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Cns Infection: Dr. Sri Indah Aruminingsih, SP - Rad
Cns Infection: Dr. Sri Indah Aruminingsih, SP - Rad
Infectionsite
1.parenchyma: encephalitis , myelitis
encephalomyelitis.
2.meninges: meningitis, pachymeningitis,
leptomeningitis.
3.both of parenchyma and meninges :
meningoencephalitis.
Infections pathway
1.infection through circulation
2.direct infection : trauma ,otitis media
3.retrograde along peripheral nerves
ASEPTIC MENINGITIS
Viral, atypical bacteria, fungal, TB
Bartonella henslae
Bordetella pertussis
Borrelia burgdorferi
Brucella spp.
Chlamydia spp.
Ehrlichia, Leptospria spp.
Mycobacteria spp.
Mycoplasma spp.
Rickettsia spp.
Treponema pallidum
Toxoplasma gondii
Entamoeba histolytica
Acanthamoeba
Trichinella
Naegleria
TB Meningitis
Most serious complication of TB
infection
Fatal without effective treatment,
significant morbidity even with
treatment
In children CNS involvement occurs
during primary infection (rather than
reactivation)
Usually results from hematogenous
spread from a primary focus (lungs)
Variable presentation, but usually
onset is insidious
More rapid in infants and young
TB Meningitis
Clinical Staging
Stage
Stage 1 (Early)
Days to weeks
Stage 2 (intermediate)
Weeks to months
Meningeal irritation
Minor neuro deficits (CN)
Stage 3 (late)
Months to years
Abnormal movements
Convulsions
Stupor or coma
Severe neuro deficits
ENCEPHALITIS AND
MYELITIS
Encephalitis
* Refers to inflammation of the brain
parenchyma
* Pathology shows:
Inflammation and destruction of neurons
Pathogen detection by direct visualization,
staining, etc
* Referred to as postinfectious encephalitis
when in temporal association with viral
infection or immunization
ADEM when it includes spinal cord
* Can cause significant alterations in
sensorium and seizures
Many patients require ICU
Etiology
* In neonates, the most common etiology is
HSV (usually type 2), but also entero- and
adenovirus
* In older children arthropod-borne viruses
(arboviruses) and enteroviruses are the
most common
Arbo: EEE, WEE, St. Louis, West Nile, JE
Entero: polio, echo, coxsackie, etc
* Subacute sclerosing panencephalitis is a
now rare complication of measles infection
* Tick borne bacteria can also be implicated
Borrelia, Rickettsia, ehrlichiosis
Pathogenesis
* Once a virus crosses the epithelium (usually at
a mucosal surface) viral replication occurs,
followed by viremia
* Viruses can penetrate the CSF from the blood,
or by spread from peripheral neurons (rabies and
HSV)
* Once in the CNS the virus attaches to host cells
Viral genome replication takes over, affecting
the other functions of the cell
* Interferon in particular inhibits viral
penetration, replication, translation, and
assembly
The inflammatory process may turn on the host
Clinical Manifestations
* Varies depending on affected site, severity,
and host factors
May or may not involve meninges (rabies)
* Nonspecific symptoms in neonates
May not have maternal h/o HSV
* Older children have acute onset of fever,
HA, seizures, behavior changes, AMS, or
coma, +/- prodrome
Depends on site of involvement
May have paralysis or paraplegia if spinal
cord involved
Look for rashes (erythema migrans)
Neuroimaging
Etiology
HSV
Japanese encephalitis
Rabies
Eastern equine
encephalitis
Site of involvement on
MRI
Inferomedial temporal
and frontal lobes
Bilateral thalami and
basal ganglia
Hippocampal, cerebellar,
mesencephalic areas
Disseminated brain stem
and basal ganglia
HSV Encephalitis
HSV is the most common cause of
fatal encephalitis in childhood
Mostly HSV-1 after neonatal period
Encephalitis can result from both
primary and recurrent HSV infection
Primary CNS if via olfactory and
trigeminal nerves
Disseminated HSV in the neonate
affects the CNS by hematogenous
spread
Older children
Diagnosis
* Swabs from conjunctiva,
nasopharynx, rectum,
skin lesions
* MRI may show temporal
or frontal involvement
* PLEDs on EEG
* HSV PCR is 95 %
sensitive and 100%
specific (gold standard)
* Please dont do a brain
biopsy
Abscesses: Etiologies
* Most common pathogens include
anaerobes, GNs, streptococci, and staph
* Neonates most commonly get GNs:
Citrobacter, Enterobacter, Proteus
* In other populations the organism
depends on predisposing factors:
CHD a-hemolytic strep
Endocarditis strep, S. aureus
Post-trauma staph
Otitis/sinusitis strep, Bacteroides
fragilis, Proteus spp., pseudomonas,
H.flu
Abscesses:
Pathogenesis
* May occur via hematogenous or direct spread
* Cyanotic heart disease is the most common
underlying condition (esp. TOF)
Polycythemia higher viscosity
microinfarcts
Bacteria love it!
