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Micbi > Bacterial Infections of CNS > Flashcards

Bacterial Infections of CNS Flashcards

1
Q

Classification of infections

A 
Meningitis
- purulent (bacterial), lymphocytic (viral), granulomatous (mycobacterial/ fungal)
Abscess 
- brain, epidural, subdural
Encephalitis (viral)
Myelitis
Spongiform Encephalopathy
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2
Q

Definitions

A

Meningitis = meningeal infection involving leptomeninges (arachnoid and pia mater) and subarachnoid space (CSF)

Acute meningitis = onset over a few hours up to several days

Chronic meningitis = insidious onset of meningeal signs and symptoms over weeks (CSF remains abnormal for >4 weeks)

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3
Q

Recall anatomy of dural spaces and CSF drainage

A

Dura mater
- periosteal layer and meningeal layers separate at certain areas to form dural venous sinuses
Arachnoid mater
Subarachnoid space (arachnoid granulations protrude into venous sinus, drain CSF into superior sagittal sinus)
Pia mater

CSF drainage:

  • CSF produced in choroid plexus of ventricles –> flow through cerebral aqueduct from 3rd to 4th ventricle –> flow into subarachnoid space by lateral and medial apertures (also into spinal canal) –> CSF removes waste from subarachnoid space –> excess is absorbed by arachnoid villi which drains into superior sagittal sinus
  • tight BBB means few WBC and inflammatory cells at CSF –> allows uncontrolled proliferation of bacteria
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4
Q

Acute bacterial meningitis: clinical presentations

A

MEDICAL EMERGENCY!!

Non-specific: acute onset of fever and headache; irritable and vomiting in neonates

Meningeal irritation due to movement of spinal cord within the meninges:

  • nuchal rigidity: inability to flex neck
  • kernig’s sign: when thigh and knee are flexed at 90 degrees, subsequent extension of knee causes pain (also +ve in SAH)
  • brudzinski’s sign: when lying supine, lifting patient’s head off couch causes flexion of hip/ knees involuntarily (to relieve pain)

Eye effects: photophobia, diplopia/ dilated pupils (CN palsy)

Mental alterations: confusion (GCS), drowsiness, coma

Haemorrhage: petechiae (esp meningococcal rash), purpura, ecchymosis

Symptoms of raised intracranial pressure

  • early: headache, vomiting, papilloedema
  • late: lethargy, CN 3 and CN 6 palsies, hemiparesis, seizures, bulging fontanelle in neonates
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5
Q

Acute bacterial meningitis: general risk factors and transmission routes

A 
Immunocompromised 
- hereditary e.g. complement defects
- splenectomy/ splenic dysfunction, HIV
Skull base fracture
NPC
Otitis media
Cranial trauma, CSF shunts
  • peak in infants and adolescents

Transmission routes

  • bloodstream (most common - via nasopharyngeal epithelium)
  • direct spread from otitis media/ sinuses
  • direct inoculation from open skull fracture
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6
Q

Causative agents of acute bacterial meningitis - age specific aetiologies/ risk factors and prevention

A

ABLE TO CROSS BBB

Neonates and Infants <3 months

  • Grp B strep > E.coli > Listeria monocytogenes
  • risk factors: maternal grp B strep colonisation (vaginal), prematurity, prolonged rupture of membrane during labour
  • prevention: maternal screening for GBS and intrapartum penicillin (IV prophylaxis at time of delivery)

Children >3 months

  • S. pneumoniae, *H. influenzae, N. meningitidis, MTB
  • risk factors: pre-existing AOM
  • prevention: PCV13, Hib vaccine, BCG vaccine, meningococcal group C+Y

Adults

  • S. pneumoniae, N. meningitidis, Strep suis, L. monocytogenes, MTB (v common in HK)
  • listeria and pneumococcus have higher mortality
  • risk factors: debilitated, elderly, DM, HIV
  • prevention: PCV13 + booster PPSV23, meningococcal A/C/Y/W-135 (travellers to endemic areas), meningococcal grp B (teenagers)

Procedure related or intra-cranial shunts

  • S. aureus/ MRSA, GN bacilli
  • prevention: infection control
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7
Q

Pneumococcal meningitis: recap organism properties, associated risk factors, complications

A

MOST COMMON CAUSE of bacterial meningitis
(common cause of bacterial sepsis)
- affect elderly, immunosuppressed, children

Recap:

  • gram +ve cocci in pairs, capsulated
  • normal resident in naspharynx, polysaccharide capsule as virulence factor, type specific Ab protective (98 serotypes based on capsule –> target of vaccine), PCV13/ PPSV vaccine
Highest mortality (15-20%)
Enter BBB using CbpA ligand (bind to PAF receptor)

Associated with:
- sinusitis, skull fracture, pneumonia, otitis media

Complications:

