meningitis and encephalitis Flashcards

(83 cards)

1
Q

meningitis

A
inflammaton of the meninges 
aseptic meningitis (no organisms)
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2
Q

encephalitis

A

inflammation of the brain parenchyma

may be further refined anatoomically eg. cerebritis, cerebeillitis, rhombencephalitis

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3
Q

cerebritis

A

inflammation of the cerebrum

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4
Q

cerebellitis

A

inflmmmation of the cerebellum

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5
Q

rhombencephallitis

A

inflammation of the brainstem

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6
Q

meningoencephalitis

A

miningitis and encephalitis

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7
Q

myelitis

A

inflammation of the psinal cord

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8
Q

encephalomyelitis

A

encephalitis and myelitis

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9
Q

subdural empyema

A

collection of pus in the dural space between the meningies and the brain parenchyma
usually iatrogenic

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10
Q

pathogenesis of CNS infection

A

infectious agents must cross physical barriers (skull, vertebrae, meninges) and blood brain barrier
may occur due to
- trauma or surgery
- immature BBB and bloodstream infection
- direct invasion by organisms growing acrosss tissue planes eg. fungi, actinomyces
- virulence factors that cause invasion of CSSF or brain parenchyma (neurotropism)

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11
Q

neurotropism

A

organisms having virulence factors allowing them to cause infection in the CNS because they can invade CSF or brain parenchyma
many may have capsules which helps immune system invasion

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12
Q

classic triad of meningitis

A

fever
altered mental state - confusion or drowsiness
neck stiffness - nuchal rigidity.

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13
Q

meningism

A

nuchal rigidity with headache and photophobia

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14
Q

nuchal rigidity

A

neck stiffness

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15
Q

other symptoms of meningitis

A

cause and vomiting
other neurological abnormalities are less common
bacterial meningitis may also be accompanied by sepsis (tachycardia, hypotension)

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16
Q

chronic meningitis presents with

A

milld or fluctuating symptoms of meningitis, often without fever, and usually with some neurological abnormality

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17
Q

sequelae of meningitis

A
  • raised ntracranlial pressure
  • temporary or permanent neurological sequelae
  • following viral meningitiis, complete recovery is common
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18
Q

raised intracranial pressure

A

due to several oedema from inflammatory cytokines released by the immune system
causes headache, nausea and vomiting, papilloedema (bulging of the optic root)
may lead to herniation of the cerebellar tonsils through the foramen magnum leading to respiratory depression and death

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19
Q

temporary or permanent neurological sequelae

A
  • sezures
  • cranial nerve palsies, hemiparesis
  • sensorineural hearing loss
  • intellectual impairment
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20
Q

clinical featuress of encephalitiis

A

less common than meningits
presentation is smilar
headache, fever, nausea and vomiting
altered mental status is more prominent, and seizuresm focal neurological abnormalities are more common
- confusion, drowsiness/obtundation, agitation
permanent neurological sequelae are more common

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21
Q
  • focal neurological abnormalities in encephaliti
A
depends on the site of brain involvement 
weakness
hemiparesis 
speech and movement disorders 
abnormal reflexe 
personality change
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22
Q

how does encephalitis differ from meningitis clinciall

A

more prominent altering of mental status, seixzures and fical neurologcal abnormalities are more common
permanent neurological sequelae are more common

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23
Q

neisseria meningitidis

A

gram positive diplocci - meningococcus
can cause a rapdly fatal infection in previously healthy people in any age group - most commonly children and young adults
encapsulated
classified into serogroups
nasopharyngeal carriage is a precursor to onvasive infection
1-15% of healthy people carry the organism - usually non invasive strains

