The document discusses central nervous system (CNS) infections such as meningitis, encephalitis, myelitis, cerebral abscess, and subdural empyema. It describes the causes, clinical features, investigations, and management of these conditions. Some key points include that meningitis involves the meninges and subarachnoid space, while encephalitis is a diffuse brain infection. Viral meningitis is commonly caused by enteroviruses, while bacterial meningitis requires prompt treatment with antibiotics. Clinical features may include headache, fever, and altered mental status. Lumbar puncture and CSF analysis are important investigations to identify the causative organism.

2. CNS Infections
•Acute meningitis
•Chronic meningitis
•Encephalitis / myelitis
•Cerebral abscess
•Subdural empyema

3. Meningitis Infection of meninges & subarachnoid space
Encephalitis Diffuse infection of the brain parenchyma
Meningoencephalitis Combination of above
Brain abscess Focal infection of the brain parenchyma
Epidural abscess Collection of pus between the dura mater &
overlying bone in either the cranial or spinal
epidural space
Subdural empyema Collection of pus in the space between the
dura & arachnoid
Myelitis Infection of the spinal cord
Infections of the CNS

4. 1. Pada saraf tepi : Neuritis
2. Pada mening : Meningitis
3. Pada Jar. Otak : Ensepalitis
4. Pada Jar. Med. Spin : Mielitis
1. Infeksi Virus
2. Infeksi Bakteri
3. Infeksi Spirokheta
4. Infeksi Fungus
5. Infeksi Parasit (Protozoa dan Metazoa)

5. 1. Enteroviruses (echo-, coxsackieviruses)
• Most common cause of viral meningitis (80-85% of
patients)
• Fecal-oral transmission
• Most common in summer & fall; age <40
2. Arboviruses
• Vector transmission
• Includes St. Louis Encephalitis virus, Eastern Equine
Encephalitis virus, Western Equine Encephalitis
3. Mumps
• Incidence decreased due to vaccination
Viral Meningitis

6. 4. Lymphocytic choriomeningitis virus
• Transmitted via contact with hamsters, rat,
mice or their excreta
5. Herpesviruses
• Meningitis occurs in 20-30% of persons
with first episode of genital herpes
• Herpes zoster (shingles)
6. HIV
• Meningitis may be part of the acute
retroviral syndrome
Viral Meningitis

7. •Acute:
•presentation within 24 hours of meningeal
symptoms
•Most acute cases are bacterial
•Subacute:
•presentation within 1-7 days of symptoms
•Chronic:
•presentation after 7 days of symptoms
Meningitis: Tempo of Illness

9. Encephalitis / Myelitis
Aetiology
Direct viral infections:
1.Enteroviruses (Coxsackie, Echo, Poliovirus)
2.Herpesviruses (HSV 1/2, VZV, EBV, CMV, HHV-6)
3.Adenovirus
4.Measles, mumps
5.Arboviruses

10. Post viral infections:
1. Herpesviruses (VZV, EBV)
2. Measles, mumps
3. Influenza
4. Rubella
Nonviral causes
Encephalitis / Myelitis (lanjutan)

11. Causes of Viral Meningitis
Virginia A. Triant, MD, MPH
The Health Care of Homeless Persons - Part I - Viral Meningitis

12. Virginia A. Triant, MD, MPH
The Health Care of Homeless Persons - Part I - Viral
Meningitis

13. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

14. Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

15. Causative agents for acute
viral encephalitis in the United
States
Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

16. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

17. Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

18. Diseases that may mimic viral
encephalitis
Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

19. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

20. Non-viral causes of infectious encephalitis (cont.)
J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

21. Non-viral causes of infectious encephalitis (cont.)
J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

23. Pathogenesis
Direct involvement
1. haematogenous
2. neural
3. direct (cribriform plate)
Indirect involvement
1. post infection
2. post vaccinal

24. Entry of virus into host
Primary replication :
Respiratory / GI tract,skin/muscle
Secondary replication
Vascular endothelium,RES or muscle
Persistent viremia
Choroid plexus to CSF Vascular endothelitis
Pathogenesis of viral inf.of the
CNS : Hematogeneous spread
Crosses from blood to brain
Pathogenesis & pathophsyology of viral CNS infections

25. Pathogenesis of viral inf.of the CNS :
Neuronal transmission
Penetration and
Replication of virus
at mucocutaneus site
Replication at dorsal
root ganglia
Cutaneous
manifestations of
disease
Transmission to
spinal cord
Axonal transport of
virions
Centrifugal
migration of virus
Pathogenesis & pathophsyology of viral CNS infections

