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Neuro Pathology > Infections of the Nervous System > Flashcards

Infections of the Nervous System Flashcards

1
Q

Definition of meningitis

A

Inflammation/infection of meninges

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2
Q

Definition of encephalitis

A

Inflammation/infection of brain substance

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3
Q

Definition of myelitis

A

Inflammation/infection of spinal cord

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4
Q

Presentation of meningitis

A 
Fever (>38C)
Neck stiffness
Altered mental status 
Short progressive headache 
Photophobia 
Nausea and vomiting 
Cranial nerve palsy (30%)
Seizures (30%)
Focal neurological deficits (10-20%)
Petechial skin rash
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5
Q

What is the classic triad of meningitis?

A

Fever
Neck stiffness
Altered mental status

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6
Q

What is the petechial skin rash a hallmark of?

A

Meningococcal meningitis

But can also occur in viral

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7
Q

Differential diagnosis of meningitis

A

Infective; bacterial, viral, fungal
Inflammatory; sarcoidosis
Drug induced; NSAIDs, IVIG
Malignant; metastatic, haematological e.g. leukaemia, lymphoma, myeloma

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8
Q

Bacterial causes of meningitis

A 
Neisseria meningitidis (meningococcus)
Stretococcus pneumoniae (pnuemococcus)
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9
Q

Viral causes of meningitis

A

Enteroviruses

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10
Q

Presentation of encephalitis

A 
Flu like prodrome (4 - 10 days)
Progressive headache
Fever
\+/- meningism 
Progressive cerebral dysfunction (confusion, abnormal behaviour, memory disturbance, depressed conscious level)
Seziures
Focal symptoms/signs
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11
Q

Main differences of viral encephalitis vs bacterial meningitis

A

VE = Slower onset and cerebral dysfunction more prominent feature

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12
Q

Differential diagnosis of encephalitis

A

Infective; Viral (most common HSV)
Inflammatory; limbic encephlaitis (Anti VGKC Anti NMDA receptor). ADEM
Metabolic; hepatic, uraemic, hyperglycaemic
Malignant; metastatic, paraneoplastic
Migraine
Post ictal

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13
Q

What does post ictal mean?

A

Post seizure

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14
Q

What are the two important antibodies recognized in autoimmune encephalitis?

A

Anti-VGKC

Anti-NMDA receptor

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15
Q

What does anti-VGKC stand for?

A

Voltage gated potassium channels

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16
Q

Presentation of Anti-VGKC Autoimmune encephalitits

A

Frequent seizures
Amnesia
Altered mental state

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17
Q

What is amnesia?

A

Not able to retain new memories

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18
Q

Presentation of anti-NMDA receptor autoimmune encephalitis

A

Flu like prodrome
Prominent psychiatric features
Altered mental state and seziures
Progressive to movement disorder and coma

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19
Q

Investigations for meningitis

A 
Blood cultures (bacteraemia)
LP (CSF culture/microscopy)
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20
Q

Investigations for encephalitis

A

Blood cultures
Imaging (CT scan +/- MRI)
LP
EEG

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21
Q

Contraindications to 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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22
Q

What do focal symptoms and signs suggest?

A

A focal brain mass

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23
Q

What does reduced consciousness level suggest?

A

Raised intracranial pressure

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24
Q

CSF findings in bacterial meningitis

A

Opening pressure increased
Cell count high, mainly neutrophils
Glucose reduced
Protein high

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25
Q

CSF findings in viral meningitis and also encephalitis

A

Opening pressure normal or increased
Cell count high, mainly lymphocytes
Glucose normal (60% of BG)
Protein slightly increased

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26
Q

How do you assess the level of glucose in the CSF?

A

Compare it to the level of glucose in the blood

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27
Q

Which bacterial cause of bacterial meningitis is sensitive to penicillin?

A

Culture streptococcus pneumoniae

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28
Q

If not pyrexial, does the patient need a blood culture?

A

No

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29
Q

How common is HSV Encephalitis?

