  • Pure motor
  • Respiratory failure
  • Autonomic dysfunction
    • Usually pupil dilation
93
Q

What is done to diagnose botulism?

A
  • Nerve conduction studies
  • Mouse neutralisation bioassay for toxin in blood
  • Culture from debrided wound
94
Q

What is the treatment of botulism?

A
  • Anti-toxin (A, B, E)
  • Penicillin/metronidazole (prolonged treatment)
  • Radical wound debridement
95
Q

What book is good to refer to for immunisatoin against infectious disease?

A

Green book

96
Q

What are examples of post infective inflammatory syndromes?

A

Central nervous system:

  • Acute disseminated encephalomyelitis (ADEM)

Peripheral nervous system:

  • Guillain Bare Syndrome (GBS)
97
Q

What does ADEM stand for?

A
  • Acute disseminated encephalomyelitis (ADEM)
98
Q

What does GBS stand for?

A
  • Guillain Bare Syndrome (GBS)
99
Q

Does guillain bare syndrome affect the CNS or PNS?

100
Q

Does acute disseminated encephalitis affect the CNS or PNS?

101
Q

What classification of disease are post infetive inflammatory syndromes?

A

Autoimmune

102
Q

What does CJD stand for?

A

Creutzfeldt-Jakob Disease

103
Q

What are the different kinds of Creutzfeldt-Jakob Disease (CJD)?

A

Sporadic CJD

New varient CJD

Familial CJD

Acquired CJD

104
Q

What are the clinical features of sporadic CJD?

A
  • Insidious onset (usually older than 60)
  • Early behavioural abnormalities
  • Rapidly progressive dementia
  • Myoclonus
  • Progressing to global neurological decline
  • Motor abnormalities
    • Cerebellar ataxia
    • Extrapyramidal
      • Tremor
      • Rigidity
      • Bradykinesis
      • Dystonia
    • Pyramidal
      • Weakness
      • Spasticity
      • Hyper-reflex
  • Cortical blindness
  • Seizures
105
Q

What is the differential diagnosis for sporadic CJD?

A
  • Alzheimer’s disease with myoclonus
    • Usually more prolonged
  • Subacute sclerosing panencephalitis (SSPE)
  • CNS vasculitis
  • Inflammatory encephalopathies
106
Q

What is the prognosis of sporadic CJD?

A
  • Rapid progression
  • Death often within 6 months
107
Q

Does new varient CJD have younger or older onset?

A

Younger onset

108
Q

What investigations are done for CJD?

A
  • MRI
    • Pulvinar sign in variant CJD
    • Often no specific changes in sporadic CJD
  • EEG
    • Generalised periodic complexes typical
    • Often normal/non-specific in early stages
  • CSF
    • Normal or raised protein
    • Immunoassay 14-3-3 brain protein (non-specific, but very helpful in correct clinical context)
109
Q

How does CJD impact the CSF proteins?

A
  • Normal or raised protein

2A - Nervous System (48 decks)

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