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NEUROINFEKSI

Dr. Syahroni, SpS


INFEKSI SUSUNAN SARAF PUSAT
• Virus >>>
• Bakteri >>>
• Jamur
• Parasit CNS

• Sal cerna
• Sal. Nafas Darah
• Kulit Continuitatum
• organisms rarely reach the CNS
• Important protective systems :
 Reticuloendothelial system (which
nonspecifically and efficiently removes
microorganisms from the blood),
 cellular and humoral immune responses
(which destroy specific microorganisms in the
blood and at sites of infection),
 and the blood–brain barrier.
Keys to Suspecting a
Central Nervous
System Infection
The signs and symptoms of a CNS infection
depend on the site of the infection and not
the Infectious organism.
The organism determines
the time course and severity of the
infection
Clinical Features of Major Central Nervous System
Infections
Bacterial Meningitis
• Meningitis is due to inflammation of the
meninges
• the most common CNS infection.
• Commonly is due to bacteria or viruses
n can be caused by fungi, parasites
• infants, the elderly
• immunosuppressed of any age.
• The usual route of entry is via the upper respiratory
tract
• The exact location of penetration of the blood–CSF
barrier is unknown
• Once within the CSF, the bacteria again replicate and
release endotoxin
• These molecules stimulate resident macrophages and
microglia to release inflamatory factors
• As the inflammation increases, however, the
brain become irritated and damaged
Clinical Features
• The clinical hallmark of any meningitis is fever,
headache, stiff neck, and a relatively
preserved mental status
Laboratory Findings

• diagnosis of meningitis bacterial


is made from analysis of CSF (LP = Lumbal
puncture)

• When meningitis is suspected, the lumbar


puncture (LP) becomes an emergency
procedure
Treatment
• The key to etiologic treatment is the prompt
administration of appropriate antibiotics
• Without antibiotics, over 95% of patients die
• the antibiotic should be given as early
• (1) in the clinical course as possible;
• (2) the bacteria must be sensitive to the antibiotic
administered;
• and (3) the antibiotic must cross the blood–CSF
barrier and achieve sufficient concentration to kill
the bacteria.
Figure . Common bacteria that cause meningitis in the United
States.
Prognosis
• Mortality ranges from 5% to 25%, depending
on the infecting bacteria,
age of patient, and
predisposing illnesses.
• In surviving children :
15% have language disorders,
10% mental retardation,
10% hearing loss,
5% weakness or spasticity, and
3% epilepsy
Brain Abscess
• A brain abscess is a localized mass infection
within the brain parenchyma
• most commonly : bacterial infection, but
fungi, M. tuberculosis can also
• Incidence of about 1/100,000 persons per
year
• both sexes and all ages.
 Microorganisms reach the brain primarily through the
 bloodstream or
 directly from adjacent infected sinuses or mastoid
air cells.
• Less-common routes :
 depressed skull fractures or following surgical procedures
 involving the sinuses, calvarium, or brain.
 Common sources of bloodstream infection :
infections of the lungs (bronchiectasis,
empyema, and lung abscess), GI tract, urinary system,
mouth (dental abscess), heart (acute bacterial
 endocarditis and cyanotic congenital heart disease),
 intravenous drug abuse
Major Laboratory Findings
• The WBC count is elevated in 60% of patients
• the total count is elevated above 20,000
cells/mm3
• in only 10%. The ESR and serum C-reactive
protein are often elevated, indicating the p
resence of a systemic infection
• signs and symptoms of a brain abscess are
those of an expanding brain mass that
develops over 1 to 2 weeks
Common symptoms
• Increased intracranial pressure (ICP) :
 headache (75%),
 lethargy and confusion (50%),
 nausea and vomiting(50%), a nd
 CN palsies (30%).

Less-common
• papilledema (10%–25%)
• stiff neck (25%).
• Focal neurologic signs (40%)
• aphasia, homonymous hemianopsia
• Ataxia,
• Focal or generalized seizures
Brain abscess (computed tomography and magnetic
resonance imaging scans).
Prognosis
• Mortality of a brain abscess 10% - 20%.
• In survivors 20% to 60% are left with
neurologic sequelae :
 hemiparesis
 aphasia, ataxia, and
 visual loss
 Chronic seizures : focal or generalized
 difficult to suppress with anticonvulsants.
Herpes Simplex Virus Encephalitis

• Encephalitis is a diffuse infection of the brain


• parenchyma.
• Viruses are the most common infectious agents, but
bacteria (e.g., general paresis
• from T. pallidum), and protozoa (e.g.,
toxoplasmosis) also cause diffuse brain infections.
• There are numerous viruses that cause encephalitis
most common :
• herpes simplex virus (HSV)
• group of arboviruses (for arthropod-borne viruses)
Pathophysiology
• HSV type 1 is most often acquired during early
Childhood
• During that infection, the virus travels up the sensory
axons of the trigeminal nerve from the mouth to the
trigeminal ganglia.
• In the corresponding ganglion neuron
• the virus becomes latent in the nucleus.
• During latency, no viral proteins appear on the
neuronal membranes so the host immune system
cannot detect and
• How HSV reaches the brain is poorly understood.
Since HSE usually develops in healthy individuals
who have been previously infected with HSV
activated latent virus appears to reach the
brain.
• One hypothesis proposes that a latently infected
neuron in the trigeminal ganglion innervates the
base of the brain rather than the face
Clinical Features
• HSE develops equally in both sexes and in all
ages without a prodromal illness.
• Acute encephalitis is characterized by the abrupt
onset of fever, headache, and mental
obtundation
• Encephalitis differs from meningitis in that
patients present with prominent mental changes
and minimal or absent stiff neck
Laboratory Findings
• WBC count is elevated
with a shift to the left
• CSF protein level is mildly to moderately
elevated
• Definitive diagnosis is usually made by
detection of HSV DNA in CSF by a PCR test
• positive in over 95% of HSE
• EEG in theHSE, demonstrates
 high-voltage complexes that originate from
the temporal lobes in a semiperiodic
nature that are suggestive but not diagnostic
• The MRI scan is very helpful in HSE
• changes are seen in the medial temporal
lobe
• CT abnormalities include low-density lesions in
one or both temporal lobes and areas of
hemorrhagic necrosis
Treatment

• Treatment with the antiviral drug acyclovir


dramatically improves morbidity and mortality
• sooner given, better the outcome
• Unfortunately no satisfactory drugs for the
common RNA viruses (arboviruses, measles,
and rabies)  symptomatic treatment
Prognosis

• Without acyclovir  HSE has a mortality rate


of 70%.
• With acyclovir : Currently about 70% of
patients with HSE survive and 30% of survivors
make a good recovery
• Mortality from encephalitis from arboviruses
ranges as high as 50%