JC24 (Medicine) - Meningitis and Encephalitis Flashcards

Question

Dx and Mx of fungal meningitis

Answer 1

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

Answer 2

**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

Answer 3

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

Answer 4

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

Answer 5

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)

Answer 6

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

Answer 7

IV dexamethasone ×2-4d for S. pneumoniae, S. suis only (no effect in others) Effect: shown to ↓mortality and ↓hearing loss

Answer 8

Encephalitis: brain parenchymal infection (mostly viral), Usually accompanied with meningitis (meningoencephalitis) Pathophysiology: direct invasion of host cells, post-infectious immune-mediated changes (ADEM)

Answer 9

□ 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

Answer 10

□ Bacterial: Legionella, L. monocytogenes, Mycoplasma pnemoniae, Rickettsia □ Parasitic: Plasmodium falciparum, Toxoplasma gondii, Trypnaosomiasis, Strongyloides stercoralis

Answer 11

□ Creutzfeldt-Jakob disease (CJD) due to **prions** □ Progressive multifocal leukoencephalopathy (PML) due to **JC virus** □ Subacute sclerosing panencephalitis due to **measles**

Answer 12

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)*

Answer 13

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

Answer 14

* 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

Answer 15

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

Answer 16

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)

Answer 17

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

Answer 18

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

Answer 19

□ 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

Answer 20

* **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)

Answer 21

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

Answer 22

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

Answer 23

* *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

Answer 24

Depends on route of spread: ## Footnote □ 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

Answer 25

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

Answer 26

**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

Answer 27

*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

Answer 28

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

Answer 29

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**

Answer 30

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

Answer 31

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)

Answer 32

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

Answer 33

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

JC24 (Medicine) - Meningitis and Encephalitis Flashcards

(57 cards)