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MBBS IV - Junior Clerkship WCS > JC24 (Medicine) - Meningitis and Encephalitis > Flashcards

JC24 (Medicine) - Meningitis and Encephalitis Flashcards

1
Q

Differentiate Meningitis and Meningism

A

Meningitis = inflammation of leptomeninges (defined by ↑WBC in CSF)

meningism = S/S of meningeal irritation w/o meningitis

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2
Q

Causes of meningitis

A

infection, neoplastic infiltration, irritation by drugs, contrast medium and blood

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3
Q

Primary sources of infection that spread to meninges

A

□ Local spread from nearby structures
→ From: sinuses, middle ear, mastoid, orbit, nasopharynx

□ Direct spread via skull or meningeal defect
→ From: head injury, neurosurgery

□ Haematogenous spread from bacteremia/distant septic foci
→ From: lung abscesses, pneumonia, IE, septicaemia, bacteraemia

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4
Q

Causative agents of acute pyogenic meningitis (neonate, infant, children)

A

□ Neonates: G- bacilli (E. coli, Proteus), S. agalactiae (GBS), Listeria monocytogenes
□ Infants: H. influenzae serotype b, N. meningitidis, S. pneumoniae, Salmonella
□ Children/young adults: N. meningitidis, S. pneumoniae

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5
Q

Causative agents of acute pyogenic meningitis (adults, elderly)

A

□ Young adults: N. meningitidis, S. pneumoniae
□ Older adults: S. pneumoniae
□ Elderly: N. meningitidis, S. pneumoniae, G- bacilli, L. monocytogenes

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6
Q

Causative bacteria of acute pyogenic meningitis (direct spread)

A

Direct spread (eg. skull injury, surgery, indwelling catheter): S. aureus, S. epidermidis, aerobic G- bacilli

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7
Q

Causative bacteria of acute pyogenic meningitis (immunocompromised)

A

L. monocytogenes, P. aeruginosa, G- bacilli, fungal etc

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8
Q

S/S of meningeal irritation

A

□ Severe headache: generalized, usually frontal/occipital (innervation)

□ Neck stiffness: gentle flexion of neck met with board-like stiffness
→ D/dx: cervical spondylosis usu generalized (not just flexion-extension)

□ Photophobia, nausea and vomiting

□ Kernig’s sign: stretching lumbar roots produces painful hamstring spasms
□ Brudzinski’s sign: spontaneous flexion of hips during attempted passive flexion of neck

□ Bulging anterior fontanelles in infants (w/o neck stiffness)

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9
Q

Classical triad of signs for meningitis

A

Fever, Neck stiffness, Altered mental status

  • Non-specific symptoms: fever (>38oC), chills, malaise, lethargy

(Up to 25% may have no fever)

  • Mental obtundation
  • S/S of meningeal irritation
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10
Q

S/S of complications of meningitis

A

Raised ICP: nausea, vomiting, papilloedema, ↓consciousness, coma

Focal S/S: seizures, CN palsies, SN deafness, hemiparesis, dysphasia, hemianopia
due to infarction (esp S. pneumoniae), abscess formation or subdural collection

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11
Q

Meningococcus meningitis

  • Transmission
  • S/S
  • Complications
  • Management and prophylaxis
A

Transmission: asymptomatic carriers, droplet transmission

S/S:
→ Often preceded by URTI or GE S/S
→ Usually abrupt in onset (short incubation)
→ A/w skin petechiae and arthralgia

Complications: septic shock, DIC, adrenal haemorrhage (Waterhouse-Friedrichsen syndrome)

Mx: IV benzylpenicillin

Chemoprophylaxis: rifampicin

Immunoprophylaxis: vaccination

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12
Q

Pneumococcus meningitis

  • Epidemiology
  • Preceding conditions
  • Course
A
  • predominantly adult, associated with debilitation and infarction
  • result from pneumonia, otitis media, sinusitis or post-splenectomy
  • rapid onset and progression to death in hours (Mortality: 20%)
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13
Q

Streptococcus suis meningitis

  • Transmission
  • S/S
  • Management
A

□ Transmission: a/w exposure to pigs or raw pork, through skin wounds → hematogenous spread
□ S/S: SN deafness (due to frequent organizing exudate in subarachnoid space), DIC with bleeding, skin blisters
□ Mx: IV benzylpenicillin

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14
Q

Haemophilus influenza meningitis

  • Epidemiology
  • S/S
  • Prophylaxis
A
  • Epidemiology: small children
  • S/S: preceded by URTI, abrupt onset with brief prodrome
  • Prophylaxis: Rifampicin, Hib vaccine
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15
Q

