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Nervous System > Infections of the Nervous System > Flashcards

Infections of the Nervous System Flashcards

1
Q

Clinical features of encephalitis

A 
Flu-like symptoms for 4-10 days 
Fever and progressive headache 
Progressive cerebral dysfunction - confusion, abnormal behaviour, memory disturbance, depressed conscious level 
Seizures 
Focal signs
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2
Q

Differential diagnoses for encephalitis

A 
Infective e.g. viral 
Inflammatory e.g. limbic encephalitis 
Metabolic e.g. uraemic 
Malignancy e.g. metastases 
Migraine 
Post-ictal
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3
Q

Antibodies present in autoimmune encephalitis

A

Anti-VGKC and anti-NMDA receptor antibodies

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4
Q

Features of Anti-VGKC autoimmune encephalitis

A

Frequent seizures
Amnesia
Altered mental state

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5
Q

Features of Anti-NMDA receptor autoimmune encephalitis

A 
Flu-like prodrome 
Prominent psychiatric features 
Altered mental state 
Seizures 
Progression to movement disorder and coma
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6
Q

How is encephalitis caused by HSV (herpes simplex virus) diagnosed?

A

Lab diagnosis by PCR of CSF for viral DNA

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7
Q

Treatment of encephalitis caused by HSV

A

Acyclovir on strong clinical suspicion

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8
Q

Morbidity/mortality rate of encephalitis caused by HSV

A

over 70% mortality and high morbidity if untreated

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9
Q

Where does the HSV lie latent after primary infection and what does this mean there is a risk of?

A

Lies latent in trigeminal or sacral ganglion after primary infection, risk of reactivation

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10
Q

Investigation of encephalitis

A

Blood cultures
Imaging - CT, MRI
LP
EEG

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11
Q

Encephalitis treatment

A

Acyclovir

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12
Q

What is a brain abscess?

A

Localised area of pus within the brain which causes high-pressure symptoms

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13
Q

When would a fever be present in brain abscess?

A

If there was systemic infection

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14
Q

Clinical features of brain abscess

A 
Fever 
Headache 
Seizures 
Dysphasia 
Hemiparesis 
Papilloedema 
False localising signs 
Depressed conscious level 
Meningism 
Features of underlying source of infection e.g. poor dentition
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15
Q

Differential diagnoses for brain abscess

A

Any focal lesion, most commonly a tumour

Subdural haematoma

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16
Q

Causes of brain abscess

A

Penetrating head injury
Spread from adjacent infection e.g. dental, sinusitis
Blood borne infection e.g. bacterial endocarditis
Neurosurgical procedure

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17
Q

Brain abscess investigation

A

MRI, CT
Investigate source
Blood cultures
Biopsy

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18
Q

What is the risk of a biopsy of a brain abscess?

A

Drainage of pus and removal of needle puts patient at risk of spread of infection

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19
Q

Infective organisms in brain abscess

A

Streptococci - 70%, especially streptococcus Milleri group

Anaerobes

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20
Q

Treatment of brain abscess

A

Surgical drainage if possible
Penicillin or ceftriaxone to cover strep infection
Metrondiazole for anaerobe infection

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21
Q

What is meningitis?

A

Inflammation/infection of the meninges

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22
Q

Clinical features of meningitis

A 
Fever, neck stiffness, altered mental status 
Short history of progressive headache 
May be associated with fever and meningism 
Cerebral dysfunction 
Cranial nerve palsy 
Seizures 
Focal neurological deficits 
Petechial skin rash
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23
Q

Differential diagnoses of meningitis

A

Infective - bacterial, viral or fungal
Inflammatory - sarcoidosis
Drug induces - NSAIDs, IVIG
Malignant - metastatic, haematological

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24
Q

Causes of meningitis

A

Bacterial

Viral (enteroviruses)

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25
Q

Bacterial organisms that cause meningitis

A

Neisseria meningitidis

Streptococcus pneumoniae

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26
Q

Investigation of meningitis

A

Blood cultures

Lumbar puncture

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27
Q

Opening pressure in LP of bacterial meningitis

A

Increased

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28
Q

Opening pressure in LP of viral meningitis and encephalitis

A

Normal or increased

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29
Q

Cell count in LP of bacterial menignitis

A

High, mainly neutrophils

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30
Q

Cell count in LP of viral meningitis

A

High, mainly lymphocytes

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31
Q

Glucose in LP of bacterial meningitis

A

Reduced

32
Q

Glucose in LP of viral meningitis

A

Normal

33
Q

Protein in LP of bacterial meningitis

A

High

34
Q

Protein in LP of viral meningitis

A

Slightly increased

35
Q

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
36
Q

Brain infections in HIV patients with low CD4 counts

A 
Cryptococcur neoformans 
Toxoplasma gondii 
Progressive multifocal Leukoencephalopathy 
Cytomegalovirus 
HIV encephalopathy
37
Q

How are cryptococcal infections established?

A

Following inhalation of airborne organisms into the lungs

38
Q

How do most cases of cryptococcal infections present?

A

With meningoencephalitis

Most patients will have defects in immune function

39
Q

Spirochaete infections in the CNS

A

Lyme disease
Syphilis
Leptospirosis

40
Q

Causative organism of Lyme disease

A

Borrelia burgdorferi

41
Q

How is Lyme disease transmitted

A

Vector borne via ticks

42
Q

What parts of the body are affected by Lyme disease?

