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Systems: Neurology AB > Infections of the Nervous System > Flashcards

Infections of the Nervous System Flashcards

1
Q

Meningitis

A

Inflammation / infection of meninges

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2
Q

Encephalitis

A

Inflammation / infection of brain substance

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3
Q

Myelitis

A

Inflammation / infection of spinal cord

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4
Q

What is the classic triad of meningitis?

A
  • Fever
  • Neck stiffness
  • Altered mental state
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5
Q

How do meningitis patients usually present?

A

Present with a short history of progressive headache associated with

  • Fever (>38º) and
  • Meningism (neck stiffness, photophobia, nausea and vomiting)
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6
Q

What should you look for on the skin in meningitis?

A

-Look for a petechial skin rash (Tumbler test)

It is hallmark of meningococcal meningitis, but can also occur in viral meningitis

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7
Q

What are the clinical features of meningitis?

A
  • Classic triad
  • Cerebral dysfunction (confusion, delirium, declining conscious level) is common and GCS is <14 in 69%
  • Cranial nerve palsy (30%), seizures (30%), focal neurological deficits (10-20%) may also occur
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8
Q

What is the differential diagnosis for meningitis?

A

Infective
-Bacterial, viral, fungal

Inflammatory
-Sarcoidosis

Drug induced
-NSAIDs, IVIG

Malignant
-Metastatic, haematological

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9
Q

What bacterial causes of meningitis are there?

A
  • Neisseria meningitidis (meningococcus)

- Streptococcus pneumoniae (pneumococcus)

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10
Q

What viral causes of meningitis are there?

A

Enteroviruses

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11
Q

What are the clinical features of encephalitis?

A
  • Flu-like prodrome (4-10days)
  • Progressive Headache associated with fever
  • +/- meningism
  • Progressive cerebral dysfunction
  • Seizures
  • Focal symptoms / signs
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12
Q

How can viral and bacterial encephalitis be differentiated?

A

Onset of a viral encephalitis is generally slower than for bacterial
meningitis and cerebral dysfunction is a more prominent feature

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13
Q

What progressive cerebral dysfunction may be present in encephalitis?

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

What is the differential diagnosis for encephalitis?

A

Infective
-Viral (most common HSV)

Inflammatory
-Limbic encephalitis (Anti VGKC, Anti NMDA receptor), ADEM

Metabolic
-Hepatic, uraemic, hyperglycaemic

Malignant
-Metastatic, paraneoplastic

Migraine

Post ictal

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15
Q

What 2 antibodies are associated with auto-immune encephalitis?

A
  • Anti-VGKC (Voltage Gated Potassium Channel)

- Anti NMDA receptor

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16
Q

How does anti-VGKC auto-immune encephalitis present?

A
  • Frequent seizures
  • Amnesia (not able to retain new memories)
  • Altered mental state
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17
Q

How does anti-NMDA receptor auto-immune encephalitis present?

A
  • Flue like prodrome
  • Prominent psychiatric features
  • Altered mental state and seizures
  • Progressing to a movement disorder and coma
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18
Q

How should meningitis be investigated?

A
  • Blood cultures (bacteraemia)
  • Lumbar puncture (CSF culture/microscopy)
  • No need for imaging if no contraindications to LP
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19
Q

How should encephalitis be investigated?

A
  • Blood cultures
  • Imaging (CT scan +/- MRI)
  • Lumbar puncture
  • EEG
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20
Q

What are the contraindications for LP?

A
  • Focal neurological deficit, not including cranial nerve palsies
  • New-onset seizures
  • Papilloedema
  • Abnormal level of consciousness, interfering with proper neurological examination (GCS<10)
  • Severe immunocompromised state
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21
Q

What do focal symptoms or signs suggest?

A

Focal brain mass

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22
Q

What does a reduced conscious level suggest?

A

Raised intracranial pressure

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23
Q

What is the opening pressure in bacterial meningitis?