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24
Q

neisseria meningitidis spread by

A

person to person via contact with respiratory secretions

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25
invasive strain of neisseria meningitidis
spread of an invasive strain may cause outbreaks not everyone who is expossed willl get invasove infection most cases in WA are sporadic or in small clusters
26
serogroups of neisseria meningitidis
classified on the basis of capsular antigens | A, B, C, W, X, Y, Z
27
most common manifestations of invasive meningococcal disease
meningitis and bacteraemia (bloodstream) | patients may present with one or both
28
neisseria meningitidis bacteraemia
bacteraemia usually causes a rash due to low platlets petechiae (non-blanching, due to low platelets), purpura, ecchymoses mortality 13% even with treatment, other serious neurological or necrotic sequelae may result
29
less commonmenifestations of neisseria meningitidis
septic arthritis | pericarditis
30
less commonmenifestations of neisseria meningitidis
septic arthritis | pericarditis
31
treatment of neisseria meningitidis
5 days high-dose intravenous ceftriaxone
32
sequelae of invasive meningococcal disease
shock - hypotension purpura fulminans permanent neurological abnormalities less common than in other bacterial meningitidis outcome is hard to predict, but is probably better when treatment is initiated early
33
purpura fulminans
disseminated intravascular coagulation | thrombosis and haemorrhage leading to gangrenous necrosis of extremities requiring amputation
34
new common serogroup of meningococcal
serogroup W (and Y)
35
vaccination for meningococcal
routine meningococcal serogroup C introduced in australia in 2003 in 2018, changed to quadrivalent vaccine against serogroups A, C, W, Y serogroup B vaccine also available
36
contact tracing of meningococcal disease
when a case occurs, household and other close contacts are also at rissk of invasive maningococcal disease usually within 7 days giving antibiotics to contacts may prevent infection special meassures are used for patients in hospital to prevent the organism spreading to staff and othe rpatients
37
streptococcu pneumoniae
pneumococcus gram positve diplococci most common bacterial cause of community acquired pneumonia most common cause of bacterial meningitidis in older adults and indigenous australians nasopharyngeal carriage is very common and is a precursor to infection
38
pneumococcus
streptococcus pneumoniae
39
most common bacterial cause of community aquired pneumonia
streptococcus pneumoniae
40
strep pneumoniae immunisation
vaccine for infants, and regular boosters for indigenous people over 50 and all adults over 65
41
strep pneumoniae mortality
pften very aggresssive with treated mortality of 20-30% | treatment is with 10-14 days high-dose intravenous ceftriaxone
42
listeria monocytogenes
gram-positive bacillus | listera infection may be asymptomatic or cause a non-specific, self-limiting febrile illness
43
lsteria monocytogenes in pregnancy
usually mild but can lead to amniotic infection and fetal loss
44
listeria monocytogenes outbreaks
not a commensal organism, outbreaks associated with contaminated vegetables, cold meats, salads, milk, cheese
45
CNS listeria infection
rare in healthy young adults rsk of CNS infection increases with immunocompromise and age oover 50 usually causes and miningoencephalitis
46
treatment of listeria monocytogenes
not treatable by ceftriaxone, needs different antibiotics
47
most common causes of bacterial meningitidis in neonates
S. agallactiae (GBS) E coli other gram negative bacillii listeria
48
mot common causes of bacterial meningitis in children
N meningitidis S pneumoniae H influenzeae serotype B
49
most common cause of bacteral meningitidis in young adults
N meningitidis | S pneumoniae
50
most common cause of bacterial meningitidis in older adults
S pneumoniae N meningitidis listeria
51
bacterial meningitis in neonates
more common in the first month of life than at any other time 10-15% mortality, with neurological sequelae common the neonatal immune system and blood brain barrier is immature, allowing bacteria to cause CNS infection where they wouldnt be in older children
52
maternal screening for GBS
strep agalactiae metrnal screening for GBSS at 36 weeks is now routine and has significantly reduced rates of neonatal GBS infection if positive, intrapartum antibiotics are given
53
enterovirus
commonest cause of viral meningitis 85-95 of all viral meningitis large group of viruses infection common worldwide, especially n children
54
spread of enterovirus
spreads via contact with resspiratory of GI secretions | in australia, most infections occur in summer
55
clinical symptoms of enterovirus
most infections cause a mild, self limiting viral illness enterovirus infection may cause a rash usually very different to the rash of nvase menngooccal disease (is blanching) usually self limiting meningitis with no sequelae can be more severe eg. polio
