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microbiology 3 > meningitis and encephalitis > Flashcards

meningitis and encephalitis Flashcards

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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
Q

invasive strain of neisseria meningitidis

A

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

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26
Q

serogroups of neisseria meningitidis

A

classified on the basis of capsular antigens

A, B, C, W, X, Y, Z

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27
Q

most common manifestations of invasive meningococcal disease

A

meningitis and bacteraemia (bloodstream)

patients may present with one or both

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28
Q

neisseria meningitidis bacteraemia

A

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

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29
Q

less commonmenifestations of neisseria meningitidis

A

septic arthritis

pericarditis

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30
Q

less commonmenifestations of neisseria meningitidis

A

septic arthritis

pericarditis

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31
Q

treatment of neisseria meningitidis

A

5 days high-dose intravenous ceftriaxone

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32
Q

sequelae of invasive meningococcal disease

A

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

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33
Q

purpura fulminans

A

disseminated intravascular coagulation

thrombosis and haemorrhage leading to gangrenous necrosis of extremities requiring amputation

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34
Q

new common serogroup of meningococcal

A

serogroup W (and Y)

35
Q

vaccination for meningococcal

A

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
Q

contact tracing of meningococcal disease

A

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
Q

streptococcu pneumoniae

A

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
Q

pneumococcus

A

streptococcus pneumoniae

39
Q

most common bacterial cause of community aquired pneumonia

A

streptococcus pneumoniae

40
Q

strep pneumoniae immunisation

A

vaccine for infants, and regular boosters for indigenous people over 50 and all adults over 65

41
Q

strep pneumoniae mortality

A

pften very aggresssive with treated mortality of 20-30%

treatment is with 10-14 days high-dose intravenous ceftriaxone

42
Q

listeria monocytogenes

A

gram-positive bacillus

listera infection may be asymptomatic or cause a non-specific, self-limiting febrile illness

43
Q

lsteria monocytogenes in pregnancy

A

usually mild but can lead to amniotic infection and fetal loss

44
Q

listeria monocytogenes outbreaks

A

not a commensal organism, outbreaks associated with contaminated vegetables, cold meats, salads, milk, cheese

45
Q

CNS listeria infection

A

rare in healthy young adults
rsk of CNS infection increases with immunocompromise and age oover 50
usually causes and miningoencephalitis

46
Q

treatment of listeria monocytogenes

A

not treatable by ceftriaxone, needs different antibiotics

47
Q

most common causes of bacterial meningitidis in neonates

A

S. agallactiae (GBS)
E coli
other gram negative bacillii
listeria

48
Q

mot common causes of bacterial meningitis in children

A

N meningitidis
S pneumoniae
H influenzeae serotype B

49
Q

most common cause of bacteral meningitidis in young adults

A

N meningitidis

S pneumoniae

50
Q

most common cause of bacterial meningitidis in older adults

A

S pneumoniae
N meningitidis
listeria

51
Q

bacterial meningitis in neonates

A

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
Q

maternal screening for GBS

A

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
Q

enterovirus

A

commonest cause of viral meningitis
85-95 of all viral meningitis
large group of viruses
infection common worldwide, especially n children

54
Q

spread of enterovirus

A

spreads via contact with resspiratory of GI secretions

in australia, most infections occur in summer

55
Q

clinical symptoms of enterovirus

A

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
Q

treatment for enterovirus

A

no specific treatment exists

57
Q

3 types of enterovirus

A

echovirus, coxsackieviruses, poliovirus

58
Q

hand foot and mouth disease

A

vessicles/blisters on hands feet mouth and palate

look like lesions of herpes

59
Q

herpex simples vrus

A

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
Q

herpes simplex virus encephalitis

A

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
Q

neonatal infection with maternal HSV1 or HSV2

A

can cause disseminated infection including encephalitis

maternal herpes at the time of delivery is a risk factor

62
Q

arbovirusses

A

arthropod borne vral nfectons
usually a mosquito
usually zoonotic (circulate in birds and mammals)
usually limited to specifc geographic areas and may be seasonal

63
Q

australia arbovirus

A

murray valley encephalits vrus and Kujin virus (west nile virus)

64
Q

non australia arboviruses

A

japanese encephalitis vruses, west nile virus

65
Q

arbovirus encephalits

A

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
Q

treatment for arboviral encephalitis

A

no specific treatment available

67
Q

cryptococcus meningitis

A

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
Q

cryptococcus meningitis examples

A

C neoformans has worldwide distribution in soil and bird guano
G gattii usually associated with red gum trees

69
Q

diagnosis of crytococcus meningitis

A

requires special diagnostic techniques

special microscopy, antigen testing, special agar

70
Q

meningitis/encephalitis in immunocompromised patients

A

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
Q

radiology diagnosis of meningitiss/encephalitis

A

CT
- usually normal in meningitis/encephalitiss
- can exclude alternate diagnosis eg. heamorrhage
MRI
- more sensitive than CT for meningitis/encephalitis

72
Q

lumbar puncture being used for diagnosis of meningitis/encephalitis

A

opening pressure
cerebrospinal fluid (CSF)
- protein and glucose
- microscopy, culture, and sensitivities (MC&S)
- PCR
- other tests (e.g. antibodies, cytology)

73
Q

CFS microscopy, culture and sensitivities - appearance

A

normal CSF is clear and colourless

if enough white cells are present, it goes turbid

74
Q

white cell count of CSF

A

raised is called pleocytosis

normal CSF sshould have no more than 5 white cells

75
Q

differential white cell count of CSF

A

differentiated neutrophils and mononuclear cels based on morphology
neutrophilic pleocytosis suggests bacterial infection
mononuclear plleocytosis suggests viral infection

76
Q

red cell count of CSF

A

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
Q

red cell count of CSF

A

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
Q

normal CSF

A 
colourless and clear 
white cel count <5 
no neutrophils 
0.2-0.4 g/L protein 
>50% glucose
78
Q

viral pattern of CSF

A 
clear/turbid 
10-500 white cells 
no neutrophils 
0.4-0.8 g/L protein 
>50% glucose
79
Q

bacterial infection CSF

A 
turbd/purulent 
200-5000 white cells 
80-95% neutrophils 
0.5-2 g/L protein 
<50% glucose
80
Q

TB CSF

A 
turbid/vicous 
100-500 white cells
0-60% neutrophil
05-3 protien 
<33% glucsoe
81
Q

PCR tests

A

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
Q

speed of PCR tests

A

molecular results are usually available within 24 hours but can be as rapid as 2 hours if testing is urgent

microbiology 3 (10 decks)

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