A

Increased

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24
Q

What is the opening pressure in viral meningitis and encephalitis?

A

Norma/ increased

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25
Q

What is the cell count in bacterial meningitis?

A

High, mainly neutrophils

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26
Q

What is the cell count in viral meningitis and encephalitis?

A

High, mainly lymphocytes

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27
Q

What is the glucose level in bacterial meningitis?

A

Reduced

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28
Q

What is the glucose level in viral meningitis and encephalitis?

A

Normal (60% of BG)

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29
Q

What is the protein level in bacterial meningitis?

A

High

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30
Q

What is the protein level in viral meningitis and encephalitis?

A

Slightly increased

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31
Q

What will be seen on blood culture gram stain of bacterial meningitis?

A

Gram positive cocci in chains - looks like streptococci

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32
Q

What is streptococcus pneumonia sensitive to?

A

Penicillin

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33
Q

What is the commonest cause of encephalitis in Europe?

A

Herpes simplex virus

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34
Q

How is Herpes simplex encephalitis diagnosed?

A

Lab diagnosis by PCR of CSF for viral DNA

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35
Q

How is HSV encephalitis treated?

A

Treat with aciclovir on clinical suspicion

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36
Q

What is the prognosis of untreated HSV encephalitis?

A

Over 70% mortality and high morbidity if untreated

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37
Q

What do the 2 types of HSV cause?

A
  • Cold sores (type 1&raquo_space; 2)

- Genital herpes (type 1 & 2)

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38
Q

Where does the HSV remain latent?

A

-Virus remains latent in the trigeminal or sacral ganglion after primary infection (as with all herpesviruses, once infected, always infected)

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39
Q

What type of HSV is associated with encephalitis?

A
  • Encephalitis is a rare complication of HSV

- Other than neonates, nearly all caused by type 1

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40
Q

What are enteroviruses?

A

Large family of RNA viruses

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41
Q

What do enteroviruses have a tendency to cause?

A

Tendency to cause CNS infections (neurotropic) Human infections, no animal reservoir

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42
Q

How are enteroviruses spread?

A

Faecal-oral route

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43
Q

What do enteroviruses NOT cause?

A

Gastroenteritis

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44
Q

What can many enteroviruses cause?

A

Non-paralytic meningitis

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45
Q

Give examples of enteroviruses

A

Include polioviruses, coxsackieviruses and echoviruses

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46
Q

How are arbovirus encephalitides transmitted?

A

Transmitted to man by vector (mosquito or tick) from non-human host

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47
Q

Give examples of arbovirus caused infection.

A
  • West Nile virus
  • St Louis Encephalitis
  • Western Equine Encephalitis
  • Tick Borne Encephalitis
  • Japanese B Encephalitis
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48
Q

What are arbovirus encephalitides named after?

A

Generally relate to where first described and NOT to current geographical distribution

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49
Q

Where do arboviruses get their name from?

A

Called Arbo as arthropod borne

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50
Q

Brain abscess

A

Localised area of pus within the brain

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51
Q

Subdural empyema

A

Thin layer of pus between the dura and arachnoid membranes over the surface of the brain

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52
Q

What are the clinical features of brain abscess and empyema?

A

-Fever, Headache
-Focal symptoms / signs (Seizures, dysphasia, hemiparesis, etc)
-Signs of raised intracranial pressure (Papilloedema, false localizing signs,
depressed conscious level)
-Meningism may be present, particularly with empyema
-Features of underlying source (e.g dental, sinus or ear infection)

53
Q

What is the differential diagnosis for brain abscess and empyema?

A
  • Any focal lesion, but most commonly tumour

- Subdural haematoma

54
Q

What can cause brain abscess and empyema?

A
  • Penetrating head injury
  • Spread from adjacent infection (Dental, Sinusitis, Otitis media)
  • Blood borne infection (e.g. Bacterial endocarditis)
  • Neurosurgical procedure
55
Q

How is brain abscess and empyema diagnosed?