27. Clinical Features
‘Meningoencephalitis’
Headcahe
Nuchal rigidity
Signs of hydrocephalus
Focal neurological signs
Altered mental status
Seizures
Hypothalamic dysregulation
‘Myelitis’
Signs of cord involvement
Systemic findings may give clues to aetiology

28. Meningitis: Clinical Manifestations
•Headache
•Nuchal rigidity
•Fever and chills
•Photophobia
•Vomiting
•Seizures
•Focal neurologic symptoms
•Altered sensorium (confusion, delirium, or declining level
of consciousness)
•Rash

29. In meningitis, the stiff
neck is a problem of
forward flexion only;
resistance to lateral
flexion, rotation, or
extension must be due
to some other etiology
(Sapira, 2nd ed., p. 548)
Physical Examination: Nuchal Rigidity

30. Flexing neck 
involuntary hip
&
knee flexion
Physical Examination: Brudzinski Sign
http://health.allrefer.com/pictures-images/brudzinskis-sign-of-meningitis.html

31. Flex knee & hip to
90°, then extend
knee  pain in
hamstrings
Physical Examination: Kernig Sign
http://health.allrefer.com/pictures-images/kernigs-sign-of-meningitis.html

33. Investigations
Lumbar puncture
CT/MRI brain
EEG
Serology

34. •If acute bacterial
meningitis is suspected,
obtain CSF & blood
cultures before
neuroimaging
•If diagnosis is uncertain, a
repeat spinal tap should be
repeated in 8-12 hours
•12-39% of patients
undergoing LP develop
headache
http://health.allrefer.com/pictures-images/lumbar-puncture-spinal-tap.html
Lumbar Puncture

35. The
Evaluation
Normal Findings What abnormal findings may indicate
Pressure Less than 200cm
H2O
tumors, hydrocephalus, intracranial bleeding
Color Clear and
colorless
Cloudy-bacteria, WBCs
Red-tinged--subarachnoid bleeding
Blood None Cerebral hemorrhage or Traumatic tap (inadvertant
rupturing a blood vessel )
Cells No Red blood
cells,
<5
lymphocytes/mm2
Red blood cells-- blood within the spinal canal,
White blood cells--infection
Culture &
Sensitivity
No organisms
present
Bacterial or fungal infection
Protein 15 - 45 mg/dl
up to 70mg/dl for
elderly and
children
Meningitis, encephalitis, myelitis, tumors, inflammatory
processes
Glucose 50 - 75 mg/dl
or 60 to 70% of
blood glucose
level
Meningitis, neoplasm
Chloride
(not
routinely
evaluated)
700 - 750 mg/dl Meningeal infections, tubercular meningitis
Lumbal Pungsi dan LCS

37. Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

38.  Metode in vitro untuk menjelaskan rangkaian
suatu asam nukleat
 Terdiri dari beberapa siklus : denaturasi
DNA,primer annealing, dan ekstensi oleh
DNA polimerase
 Untuk menjelaskan sebuah segmen
DNA,digunakan 2 bahan
dasar(as.nukleat)untuk mengikatkan
rangkaian tambahan dari target gen
Zeev`Ronai,Ph.D.PCR in early detection and monitoring of cancer

39.  Dua bahan dasar ini,dicangkokkan pada
rangkaian lain dari DNA target pada arah
yang berlawanan,sehingga memungkinkan
DNA polimerase untuk menyambung
rangkaian tersebut
 Setiap siklus menghasilkan rangkaian DNA
yang saling melengkapi, dimana primer terikat
sebelum polimerase mempengaruhi
rangkaian lain di siklus berikutnya

40. Hasil dari setiap siklus adalah ganda
Hasil yang sangat sensitiv,sehingga
menyebabkan reaksi yang beragam dari
sebagian kecil dari rangkaian DNA awal
Zeev`Ronai,Ph.D.PCR in early detection and monitoring of cancer

41. Polymerase Chain Reaction

42. Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town

43. Langkah – langkah pemeriksaan PCR

45. Management
Empirical therapy
Acyclovir
Antibacterial
Presumptive/specific therapy
Supportive therapy

46. J Neurol Neurosurg Psychiatry 2003;74:1016–1022

47. Virginia A. Triant, MD, MPH
The Health Care of Homeless Persons - Part I - Viral Meningitis

48. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

49. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

50. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

51. J Neurol Neurosurg Psychiatry 2004;75(Suppl I):i29–i35. doi: 10.1136/jnnp.2003.034348

52. J Neurol Neurosurg Psychiatry 2003;74:1016–1022

53. J Neurol Neurosurg Psychiatry 2003;74:1016–1022

54. Carolyn V Gould, Ebbing Lautenbach “Meningitis and
encephalitis”

55. Differential diagnosis of acute meningitis
(cont.)
Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

56. Differential diagnosis of acute meningitis (cont.)
Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”
Carolyn V Gould, Ebbing Lautenbach “Meningitis and encephalitis”

