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MED627 > Meningitis and Encephalitis > Flashcards

Meningitis and Encephalitis Flashcards

1
Q

what is the difference b/w meningitis and encephalitis?

A

meningitis - inflammation of the meninges

encephalitis - inflammation of the brain (parenchyma)

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2
Q

what is the carriage and transmission of neisseria meningitis?

A
  • throat carrier in approx. 10% population: 25% of 15-19yrs
  • person-person spread
  • inhalation of respiratory secretions
  • lose prolonged contact e.g. household members
  • direct contact (kissing)
  • disease in minority (patients needs to be immune-susceptible and the strain of bacteria needs to be present in the throat)
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3
Q

what are the types of meningococcal disease and how prevalent are they?

A
  1. septicaemia (25%) - blood stream infection, symptoms like fever, hypothermia, headache (may be), low BP, rapid spreading rash at periphery (e.g. toes)
  2. meningitis (15%) - similar symptoms as septicaemia but no rash
  3. both septicaemia and meningitis (65%)
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4
Q
  1. what are the rate of prognosis (or fatality) of meningococcus (meningitis, septicaemia and if left untreated)?
  2. if survived what are morbidity cases? and
  3. what is impact of antibiotics?
A
  1. fatal in
    - meningococcal: 10%
    - with meningitis: 5%
    - septicaemia: 50%
    - untreated: 100%
  2. if survived, 1 in 8 suffer from long term morbidity like headache, joint stiffness, epilepsy, learning loss and learning difficulties
  3. early antibiotics improve prospect of recovery
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5
Q

why is hearing loss a common long term neurological problem in meningococcal diseases?

A

because the cranial nerves pass through the meninges which gets inflamed and damaged

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6
Q

what is the treatment for bacterial (Neisseria) meningitis?

A
  • antibiotics: IV ceftriaxone or cefotaxime, after blood cultures or lumbar puncture
  • Aurburtin M et al. 1993, Proulx et al. 2005 showed delayed administrations associated w increased mortality
  • role of corticosteroid unclear?
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7
Q

how common is neisseria meningitides?

A
  • England: groups B,C,W,Y
  • common in children <4yrs
  • at peak in 5-6m olds
  • 2nd highest incidence in teens (15-19yr)
  • meningococcal cases in England:
  • 1999/00: 2595 cases
  • 2016/17: 747 cases
  • significant reduction since meningococcal C vaccine introduction in 1999/2000
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8
Q

at what age is meningitis B and ACYW given?

A

since 2015

  • Men B:2-4m, booster: 1-3yrs
  • MenACYW-135: teenagers + uni students
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9
Q

how common is meningitis in foreign countries?

A
  • African meningitis belt
  • Saudi Arabia, Hajj (Men ACYW-135), travellers going to hajj need to present vaccination certificate (medical cases exempted)
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10
Q

pneumococcal meningitis

  1. Prevalent in which age
  2. Mode of spread
  3. Treatment
A
  1. Elderly: main cause of bacterial meningitis
  2. contiguous spread: sinuses (infection) -> middle ear
    - (sequel) previous history of neurological condition
  3. similar to meningococcal meningitis i.e cephalosporins: IV ceftriaxone or cefotaxime (antibiotics)
    - alternative meds for penicillin resistant pneumococcus like vancomycin
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11
Q

are corticosteroids helpful in treating bacterial meningitis?

A
  • dexamethasone for 4 days if organism unknown or streptococcus pneumonia confirmed
    A. De Gans J et al. 2002, RCT of 301 pts w bacterial meningitis in Europe,
    1. dex significantly reduced mortality + neurological disability at 8wks in pts with Strep pneumonia w GCS<11 on admission
    2. meningococcal meningitis: much lower mortality + morbidity rates independent of the use of dex
  • no diff in groups for hearing loss
  • effective: intermediate>mild neurological problems
    3. dex reduced mortality + incidence of deafness in children w Haemophilus influenzae meningitis + pneumococcal meningitis
  • dex safe except cerebral malaria cases, therefore, the use of steroids could be beneficial
    B. Scarborough M et al. 2007, contrastingly a Malawi study w 95% HIV +ve pts had
    1. no benefits from dex even for pneumococcal meningitis
    C. Van de Beek D et al. 2010, metaanalysis w 81% bacterial meningitis, 29% HIV +ve + 41% <15yrs does not significantly reduce death or neurological disability and benefit for all or any subgroup of patients remains unproven
  • highlighting,
    1. variance of efficacy across race (cross-check?)
    2. poor/some evidence to reduce mortality + morbidity in step. pneumonia meningitis but not in other bacterial meningitis
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12
Q