A
  • Imaging: CT or MRI
  • Investigate source
  • Blood cultures
  • Biopsy (drainage of pus)
56
Q

What organisms are usually present in brain abscesses?

A
  • Often a mix
  • Streptococci in 70% of cases, especially the penicillin-sensitive “Strep milleri” group (Strep anginosus, Strep intermedius, Strep constellatus)
  • Anaerobes in 40 - 100% of cases (Bacteroides, Prevotella)
57
Q

How should brain abscess be managed?

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
58
Q

What brain illnesses may indicate HIV?

A
  • Cerebral toxoplasmosis
  • Aseptic meningitis/encephalitis
  • Primary cerebral lymphoma
  • Cerebral abscess
  • Cryptococcal meningitis
  • Space occupying lesion of unknown cause
  • Dementia
  • Leucoencephalopathy
59
Q

What brain infections are common in HIV patients with low CD4 counts?

A
  • Cryptococcus neoformans
  • Toxoplasma gondii
  • Progressive multifocal leukoencephalopathy (PML)
  • Cytomegalovirus (CMV)
  • HIV-encephalopathy (HIV-associated dementia)
60
Q

What diagnostics are there for HIV related brain infections?

A
  • India Ink, cryptococcal antigen
  • Toxoplasmosis serology (IgG)
  • JC virus PCR
  • CMV PCR
  • HIV PCR
61
Q

How are people exposed to Cryptococci infections?

A

Exposure occurs following inhalation of airborne organisms into the lungs.

62
Q

What do most clinical cases of cryptococcal infections present with?

A

Most clinical cases present with meningoencephalitis

63
Q

What are the risk factors for cryptococcal infection?

A
  • Defects in immune function
  • AIDS
  • Transplant patients
64
Q

What spirochaetes can cause CNS illness?

A
  • Borrelia burgorferi
  • Trepomena pallidum
  • Leptospira interrogans
65
Q

What is the causative agent of Lyme disease?

A

Borrelia burgorferi

66
Q

What is the causative agent of syphilis?

A

Trepomena pallidum

67
Q

What is the causative agent of leptospirosis?

A

Leptospira interrogans

68
Q

What is the vector in Lyme disease?

A

Tick

69
Q

How many stages are there in Lyme disease?

A

3

70
Q

What is meant by Lyme disease being multi-system?

A
  • Skin, rheumatological, neurological / neuropsychiatric, cardiac and ophthalmological involvement
  • Untreated 80% will develop multi-system disseminated disease
71
Q

What is stage 1 of Lyme disease?

A
  • Early localized infection (1-30d)
  • Characteristic expanding rash at the site of the tick bit known as erythema migrans
  • 50% flu like symptoms lasting days (fatigue, myalgia, arthralgia, headache., fever, chills, neck stiffness)
72
Q

What is stage 2 of Lyme disease?

A

-Early disseminated infection (weeks – months)
-One or more organ systems become involved
Haematologic or lymphatic spread
-Musculoskeletal and neurologic involvement most common
-Neurologic involvement (10-15%) untreated patients

73
Q

What neurological involvement may there be in stage 2 Lyme disease?

A

PNS> CNS

  • Mononeuropathy
  • Mononeuritis multiplex
  • Painful radiculoneuropathy
  • Cranial neuropathy
  • Myelitis
  • Meningo-encephalitis
74
Q

What is stage 3 of Lyme disease?

A

Chronic infection
-Months to years occuring after a period of latency

Musculoskeletal and neurologic involvement most common

Neurologic involvement

  • As described for stage 2
  • Subacute encephalopathy
  • Encephalomyelitis
75
Q

What does Lyme disease not cause?

A

Chronic fatigue syndrome

76
Q

What is the investigation for Lyme disease?

