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Nervous System > Infections of the nervous system > Flashcards

Infections of the nervous system Flashcards

1
Q

what is meningitis?

A

inflammation / infection of meninges

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2
Q

what is encephalitis?

A

inflammation / infection of brain substance

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3
Q

what is myelitis?

A

inflammation / infection of spinal cord

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4
Q

what are 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 (>38º) and
Meningism (neck stiffness, photophobia, nausea and vomiting)
Neck stiffness is examined by passively bending the neck forward

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

Look for a petechial skin rash (Tumbler test)
hallmark of meningococcal meningitis, but can also occur in viral meningitis

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5
Q

what is the classid triad of symptoms for meningitis?

A

fever, neck stiffness and altered mental status

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6
Q

what test is used to check for a rash in meningitis?

A

Tumbler test

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7
Q

what typpe of rash is seen in meningitis?

A

petechial skin rash

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8
Q

what are 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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9
Q

what are bacterial causes of meningitis?

A

Neisseria meningitidis (meningococcus)
Streptococcus pneumoniae (pneumococcus)

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10
Q

what are viral causes of meningitis?

A

enteroviruses

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11
Q

what are clinical features of encephalitis?

A

Flu-like prodrome (4-10days)

Progressive Headache associated with fever
+/- meningism
Progressive cerebral dysfunction
Confusion
Abnormal behaviour
Memory disturbance
Depressed conscious level
Seizures
Focal symptoms / signs

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12
Q

how does the onset of viral encephalitis compare to bacterial meningitis?

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 are differential diagnosis of 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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14
Q

what is auto-immune encephalitis?

A

acute to subacute, progressive inflammation of the brain associated with antibodies against neuronal cell surface and synaptic protein, most commonly being anti - NMDA receptor encephalitis

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15
Q

what is anti-VGKC auto-immune encephalitis?

A

Anti-VGKC-complex encephalitis are caused by antibodies against the voltage gated potassium channel-complex (VGKC-complex) and are implicated in several autoimmune conditions including limbic encephalitis, epilepsy and neuromyotonia (i.e. Isaacs’ Syndrome).

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16
Q

symptoms of Anti-VGKC (Voltage Gated Potassium Channel) autoimmune encephalitis?

A

Frequent seizures
amnesia (not able to retain new memories)
Altered mental state

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17
Q

what is anti-NMDA receptor encephalitis?

A

Anti-NMDA receptor encephalitis is a neurologic disease first identified by Dr. Josep Dalmau and colleagues at the University of Pennsylvania in 2007. It is an autoimmune disease, where the body creates antibodies against the NMDA receptors in the brain.

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18
Q

what are symptoms of Anti-NMDA receptor
auto–immune encephalitis?

A

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

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19
Q

what are investigations for meningitis?

A

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

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20
Q

what are investigations for encephalitis?

A

blood cultures
Imaging (CT scan +/- MRI)
Lumbar puncture
EEG

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21
Q

what are indications for CT brainscanning before lumbar puncture?

A

focal neurological deficit (cranial N palsies)
new onset seizures
abnormal levek conciousness
severe immunocomprimised state

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22
Q

what do Focal symptoms or signs suggest?

A

focal brain mass

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23
Q

what do reduced conciousness levels suggest?

A

raised intracranial pressure

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24
Q

describe the opening pressure, cell count, glucose and protein of CSF in bacterial meningitis?

A

increased
High - mainly neutrophils
reduced
high

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25
Q

describe the opening pressure, cell count, glucose and protein of CSF in viral meningitis and encephalitis?

A

normal/increased
High mainly lymphocytes
normal
slightly increased

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26
Q

which gram stains and cultures do you do for bacterial meningitis?

A

Blood culture Gram stain: Gram positive cocci in chains - looks like streptococci

Culture streptococcus pneumoniae sensitive to penicillin

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27
Q

what is herpes simplex encephalitis?

A

Relatively rare, but commonest cause of encephalitis in Europe
Lab diagnosis by PCR of CSF for viral DNA

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28
Q

how is herpes simplex virus encephalitis treated?