Listeria monocytogenes

  • Source
  • Transmission
  • S/S
A
  • found in soil, decayed vegetables
  • transmitted by contaminated meat/cheese
  • S/S: ↑risk of early seizures, focal neurology (rhombencephalitis picture)
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16
Q

D/dx of bacterial meningitis

A
  • Other infective meningitis and meiningoencephalitis (viral, TB, fungal, leptospiral, amoebic)
  • Viral encephalitis
  • Brain abscess
  • Spinal epidural abscess
  • Parameningeal infection (cranial osteomyelitis, subdural empyema)
  • Aseptic meningitis (eg. SLE, Behcet’s, sarcoidosis)
  • Chemical meningitis (eg. after human IVIg, SAH) [very rare]
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17
Q

List causative viruses of viral meningitis/ meningoencephalitis

A

Enterovirus (>75%): coxsackie A/B, poliovirus, echovirus, EV68-72
□ Mainly in young children, transmitted by feco-oral route

Others (less common):
□ Paramyxovirus (mumps, measles)
□ Herpesvirus (EBV, HSV)
□ Arenavirus (lymphochorionic virus)
□ HIV, influenza

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18
Q

S/S of viral meningitis/ meningoencephalitis

A

Non-specific ‘viral’ syndrome: fever, URTI, diarrhea, myalgia, parotitis, exanthemata

Meningeal irritation: headache, nausea/vomiting, photophobia…

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19
Q

Causes of chronic meningitis

A

Infective:
□ TB
□ Fungal: Cryptococcus neoformans (can uncommonly affect normal ppl)
□ Bacterial: Brucella, Actinomyces, Listeria…
□ Protozoal: cysticercosis, amoeba (rare)

Non-infective
□ Malignant meningitis: CA breast, CA lung, leukaemia, lymphoma
□ Inflammatory: sarcoidosis, SLE, Behcet’s disease

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20
Q

S/S of tuberculous meningitis

A

classically triphasic

□ Prodrome: insidious onset of malaise, anorexia, low-grade fever, night sweats, headache
(Up to 40% afebrile, suspect when unexplained neurological deficit)

□ Meningitic: meningism’s, protracted headache, vomiting, lethargy, confusion, ± CN and long tract signs

□ Paralytic: accelerated confusion, stupor, coma, seizures, hemiparesis, death

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21
Q

Complications of tuberculous meningitis

A

□ Basal meningeal adhesions: CN palsies (3, 4, 6, 8), hydrocephalus
→ Think TBM in CN palsy combinations that doesn’t make sense

□ Infarction due to endarteritis obliterans

□ Parenchymal damage

□ Spinal spread: myelitis, arachnoiditis (SC compression by thickened meninges → paraparesis)

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22
Q

Investigations for suspected tuberculous meningitis

A

□ LP: low glucose, Extremely high protein (up to 2-6g/dL), high WBC (lymphocyte predominant)

□ Microbiology: CSF AFB smear/culture, PCR (Sens 82% Spec 99%), ADA

□ Imaging: meningeal enhancement (esp basal), hydrocephalus, tuberculoma with rim enhancement ± cerebral infarction

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23
Q

Management of tuberculous meningitis

A

□ Anti-TB: 3HREZ ±S / 9HR±E (i.e. 3mo× 4 drugs + 9mo× 2 drugs)
□ Corticosteroids ×6mo

24
Q

Name of most common fungal meningitis

S/S

Epidemiology

A

Cryptococcal Meningitis

Caused by Cryptococcal neoformans

Symptomatology: >1/2 immunocompromised, most have cell-mediated deficiency
□ Non-specific: fever, headache, irritability
□ Meningitis: mental confusion, seizures, CN palsies

25
Q

Dx and Mx of fungal meningitis

A

Dx:
□ LP: ↑protein, ↓Glc, ↑WBC (lymphocyte predominant)
□ Microbiology: +ve Indian ink smear of CSF, cryptococcal Ag in CSF and serum

Mx:

□ Induction: IV amphotericin infusion for 6 hours AND IV 5-flucytosine for 2 weeks
□ Consolidation: PO fluconazole for ≥8w until CSF normal

26
Q

Complications of pyogenic meningitis

A

Basal meningeal adhesions due to incomplete organization of inflammatory exudates
□ Hydrocephalus raise ICP
□ CN palsies: III, IV, VI commonest, VIII involvement tends to persist

Arteritis/thrombophlebitis leading to cerebral infarction

Parenchymal damage
□ Neurological sequelae: intellectual impairment, mental retardation or cerebral palsy
□ Seizures: occur in 10% of acute bacterial meningitis, ~5% develops epilepsy

