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Central Nervous System

Infection
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(Infeksi
susunan saraf pusat)
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Foreword

Central Nervous System Infections is a

serious Illness
 Late diagnosis and proper Management
leads to death or serious disabilities
 Early diagnosis and treatment is
important

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CNS Infection may involve :

• The leptomeninges and CSF space

(meningitis)
• The gray and white matter of the brain
(encephalitis)
• The spinal cord (myelitis)

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Route Infection
 Open Wound around cephalic
 Direct contiguous infection from otitis media, sinus-
sinus paranasal, skin infection around cephalic and
face.
 Septisemia/ bakteriemia
 Abses cerebri.
 Retrograde infection along nerve.
 Direct infection to CSF by non steril lumbal
punction.

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Etiology of CNS Infections

 In case of suspected CNS Infections, we have to

differentiate between:
 Bacterial : Specific /non-specific
 Parasites : Malaria / Toxoplasma
 Fungal : Cryptococcus/Aspergillus's
 Viral : Japanese Encephalitis HIV, Herpes
 Prion Disease : TSE , CJD
 Look for the possibility of MIXED infections

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Special to look for

 Tuberculosis
 HIV / AIDS
 AIDS related opportunistic infections:
 Toxoplasma , Cryptococcus.
 Cysticercosis in endemic areas
 Malaria
 Typhoid
 New diseases ( Nipah E. , SARS )

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Clinical Sign and Symptoms

 Neurological Deficits

 Sign of Increased Intracranial Pressure:

 Papil edema
 Severe headache

 With or without fever

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Clinical Presentation

 Acute Meningo-Encephalitis
 Intracranial tumor Like : Brain abscess,
tuberculoma,Toxoplasma etc.
 First sign as Epilepsy : Cystecercosis
 Degenerative disease Like : SSPE,TSE

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LOGO Clinical presentation of
infective agents
 Meningitis: Bacterial / viral / fungal
 Encephalitis: Viral
 Brain abscess: Bacterial, fungal, parasitic
 Sinus thrombosis: Bacterial

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Physical Examination, Neurological

 Any sign of Infections ? Fever ,with headache,

muscle pain ?
 Lowering of Consciousness
 Alteration of Consciousness
 Cranial nerve palsies
 Neck stiffness/ meningeal signs
 Limb paralysis / hemiplegia

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Physical examination, Internal

 Skin abnormalities , exanthema , bleedings.

 Body temperature ? Fever ?
 Vital signs ; Blood pressure ,pulse, respiration,
 Respiratory abnormalities : Dyspnoeic ?
 Abdomen : tenderness , stiffness . Liver /spleen
palpable ?

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Diagnostic

 History taking
 General Examination
 Neurological Examination
 Neurological Investigation :
 EEG
 Chest x-ray
 CT Scan
 MRI
 Laboratory Examinaton :

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Diagnostic (Cont’)

 Laboratory Examinaton :
 Blood Leukocyte and differential count
 Blood test for micro-organism :
• culture / staining
• serological
• staining
• PCR
 Lumbar Puncture

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Lumbar Puncture

 Contraindications
 Infection in overlying skin
 Signs of intracranial mass lesion/ papil edema
 If an intracranial mass/hydrocephalus is
suspected.
 NEURO IMAGING is indicated, before CSF
examination
 Relative
• Coagulopathy
• Thrombocytopenia
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CSF analysis

 Examination followed by for protein and glucose

levels, cellular analysis, and identification of the
pathogen by polymerase chain reaction
amplification (recommendation level A) and
serology (level B)

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CSF Examination

In Viral infections:
 Cell count, Protein and Glucose content are not
so prominently altered.

In Bacterial and Fungal /Parasitic Meningitis:

 Cell count, protein content are much more
pronouncedly alleviated, and glucose content
lowered.

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CSF Abnormalities

Bacterial Serous Viral Meningitis/

Meningitis Meningitis Encephalitis

Appearance Purulent Turbid/Xanth Clear

Cell > 10,000 < 500 < 100

Diff count PMN >> MN >> MN >

­

Protein ­­

Glucose -0 N

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Viral Meningoencaphalitis

 Viral encephalitis is a medical emergency. The

prognosis depends mainly on the pathogen and
host immunologic state.
 Correct immediate diagnosis and introduction of
symptomatic and specific therapy has a
dramatic influence upon survival and reduces
the extent of permanent brain injury.

