Infections of the Nervous System Flashcards

1
Q

Define Meningitis

A

Inflammation/infection of meninges

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2
Q

What is the classic triad of meningitis

A

Fever
Neck stiffness
Altered mental status

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3
Q

What is the clinical features associated with meningitis

A

Short history of a
Progressive headache with fever and meningism

Cerebral dysfunction

Cranial nerve palsy

seizures

focal neurological deficits

Petechial skin rash

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4
Q

A tumbler test indicates a petechial skin rash, what does this usually indicate

A

Meningococcal meningitis

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5
Q

What is the differential diagnosis for meningitis

A

Infective

Inflammatory - sarcodosis

Drug induced (NSAIDs, IVIG)

Malignant

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6
Q

What bacterial cause meningitis

A
Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)
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7
Q

What virus cause meningitis

A

enteroviruses

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8
Q

Define encephalitis

A

Inflammation/ infection of brain substance

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9
Q

What is the clinical features of encephalitis

A

Flu like prodrome

Progressie headache with associated fever

Progressive cerebral dysfunction

seizures

focal symptoms

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10
Q

What is the similarities to encephalitis and meningitis

A

Both have classic triad of meningism symptoms but encephalitis has more brain problems and is a more prominent feature

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11
Q

What is the differential diagnosis of encephalitis

A

Infective - viral

Inflammatory
(limbic encephalits,
Acute disseminated encephalomyelitis)

Metabolic
(Hepatic, uraemic, hyperglycaemic)

malignant
(metastatic, paraneoplastic)

migraine

After seizure

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12
Q

What is the most common cause of encephalitis

A

Herpes simplex virus

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13
Q

What are two important antibodies causing autoimmune encephalitis

A

Anti VGKC (voltage gates potassium channel)

Anti NMDA receptor

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14
Q

What is the the investigation for meningitis

A

Blood cultures (bacteraemia)

Lumbar puncture (CSF culture/microscopy)

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15
Q

When would imaging be needed in investigating meningitis

A

If there was contradictions to lumbar puncture

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16
Q

What is the CSF finding in Bacterial meningitis

A

Increased opening pressusre

High cell count - mainly neutrophils

Reduced glucose

High protein

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17
Q

What is the CSF findings in viral meningitis

A

Opening pressure is normal or increased

High cell count- mainly lymphocytes

Normal glucose levels

Protein slightly increased

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18
Q

What occurs after CSF findings

A

Gram stain and culture

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19
Q

how is bacterial meningitis diagnosed from gram stain and culture (blood/CSF)

A

Gram stain shows - gram positive cocci in chains

= streptococci

Culture and check is allergic to penicillin

= streptococcus pneumonia

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20
Q

What is the first line treatment for suspected meningitis

A

IV ceftriaxone

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21
Q

What is the investigations for encephalitis

A

Blood culture

Imaging (CT scan +/- MRI)

Lumbar punture

EEG

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22
Q

What is first line treatment of suspected herpes simplex encephalitis

A

Aciclovir

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23
Q

How do you specifically diagnose herpes simplex encephalitis

A

Lab diagnosis by PCR of CSF for viral DNA

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24
Q

Where does herpes simplex virus lay dormant after primary infection

A

Trigeminal or sacral ganglion

then patients is always affected with virus becoming active again when patient is under immune pressure

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25
Q

Enterovirus, has a tendency to cause what

A

CNS infections

eg non -paralytic meningitis

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26
Q

How do enteroviruses spread

A

Faecal-oral route

no animal reservoir - only human

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27
Q

How do diagnose enterovirus

A

Stool sample

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28
Q

What additional virus groups can cause encephalitis

A

Arbovirus encephalitis which is transmitted to man by a non human vector

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29
Q

What part of the history is important in arbovirus encephalitis

A

Travel history

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30
Q

Arborvirus encephalitis organisms are named dependant on where they were first described, name 5 arbovirus encephalitis