A
  • Complex range of serological tests
  • CSF lymphocytosis
  • PCR of CSF
  • MRI brain / spine (if CNS involvement)
  • Nerve conduction studies / EMG (if PNS involvement)
77
Q

How should Lyme disease be treated?

A
  • Prolonged antibiotic treatment
  • Intravenous ceftriaxone
  • Oral doxycycline
78
Q

What are the stages of syphilis?

A
  • Primary
  • Secondary
  • Latent
79
Q

What is tertiary syphilis?

A

Tertiary disease (neurosyphilis) years/decades after primary disease - not common

80
Q

What investigation is there for syphilis?

A
  • Treponema specific and non-treponemal specific (VDRL) antibody tests
  • CSF lymphocytes increased, evidence of intrathecal antibody production, PCR
81
Q

How is syphilis treated?

A

High dose penicillin

82
Q

What is poliomyelitis caused by?

A
  • Poliovirus 1, 2 or 3

- All enteroviruses

83
Q

How does poliovirus infection present?

A
  • 99% of infections are asymptomatic

- Paralytic disease in ~1%

84
Q

When does paralytic disease occur in poliovirus infection?

A

When it infects anterior horn cells of lower motor neurones

85
Q

Why did the polio vaccine change from oral to injected administration?

A
  • Risk of vaccine-associated polio from oral vaccine
  • Indigenous polio due to wild (ie non-vaccine) polio eliminated from UK
  • Given combined with other antigens (IPV)
86
Q

What is rabies?

A

Acute infectious disease of CNS affecting almost all mammals

87
Q

How is rabies transmitted?

A

Transmitted to human by bite or salivary contamination of open lesion

88
Q

How does rabies present?

A
  • Paraesthesiae at site of original lesion

- Ascending paralysis and encephalitis

89
Q

How does the rabies virus spread in the body?

A

Neurotropic - virus enters peripheral nerves and migrates to CNS

90
Q

How is rabies encephalitis diagnosed

A
  • No useful diagnostic tests before clinical disease apparent
  • Diagnosis: culture, detection or serology
91
Q

What are important sources of rabies encephalitis?

A
  • Dogs in Africa/Asia
  • Bats in the developed world. In 2003 it was recognised that UK bats may carry a rabies-like virus, European Bat Lyssavirus 2 (EBL2).
92
Q

What rabies pre-exposure prevention is there?

A

Active immunisation with killed vaccine

93
Q

Who is the rabies immunisation given to in the UK?

A
  • Bat handlers
  • Regular handlers of imported animals
  • Selected travellers to enzootic areas
94
Q

What is the rabies post-exposure treatment?

A
  • Wash wound
  • Give active rabies immunisation
  • Give human rabies immunoglobulin (passive immunisation) if high risk
95
Q

What is the causative agent of tetanus?

A

Clostridium tetani

96
Q

What is clostridium tetani?

A

-Anaerobic Gram positive bacillus, spore forming

97
Q

How does tetanus present?

A
  • Wound may not be apparent

- Rigidity and spasm (risus sardonicus)

98
Q

What is the pathology behind tetanus?

A

Toxin acts at neuro-muscular junction and blocks inhibition of motor neurones

99
Q

How is tetanus prevented?

A
  • Immunisation (toxoid)
  • Given combined with other antigens (DTaP}
  • Penicillin and immunoglobulin for high risk wounds/patients
100
Q

What is the causative agent of botulism?

A

Clostridium botulinum

101
Q

What is clostridium botulinum?

A

Anaerobic spore producing gram positive bacillus

102
Q

Where is clostridium botulinum naturally present?

A

Naturally present in soil, dust and aquatic environments

103
Q

Why is clostridium botulinum considered a neurotoxin?

A
  • Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
  • Toxin binding blocks acetylcholine release
  • Recovery is by sprouting new axons
104
Q

What are the 3 modes of infection of clostridium botulinum?