58. Abses serebri adalah kumpulan material
piogenik dibatasi struktur melingkar yang
berlokasi pada perenkim otak.
Diperkirakan insiden abses serebri pada
negara industri adalah 1 dalam 10.000 orang.
Lebih banyak pada laki-laki dibanding
perempuan dengan perbandingan 1,7 : 1
sampai 3 : 1. Abses serebri terjadi pada
semua umur, nilai tengah umur yaitu 30
sampai 40 tahun, 25 % terjadi pada umur 50
sampai 60 tahun dan umur yang lebih muda
dari 15 tahun.

59. Pulmonary abnormalities
Congenital cyanotic heart disease
Bacterial endocarditis
Penetrating head trauma
AIDS
Greenberg, 2001

60. Mikrobiologi penyebab abses otak
( Infections of the Central Nervous System, 1991 )
Organisma Total ( % )
Aerob 61,2
Staphylococcus aureus 13,4
Gram negative bacilli 15,7
Streptococci 32,1
Anaerob 32,1
Streptococci 9,6
Species Bacteriodes 10,8
Lain-lain 11,7
Miscellaneous 6,7

61. Abses otak : penyakit pendahulu, lokasi abses, dan mikrobiologi
(Infections of the Central Nervous System, 1991)
Penyakit pendahulu Lokasi abses Isolasi kuman dari abses
Penyebaran dari lokasi infeksi primer
pada otitis media dan mastoiditis
Lobus temporalis, hemisfer
cerebellar
Streptococci (anaerobic atau aerobic),
Bacteriodes fragilis, Enterobacteriaceae
Sinusitis frontoethmoidal Lobus frontalis Predominan streptococci, Bacteriodes,
Enterobacteriaceae, Staphylococcus
aureus, species Haemophilus
Sinusitis sphenoidal Lobus frontalis, lobus temporalis Predominan streptococci, Bacteriodes,
Enterobacteriaceae, Staphylococcus
aureus, species Haemophilus
Sepsis dental Lobus frontalis Campuran Fusobacterium, Bacteriodes,
dan species Streptococcus
Penetrasi trauma kepala, infeksi
pasca bedah, pelebaran dari infeksi
primer
Berhubungan dengan luka Staphylococcus aureus, streptococci,
Enterobacteriaceae, Clostridium sp
Penyakit jantung kongenital Abses multiple, lazimnya distribusi
mengikuti arteri cerebri media
Viridans, anaerobic, dan microaerophilic
streptococci, species Haemophillus
Abses paru, empyema,
bronchiectases
Abses multiple, lazimnya distribusi
mengikuti arteri cerebri media
Fusobacterium, Actinomyces,
Bacteriodes, streptococci, Nocardia
asteroides
Endocarditis bacterial Abses multiple, lazimnya distribusi
mengikuti arteri cerebri media
Staphylococcus aureus, streptococci
Daya tahan tubuh lemah (terapi
imunosupresif, keganasan)
Abses multiple, lazimnya distribusi
mengikuti arteri cerebri media
Toxoplasma, fungi, Enterobacteriaceae,
Nocardia

62. Penyebaran langsung dari fokal infeksi
yang berdekatan
Penyebaran hematogen dari fokus infeksi
yang jauh
Infeksi postraumatik, infeksi kriptogenik
Infeksi pada pasien immunocompromised
oleh opportunistic pathogen.

63. Diabetes
Sarcoidosis
Malignancy
Recipiens transplant organ
Corticosteroid
AIDS

64. Penyebaran dari fokus infeksi yang jauh
Lokasi distribusi pada arteri serebri media
Lokasi awal pada gray matter-white
matter junction
Pengkapsulan tidak sempurna
Mortalitas tinggi

65. Penyebaran langsung dari area yang
berhubungan dengan osteitis atau
osteomielitis
Penyebaran retrograd dari
thromboflebitis melalui vena diploica
atau emissaria

67.  A 3rd generation cephalosporin
(cefotaxime, ceftriaxone, ceftizoxime)
Plus
 Metronidazole : adult 30mg/kg/d usually IV q 12
hr or q 6 hr
Or
 Chloramphenicol : 1 gm IV q 6 hr
If culture shows only streptococcus : Penicillin G
high dose 5 M units IV q 6 hr