Spread of infection:
□ Locally → cerebritis, cerebral abscess, subdural effusion/empyema
□ Systemic → arthritis, IE

SIADH → hyponatremia

27
Q

First line investigations for suspected meningitis

A
  1. Blood: CBC with WBC differential, Clotting profile (DIC), Electrolytes (SIADH)
  2. Blood culture (2 sets before antibiotics)
  3. Lumbar Puncture: CSF analysis: Opening pressure, WBC, protein, glucose, microbiology (C/ST, AFB and TB PCR, Indian ink and cryptococcal antigen)
  4. Imaging: CT/MRI brain if suspect mass lesion or raised ICP, altered consciousness, seizure, papilledema, focal signs
28
Q

Describe morphology of these bacteria in CSF

  • S. pneumoniae
  • N. meningitidis
  • H. influenzae
  • Listeria
A
  • S. pneumoniae: G+ diplococci
  • N. meningitidis: G- diplococci
  • H. influenzae: small pleomorphic G- coccobacilli
  • Listeria spp: G+ coccobacilli
29
Q

Outline management of bacterial meningitis

  • Duration for different bacteria
  • Choice of Abx
  • Monitoring methods
A

Empirical IV Abx (at meningitic dose)

Duration: ≥7d for H. influenzae, 10-14d for S. pneumoniae, 14-21d for L. monocytogenes and S. agalactiae, 21d for G- bacilli

  • 3G cephalosporin for meningococcus and pneumococcus
    → Cefotaxime/ Ceftriaxone
  • Vancomycin (and/or broad-spectrum penicillins) for pneumococcus
  • Vancomycin + Ampicillin for Listeriosis

Repeat LP and optional neuroimaging after 48 hours for response to Abx

Repeat LP to assess response when poor clinical response or persistent fever >8d

± consult neurosurgery for control of ICP (eg. EVD, mannitol)

30
Q

Causes of poor response to Abx in bacterial meningitis

A

Persistence of primary cause, eg. pneumonia, SBE, mastoiditis, otitis

Cerebritis or small early cerebral abscess → bacteria partially resistant

Inadequate immunity → prolonged Abx required for I/C patients

31
Q

Indications for steroid use in bacterial maningitis

A

IV dexamethasone ×2-4d for S. pneumoniae, S. suis only (no effect in others)

Effect: shown to ↓mortality and ↓hearing loss

32
Q

Define encephalitis

Outline Pathophysiology

A

Encephalitis: brain parenchymal infection (mostly viral), Usually accompanied with meningitis (meningoencephalitis)

Pathophysiology: direct invasion of host cells, post-infectious immune-mediated changes (ADEM)

33
Q

List causative agents for acute viral encephalitis

A

□ Epidemic: Japanese B encephalitis, dengue fever, influenza, West Nile virus, Nipah virus

□ Sporadic:
→ Herpesviridae: HSV I, CMV, VZV, EBV
→ Enteroviruses: coxsackie, echovirus, poliovirus
→ Paramyxovirus: measles, mumps, rubella
→ Retroviruses: HIV
→ Others: adenovirus, lymphochorionic virus, rabies

34
Q

List non-viral agents that cause infectious meningoencephalitis

A

□ Bacterial: Legionella, L. monocytogenes, Mycoplasma pnemoniae, Rickettsia

□ Parasitic: Plasmodium falciparum, Toxoplasma gondii, Trypnaosomiasis, Strongyloides stercoralis

35
Q

List causative agents for ‘slow-virus’ encephalitis

A

□ Creutzfeldt-Jakob disease (CJD) due to prions

□ Progressive multifocal leukoencephalopathy (PML) due to JC virus

□ Subacute sclerosing panencephalitis due to measles

36
Q

List causative agents that cause post-infectious encephalitis

A

Post-infectious encephalitis (acute disseminated encephalomyelitis, ADEM):

□ Common viral infections: childhood exanthemata*

□ From Vaccinations: rabies, smallpox, influenza and pertussis

Exanthem = widespread rash, usually occurring in children. Classically caused by measles, rubella, parvovirus B19 and HHV6/7 (human herpesvirus), but can result from other illnesses (eg. mumps, S. pyogenes, VZV)

37
Q

S/S of viral encephalitis

A

Non-specific prodrome:
□ General: fever, viral syndrome, nausea, malaise
□ Virus-specific, eg. zoster vesicles

 Features of brain parenchymal involvement:
Focal:
→ +ve: seizures (focal or generalized)
→ -ve: hemiplegia, aphasia, VF defects, UMN signs, cerebellar ataxia (esp in VZV)
Global: ↓conscious level, confusion, agitation, mental obtundation