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Epidemiology

 Incidence is 1/10 of bacterial meningitis

 HSV-1, zoster, EBV,CMV, rabies, arbo
 Arbo
• LAC (La Crosse)-diagnosed most frequently
• SEE(St Louis)-20% mortality in elderly
• WEE(Western)- causes seizures in 90% of infected
infants, permanent neuro deficits in 50%
• EEE(Eastern)- most devastating, mortality 70%
• WNV(West Nile)
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 Benigne, symptoms are sometimes very mild

 Severe conditions give symptoms:
 Headaches
 Stiff kuduk
 LP : Pleiositosis lymphocytes. clear liquor
 Causes: most often from the enterovirus group:
 V. polyomyelitis
 V. coxsakie
 V. ECHO (Entero Cytophatic Human Orphan)
 Penetration through oral fecal trajectory / droplet spray

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V. Coxsakie is known for:

 Group A :
• Causes meningitis
• Rubeliform exantema with herpangina in the
hands, feet, mouth
 Group B
• Causes meningitis accompanied by muscle fatigue
to paralysis.
• Rhinitis, laryngitis, bronchitis.
• Exoantema was not found.

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 V. Echo :
 Scattered all over the world
 More often in children
 Children are often fussy/ whiny
 Often more prominent symptoms of exotelma
 Headaches
 Vomiting, muscle weakness of the limbs
 ± 24 hours of red patches ranging from the face
to the body.
 Stiff neck & pain

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Clinical features

The diagnosis of viral encephalitis is

suspected in the context of a febrile
disease accompanied by headache,
altered level of consciousness and
symptoms, and signs of cerebral
dysfunction.
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Clinical features
These may consist of abnormalities that can be
categorized into four:
 cognitive dysfunction (acute memory, speech
and orientation disturbances, etc.),
 behavioral changes (disorientation,
hallucinations, psychosis, personality changes,
agitation),
 focal neurological abnormalities (such as
anomia, dysphasia, hemiparesis), and
 seizures.

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Diagnosis

 MRI-more sensitive than CT

 CT Scan
 EEG
 LP-findings consistent with aseptic meningitis
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Differential

 Exclude the killers

 Bacterial meningitis & SAH
 More meningeal symptoms
 Lyme, TB, fungal, bacterial, viral, neoplastic
 More parenchymal symptoms
 Abscess, bacterial endocarditis, post-infectious
encephalomyelitis, toxic or metabolic
encephalopathy
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Treatment

 HSV: acyclovir 10mg/kg IV

 CMV: ganciclovir
 Rabies/EEE/HSVdevastating & usually fatal or
residual deficits
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Bacterial Meningitis
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Epidemiology

 400 per 100,000 in neonates

 1-2 per 100,000 in adults
 S pneumoniae & N meningitidis m/c
 HIB vaccine has been very effective
 Mortality
 5% in children beyond infancy
 25% in neonates and in adults
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Pathophysiology

S. pneumonia and N. meningitidis (and H.

influenzae) are encapsulated which provides
them with increased ability to invade BBB
Upper airway bloodstream subarachnoid
space subcapsular constituents trigger
inflammation fever, meningimus, change in
MS brain/meningeal edema decreased
CSF drainage hydrocephalus increased
ICP ICP>CPP
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Clinical Features

 25% of adult cases “classic”

 Rapid development of
• Fever
• Headache
• Stiff neck
• Photophobia
 Nonspecific signs/symptoms in very young/old
 25% will develop seizures
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BAKTERIAL AKUT

In neonates, purulent meningitis shows symptoms:

 Acute, heat high
 dyspnoe
 don't want to cheat
 icterus, decreased awareness
 seizures & coma.
 Often caused by:
 E Coli
 Streptococcal
 Stafilokokus
 Pneumococcal

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In infants and older children show symptoms:

 don't want to eat
 irritable
 confuse & letargy
 seizures & coma.
Often caused by:
 H. Infulenza
 Meningococcal
 Pneumococcal
 E Coli
 Streptococcal

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LOGO MENINGITIS
BAKTERIAL AKUT

In adults it is often caused by:

 Pneumococcal
 Meningococcal
 Streptococcal
 Stafilokokus
 H. Infulenza

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Clinical Features

 History
 Living conditions
• College dorm/barracksN meningitidis
 Trauma
• Recent neurosurgeryStaph/gram(-) rod
 Immunocompetence
 Immunization hx
• NoneHiB
 Antibiotic use
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Clinical Features