A 
Multi-system involvement 
Skin 
Rheumatological 
Neurological/neuropsychiatric 
Cardiac
Opthalmological
43
Q

Consequence of untreated Lyme disease

A

80% will develop disseminated disease

44
Q

Describe stage 1 Lyme disease

A

Early localised infection 1-30 days
Expanding rash at site of tick bite - erythema migrans
Flu-like symptoms (50%) - fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness

45
Q

Treatment of stage 1 Lyme disease

A

doxycycline

46
Q

Describe stage 2 Lyme disease

A

Early disseminated infection (weeks-months)
One or more organ systems become involved - haematological or lymphatic spread
Musculoskeletal and neurological involvement most common

47
Q

Possible presentations of neurological involvement in Lyme disease

A 
Meningo-encephalitis 
Cranial neuropathy 
Painful radiculopathy 
Plexopathy 
Diffuse or focal mononeuritis multiplex 
Mononeuropathy 
Myelitis
48
Q

Describe stage 3 Lyme disease

A

Chronic infection months - years, occurring after a period of latency
Musculoskeletal and neurological involvement most common
Neurological involvement - subacute encephalopathy, encephalomyelitis

49
Q

Investigation of Lyme disease

A 
Serological tests 
CSF lymphocytosis 
PCR of CSF 
MRI brain/spine if CNS involvement 
Nerve conduction studies/EMG if PNS involvement
50
Q

Lyme disease treatment

A

Prolonged antibiotic treatment IV, 3 weeks-1 month
IV ceftriaxone
Oral doxycyclin

51
Q

Treatment of neurosyphilis

A

High dose penicillin

52
Q

Aetiologies of Creutzfeldt-Jakob disease (CJD)

A

Sporadic
New variant
Familial
Acquired

53
Q

Clinical features of sporadic CJD

A 
Rapidly progressive dementia 
Insidious onset, usually over 60s 
Behavioural abnormalities 
Myoclonus 
Global neurological decline 
Motor abnormalities 
Cortical blindness 
Seizures
54
Q

Sporadic CJD differential diagnoses

A 
Alzheimer's disease with myoclonus 
Subacute sclerosing panencephalitis 
CNS vasculitis 
Non-convulsive status 
Toxic/metabolic encephalopathies
55
Q

Sporadic CJD prognosis

A

Rapid progression

Death, often within 6 months

56
Q

Features of new variant CJD

A

Younger onset (< 40)
Linked to bovine spongiform encephalopathy in cattle - eating infected material
Early behavioural changes more prominent
Longer course, around 13 months

57
Q

Investigation of CJD

A

MRI - Pulvinar sign present in variant CJD, often no specific signs in sporadic CJD
EEG - generalised periodic complexes typical, often normal/non-specific in early stages
CSF - normal or raised protein

58
Q

Cause of poliomyelitis

A

Polioviruses type 1, 2 and 3 (enteroviruses)

59
Q

What percentage of poliomyelitis will result in paralytic disease?

A

1%, 99% are asymptomatic

60
Q

Features of poliomyelitis

A

Infects anterior horn cells of lower motor neurones
Asymmetric, flaccid paralysis, especially of the legs
No sensory features

61
Q

Transmission of rabies

A

By bite or salivary contamination of an open lesion

62
Q

Features of rabies

A

Virus enters peripheral nerves and migrates to CNS
Paraesthesiae at the site of the original lesion
Ascending paralysis and encephalitis

63
Q

Diagnosis of rabies encephalitis

A

Culture
Detection
Serology

64
Q

Treatment of rabies encephalitis

A

Condition has 100% mortality, sedation and intensive care

65
Q

Main sources of rabies encephalitis

A

Dogs and bats

66
Q

How is rabies pre-exposure prevention carried out?

A

Active immunisation with killed vaccine

67
Q

Rabies post-exposure treatment

A

Wash wound
Give active rabies immunisation
Give human rabies immunoglobulin if high risk

68
Q

Organism causing tetanus

A

Clostridium tetani

Anaerobic gram-positive bacillus, spore forming

69
Q

Clinical features of tetanus

A

Rigidity and spasm

70
Q

Treatment of tetanus

A

Immunisation combined with other antigens

Penicillin and immunoglobulin for high risk wounds/patients

71
Q

Infective organism causing botulism

A

Clostridium botulinum

Anaerobic sporre producing gram positive bacillus

72
Q

How does clostridium botulinum work?

A

Neurotoxin, binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
Toxin binding block ACh release

73
Q

Modes of infection of clostridium botulinum

A

Infantile
Food-borne
Wound

74
Q

Clinical presentation of botulism

A 
Incubation period 4-14 days 
Descending symmetrical flaccid paralysis 
Pure motor 
Respiratory failure 
Autonomic dysfunction
75
Q

Botulism diagnosis

A

Nerve conduction studies
Mouse neutralisation bioassay for toxin in blood
Culture for debrided wound

76
Q

Botulism treatment

A

Anti-toxin
Penicillin/metronidazole
Radical wound debridement

Nervous System (44 decks)

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