A

West Nile virus

St Louis Encephalitis

Western Equine
Encephalitis

Tick Borne Encephalitis

Japanese B Encephalitis

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31
Q

Define Brain abscess

A

localized area of pus within the brain

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32
Q

Define subdural empyema

A

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

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33
Q

What is the symptoms of brain abscess

A

Fever

headache

Focal symptoms

Papilloedema

Depressed conscious level

Meningism

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34
Q

What symptoms are particulate present in empyema

A

Meningism

  • neck stiffness, -photophobia,
  • headache
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35
Q

What is the pathological affect of brain abscess and subdural empyemma

A

Raised intracranial pressure

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36
Q

What is the differential diagnosis of brain abscess and empyema

A

Any focal lesion - tumour

Subdural haematoma

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37
Q

What is the potential causes of brain abscess and empyema

A

Penetrating head injury

Spread from adjacent infection

Blood borne infection
e.g. Bacterial endocarditis

Neurosurgical procedure

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38
Q

How do you diagnose brain abscess and empyema

A

Imaging: CT or MRI

investigate source

blood cultures

Biopsy (drainage of pus)

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39
Q

What is the contradiction with taking a biopsy in brain abscess diagnosis

A

Depends where abscess is as brain stem has a higher threshold for taking biopsy compared to the periphery

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40
Q

What is the microbiology of brain abscess

A

Often a mixture of organisms present

Streptococci:
“strep milleri” group

Anerobes:
Bacteriodes, prevotella

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41
Q

What is the management of brain abscess

A

Surgical drainage

Antibiotics

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42
Q

What antibiotics are given in brain abscess based on the microbiology

A

Streps - penicillin or ceftriaxone

Anaerobes - metronidazole

High dose required for penetration

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43
Q

What gives a useful guid on how to manage brain abscess

A

Culture and sensitive tests on aspirate sample

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44
Q

What are three different forms of streptococci in the penicillin sensitive strep milleri group

A

Strep anginosus,
strep intermedius ,
strep constellatus

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45
Q

What is the characteristic of strep miller groups

A

Causes many abscess elsewhere

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46
Q

What are 8 examples of neurological illnesses that can result from HIV

A

Cerebral toxoplasmosis

Aseptic meningitis /encephalitis

Primary cerebral
lymphoma

Cerebral abscess

Cryptococcal meningitis

Space occupying lesion of unknown cause

Dementia

Leucoencephalopathy

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47
Q

What cells does the HIV virus affect, and what does this result in

A

HIV virus kills CD4 cells, this result in HIV patients becoming immunocompromised

48
Q

What is the main cause of morality in HIV patients

A

Opturmistic infection on the immunocompromised patient

49
Q

What are the brain infection that can occur in a HIV patient with low CD4 count

A

Cryptococcus neoformans

Toxoplasma gondii

Progressive multifocal leukoencephalopathy (PML)

Cytomegalovirus (CMV)

HIV-encephalopathy

50
Q

What brain infections can lead to HIV associated dementia

A

HIV - encephalopathy

51
Q

What is the diagnostic for infection in HIV patients

A

India Ink, cryptococcal antigen

Toxoplasmosis serology (IgG)

JC virus PCR

CMV PCR

HIV PCR

52
Q

What is the JC virus an early indication of

A

Progressive leukoecnephalopathy

53
Q

What is the main cause of cryptococcal infection

A
Cryptococcal neoformans (in soil and avian habitats) and rarely C.gatti (trees)
Inhaled as airborne organisms (spores and yeast) into the lungs
54
Q

What is the clinical presentation of cryptococcal infections

A

Patient present with Cryptococal Meninigencephalitis

Has defects in immune function

55
Q

What is a major risk factor in cryptococcal infections

A

AIDS

56
Q

How do you diagnose cryptococcal infections

A

Mucicarmine stain
-pink stained fungi

India ink stain
-add drop to CSF, blue stain to confirm the morphology

57
Q

Name three spirochetes disease (spiral twisted bacteria) in the CNS

A

Lyme disease
Syphilis
Leptospirosis

58
Q

What causes Lymes

A

The bacterial species borrelia burgdorferi which is found in ticks

59
Q

How does lymes disease become a multi system disease

A

due to Skin, rheumatological, neurological / neuropsychiatric, cardiac and ophthalmological involvement