listeria monocytogenes

  1. how common is it?
  2. causes
  3. which are the risk groups
  4. likelihood of developing of meningitis
  5. mortality rate
  6. treatment
A
  1. 60 cases/year in England + Wales, third common cause in adults in UK
  2. acquired by ingestion for meats or dairy
  3. high risk groups (via blood)
    - >55yrs
    - immunocomprised
    - pregnant women
    - neonates
  4. can develop meningitis in 55-70% (if enters the blood)
  5. mortality rate: 25%
  6. treatment: IV amoxicillin +/- gentamicin
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13
Q

what are the viral and non-viral causes of meningitis?

A
  1. viral: enterovirus, herpes simplex virus (HSV 1 +2 - recurrent) (mollaret’s syndrome), mumps, measles (rash), adenovirus, HIV
  2. non-viral: Lyme disease, syphilis, drugs (used to treat UTI, mostly benign and self-limiting)
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14
Q

enterovirus meningitis

  1. days of incubation
  2. location of replication
  3. mode of transmission
  4. diagnosis
  5. prognosis
  6. treatment
A
  1. incubates for 2-5days
  2. replication in reparatory or GI epithelial cells
  3. transmission via respiratory or conjunctival secretion, face-oral
  4. diagnosis: PCR (CSF (most common),throat swab, faeces)
  5. prognosis: self limiting
  6. treatment: symptomatic
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15
Q

gram stain is useful for which meningitis and why?

A

for bacterial meningitis because viruses too small to be seen

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16
Q

TB meningitis

  1. days of presentation
  2. risk factors
  3. diagnosis (imaging?)
  4. treatment
A
  1. presentation: chronic days-wks (unlike bacterial meningitis)
  2. risk factors - HIV (immunosuppressed -> increases the likelihood of heamatogenous TB spread), alcoholism, diabetes, steroids, anti-TNF agents (anti-TNF -> switcher off cytokine, essential for immune control to TB, thus inactive TB -> active -> replicate +spreads), immigration to area of high prevalence (India)
  3. diagnosis: imaging used
    - chest x-ray: suggestive of active or previous pulmonary TB in 50%
    - contrast CT head: hydrocephalus, basal enhancement, infarction, tuberculoma
  4. treatment:
    - 12m (pulmonary TB6m but CNS TB longer): antibiotics used to treat TB, rifampicin, isoniazid, pyrazinamide, ethambutol
    - dexmeth (Thwaites regimen)
    - communicating hydrocephalus: acetazolamide + frusemide or repeated LP
    - non-communicating hydrocephalus: consider early ventriculo-peritoneal shunting
17
Q

cryptococcal meningitis

  1. symptoms
  2. commonly found in
  3. cause
  4. CD4 count that results in disease
  5. treatment
A
  1. classic meningitis symptoms usually absent
  2. global distribution - bird dropping (breathing it all the time but does not cause disease)
  3. cause: inhalation of Yeats
  4. CD4 >100cells/μL otherwise disease rare
  5. treatment
    - uniformly fatal if left untreated
    - controlling raised ICP: major factor in reducing mortality and morbidity
18
Q

True or False

  1. Neisseria meningitis infection is always associated with a non-blanching rash
  2. Neisseria meningitis serogroup C is vaccine preventable
  3. Listeria meningitis can be treated with ceftriaxone
  4. Enterovirus is the commonest cause of viral meningitis
  5. Cryptococcal meningitis should be treated with adjuvant corticosteroids
A
  1. FALSE, N. meningitis may present rash but not always
  2. TRUE since introduction of vaccine in
  3. FALSE, listeria is resistant to cephalosporins (class of ABs w ceftriaxone) thus, combination of amoxicillin + gentamicin is used
  4. TRUE
  5. FALSE corticosteroids may be effective only for step. pneumococcal meningitis
19
Q

how does the lab results differ for bacterial and viral meningitis?

A

refer

20
Q

how to distinguish meningitis and encephalitis?

A
  • by brain abnormalities in brain function, encephalitis associated w
    1. altered mental status
    2. motor or sensory deficits (frontal)
    3. altered behaviour/personality (parietal)
    4. speech or movement disorder
    5. may be lethargic or have seizures
  • distinction blurred if features of both preset - meningoencephalitis
  • markers: inflammatory cells in CSF or inflammation on imaging
21
Q

what are the causes of encephalitis?