  • cerebral oedema (invasion into CNS induces permeability of BBB –> oedema and increase ICP)
  • cranial nerve palsies (pro inflammatory cytokines cause neuronal injury) e.g. deafness, mental retardation
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8
Q

Pneumococcal meningitis: treatment and prophylaxis

A

Treatment:
- Empirical IV cefotaxime –> change to IV penicillin G (benzylpenicillin) if sensitive; change to IV vancomycin if resistant to cefotaxime
(- IV dexamethasone may reduce mortality and hearing loss)

Prophylaxis:

  • protein conjugate vaccines (PCV13, PPSV23)
  • <2 yrs, >65 yrs or 2-65 with hx of invasive pneumococcal disease or immunocompromised or chronic disease e.g. DM, CVS/ Lung/ Liver/ Renal or cochlear implants
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9
Q

Pathogenesis of acute bacterial meningitis

A

Haematogenous spread by nasopharyngeal epithelium most common
- possible direct contiguous spread (sinusitis), direct inoculation (open skull fracture), vertical transmission (newborn)

–> local invasion and bacteraemia –> meningeal invasion via BBB receptors –> bacterial replication in subarachnoid space –> immune system activation and release of cytokines

Cerebral Microvascular endothelium

  1. increase BBB permeability ==> VASOGENIC OEDEMA
  2. increased CSF outflow resistance (due to WBC and protein) –> hydrocephalus ==> INTERSTITIAL OEDEMA

Macrophages (subarachnoid inflammation)

  1. bacterial toxins and ROS ==> CYTOTOXIC OEDEMA
  2. cerebral VASCULITIS affecting auto regulation and cerebral blood flow ==> DECREASE PERFUSION PRESSURE

All these results in INCREASE ICP and DECREASED BLOOD FLOW ==> CEREBRAL ISCHAEMIA (+/- herniation) with neuronal injury

VICIOUS CYCLE (high ICP leads to further oedema and metabolic disturbances etc.)

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10
Q

Meningococcal meningitis: organism, serotypes, epidemiology, presentation, complications

A

N. meningitidis

  • fastidious gram -ve diplococci
  • groups A/B/C/Y/ W135
  • reservoir from human nasopharynx

Affects all ages, commonly young adults

Presentation:

  • rapid progression of high fever and rash (non-blanching)
  • 50% PETECHIAE/ PURPURA

Complication:WATERHOUSE - FRIEDERICKSON SYNDROME
- meningococcaemia causing overwhelming sepsis ==> endotoxic SHOCK, DIC, widespread vasculitis ==> organ necrosis and BILATERAL ADRENAL GLAND HAEMORRHAGE (leading to adrenocortical insufficiency)

  • poor oxygenation can affect any organ e.g. ARDS, DIC, ARF (renal failure), liver failure, intestinal bleeding, CNS dysfunction, heart failure/ acute myocarditis ==> death
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11
Q

Meningococcal meningitis: treatment and prophylaxis

A

IV Ceftotaxime, 14 days (pen G if susceptible)

Prophylaxis:

  • group A/C/Y/W135 vaccine for travellers
  • group B vaccine (protein conjugate) for teenagers
  • Rifampicin (2 days) for close contacts (not necessary for health care professionals); alternatives include cefotaxime, ciprofloxacin, ceftriaxone
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12
Q

H. influenzae meningitis: organism, associated risk factors, epidemiology, treatment, prophylaxis

A

Pleomorphic GN bacilli, capsular type b most virulent

Associated with:
- pre-exisitng otitis media, pharyngitis, pneumonia

Affects infants 1 mth to 3 yrs

Complications:
- cerebral oedema, hydrocephalus, cranial nerve palsies

Treatment:
- Empirical IV cefotaxime –> change to IV ampicillin if sensitive (10-30% resistant)

Prophylaxis:

  • Rifampicin 4 days for close contacts
  • Hib vaccine available (not part of CIP as type b uncommon in HK)
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13
Q

Streptococcus suis meningitis: organism, source, at risk groups, other presentations, complications, treatment

A

gram +ve cocci in short chains
(grp R/S strep; serotype 2)

  • found in pigs –> affect butchers

Presentations:
- septicaemia, meningitis, infectious arthritis

Complications
- high incidence of deafness associated with meningitis

Treatment:
- high dose IV penicillin G for 14-21 days

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14
Q

Management of bacterial meningitis

A

Hx, PE
Identification of papilloedema, focal neurological deficits (pupils, gaze palsy etc)
–> if present: CT scan for MASS LESION, BLOOD CULTURE and EMPIRIC ANTIBIOTICS
–> if absent: BLOOD CULTURE and LUMBAR PUNCTURE

If no mass lesion on CT scan –> lumbar puncture
** don’t do LP if have mass or else risk of herniation!!

