This document discusses meningitis and brain abscess. It defines meningitis as inflammation of the meninges due to infection, which can be caused by bacteria, viruses, fungi or protozoa. Common bacterial causes include Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b. Symptoms vary depending on age but include fever, headache, neck stiffness, vomiting, and confusion. Treatment involves antibiotics, steroids, and supportive care. Brain abscesses are usually secondary to infections elsewhere, like sinusitis or otitis media. Common causative agents are streptococci, staphylococci, and anaerobic bacteria. Diagnosis involves imaging and treatment

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Definition of meningitis: Inflammation of the meninges due to infection
 Causes of meningitis:
1) Bacteria (more severe)
2) Viruses
-Mild
-Enteroviruses and Mumps (common)
3) Fungi (very occasionally) – Cryptococcus neoformans meningitis in
immunocompromised patients
4) Protozoa – Toxoplasma gondii (also causing brain abscess and encephalitis)
 Route of infection:
1) Haematogenous
2) Direct (particularly from an open skull fracture or from paranasal sinuses and middle
ear infection)
3) Iatrogenic (from lumbar puncture procedure)
 Symptoms:
Infant and young child (<5y/o) – non
specific symptoms
i. Low grade fever
ii. Vomiting
iii. Reluctance to feed
iv. Irritability
v. Rash (purpural or petechial)
Older child and adult
i. Fever
ii. Vomiting
iii. Headache
iv. Neck stiffness
v. Photophobia
vi. Confusion
vii. Rash (purpural or petechial)

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 Risk factors:
i. Splenectomy – infection with Haemophilus influenza type b
ii. Diabetes Mellitus – infection with S. pneumoniae
iii. Alcoholism – infection with S. pneumoniae
iv. Immunosuppressed – infection with Listeria monocytogenes
v. Fractured skull- infection with S. pneumoniae
vi. Inherited defects in late complement components – infection with Neisseria
meningitidis
vii. Pregnant woman – infection with Neisseria meningitidis
A. BACTERIAL MENINGITIS
 Most common in infants and young child
 Pattern of infection:
i. Colonisation
ii. Carriers
iii. Invasive
iv. Post-infection sequelae – post-infectious autoimmune disease and CNS
abscess
 Causative agents depends on geography and age-related differences
 TYPICAL pathogens:
All ages
i. N.meningitidis
ii. S.pneumoniae
iii. H.influenzae type b, in
pre-school child who are
not vaccinated
Neonate
i. Group B strep
ii. E.coli and aerobic GNB
iii. Listeria monotcytogenes
Teenagers and children
i. N.meningitidis
Elderly
i. S.pneumoniae
Immunocompromised
i. Listeria monocytogenes
WORLDWIDE!!
A. Neisseria Meningitidis
B. Streptococcus pneumoniae

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 Investigations:
a) Clinical – assess vaccine Hx + symptoms and signs of meningitis
b) Lab (sample: blood , CSF and rash)
i. Blood
-Culture
-PCR
-EDTA blood sample for peripheral WCC
-Blood sugar level (to compare with CSF sugar level; normal CSF sugar is
>60% of blood sugar!!!)
ii. CSF
-Physical appearance of fluid, i.e color! Bacterial infection: turbid or cloudy
fluid and NORMAL fluid is colourless
-Microscopy: Gram stain, cell count and differential
-Culture
-PCR for N.meningitidis, S. pneumonia, Haemophilus influenza
-Biochemistry: glucose and protein level (high in meningitis!)
iii. Rash
-Microscopy: presence of INTRACELLULAR gram –ve diplococcic will
confirm a diagnosis of meningococaemia (BSI of meningococcus)
-Sample of skin rash is indicated IF lumbar puncture is contraindicated, i.e
in RIP patient
iv. Nasopharyngeal swab will indicate colonisation not diagnostic of infection
v. Antigen detection for N.meningtidis, S.pneumoniae, Hib, E.coli and group
B strep
 Mx of bacterial meningitis:
1) Airway: ventilation may be required if patient is interrupted
2) Intensive care: organ support IF bloodstream infection is indicated
3) Steroids: administer before antibiotic or with first dose antibiotic to
reduce inflammation
-Hib meningitis: steroids reduce overall mortality
-Pneumococcal meningitis: steroids may reduce mortality in adults
-TB meningitis: steroids is used to reduce fibrosis and risk of
hydrocephalus
-Meningococcal meningitis: NO DATA!
4) Antibiotics: empirical and quickly (before blood or CSF cultures)
-Empirical:
 0-3mths: ampicillin + cefotaxime +gentamicin
 >3 mths: cefotaxime +/- vancomycin
-Definitive:
 Strep pneumoniae: cefotaxime + vancomycin IF penicillin
resistant
 N.meningitidis: benzyl penicillin
 TB: RIPE initially
5) Fluid: Fluid resuscitation for shock patient and fluid restriction for RIP