56
treatment for enterovirus
no specific treatment exists
57
3 types of enterovirus
echovirus, coxsackieviruses, poliovirus
58
hand foot and mouth disease
vessicles/blisters on hands feet mouth and palate | look like lesions of herpes
59
herpex simples vrus
HSV-1 is the commonest cause of sporadic viral encephalitis worldwide can occur in healthy people at any age 90% of people are infected by the 4th decade of life
60
herpes simplex virus encephalitis
encephalitis may occur in primary infection or upon reactivation primarily effects temporal lobe - seem on MIR treated with antiviral medications (aciclovir) treated mortality in 10-30%, up to 70% if untreated permenent cognitive impairment may occur
61
neonatal infection with maternal HSV1 or HSV2
can cause disseminated infection including encephalitis | maternal herpes at the time of delivery is a risk factor
62
arbovirusses
arthropod borne vral nfectons usually a mosquito usually zoonotic (circulate in birds and mammals) usually limited to specifc geographic areas and may be seasonal
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australia arbovirus
murray valley encephalits vrus and Kujin virus (west nile virus)
64
non australia arboviruses
japanese encephalitis vruses, west nile virus
65
arbovirus encephalits
between them, they are assocated with s similar worldwise encephalitis incidence to HSV1 most infections are mild and self limiting, sometimes with rash and/or arthralgia/myalgia encephalitis attack rate varies mortality is up to 33% with permanent neurological abnormalities common
66
treatment for arboviral encephalitis
no specific treatment available
67
cryptococcus meningitis
widespread environmental fungues produces a capsule - virulence factor usually causes a chronic or subacute meningts can also cause lung or disseminated infection rarely causes infection in immunocompetent people immunocompromised patients are more susceptible may reactve from latent infection
68
cryptococcus meningitis examples
C neoformans has worldwide distribution in soil and bird guano G gattii usually associated with red gum trees
69
diagnosis of crytococcus meningitis
requires special diagnostic techniques | special microscopy, antigen testing, special agar
70
meningitis/encephalitis in immunocompromised patients
the immune system prevents most CNS infections the immune system may be imparied due to primary insufficiency, acquired insufficiency, iatrogenic insufficiency immunocompromised patients are at risk of unusualy CNS infections - cryptococcus meningitis - toxoplasma encephalitis - JC virus encephalitis - CMV meningitis/encephalitis
71
radiology diagnosis of meningitiss/encephalitis
CT - usually normal in meningitis/encephalitiss - can exclude alternate diagnosis eg. heamorrhage MRI - more sensitive than CT for meningitis/encephalitis
72
lumbar puncture being used for diagnosis of meningitis/encephalitis
opening pressure cerebrospinal fluid (CSF) - protein and glucose - microscopy, culture, and sensitivities (MC&S) - PCR - other tests (e.g. antibodies, cytology)
73
CFS microscopy, culture and sensitivities - appearance
normal CSF is clear and colourless | if enough white cells are present, it goes turbid
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white cell count of CSF
raised is called pleocytosis | normal CSF sshould have no more than 5 white cells
75
differential white cell count of CSF
differentiated neutrophils and mononuclear cels based on morphology neutrophilic pleocytosis suggests bacterial infection mononuclear plleocytosis suggests viral infection
76
red cell count of CSF
not usually raised in meningitis presence suggests 'bloody tap' or subarachnoid heamorrhage - meaning a vein or artery has been puctured during CSF collection microscopy s difficult to interpret in bloody taps - 500:1 or 1000:1 red cell:white cell ratio is usually best
76
red cell count of CSF
not usually raised in meningitis presence suggests 'bloody tap' or subarachnoid heamorrhage - meaning a vein or artery has been puctured during CSF collection microscopy s difficult to interpret in bloody taps - 500:1 or 1000:1 red cell:white cell ratio is usually best
77
normal CSF
``` colourless and clear white cel count <5 no neutrophils 0.2-0.4 g/L protein >50% glucose ```
78
viral pattern of CSF
``` clear/turbid 10-500 white cells no neutrophils 0.4-0.8 g/L protein >50% glucose ```
79
bacterial infection CSF
``` turbd/purulent 200-5000 white cells 80-95% neutrophils 0.5-2 g/L protein <50% glucose ```
80
TB CSF
``` turbid/vicous 100-500 white cells 0-60% neutrophil 05-3 protien <33% glucsoe ```
81
PCR tests
viral culture is slow and often not clinically useful nucleic acid aplifcation tests, such as PCR, are rapid and more sensitive commonly performed PCR tests for viral cuases of meningitis/encephalitis - enterovirus, HSV1, HSV2 and VZV can also detect common bacterial pathogens
82
speed of PCR tests
molecular results are usually available within 24 hours but can be as rapid as 2 hours if testing is urgent