* Chronic pulm infection, bacterial endocarditis,
and immune compromise also increase risk
* Direct spread may occur from chronic otitis,
mastoiditis, sinusitis, trauma, NS procedures
* Meningitis is a rare cause if treated
appropriately
Except in neonates with GN meningitis
Abscesses:
Pathogenesis
* Bugs localize at the gray-white junction
cerebritis
* Stage 1: Early cerebritis (Day 1-3)
Leukocyte infiltration, focal edema, no
clear demarcation
* Stage 2: Late cerebritis (Day 4-9)
Central liquefaction necrosis (yum!),
fibroblast infiltration, capsule formation
* Stage 3: Early capsule formation
* Stage 4: Late capsule formation (2
weeks out)
Dense fibrous capsule, marked edema
Abscesses:
Pathogenesis
Entire process may take 4-6 weeks
May progress faster or rupture into
ventricular system
Sites of infection vary but cerebral
are most common
Kids with CHD get them in MCA
distribution
Otitis can spread to unilateral
temporal lobe or cerebellum
Abscesses: Diagnosis
LP would be contraindicated in a
patient with brain or spinal cord
abscess
ButCSF may show pleocytosis,
protein, normal glc
Blood cultures and cultures from
other potential foci would help
Get imaging
Pathogenesis
Direct spread from contiguous foci (4050%)
Hematogenous (25-35%)
Penetrating trauma/surgery (10%)
Cryptogenic (15-20%)
27
CTID,2001
IMAGING STUDIES
MRI
more sensitive for early
cerebritis, satellite lesions,
necrosis, ring, edema,
especially posterior fossa &
brain stem
CT scan
99m Tc brain scan
Abscesses: Imaging
Abscesses: Imaging
Cerebritis Vasculitis
Shunt Infections
2/3 of all shunt infections are caused
by staph spp
Staph epi, aureus, and other coagnegative types have been
frequently isolated in several
series
GN enterics (E.coli, Klebsiella,
Proteus, Pseudomonas) make up 620%
Strep causes 8-10%
Multiple organisms are found in 1015%
Incidence has declined over the past
Pathogenesis
* Shunts are foreign bodies and interfere
with natural host defense mechanisms
Chemotaxis and phagocytosis
* Staph can also form biofilm which
increases bacterial adherence and
decreases effect of antibiotics
* Infection may occur through different
mechanisms:
Wound or skin breakdown over shunt
Colonization at the time of surgery
Retrograde from the distal end of shunt
Hematogenous seeding (infrequent)
Clinical Presentation
Fever, headache, vomiting, lethargy,
altered mental status
Check for wounds and look for
cellulitis along the shunt
Infection may spread to the distal
end of the shunt and cause
peritonitis
Fungal Pathogen
Prematurity
Candida albicans
Candida, Cryptococcus,
Aspergillus
Corticosteroids
Cryptococcus, Candida
Cytotoxic agents
Aspergillus, Candida
Secondary immunodeficiency
(AIDS)
Cryptococcus, Histoplasma
Zygomycetes
IV drug abuse
Candida, Zygomycetes
Zygomycetes (Mucor)
Candida
Fungal Meningitis
Most common causes are
Cryptococcus neoformans, C.
immitis, Candida, and Aspergillus
Fungal meningitis in general has a
more insidious onset than bacterial
Symptoms may develop over days
Always consider it with
subacute/chronic presentation
C.neoformans may develop more
quickly in patients on high-dose
steroids or with HIV
Fungal Meningitis
Rhinocerebral syndrome is a major
presentation of zygomycosis
Rhizopus and Mucor spp
Associated with poorly controlled
DM
Orbital pain, nasal discharge, facial
edema, proptosis
May invade carotids, trigeminal nerve
and adjacent brain structures
May also present with sudden
neuro deficit due to vasculitis
Can rarely cause mycotic
aneurysmal bleed
PARASITIC CNS
INFECTIONS
Neurocysticercosis
and Cerebral Malaria
Neurocysticercosis
- Most common parasitic
CNS infection.
Important cause of epilepsy in
the tropics.
Neurocysticercosis
Parenchymal
Extraparenchymal
Seizures in 70-90% of
patients
1/3 will have raised
ICP
4% have focal neuro
deficits
May have encephalitis
Rare in children
Obstructive
hyrdocephalous or
chronic meningitis
Spinal involvement
Numerous cysts
Diffuse cerebral edema
Poor prognosis
Radicular pain
Cord compression
Transverse myelitis
Ophthalmic
involvement
Vision deficits
Neurocysticercosis
Organisme
bentuk kalsifikasi
Toxoplasmosis
Rubella
CMV
HSV
Toxoplasmosis
Gambaran radiologis
1.
Rubella
Gambaran radiologis
2.
3.
CMV
Gambaran radiologis
1.
2.
3.
4.
5.
Kalsifikasi : curvilinear,
periventrikuler
Cerebral atrophy + gliosis + ggn.
myelinasi
Hydrocephalus / ventriculomegaly.
Hypoplasia cerebellar
Microcephaly + cortical dysplasia
( relatif sering ) polymicrogyria
lissencephaly
Herpes Simplex
Virus
Gambaran radiologis
Herpes
Simplex
Virus
Terima kasih