60
Q

What can be seen in stage 1 lymes disease (

A

Early localised infection

Characterised by expanding rash at the site of the tick bite

Flu like symptoms

61
Q

What occurs in stage 2 lymes disease

A

Early disseminated infection

One or more organ system become involved

Musculoskeletal and neurological involvement most common

62
Q

How does lymes disease spread from stage 1 to stage 2

A

haematological or lymphatic spread

63
Q

What does the neurological involvement of lymes disease potentially cause

A

Mononeuropathy

Mononeuritis multiplex	
(peripheral neuropathy)	

Painful radiculoneuropathy

Cranial neuropathy

Myelitis

Meningo-encephalitis

64
Q

What occurs in stage 3 lymes disease

A

Chronic infection
(months - years, or occurring after period of latency)

musckuloskeletal and further neurological involvement

does not cause chronic fatigue symptoms

65
Q

What is the further neurological involvement in stage 3 lymes disease

A

Subacute encephalopathy

Encephalomyelitis

66
Q

What is the overall investigations for Lymes 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)

67
Q

What is the treatment of lymes disease

A

Prolonged antibiotic treatment (3-4 weeks)

Intravenous cefrtriaxone

oral doxycycline

68
Q

What cause syphilis

A

The spirochaete bacterium treponema pallidum

69
Q

How many stage presentation does syphils have

A

Primary
Secondary
Latent /tertiary

70
Q

When does syphilis become neurosyphilis

A

In the territory disease, years and decades later after primary disease

71
Q

How do you diagnose syphilis

A

Serology-Treponema specific and non-treponemal specific (VDRL) antibody tests

PCR

72
Q

What is indication of syphilis in testing

A

CSF lymphocytes increased

Evidence of intrathecal antibody production (CSF)

73
Q

What is the treatment for syphilis

A

High dose penicillin

74
Q

What is the cause of leptospirosis

A

The spirochaete bacterium leptospira interrogans

75
Q

What is 3 important vaccines for the the nervous system

A

Polio immunisation

Rabies immunisation

Tetanus immunisation

76
Q

What causes poliomyelitis

A

Poliovirus types 1,2 and 3 which are all enteroviruses

77
Q

99% of poliovirus infections are asymptomatic, what happens in the 1%

A

Paralytic disease as affects the anterior horn cells of the lower motor neurones

78
Q

What is the symptoms of poliomyelitis

A

Asymmetric
flaccid paralysis especially legs

no sensory features

79
Q

What occurs in rabies, and how does it occur

A

Acute inflammation disease of CNS affecting almost all mammals, transmitted to human by bite or salivary contamination of open lesion

80
Q

How is rabies a neurotropic virus

A

enters peripheral nerves and migrates to the CNS

81
Q

What is the effect of rabies

A

Parathesia at site of original lesson

ascending paralysis and encephalitis

82
Q

How do you diagnose rabies encephalitis

A

Culture
detection
serology

No useful diagnostic test before clinical disease is apparent

83
Q

How do we prevent rabies

A

Rabies pre-exposure prevention through active immunisation with killed vaccine

84
Q

Who is given rabies immunisation

A

bat handlers

regular handlers of imported animals

selected travellers to enzootic areas

85
Q

What is the treatment of rabies post exposure

A

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

86
Q

What causes tetanus

A

Infection of clostridium tetani - an aerobic gram positive bacillus (spore forming) coming into contact with a wound

87
Q

What is the pathology of tetanus

A

The bacterium releasing toxin at nerve-muscular junction blocking the inhibition of motor neurones

resulting in rigidity and spasms

88
Q

How is tetanus prevented

A

Immunisation which contains toxoid and combined with other antigens (DTaP)

89
Q

What is given to high risk wound/patients for prevention of tetanus

A

Penicillin and immunoglobulin

90
Q

What causes botulism

A

Clostridium botulinum

an anaerobic spore producing gram postive bacillus naturally present in soil, dust and aquatic environment