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 Prevention of meningitis: by chemoprophylaxis
-Rifampicin oral (first choice) and alternatives: ceftriaxone IM or
ciprofloxacin oral
I. Invasive meningococcal meningitis: close contacts of index case
II. Invasive Hib meningitis: close contacts IF there is an at-risk child
(<48mths @ <2y/o) in the contact network
III. Invasive pneumococcal meningitis: NO PROPHYLAXIS
By immunisation:
I. Hib vaccine for infants
II. MenC vaccine added for infant routine immunisation
III. Pneumococcal vaccine for at-risk groups (CSF leak, skull fracture,
elderly)
IV. No vaccines for neonatal bacterial meningitis (Listeria
monocytogenes, E.coli, Group B strep)
 Complications of bacterial meningitis:
I. Subdural abscess
II. Ventriculitis
III. Cranial nerve palsies especially the 6th
IV. Secondary vasculitis
V. Hydrocephalus (due to obstructed CSF drainage)
VI. Intellectual handicap
VII. RIP
VIII. Cerebral oedema
IX. Seizure and blindness
X. Herniation!

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Type of
Bacterial
Meningitis
Listeria monocytogenes Leptospira canicola
or Leptospira
icterhaemorrhagica
(Weil’s disease)
TB
Zoonosis Zoonosis TB meningitis usually secondary
haematogenous spread from a
focus elsewhere and the onset is
stealthy
In infants, the onset may be
acute
May occur during primary
haematogenous spread (miliary
TB) in infancy in particular
Route of
transmission
I. Ingestion of contaminated
meat, vegetables or dairy
products
II. Direct contact with infected
animals
I. Direct contact
with skin
openings such
as wounds
and mucous
membranes
I. Inhalation
Individuals at
risk?
I. Foetus
II. Neonate
III. Pregnant women
IV. Elderly
V. Immunocompromised
(due to neoplasia, high
steroids, transplant)
VI. Occupational Xposure
I. Farmer
II. Water
sports
Clues for diagnosis
-Jaundice
-Conjunctival
injection
I. Immigrants from areas
with TB endemic (Africa)
II. Child with malnutrition
III. Immunocompromised
IV. Non-vaccinated with BCG
V. Fever for mths or wks
Tx Ampicilin + gentamicin (resistant
to cephalosporin)
Benzyl penicillin RIPE tx
Investigation CSF with high
lymphocytes;
consider CSF if
renal/ hepatic
failure and
meningism
CSF clear
CSF with high protein and low
glucose and high lymhocytes
A fibrin clot may occur after a
short time of standing
ZN/Auramine stain and culture
Biopsy of meninges
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B. BRAIN ABSCESS
a) Clinical presentations: (can also be seen in encephalitis, meningitis, head trauma, stroke,
tumour)
i. Headache
ii. Seizure
iii. Nausea and vomiting
iv. Altered mental status
b) Sites:
i. Frontal lobe
ii. Temporal lobe
iii. Parietal lobe
c) Pathogenesis:
i. Secondary to a focus elsewhere
 Sinusitis
 Otitis media
 Penetrating head wound
 Fractured skull
 Post-op surgical sepsis
 Metastatic spread; S.aureus BSI with endocarditis
 IV drug use
 Immunosuppresion
 DM
d) Causative agents:
i. Bacterial
 Strep + anaerobes (commonest!!), polymicrobial
 Streptococcus (Str. Milleri or Str. Anginosus) 35%
 Staphylococcus (including MRSA) 20%
 Aerobic GN bacilli (E.coli) 23%
 Anaerobes (Bacteroides spp) 14%
ii. Fungal
 Aspergillus (in immunocompromised patients, eg neutropenia)
iii. Protozoa
 Toxoplasma gondii (in poorly controlled HIV infection)
e) Investigations:
i. Clinical:
-Signs and symptoms of underlying condition (eg sinusitis)
-Signs of RIP
ii. Imaging:
-CT
-MRI
f) Tx:
i. Craniotomy
ii. Burr hole aspiration + antibiotics (>2 types) , eg cefotaxime + metronidazole +
flucloxacillin
LESS COMMON