 Physical Exam
 Brudzinski
• Passive neck flex hips & knees flex
 Kernig
• Flex hip, ext knee hamstrings contract
 Skin
• Purpura
• Petechiae/splinter hem, pustular lesionsmicroemboli
 Funduscopy
 Neurology Examination
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Diagnosis

 Parenchymal
 CT is the imaging of choice
• Brain abscess, encephalitis, toxoplasmosis
 Meningeal
 Lumbar puncture
• Neoplasm, CNS vasculitis, SAH
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CEREBROSPINAL FLUID (CSF) ABNORMALITIES IN BACTERIAL MENINGITIS

Opening pressure; >180 mmH2O
White blood cells 10/µL to 10,000/µL; neutrophils predominate
Red blood cells Absent in nontraumatic tap
Glucose < 2.2 mmol/L (< 40mg/dl)
CSF/serum glucose < 0.4
Protein 0.45 g/L (>45 mg/dL)
Gram’s stain Positive in >60%
Culture Positive in >80%
Latex agglutination May be positive in patients with meningitis due to
Streptococcus pneumoniae, Neisseria meningitidis,
Haemophilus in uenzae type b, Escherichia coli, group B
streptococci
Limulus lysat Positive in cases o gram-negative meningitis
PCR Detects bacterial DNA
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Treatment
 First priority
 Antibiotics
 Second priority in some cases
 Anti-inflammatories
 Third priority
 Counter the adverse effects of increased ICP &
vasculopathy
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ANTIBIOTICS USED IN EMPIRICAL THERAPY OF

BACTERIAL MENINGITIS AND FOCAL CENTRAL NERVOUS SYSTEM INFECTIONS

INDICATION ANTIBIOTIC

Preterm infants to infant < 1 month Ampicillin + cefotaxime

Infants 1–3 months Ampicillin + cefotaxime or ceftriaxone

Immunocompetent children >3 months Cefotaxime, ceftriaxone, or

and adults <55 cefepime + vancomycin

Adults >55 and adults o any age with Ampicillin + cefotaxime, ceftriaxone or
alcoholism or other debilitating illnesses cefepime + vancomycin

Hospital-acquired meningitis, posttraumatic or Ampicillin + ceftazidime or

postneurosurgery meningitis, neutropenic meropenem + vancomycin
patients, or patients with impaired cell-mediated
immunity
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ANTIMICROBIAL THERAPY OF CENTRAL NERVOUS SYSTEM BACTERIAL INFECTIONS
BASED ON PATHOGENA
ORGANISM ANTIBIOTIC
Neisseria meningitides
Penicillin-sensitive Penicillin G or ampicillin
Penicillin-resistant Ceftriaxone or cefotaxime
Streptococcus pneumoniae
Penicillin-sensitive Penicillin G
Penicillin-intermediate Ceftriaxone or cefotaxime or cefepime
Penicillin-resistant Ceftriaxone (or cefotaxime or cefepime) + vancomycin
Gram-negative bacilli (except Ceftriaxone or cefotaxime
Pseudomonas spp.)
Pseudomonas aeruginosa Ceftazidime or cefepime or meropenem
Staphylococci spp.
Methicillin-sensitive Nafcillin
Methicillin-resistant
Vancomycin
Listeria monocytogenes Ampicillin + gentamicin
Haemophilus influenzae Ceftriaxone or cefotaxime or cefepime
Streptococcus agalactiae Penicillin G or ampicillin
Bacteroides ragilis Metronidazole
Fusobacterium spp. Metronidazole
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TOTAL DAILY DOSE AND DOSING INTERVAL

ANTIMICROBIAL AGENT CHILD (>1 MONTH) ADULT
Ampicillin 300 (mg/kg)/d, q6h 12 g/d, q4h
Cefepime 150 (mg/kg)/d, q8h 6 g/d, q8h
Cetotaxime 225-300 (mg/kg)/d, q6h 12 g/d, q4h
Cettriaxone 100 (mg/kg)/d, q12h 4 g/d, q12h
Cettazidime 150 (mg/kg)/d, q8h 6 g/d, q8h
Gentamicin 7.5 (mg/kg)/d, q8hb 7.5 (mg/kg)/d, q8h
Meropenem 120 (mg/kg)/d, q8h 6 g/d, q8h
Metronidazole 30 (mg/kg)/d, q6h 1500–2000 mg/d, q6h
Nafcillin 100–200 (mg/kg)/d, q6h 9–12 g/d, q4h
Penicillin G 400,000 (U/kg)/d, q4h 20–24 million U/d, q4h
Vancomycin 45-60 (mg/kg)/d, q6h 45-60 (mg/kg)d, q6–12hb
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Complications