A

Relatively rare

Commonest cause of encephalitis in Europe

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30
Q

Investigations of HSV Encephalitis

A 
CSF
- PCR for Viral DNA
- Lymphocytosis 
- elevated protein 
CT
- medial temporal and inferior frontal lobe changes (e.g. petechial changes)
MRI (better)
EEG
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31
Q

Treatment of HSV Encephalitis

A

Aciclovir on clinical suspicision

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32
Q

Types of HSV

A

Type 1

Type 2

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33
Q

What do both types of HSV cause?

A 
Cold sores (type 1 > 2)
Genital herpes (both types)
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34
Q

Where does the HSV virus lie in the body?

A

Remains latent in the trigeminal or sacral ganglion after primary infection

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35
Q

What type of HSV usually causes HSV encephalitis?

A

Type 1 (other than neonates)

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36
Q

What type of viruses are enteroviruses?

A

RNA viruses

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37
Q

Spread of entero-viruses

A

Faecal oral route

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38
Q

What do enteroviruses have the tendency to cause?

A

CNS infections (neurotrophic)

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39
Q

Do enteroviruses also cause gastroenteritis?

A

NO

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40
Q

Examples of enteroviruses

A

Polioviruses
Coxsackieviruses
Echoviruses

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41
Q

Causes of encephalitis

A

HSV
Enteroviruses
Arbovirus

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42
Q

Where is arbovirus encephalitis common?

A

Certain areas of the world where there is certain types of ticks/mosquitos - therefore have to have travel history

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43
Q

Types of arbovirus encephalitis

A

West nile virus
St Louis encephalitis
Tick borne encephalitis
Japanese B encephalitis

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44
Q

Definition of brain abscess

A

Localized area of pus within the brain

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45
Q

Definition of subdural empyema

A

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

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46
Q

Presentation of brain abscess/empyema

A 
Fever
Headache
Focal symptoms
- seizures 
- dysphagia
- hemiparesis
Signs of raised ICP
- papilloedema
- false localising signs
- depressing conscious level 
Meningism may be present, particularly with empyema 
Features of an underlying source
- dental, sinus or ear infection
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47
Q

Differential diagnosis of brain abscess/empyema

A

Any focal lesion but most commonly tumour

Subdural haematoma

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48
Q

Causes of brain abscess/empyema

A 
Penetrating head injury 
Spread from adjacent infection 
- dental 
- sinusitis
- otitis media
Blood borne infection e.g. bacterial endocarditis
Neurosurgical procedure
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49
Q

Investigations for brain abscess and empyema

A

Imaging; CT or MRI
Investigate source
Blood cultures
Biopsy (drainage of pus)

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50
Q

Causative organisms of a brain abscess

A 
Often a mixture present - depends on predisposing condition 
Streptococci (70% of cases) 
- Strep anginousus
- Strep intermediuss
- Strep constellatus 
Anaerobes in 40-100% of cases
- bacteriodes
- prevotella
51
Q

Treatment of brain abscess

A

Surgical drainage if possible
Penicillin or ceftrixazone to cover streps
Metronidazole for anaerobes
HIGH DOSES REQUIRED FOR PENETRATION

52
Q

HIV indicator illnesses of the brain

A 
Cerebral toxoplasmosis
Aseptic meningitis/encephalitis
Primary cerebral lymphoma
Cerebral abscess 
Cryptococcal meningitis
Space occupying lesion of unknown cause
Dementia
Leucoencephalopathy
53
Q

Brain infections in HIV patients with low CD4 counts

A

Cryptococcus neoformans
Toxoplasma gondii
Progressive multifocal leykoencephalopathy (PML)
CMV
HIV encephalopathy (HIV-associated dementia)

54
Q

Investigations of brain infections in HIV patients with low CD4 counts

A 
India ink, cyptococcal antigen 
Toxoplasmosis serology (IgG)
JC virus PCR
CMV PCR
HIV PCR
55
Q

Causative organisms of cryptococcal infections

A

Cryptococcus neoformans

56
Q

Exposure of cryptococcus organisms is due to what?

A

Inhalation of airborne organisms into the lungs

57
Q

Most clinical cases of cryptococcal infections present with what?

A

Meningoencephalitis

58
Q

What do most patients with cryptococcal infections also have?