91
Q

What is the affect of clostridium botulinium

A

Is a neurotoxin
Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
and toxin binding blocks acetylcholine release

92
Q

How does the nervous system recover form the neurotoxin affects of botulism

A

Recovery is by sprouting new axons

93
Q

What is the three modes of infection from clostridium botulinum

A

Infantile (intestinal colonization)

Food-borne (outbreaks)

Wound: Almost exclusively
injecting or “popping” drug users

94
Q

What is the symptoms of botulism

A

Descending symmetrical flaccid paralysis

Respiratory failure

Autonomic dysfunction

95
Q

How do you diagnose botulism

A

Nerve conduction studies

Mouse neutralisation bioassay for toxin in blood

Culture from debrided wound

96
Q

How long is the incubation period for botulism

A

4-14 days

97
Q

What is the treatment for botulism

A

Anti-toxin (A,B,E)

Penicillin / Metronidazole (prolonged treatment)

Radical wound debridement

98
Q

What is a post infective inflammatory syndrome of the CNS

A

Acute disseminated encephalomyelitis (ADEM)
- rare autoimmune disease marked by a sudden, widespread attack of inflammation in the brain and spinal cord (encephalitis)

99
Q

What is a post infective inflammatory syndrome of the PNS

A

Gullian barre syndrome
-an acute autoimmune disorder of the peripheral nerves, often preceded by a respiratory infection, causing weakness and often paralysis of the limbs (radiculoneuropathy)

100
Q

How does post infective inflammatory syndromes arise

A

Due to preceding infection (viral, bacterial) or through immunisation

causing a latent arrival between precipitating infections and onset of neurological symptoms due to autoimmune disorder

101
Q

What is the cause of Creutzfeldt-Jakob Disease (CJD)

A

Prion - a transmissible proteinaceous particle

disease causing small infectious particle

102
Q

What is the aetiology of Creutzfeldt-Jakob Disease (CJD) prion

A

Sporadic CJD

New variant CJD

Familial CJD (10-15%)

Acquired CJD (<5%)

103
Q

What aetiology of CJD is considered in rapid progressive dementia

A

Sporadic CJD

104
Q

What is the clinical presentation of sporadic CJD

A

Insidious onset - gradual with detrimental affects

Early behavioural abnormalities

Rapidly progressive dementia

Myoclonus

Progressing to global neurological decline

Motor abnormalities

cortical blindness

seizures

105
Q

What is the motor abnormalities seen in CJD

A

Cerebellar ataxia - loss of movement

Extrapyramidal:
tremor, rigidity, bradykinesis, dystonia

Pyramidal: weakness, spacticity, hyper-refexia

106
Q

What is a differential diagnosis to sporadic CJD

A

Alzheimer’s disease with myoclonus

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

CNS vasculitis

Inflammatory encephalopathies

107
Q

What is the difference between sporadic CJD and Alzheimer’s

A

Alzheimers us usually more prolonged

108
Q

What is the prognosis of sporadic CJD

A

Rapid progression

Death often within 6 months

109
Q

When is usually the onset for sporadic CJD

A

Over 60 years

110
Q

What is the difference between new variant CJD and sporadic CJD

A

New variant CJD has younger onset (<40 years)

early behavioural changes more prominent

Longer prognosis course - average 13 months

may be genetically susceptibility

111
Q

What is new variant CJD linked to

A

Bovine spongiform encephalopathy in cattle

- eating this infected material

112
Q

What is the investigations for CJD

A

MRI
EEG
CSF

113
Q

What can be seen in a MRI of CJD

A

Pulvinar sign in variant CJD

Often no specific changes
in sporadic CJD

114
Q

What is typical in an EEG of CJD

A

Generalised periodic
complexes

Often normal / non-specific in initial stages

115
Q

What can be seen in a CSF sample of CJD

A

Normal or raised protein

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

116
Q

How does acquired CJD arise

A
  • Cadeveric Growth Hormone
  • Dura matter grafts
  • Blood transfusion