A
  1. viruses
    - direct invasion of CNS: herpes virus, arboviruses (arthropod borne viruses)
    - immune mediated post infection/vaccination: ADEM (acute disseminated encephalomyelitis) and mumps, measles, rubella, influenza
  2. bacteria: listeria, mycoplasma, lyme, syphilis
  3. TB
  4. parasites: cerebral malaria (topical areas)
  5. fungi
22
Q

what are the causes of viral encephalitis?

A
  1. herpes virus: HSV 1 +2 (common in industrialised), Epstein-Barr virus, HHV 6 + 7
    - HSV2 encephalitis neonates and immunocompromised
    - HSV2 meningitis in adults
  2. enteroviruses: coxsackie, poliovirus
    - normally do not cause encephalitis but not possible
  3. paramyxoviruses: weasels, umps
  4. rarer: influenza, adenovirus, parvovirus, rubella
23
Q

why is it essential to enquire the travel history off patients while examining viral encephalitis? what is significance the west nile virus?

A
  • geographically restricted
  • west nile encephalitis in America, supre, Middle East, Africa and Asia
  • Murray valley is Australasia
  • all arboviruses except rabies
  • therefore, essential to ask the travel history
  • west nile virus: mosquito borne infection -> kills birds
24
Q

HSV encephalitis

  1. number of cases per year
  2. age group affected
  3. mortality rate in untreated
  4. neuropsychiatric sequelae
A
  1. 1-2 cases/ 250,00/ year
  2. all age groups
  3. 70% mortality in untreated
  4. 2/3 survivors
    - 70% memory impairement
    - 45% personality/behavioural change
    - 40% dysphasia
    - 25% seizures (risk of those w seizure during acute period higher)
    - disinhibition/depression
25
Q

what are the clinical presentation of HSV encephalitis?

A 
Acute presentation
Flu-like prodrome
Fever (90%)
Headache
Altered consciousness 
Disorientation (76%)
Seizures in 1/3 of patients with HSV-1 encephalitis
Focal neurological signs common
Speech disturbance (59%)
Behavioural change, e.g. hypomania, irritability (41%)
Memory impairment
26
Q

what are the common misdiagnosis of encephalitis?

A
  1. fever + confusion - urinary/chest infection
  2. fever + seizures (febrile) - post-octal pyrexia (febrile illness - CNS infection investigation)
  3. altered consciousness or behaviour - drugs/alcohol/psychiatric illness
27
Q

how is HSV diagnosed?

A
  1. lab tests
    - CSF HSV-1 DNA PCR: sensitivity >95% within 10days from onset but can be -ve initially
    - CSF antibody: sensitivity 50%, detection from 10days
  2. Imaging: MRI > CT, imaging could be normal initially, MRI w DWI might help
    - unilateral temporal abnormality suggest HSV encephalitis
  3. EEG: non-specific focal findings in >80% HSV encephalitis, periodic lateralised epileptiform discharges
28
Q
  1. what is aciclovir?
  2. what are the pros and cons associated
  3. when to administer it?
A
  1. antiviral used for treating HSV encephalitis
  2. pros: reduces mortality from 70% to 28% + limits postendephaltiic impairment
    cons: poor outcome if delay>2days b/w admitting and starting the treatment
  3. in suspected EC, first perform LP (proving no contradictions) then start acyclovir antibiotics
    - if LP likely to delayed or patient deteriorating start presumptive aciclovir at once
29
Q

when to stop acicclovir for HSV encephalitis ?

A
  1. confirmed HSV E: stop at 14-21 days
  2. high suspicion but initial CSF PCR -ve, continue acyclovir and repeat LP after 48hrs
  3. if PCR again -ve but suspicion persists then continue IV acyclovir for 10 days
  4. low suspicion or alternative diagnosis apparent then stop after 2.d -ve PCR
30
Q

what is the significance of corticosteroids in HSV encephalitis?

A
  • retrospective non-randomised data – corticosteroid administration improved outcome in 22 of 45 patients with HSV encephalitis w combination therapy for aciclovir and corticosteroids
  • Efficacy not yet proven
  • Optimal timing unclear
  • Often used if significant brain oedema or if deterioration despite appropriate antiviral treatment
  • however, mannitol and decompressive hemicraniectomy sometime preferred
  • prospective RCT 2015, following standard treatment w IV ACV for PCR-confirmed HSE, an additional 3-month course of oral (valacyclovir) VACV therapy did not provide added benefit

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