A

Defects in immune function

59
Q

Major risk factor for cryptococcal infections

A

AIDs

60
Q

Risk factors for cryptococcal infections

A

AIDs
Immunosuppressive medications
- particularly in the setting of solid organ transplantation

61
Q

What spirochaeates can be found in the CNS?

A

Borrelia Burgorferi
Trepomena pallidum
Leptospira interrogans

62
Q

What does borrelia burgorgeri cause?

A

Lymes disease

63
Q

What does trepomena pallidum cause?

A

Syphillis

64
Q

What does leptospira interrogans cause?

A

Leptospirosis

65
Q

How do you get lyme disease?

A

Vector borne; tick (wooded areas)

66
Q

3 stages of lymes disease

A

Stage 1 , 2, 3

67
Q

Presentation of stage 1 lymes disease

A

Early localised infection (1 - 30 days)
Characteristic expanding rash at the site of the tick bites - erythema migrans
50% flu like symptoms (days - 1 week)
- fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness

68
Q

Presentation of stage 2 lymes disease

A

Early disseminated infections (weeks - months)
One or more organ systems involved - hematological or lymphatic spread
MSK and neurological involvement most common
Neurological involvement in 10 - 15% of untreated patients
- mononeuropathy
- mononeurtis multiplex
- painful radiculoneuropathy
- cranial neuropathy
- myeltiis
- meningo-encephalitis
PNS > CNS

69
Q

When does stage 3 lymes disease occur?

A

Chronic infection - months to years

Occurring after a period of latency

70
Q

Presentation of stage 3 lymes disease

A

MSK and neurological involvement most common
Neurological involvement as per stage 2 plus
- subacute encephalopathy
- encephalomyeltiis

71
Q

Does stage 3 lymes disease cause chronic fatigue syndrome?

A

NO

72
Q

Investigations for lymes disease

A 
Serological testing
CSF Lymphocytosis
PCR of CSF
MRI brain spine if CNS involvement 
Nerve conduction studies/EMG if PNS involvement
73
Q

Treatment of lymes disease

A

IV ceftrixazone

Oral doxycycline

74
Q

Stages of syphillis

A

Primary
Secondary
Latent

75
Q

What stage of syphillis can affect the CNS? When does this occur?

A 
Tertiary disease (neurosyphillis) 
Years / decades after primary disease
76
Q

Investigations of syphillis

A

Treponema specific and non teponema specific (VDRL) antibody tests
CSF lymphocytes increased
Evidence of intrathecal antibody production
PCR

77
Q

Treatment of syphillis

A

High dose penicillin

78
Q

What is poliomyelitis caused by?

A

Poliovirus types 1, 2 or 3

79
Q

What % of poliomyelitis infections are asymptomatic? What happens to the symptomatic group?

A

99%

1% symptomatic - paralytic disease as infects anterior horn cells of LMNs

80
Q

Presentation of symptomatic poliomyelritis

A

Asymmetric, flaccid paralysis, especially on the legs

No sensory features

81
Q

In the UK, what is done to prevent poliomyelitis?

A

Polio immunization against all 3 poliovirus types

82
Q

What is rabies?

A

Acute infectious diseases of the CNS affecting almost all mammals

83
Q

How are rabies transmitted from animal to human?

A

Bite

Salivary contamination of an open lesion

84
Q

Features of the rabies virus

A

Neurotropic

Virus enters peripheral nerves and migrates to the CNS

85
Q

Presentation of rabies

A

Paraesthesia at site of original lesion
Ascending Paralysis
Encephalitis

86
Q

Investigations of rabies encephalitis

A

No useful diagnostic tests before clinical disease apparent
Culture
Detection or serology

87
Q

What animals often carry rabies?

A

Dogs in Asia/Africa

Bats in developed world

88
Q

What can be done for rabies pre-exposure prevention?

A

Active immunization with killed vaccine

89
Q

Who is the rabies vaccine given to in the UK?

A

Bat handlers
Regular handlers of imported animals
Selected travelers to enzoonotic areas

90
Q

Rabies post exposure treatment

A

Wash wound
Give active rabies immunisation
Give human rabies immunoglobulin (passive immunisation) if high risk

91
Q

What is the causative organism of tetanus?