A

Treat with aciclovir on clinical suspicion

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29
Q

if HSV is left untreated what is the mortality rate?

A

Over 70% mortality and high morbidity if untreated

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30
Q

what is herpes simplex virus?

A

One of the herpes group of viruses (VZV, EBV, CMV)
HSV types 1 & 2 cause
cold sores (type 1&raquo_space; 2)
genital herpes (type 1 & 2)

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

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31
Q

which types of herpes is cold sores?

A

(type 1&raquo_space; 2)

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31
Q

which type of herpes is genital herpes?

A

(type 1 & 2)

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32
Q

what is a rare complication of HSV?

A

Encephalitis is a rare complication of HSV other than neonates, nearly all caused by type 1

33
Q

what do enteroviruses have a tendency of causing?

A

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

34
Q

how do enteroviruses spread?

A

faecal-oral route

35
Q

what conditions do enteroviruses cause?

A

Many can cause non-paralytic meningitis
They do NOT cause gastroenteritis
Include polioviruses, coxsackieviruses and echoviruses

36
Q

what is arbovirus encephalitides?

A

Common in other parts of the world

Variety of virus groups

Transmitted to man by vector (mosquito or tick) from non-human host e.g. :
West Nile virus
St Louis Encephalitis
Western Equine Encephalitis
Tick Borne Encephalitis
Japanese B Encephalitis

37
Q

by what mechanism is arbovirus encephalitides formed?

A

Called Arbo as arthropod borne
Relevant to travel
travel history important
some preventable by immunisation

Place names of organisms
generally relate to where first described and NOT to current geographical distribution

38
Q

what is a brain abscess?

A

localized area of pus within the brain

39
Q

what is subdural empyema?

A

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

40
Q

what are 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

41
Q

what is a differential diagnosis of brain abscess and empyema?

A

Any focal lesion, but most commonly tumour

Subdural haematoma

42
Q

what are causes of brain abcess and empyema?

A

Penetrating head injury
Spread from adjacent infection
Dental, Sinusitis, Otitis media
Blood borne infection
e.g. Bacterial endocarditis
Neurosurgical procedure

43
Q

how is brain abscess and empyema diagnosed?

A

imaging: CT or MRI

investigate source

blood cultures

Biopsy (drainage of pus)

44
Q

what organisms are ussually present in a brain abscess?

A

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

45
Q

what is management of 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

46
Q

what are indicator illnesses for HIV?

A

Cerebral toxoplasmosis
Aseptic meningitis /encephalitis
Primary cerebral lymphoma
Cerebral abscess

47
Q

what are you looking for in HIV patients with low CD4 counts?

A

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

48
Q

how do you diagnose HIV indicator illness patients?

A

Cryptococcal antigen
Toxoplasmosis serology
CMV PCR
HIV PCR

49
Q

how is spirochaetes in the CNS spread?

A

Lyme Disease (Borrelia burgdorferi)
Syphilis (Trepomena pallidum)
Leptospirosis (Leptospira interrogans)

50
Q

how is lyme disease borne?

A

Vector borne: Tick (wooded areas)

51
Q

what is the spirochate og lymes disease?

A

Borrelia burgdorferi

52
Q

what systems are involved in llymes diseaae?

A

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

53
Q

what is stage one of lymes disease?

A

Early localized infection (1-30d)

Characteristic expanding rash at the site of the tick bite: erythema migrans

50% flu like symptoms (days – 1 week)
Fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness

54
Q

what is stage 2 of lymes 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
Mononeuropathy
Mononeuritis multiplex
Painful radiculoneuropathy PNS > CNS
Cranial neuropathy
Myelitis
Meningo-encephalitis

55
Q

what is stage 3 of lymes 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

56
Q

how is lymes disease investigated?

A

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

57
Q

how is lymes disease treated?

A

Prolonged antibiotic treatment
intravenous ceftriaxone
oral doxycycline

58
Q

what three stages does neurosyphilis present as?

