meningitis and encephalitis Flashcards
meningitis
inflammaton of the meninges aseptic meningitis (no organisms)
encephalitis
inflammation of the brain parenchyma
may be further refined anatoomically eg. cerebritis, cerebeillitis, rhombencephalitis
cerebritis
inflammation of the cerebrum
cerebellitis
inflmmmation of the cerebellum
rhombencephallitis
inflammation of the brainstem
meningoencephalitis
miningitis and encephalitis
myelitis
inflammation of the psinal cord
encephalomyelitis
encephalitis and myelitis
subdural empyema
collection of pus in the dural space between the meningies and the brain parenchyma
usually iatrogenic
pathogenesis of CNS infection
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)
neurotropism
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
classic triad of meningitis
fever
altered mental state - confusion or drowsiness
neck stiffness - nuchal rigidity.
meningism
nuchal rigidity with headache and photophobia
nuchal rigidity
neck stiffness
other symptoms of meningitis
cause and vomiting
other neurological abnormalities are less common
bacterial meningitis may also be accompanied by sepsis (tachycardia, hypotension)
chronic meningitis presents with
milld or fluctuating symptoms of meningitis, often without fever, and usually with some neurological abnormality
sequelae of meningitis
- raised ntracranlial pressure
- temporary or permanent neurological sequelae
- following viral meningitiis, complete recovery is common
raised intracranial pressure
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
temporary or permanent neurological sequelae
- sezures
- cranial nerve palsies, hemiparesis
- sensorineural hearing loss
- intellectual impairment
clinical featuress of encephalitiis
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
- focal neurological abnormalities in encephaliti
depends on the site of brain involvement weakness hemiparesis speech and movement disorders abnormal reflexe personality change
how does encephalitis differ from meningitis clinciall
more prominent altering of mental status, seixzures and fical neurologcal abnormalities are more common
permanent neurological sequelae are more common
neisseria meningitidis
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
neisseria meningitidis spread by
person to person via contact with respiratory secretions
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
serogroups of neisseria meningitidis
classified on the basis of capsular antigens
A, B, C, W, X, Y, Z
most common manifestations of invasive meningococcal disease
meningitis and bacteraemia (bloodstream)
patients may present with one or both
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
less commonmenifestations of neisseria meningitidis
septic arthritis
pericarditis
less commonmenifestations of neisseria meningitidis
septic arthritis
pericarditis
treatment of neisseria meningitidis
5 days high-dose intravenous ceftriaxone
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
purpura fulminans
disseminated intravascular coagulation
thrombosis and haemorrhage leading to gangrenous necrosis of extremities requiring amputation
new common serogroup of meningococcal
serogroup W (and Y)
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
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
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
pneumococcus
streptococcus pneumoniae
most common bacterial cause of community aquired pneumonia
streptococcus pneumoniae
strep pneumoniae immunisation
vaccine for infants, and regular boosters for indigenous people over 50 and all adults over 65
strep pneumoniae mortality
pften very aggresssive with treated mortality of 20-30%
treatment is with 10-14 days high-dose intravenous ceftriaxone
listeria monocytogenes
gram-positive bacillus
listera infection may be asymptomatic or cause a non-specific, self-limiting febrile illness
lsteria monocytogenes in pregnancy
usually mild but can lead to amniotic infection and fetal loss
listeria monocytogenes outbreaks
not a commensal organism, outbreaks associated with contaminated vegetables, cold meats, salads, milk, cheese
CNS listeria infection
rare in healthy young adults
rsk of CNS infection increases with immunocompromise and age oover 50
usually causes and miningoencephalitis
treatment of listeria monocytogenes
not treatable by ceftriaxone, needs different antibiotics
most common causes of bacterial meningitidis in neonates
S. agallactiae (GBS)
E coli
other gram negative bacillii
listeria
mot common causes of bacterial meningitis in children
N meningitidis
S pneumoniae
H influenzeae serotype B
most common cause of bacteral meningitidis in young adults
N meningitidis
S pneumoniae
most common cause of bacterial meningitidis in older adults
S pneumoniae
N meningitidis
listeria
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
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
enterovirus
commonest cause of viral meningitis
85-95 of all viral meningitis
large group of viruses
infection common worldwide, especially n children
spread of enterovirus
spreads via contact with resspiratory of GI secretions
in australia, most infections occur in summer
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
treatment for enterovirus
no specific treatment exists
3 types of enterovirus
echovirus, coxsackieviruses, poliovirus
hand foot and mouth disease
vessicles/blisters on hands feet mouth and palate
look like lesions of herpes
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
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
neonatal infection with maternal HSV1 or HSV2
can cause disseminated infection including encephalitis
maternal herpes at the time of delivery is a risk factor
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
australia arbovirus
murray valley encephalits vrus and Kujin virus (west nile virus)
non australia arboviruses
japanese encephalitis vruses, west nile virus
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
treatment for arboviral encephalitis
no specific treatment available
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
cryptococcus meningitis examples
C neoformans has worldwide distribution in soil and bird guano
G gattii usually associated with red gum trees
diagnosis of crytococcus meningitis
requires special diagnostic techniques
special microscopy, antigen testing, special agar
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
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
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)
CFS microscopy, culture and sensitivities - appearance
normal CSF is clear and colourless
if enough white cells are present, it goes turbid
white cell count of CSF
raised is called pleocytosis
normal CSF sshould have no more than 5 white cells
differential white cell count of CSF
differentiated neutrophils and mononuclear cels based on morphology
neutrophilic pleocytosis suggests bacterial infection
mononuclear plleocytosis suggests viral infection
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
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
normal CSF
colourless and clear white cel count <5 no neutrophils 0.2-0.4 g/L protein >50% glucose
viral pattern of CSF
clear/turbid 10-500 white cells no neutrophils 0.4-0.8 g/L protein >50% glucose
bacterial infection CSF
turbd/purulent 200-5000 white cells 80-95% neutrophils 0.5-2 g/L protein <50% glucose
TB CSF
turbid/vicous 100-500 white cells 0-60% neutrophil 05-3 protien <33% glucsoe
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
speed of PCR tests
molecular results are usually available within 24 hours but can be as rapid as 2 hours if testing is urgent