A

Clostridium tetani

92
Q

Pathology of tetanus

A

Toxin acts at the NMJ

Blocks the inhibition of motor neurones

93
Q

Presentation of tetanus

A

Rigidity and spam (risus sarconicus)

94
Q

Prevention of tetanus

A

Immunisation (toxoid)
Given combined with other antigens (DTaP)
Penicillin and immunoglobulin for high risk wounds/patients

95
Q

What is the causative organism for botulism?

A

Clostridium Botulinium

96
Q

Pathology of botulism

A

Neurotoxin binds irreversibly to the presynaptic membranes of peripheral neuromuscular autonomic nerve junctions
Toxin binding blocks acetylcholine release
Recovery is by sprouting new axons

97
Q

Where is clostridium botulinium naturally present?

A

Soil
Dust
Aquatic environments

98
Q

Three modes of infection of clostridium botulinium

A

Infantile (intestinal colonisation)
Food-borne (outbreaks)
Wound; almost exclusively injecting or “popping” drug users

99
Q

Presentation of botulism

A

Incubation period 4-14 days
Descending symmetrical flaccid paralysis
Pure motor
Resp failure
Autonomic dysfunction - usually pupil dilation

100
Q

Investigations of botulism

A

Nerve conduction studies
Mouse neutralisation bioassay for toxin in the blood
Culture from debrided woud

101
Q

Treatment of botulism

A

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

102
Q

Example of a CNS post infective inflammatory syndrome

A

Acute disseminated encephalomyeltitis (ADEM)

103
Q

Example of a PNS post infective inflammatory syndrome

A

Guillian Barre Syndrome (GBS)

104
Q

What does CJD stand for?

A

Cretuzfeldt-Jakob Disease

105
Q

Types of CJD

A

Sporadic
New variant
Familial
Acquired

106
Q

How do patients get acquired CJD?

A

Cadaveric growth hormone
Dura mater grafts
Blood transfusion

107
Q

Who should sporadic CJD be considered in?

A

Rapidly progressive dementia

108
Q

Presentation of sporadic CJD

A 
Insidious onset (usually older than 60) 
Early behavioral abnormalities
Myoclonus
Rapidly progressive dementia
Motor abnormalities 
- cerebellar ataxia
- extrapyramidal 
- pyramidal 
Cortical blindness 
Seizures may occur
109
Q

Features of extrapyramidal motor abnormalities

A

Tremor
Rigidity
Bradykinesis
Dystonia

110
Q

Features of pyramidal motor abnormalities

A

Weakness
Spasticity
Hyper-reflexia

111
Q

Differential diagnosis of sporadic CJD

A

Alzheimer’s disease with myoclonus - usually more prolonged
Subacute sclerosing panencephalitis (SSPE)
CNS vasculitis
Inflammatory encephalopathies

112
Q

Prognosis of sproadic CJD

A

Rapid progression

Death often within 6 months

113
Q

What age do people get new variant?

A

< 40 y/o (usually < 25 y/o)

114
Q

How do people get new variant CJD?

A

Linked to Bovine Spongiform Encephalopathy in cattle

- eating infected material

115
Q

Investigations of CJD

A 
MRI
- pulvinar sign in variant CJD 
- no specific changes in sporadic CJD
EEG
- generalised periodic complexes typical 
CSF
- normal or raised protein 
- immunoassay 14-3-3 brain protein (non specific but helpful in a clinical context)
116
Q

What lobes does HSV encephalitis tend to affect?

A

Temporal lobes

Inferior frontal lobe

117
Q

Presentation of HSV encephalitis

A 
Fever
Headache
Psychiatric symptoms
Seizures
Vomiting
Focal features e.g. aphasia
118
Q

What is CJD caused by?

A

Prion proteins

119
Q

Features of CJD

A

Rapidly progressive dementia

Myoclonus

120
Q

Investigations of CJD

A

CSF = normal
EEG
MRI

121
Q

Presentation of new variant CJD

A 
Younger patients
Psychological symptoms
- anxiety
- withdrawal 
- dysphonia
122
Q

Median survival for new variant CJD

A

13 months

123
Q

What is the most common complication of meningitis?

A

Sensorineural hearing loss

Neuro Pathology (21 decks)

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