 Seizures
 Hyponatremia
 SIADH
 CVA
 Coagulopathies
 Cognitive deficits, epilepsy, hydrocephalus,
hearing loss affect 25% of survivors
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MENINGITIS TUBERKULOSA
Berupa meningitis serosa akibat reaksi
peradangan yg disebabkan oleh kuman
tuberkulosa Terutama pada anak

 Penjalaran berasal dari :

 Paru – paru secara hematogen
 Infeksi TB di mastoid
 Spondilitis TB

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MENINGITIS TUBERKULOSA

 Pemeriksaan Fisik:
 Tanda-tanda rangsangan meningeal berupa kaku
kuduk, tanda Laseque dan Kernig
 Kelumpuhan saraf otak sering dijumpai

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LOGO MENINGITIS TUBERKULOSA

 Pemeriksaan Penunjang :
 LCS :
• Pelikel (+)/Cobweb Appearance (+)
• Peliositosis 50 – 500/mm3, dominan sel mononuklear,
protein meningkat 100-200 mg%, glukosa menurun < 50-
60%, bakteriologis Ziehl Nielsen (+), kultur BTA (+)
 IgG anti TB atau PCR
 Thorax foto
 CT Scan Kepala atau MRI

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LOGO MENINGITIS TUBERKULOSA

 Diagnosa Banding
 Meningoencephalitis karena Virus
 Meningitis bakterial yang pengobatannya tidak
sempurna.
 Meningitis oleh karena infeksi jamur/parasit
(Cryptococcus neoformans atau toxoplasma gondii),
sarcoid meningitis
 Tekanan selaput yang difus oleh sel ganas, termasuk
karsinoma, limfoma, leukemia, glioma, melanoma dan
medulablastoma.

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LOGO MENINGITIS TUBERKULOSA

 Tatalaksana :
 Umum
 Terapi kausal : kombinasi obat anti tuberkulosa
(OAT)
• INH
• Pyrazinamida
• Rifampisin
• etambutol

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LOGO MENINGITIS TUBERKULOSA

 Komplikasi :
 Hidrosefalus
 Kelumpuhan saraf kranial
 Iskemi dan infark pada otak dan mielum
 Epilepsi
 SIADH
 Retardasi mental
 Atrofi nervus optikus
 Prognosis
 Sembuh lambat dan umumnya
meninggalkan sekuele neurologis

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Brain Abscess
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Brain Abscess

 Focal pyogenic infection

 Pus-filled cavity ringed by granulation tissue &
outer fibrous capsule surrounded by edematous
brain tissue
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Epidemiology

 Paranasal sinus focus

 10-30 y/o
 Otic
 Bimodal: <20 y/o & >40 y/o
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Pathophysiology

 Hematogenous spread
 1/3 of cases
 Contiguous (middle ear, sinus, teeth)
 1/3 of cases
 Otogenic (Bacteroides)temporal
lobe/cerebellum
 Sinogenic & odontogenic(anaerobic &
microaerophilic streptococci)frontal lobe
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Clinical Features
 Classic triad
 Headache, fever, focal deficit <1/3 of cases
 Toxic appearance is rare
 Seizures, vomiting, confusion, obtundation
possible
 Frontal lobe-hemiparesis
 Temporal lobe- homonymous superior quadrant
visual field deficit or aphasia
 Cerebellum-limb incoordination or nystagmus
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Diagnosis

 CT with contrast
 LP contraindicated
 Biopsy or aspiration for confirmation
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Treatment