A

(Treponema pallidum)
primary
secondary
tertiary

59
Q

what tests are done for neurosyphilis?

A

Treponema specific and non-treponemal specific antibody tests

CSF lymphocytes increased, evidence of intrathecal antibody production

60
Q

how is neurosyphylis treated?

A

High dose penicillin

61
Q

what are causes of encephalitis?

A

Herpes Simplex
Enteroviruses
Arbovirus encephalitides
Brain Abscess and Empyema
HIV indicator illnesses (brain)
Lyme disease
Neurosyphilis

62
Q

what is poliomyelitis?

A

Caused by poliovirus types 1, 2 or 3
all enteroviruses
99% of infections are asymptomatic
Paralytic disease in ~1%
infects anterior horn cells of lower motor neurones
Asymmetric, flaccid paralysis, esp legs
No sensory features

63
Q

describe the polio immunisation?

A

In UK, both contain all three poliovirus types
UK 2004 changed from oral to injected vaccine
because of risk of vaccine-associated polio from oral vaccine
because indigenous polio due to wild (ie non-vaccine) polio eliminated from UK
given combined with other antigens (IPV)

64
Q

what is rabies?

A

Acute infectious disease of CNS affecting almost all mammals
Transmitted to human by bite or salivary contamination of open lesion
Neurotropic - virus enters peripheral nerves and migrates to CNS
Paraesthesiae at site of original lesion
Ascending paralysis and encephalitis

65
Q

what is rabies encephalitis?

A

No useful diagnostic tests before clinical disease apparent
Diagnosis: PCR and Serology
Sedation/intensive care/death
~ 40,000 - 50,000 deaths/year, mostly Asia
Important sources of human infection:
Dogs in Africa/Asia
Bats in the developed world.
2002: 1st indigenous case in UK since 1902 – bat handler.

66
Q

what is rpre exposure prevention for rabies?

A

Active immunisation with killed vaccine
In UK give to:-
bat handlers
regular handlers of imported animals
selected travellers to enzootic areas

67
Q

what is post exposure treatment for rabies?

A

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

68
Q

what is tetanus?

A

infection with Clostridium tetani
anaerobic Gram positive bacillus, spore forming
wound may not be apparent
toxin acts at neuro-muscular junction
blocks inhibition of motor neurones
rigidity and spasm (risus sardonicus)

69
Q

how is tetanus prevented?

A

Immunisation (toxoid)
given combined with other antigens (DTaP)

70
Q

what is given to patients at high risk of teanus?

A

Penicillin and immunoglobulin for high risk wounds/patients

71
Q

what is botulism?

A

Anaerobic spore producing gram positive bacillus
Neurotoxin
Binds irreversibly to the presynaptic membranes of peripheral neuromuscular and autonomic nerve junctions
Toxin binding blocks acetylcholine release
Recovery is by sprouting new axons
Naturally present in soil, dust and aquatic environments

72
Q

what are the three modes of infection or botulism?

A

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

73
Q

what is the clinical presentation for botulism?

A

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

74
Q

how is botulism diagnosied?

A

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

75
Q

how is botylism treated?

A

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

76
Q

what are post infective inflammatory syndromes?

A

Central nervous system
Acute disseminated encephalomyelitis (ADEM)

Peripheral nervous system
Guillain Barre Syndrome (GBS)

77
Q

what is Creutzfeldt-Jakob Disease (CJD)?

A

Aetiology
Sporadic CJD
New variant CJD
Familial CJD (10-15%)
Acquired CJD (<5%)
Cadeveric Growth Hormone
Dura matter grafts
Blood transfusion

78
Q

what are clinical features of CJD?

A

Clinical features
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, spacticity, hyper-refexia

Cortical blindness
Seizures may occur

79
Q

what are differential diagnosis of 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

80
Q

what is prognosis of sporadic CJD?

A

Rapid progression
Death often within 6 months

81
Q

what are investigations 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 initial stages

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

Nervous System (40 decks)

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