A
  • Infantile (intestinal colonization)
  • Food-borne (outbreaks)
  • Wound: Almost exclusively injecting or “popping” drug users
105
Q

How does botulism present?

A
  • Incubation period 4-14 days
  • Descending symmetrical flaccid paralysis
  • Pure motor
  • Respiratory failure
  • Autonomic dysfunction: Usually pupil dilation
106
Q

How is botulism diagnosed?

A
  • Nerve conduction studies
  • Mouse neutralisation bioassay for toxin in blood
  • Culture from debrided wound
107
Q

How is botulism treated?

A
  • Anti-toxin (A,B,E)
  • Penicillin / Metronidazole (prolonged treatment)
  • Radical wound debridement
108
Q

Give an example of a post-infective inflammatory syndrome affecting the CNS

A

Acute disseminated encephalomyelitis (ADEM)

109
Q

Give an example of a post-infective inflammatory syndrome affecting the PNS

A

Guillain Barre Syndrome (GBS)

110
Q

What can precede a post infective inflammatory syndrome?

A

Preceding infection (viral, bacterial) or immunization

  • “Molecular mimicry”
  • Latent interval between the precipitating infection and onset of neurological symptoms
  • Autoimmune
111
Q

What is the causative agent of Creutzfeldt-Jakob Disease?

A

Transmissible Proteinaceous particle – Prion

112
Q

What is the aetiology of CJD?

A
  • Sporadic CJD
  • New variant CJD
  • Familial CJD (10-15%)
  • Acquired CJD (<5%) (Cadeveric Growth Hormone, Dura matter grafts, Blood transfusion)
113
Q

What is the epidemiologyof CJD?

A

Very rare: sporadic 1 per million per year (incidence)

114
Q

When should sporadic CJD be considered?

A

Consider in any rapidly progressive dementia

115
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
  • Cortical blindness
  • Seizures may occur
116
Q

What motor abnormalities may be present in sporadic CJD?

A
  • Cerebellar ataxia
  • Extrapyramidal: tremor, rigidity, bradykinesis, dystonia
  • Pyramidal: weakness, spacticity, hyper-refexia
117
Q

What is the differential diagnosis for sporadic CJD?

A

Alzheimer’s disease with myoclonus
-Usually more prolonged

Subacute sclerosing panencephalitis (SSPE)
-Very rare, chronic infection with defective measles virus

CNS vasculitis

Inflammatory encephalopathies

118
Q

What is the prognosis of sporadic CJD?

A
  • Rapid progression

- Death often within 6 months

119
Q

Who is usually affected by new variant CJD?

A

Younger onset <40

120
Q

What is new variant CJD linked to?

A

Linked to Bovine Spongiform Encephalopathy in Cattle
-Eating infected material
-Less cases than predicted
-No new cases last few years
-May be a genetic susceptibility (MM, MV, VV)
-Concern about a further wave
of infection

121
Q

What length of course is associated with new-variant CJD?

A

Longer course (average 13 months)

122
Q

What clinical feature is more prominent in new variant CJD?

A

Early behavioural changes more prominent

123
Q

How is new variant CJD investigated?

A
  • MRI
  • EEG
  • CSF
124
Q

What may be seen on MRI of new variant CJD?

A
  • Pulvinar sign in variant CJD

- Often no specific changes in sporadic CJD

125
Q

What may be seen on EEG of new variant CJD?

A
  • Generalised periodic complexes typical

- Often normal / non-specific in initial stages

126
Q

What may be seen in the CSF of new variant CJD?

A
  • Normal or raised protein

- Immunoassay 14-3-3 brain protein (non-specific, but very helpful in correct clinical context)

127
Q

What is the causative agent of cryptococcal meningitis?

A

Cryptococcus neoformans

128
Q

How does paralytic disease present in poliomyelitis?

A
  • Asymmetric, flaccid paralysis, esp legs

- No sensory features

Systems: Neurology AB (51 decks)

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