Presumed Source Primary Empiric Tx Alternative Tx

Otogenic Cefotaxime 2g IV q8h Bactrim 5mg/kg IV q6h +

Flagyl 1giv then 500mg q6 or
chloramphenicol

Sinogenic or odontogenic Pen 24 million units/d IV divided Pen (same dose) +

q4h + Chloramphenicol 100mg/kg/d
Flagyl 1g IV then 500mg q6h divided q6h

Penetrating trauma or Nafcillin 2g IV q4h + Vanco 15mg/kg (max 1g)IV q6h +

Ceftazidime 2g IV q8h Ceftazidime 2g IV
neurosurgery

Hematogenous Pen 24 million units/d divided q4h Pen (same dose) +

+ Chloramphenicol 100mg/kg/d
Flagyl 1g then 500mg q6h divided q6h

No obvious source Cefotaxime 2g IV q6h + No recommendations

Flagyl 1g IV then 500mg q6h
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INFEKSI SPIROKHETAL
Sifilis
 Disebabkan oleh kuman Treponema pallidum.
 Kuman ini tidak tahan terhadap panas, mudah
terbunuh oleh sabun, antiseptika, pengeringan.
Hanya bisa bertahan hidup pada keadaan
dingin.

 Penularan melalui kontak seksual.

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INFEKSI SPIROKHETAL
Sifilis
Gambaran penyakit :
 Menyerupai organic brain syndrome.
 Gejala prodromal berupa sakit kepala, insomnia,
cepat lupa, daya konsentrasi menurun, badan
letih. Pada tahap lanjut timbul dementia dan
perubahan watak yang menyerupai psikosis.

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INFEKSI FUNGAL

 Sering disebabkan oleh kriptokokus, nokardia,

mukomikosis, koksidiomikosis, aktinomikosis,
aspergillus.
 Penyebaran secara hematogen sering berasal
dari paru – paru.
 Meningitis oleh infeksi fungal ini menyerupai
meningitis serosa.

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INFEKSI PROTOZOAL

Toxoplasmosis

Gejala Klinis :
 80 – 90 % pasien tidak menimbulkan
gejala
 jika ada tersering limpadenopati
 Hidrosephalus
 Kalsifikasi serebral
 Khorioretinitis

ada binatang peliharaan  kucing

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INFEKSI PROTOZOAL
Toxoplasmosis
Liquor :
 kronik  N
 Akut  protein & limphosit meningkat
 EEG  gelombang delta diselingi spike.
Pada keadaan kronis EEG normal
CT Scan :
 lesi multiple yang menyerap kontras
 bentruk bisa cincin atau noduler
 tumor di white matter
 dgn edema otak diffus
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MIELITIS TRANSVERSA

Yaitu radang medulla spinalis yang mengenai segmen

medulla spinalis (substansia alba & grisea).
Etiologi :
 Pasca infeksi atau parainfeksi : infeksi virus, rubeola,
varisella, variola, jarang pada rubella, mumps, influenza.
 Pasca vaksinasi : anti rabies, varisella, pertusis, polio,
tetanus.
 Nekrotik atau degeneratif
 AIDS (Aquired Immuno Deficiency Syndrom)
 Dasar terjadinya mielitis oleh karena reaksi alergi

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LOGO MIELITIS TRANSVERSA
Gambaran klinis :
 Pasca infeksi / pasca vaksinasi mulai timbul
deficit neurology setelah 5 – 10 hari
 Perjalanan penyakit akut
» ± 50% timbul dalam waktu 12 jam
» ± 75% timbul dalam waktu 24 jam
 Mula mula berupa demam, malaise, mialgia.
 Deficit neurologik berupa
» Kelemahan ekstremitas
» Gangguan sensibilitas
» Gangguan genitourinaria & defekasi
 Segmen medulla spinalis yang sering terkena
antara segmen thoracal 2 – thorakal 6.

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MIELITIS TRANSVERSA
Gejala neurologik awal :

 Parestesia anggota gerak bawah dan tubuh

dengan pola segmental
 Kadang nyeri punggung yang menjalar
sepanjang batas atas lesi medulla spinalis.
 Pada keadaan akut timbul fase syok spinal
dengan gejala paralysis flaksid ke 2 tungkai,
retensio urine & alvi, setelah 3 – 6 mg baru
muncul paralysis spastic.
 Neuritis optika  Devic disease.

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MIELITIS TRANSVERSA

Laboratorium :
Liquor :
 Hambatan aliran liquor
 Pleiositosis moderat 20 – 200 sel/mm3 . limfosit
lebih banyak.
 Protein sedikit meningkat 50 – 120 mg/dl.
 Kadar glukosa normal.

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