 ± features of meningeal irritation, i.e. meningoencephalitis

38
Q

HSV-1 encephalitis

  • Source of infection
  • Lobes involved
  • S/S
  • Ix
  • Mx
A
  • Source: Primary infection or reactivation from trigeminal ganglia
  • Temporal and frontal lobe

S/S

→ Prodromal: headache, malaise, resp symptoms, vomiting for a few days
→ Encephalitis: ↑drowsiness, confusion, hallucination, seizures, coma
→ ± focal cortical signs, eg. aphasia, hemiparesis

Ix:

→ EEG: ~60% focal or epileptic activity, esp over frontal or temporal regions
→ Microbiology: HSV PCR in blood and CSF
→ MRI: T2W hyperintensity in frontotemporal regions

Mx: IV acyclovir 10mg/kg Q8H x10d

39
Q

VZV encephalitis

List complications

A
  1. Acute cerebellar ataxia: Ataxia occurs at onset of skin rash + Fever, vomiting, headache, meningism
  2. Post-herpetic neuralgia: chronic dermatomal neuralgia persisting after herpetic skin eruption
  3. Cranial neuropathies, eg. Ramsay-Hunt syndrome, herpes zoster ophthalmicus
  4. Encephalitis

Others: leukoencephalopathy, aseptic meningitis, transverse myelitis, segmental motor neuropathies, cerebral vasculopathy

40
Q

S/S, Ix and Mx for suspected VZV encephalitis

A

S/S: fever, altered consciousness, seizures ~1w after onset of skin rash

Ix:
→ MRI: multiple T2W hyperintense lesions in subcortical white matter ± spreading to cortex
→ Microbiology: VZV PCR

Mx: supportive, PO acyclovir/valaciclovir/Famciclovir, IV acyclovir if severe (esp if I/C)

41
Q

Japanese B encephalitis:

  • Transmission
  • S/S
  • Ix
  • Mx
A

Transmission: Culex tritoaeniorhynchus (mosquito a/w rice fields), amplified in birds and pigs

S/S: commonly subclinical (1/300-400 symptomatic), a/w rapid onset psychosis, EPS, focal signs

Dx: anti-JEV IgM in CSF, predilection to bilateral thalamus

Mx: supportive, vaccination

42
Q

Nipah virus encephalitis

  • Transmission
  • S/S
  • Ix
  • Mx
A

paramyxovirus outbreak in pig farm/abattoir workers

S/S: sudden prodrome of fever, headache, myalgia, N/V ± atypical pneumonia → LOC, coma and death

Ix: serology for IgM**, multiple discrete **deep cortical lesions (MRI)

Mx: IV ribavirin

43
Q

Ddx encephalitis

A

□ Bacterial meningitis complicated by cerebral abscess, oedema or venous thrombosis
□ Metabolic encephalopathy, eg. drug OD, hypoGly, liver or renal failure, hypoNa
□ Complex partial status epilepticus from other causes

44
Q

First line investigations for suspected viral encephalitis

A
  • LP + CSF analysis: Lymphocytosis, High protein, Normal glucose, PCR for CMV, HSV, EV, VZV
  • Imaging: MRI with hypertense lesions in T2-W
  • Serology: Paired sera for Influenza, mycoplasma, mumps, measles/ Single IgM sera for JEV, EBV, CMV
  • Viral culture on urine, faeces, throat swabs
  • EEG: diffuse slowing with spike activities
  • Brain biopsy (last-line)
45
Q

Empirical management of viral encephalitis

A

Empirical Tx:
□ IV Acyclovir → cover for HSV (70% mortality if untreated)
□ Anticonvulsants if indicated
□ Dexamethasone if ↑ICP

Supportive Tx, eg. ICP management

No specific Tx if not HSV

46
Q

Possible locations of brain abscess

A

Intracranial abscess: accumulation of pus in
□ Extradural space → extradural abscess
□ Subdural space → subdural empyema
□ Brain parenchyma → cerebral abscess

47
Q

Sources of primary infection causing brain abscess

A
  • *Haematogenous spread** → multiple abscesses in MCA territory at grey-white junction
  • CVS: IE, congenital heart disease (esp when a/w R-to-L shunts)
  • Respiratory: bronchiectasis, pulmonary abscess, empyema
  • Other sites: skin infections, deep-seated abscess
  • *Local spread → single abscess**
  • Direct spread: skull fracture and meningeal defect
  • Indirect spread: extension of infected thrombus or embolic spread along veins
  • Sites: skull fractures, dental caries, sinusitis, otitis media/mastoiditis, orbit, cavernous sinus
48
Q