Mass lesino +ve –> contrast CT to rule out abscess
- organ support and surgical intervention as required

Lumbar puncture consistent with bacterial meningitis ==> EMPIRICAL ANTIBIOTICS based on gram stain/ Ag detection

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15
Q

Laboratory investigations of meningitis

A

LUMBAR PUNCTURE CSF

  • opening pressure increased (10-20 cm H20 is normal)
  • microbiology
  • – gram stain and culture (note H. influenzae may be misread as pneumococcus if inadequate decolorisation)
  • – india ink for cryptococcus
  • – ZN stain and rapid DNA detection for MTB
  • – +/- latex agglutination for common bacterial Ag/ cryptococcus antigens
  • CSF cell counts, protein and glucose levels

Others:

  • plasma glucose (to compare with CSF)
  • blood cultures
  • serology for viral studies (throat swab and stool culture if viral aetiology suspected)
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16
Q

CSF interpretation

A 
Appearance
Cells 
Type of cells (lymphocytes vs polymorphs)
Protein
Glucose
17
Q

CSF interpretation: appearance

A

Normal: Clear
Bacterial: Cloudy
Viral/ Encephalitis (mainly viral in origin): Clear
TB: Opalescent (thick, proteinaceous)
Cryptococcal: Clear/ cloudy
SAH: Xanthochromic (yellow) due to RBC degradation and haemolysis

18
Q

CSF interpretation: cells/ ml or microL??

A

Normal: <4 (neonates <30)
Bacterial: 100-2000
Viral/ Encephalitis/ TB/ Cryptococcal: 15-100
SAH: very high (may be >2000)

19
Q

CSF interpretation: type of cells

A 
Normal: L
Bacterial: P (increase >80%)
Viral/ Encephalitis: L (late)>P (early)
TB: L>P
Cryptococcal: L>P
SAH: crenated RBC
20
Q

CSF interpretation: protein (g/L)

A

Normal: 0.15-0.45
Other: >0.5
(TB and SAH very high)

21
Q

CSF interpretation: glucose (mmol/L)

A 
Normal: 60% of plasma glucose (2.8-4.2)
Bacterial: <2.2 (usually 0.1-1.1)
Viral/ encephalitis/ SAH: normal
TB: <2.2 (1.1-2.2 or <50% of plasma glucose)
Cryptococcal: <2.2

Decrease glucose due to glucose consumption and decreased glucose transport to brain

22
Q

Chronic meningitis: causative agents

A 
MTB
Cryptococcus neoformans
Treponema pallidum
Amoeba
HIV
23
Q

Granulomatous meningitis: causes, tuberculous meningitis (CSF features, presentation, location, complication, diagnosis)

A

MTB and Cryptococcus neoformans

Tuberculous meningitis

  • LYMPHOCYTIC CSF
  • insidious onset of headache, confusion and fever
  • Basal involvement, cerebellum
  • complicated by CSF blockage and hydrocephalus
  • Dx: BAL for PCR (sputum not sensitive enough), CSF for Ag detection

Cryptococcal meningitis
- HIV patients, immunocompromised

24
Q

Cryptococcal meningitis: risk factors, pathogenesis, pathology, diagnosis specimens and methods, monitoring methods, treatment, prophylaxis

A

Risk factors:

  • immunocompromised: AIDS defining disease, malignancy, steroid therapy, DM
  • SLE
  • alcoholism

Pathogenesis:
Pigeon droppings –> inhalation of yeasts –> engulfed by alveolar macrophages –> spread to LN in immune deficient patients –> blood borne –> NEUROTROPIC (grey matter ard ventricles, basal ganglia, cerebral white matter, cerebellar dentate nucleus)

Pathology: SOL with granulomas and mucinous exudate

Presentations:

  • indolent
  • similar to bacterial meningitis, weight loss, LG fever
  • cerebellar signs

Diagnosis:

  • CSF and BLOOD
  • increased CSF opening pressure
  • india ink +ve, culture on sabouraud agar without cycloheximide
  • latex agglutination test of CSF and Blood to detect capsule Ag titre for monitoring treatment response

Treatment

  • IV AMPHOTERICIN B (+ flucytosine)
  • Life-long FLUCONAZOLE prophylaxis after primary treatment in AIDS patients
25
Q

Brain abscess: risk factors, CT image, treatment

A

Risk factors:

  • haematogenous spread (MC: IE)
  • contiguous spread e.g. bronchiectasis, sinusitis, dental caries
  • direct inoculation e.g. open fracture, post-op

CT: ring enhancing lesion with surrounding vasogenic oedema

Treatment

  • drainage
  • antibiotics: 3rd generation cephalosporin + metronidazole
26
Q

DDx of CNS infections

A 
Acute meningitis (various pathogens)
Brain abscess
Rickettsial infection, parasitic infection, leptospirosis
Non-infective e.g. SAH
Malignancy

Micbi (32 decks)

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