Causative agents of brain abscesses

A

Depends on route of spread:

□ Middle ear (often mixed): S. viridans, Bacteroides, E. coli, Proteus, S. pneumoniae

□ Sinus: S. viridans, S. pneumoniae, Haemophilus spp, anaerobes

□ Blood: S. viridans, S. pneumoniae, S. aureus

□ Trauma from skin: S. aureus

□ Immunocompromised: Toxoplasma (esp in HIV), Aspergillus, Candida, Nocardia, Listeria

49
Q

Pathogenesis of brain abscess

A

Invasion:
□ Local/haematogenous spread of bacteria
□ Small vessel occlusion/surface thrombophlebitis (may precede parenchymal involvement) → ischaemia favours bacterial growth
□ Parenchymal bacterial invasion

Cerebritis:
□ Polymorph infiltration
□ Granulation tissue formation and fibrosis

Capsule formation with central necrotic zone and inflammatory cells

50
Q

S/S of brain abscesses

A

Systemic S/S: pyrexia, malaise (only 45-53% has fever → high index of suspicion)

Raised ICP: severe ipsilateral headache, vomiting → ↓consciousness, papilloedema (late)

Focal S/S (75%): hemiparesis, dysphasia, ataxia, nystagmus, seizures (30%)

S/S related to infective source

51
Q

Ix for suspected brain abscess

A

Do NOT do lumbar puncture if focal S/S present

Contrast CT/MRI brain

Microbiology workup:
□ Blood culture (10% +ve) and sample from suspected source
□ Aspirated pus for smear, culture and sensitivity

Ix for underlying septic foci: CXR, echo, XR skull, ENT examination

52
Q

Features of brain abscess on imaging

A

Contrast CT/MRI brain:
□ Cerebritis (early): normal/irregular non-enhancing hypodensity

□ Abscess (late): 3 layers
→ Liquefactive debris: hypodense on T1W
→ Capsule: rim enhancement
→ Surrounding oedema: hypodense on T2W

± midline shift/ventricular compression: abscess rupture into ventricle causes fulminant ventriculitis

± sinusitis/mastoiditis

53
Q

Empirical management of brain abscess

A

Empirical Tx: Benzylpenicillin + IV ceftriaxone/cefotaxime + metronidazole or IV meropenem

→ Skull injury/NS procedures: high dose cloxacillin or fusidic acid to cover S. aureus
→ Haematogenous spread: consider using IV vancomycin to cover MRSA

Treat for at least 6 weeks w/ clinical-radiological monitoring (serial CT head)

Neurosurgery: only for Large, single abscess/empyema → early drainage by EVD, guided aspiration, craniotomy

Prophylactic antiepileptics

54
Q

Complications of brain abscess

A

□ Gliosis → ↑risk of epilepsy
□ Herniation esp in posterior fossa abscess
□ Rupture into subarachnoid space and ventricles
□ Residual neurological deficit
□ Recurrence

55
Q

Prion encephalopathy

  • Pathophysiology
  • Sources of infection
A

Transmissible spongiform encephalopathy (TSE):

histopathological triad of cortical spongiform changes, neuronal loss and gliosis due to accumulation of amyloid deposits of an altered prion protein

spontaneous (a/w transmitted PrP) or familial (a/w inherited PrP)

56
Q

Creutzfeldt-Jakob Disease (CJD)

  • S/S
  • Ix
A

Clinical features:
□ Rapidly progressive dementia
□ Motor features: myoclonus, extrapyramidal and pyramidal signs

Ix:
□ EEG: periodic high-voltage, polyspike or triphasic sharp wave complexes (1-2Hz) w/ suppressed background activity
□ MRI: cortical ribboning (abnormal DWI/FLAIR hyperintensity in cortical gyri)
□ Brain Bx: vacuolation and loss of neurons with hypertrophy and proliferation of glial cells mostly in cerebral cortex

57
Q

Variant CJD (vCJD)

  • Source of infection
  • S/S
  • Ix
A

bovine spongiform encephalopathy (BSE, mad cow disease)

S/S:

□ Early psychiatric manifestations (most often depression) and painful sensory symptoms
□ Followed by rapidly progressive dementia, ataxia and akinetic mutism

Ix:

□ EEG: characteristic changes absent
□ MRI: pulvinar sign (hyperintensity at pulvinar nucleus)
□ Tonsillar biopsy for PrPSc
□ Brain Bx: florid plaques with dense prion protein deposits on IHC

MBBS IV - Junior Clerkship WCS (131 decks)

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