68.  IV antibiotics for 6-8 weeks (most commonly 6
weeks)
 Duration of treatment may be reduced if abscess
and capsule entirely excised surgically
 Oral antibiotic may be used following IV, course
5-20% of abscesses recur within 6 weeks of
discontinuing antibiotics
Greenberg, 2001

69. Tindakan darurat untuk menurunkan
tekanan intrakranial
Konfirmasi diagnosis
Mengambil pus untuk diagnosis
mikrobiologi
Mempertinggi efikasi terapi antibiotika
Menghindari penyebaran iatrogenik infeksi
ke dalam ventrikel

70. Keterlambatan diagnosis
Lokasi abses pada tempat yang
berbahaya
Abses multiple dan terletak dalam
Ruptur abses ke ventrikel
Koma
Etiologi dari jamur
Antibiotika tidak adekuat

71. The role of LP is very dubious.
Although LP is abnormal in > 90 %, there
is no characteristic finding diagnostic of
abscess (Greenberg,2001)
The CSF profile from a patient with brain
abscess is nonspecific ( Scheld et al, 1991)

72. - Controversial
The potential drawbacks of these agents are :
 Reduced antibiotic entry into CNS
 Decreased collagen formation and glial response
 Alteration of the CT scan appearance of ring
enhancement as inflammation subsides
Scheld et al, 1991

73. Can retard the encapsulation process
Increase necrosis
Reduce antibiotic penetration into the
abscess
Steroid used to reduce cerebral edema
Brook, 2004

74. CT Scan Brain absces
MRI Brain Absces

75. cold abscess: an abscess of comparatively slow development with
little evidence of inflammation. (= chronic a. / tuberculous a.)
hot abscess, an acute abscess with symptoms of local inflammation.

76. - Contralateral limb weakness
- Contralateral sensory loss
- Disfasia
- Disleksia, disgrafia, diskalkulia
- Disorientasi spasial
Hemianopsia
Homonim
Kontralateral
Nistagmus
Disartria
Ataksia
- Ggn saraf kranial
- Ggn fx vital
- Ggn bahasa
- Ggn memori
- Ggn mood
- Ggn perilaku
- Hearing & vision
pathways
- Demensia
- Ggn mood
- Ggn perilaku
- Inkontinensia
- disfungsi olfaktorius
- Disfungsi opticus
(Wilkinson, 1997)

78.  Demam
 Nyeri kepala hebat
 Kejang umum
 Gangguan kesadaran
 Kaku kuduk
 Brudzinky (+)
 Tanda Kernig (+)
 Mungkin terdapat bercak
merah (Neisseria)
Gejala klinik pada dewasa
dan anak lebih 5 tahun
 Nyeri kepala  tak tahu
 Kaku kuduk  mungkin tak ada
 Demam dan kejang
 Ngantuk
 Mudah terangsang
 Fontanella cembung.
Gejala klinik pada
anak-anak dan bayi

79. INFEKSI TAK MELALUI SAWAR OTAK
Infeksi pada arteri Cairan Serebospinal (SS) Piameter
Jaringan otak
Infeksi langsung
Traumatik : Luka ==> infeksi (infeksi sekitar
kepala otak
Non Traumatik : Mastoiditis ==> Otak
Saraf -saraf Tepi
Otak
Infeksi langsung cairan SS Otak

80. Meningitis piogenik akut adalah respon
inflamasi terhadap infeksi bakteri pada
membran arakhnoid dan piamater yang
membungkus otak dan medula spinalis
(Gilroy, 2000).
Insiden meningitis bacterial adalah 2 sampai 7
kasus tiap 100.000 orang pada dewasa dan
70 kasus tiap 100.000 pada anak (Weiner,
1999).

81.  Konsentrasi bakteri dalam darah tinggi
dan terjadi invasi ke susunan saraf pusat
 Anak dengan imunodefisiensi,
splenektomi dan asplenia kongenital
 Penyakit kronik seperti diabetes mellitus,
alkoholisme, sirosis hati.
 Sickle cell anemia dan hemoglobinopati
 Virulensi bakteri.

82. Gejala dan tanda
Pungsi lumbal, diikuti pemeriksaan:
* Gram’s stain
* Tes antigen bakteri
* Kultur bakteri
* Deteksi asam nukleat bakteri

83. Rash

84. INDIKASI
 PERIPHERAL NERVE DISEASE:
GBS, DIABETIC POLYNEURO
PATHY, HYPERTROPHIC
POLYNEURITIS (Dejerine-Sottas
disease)
 SUSPECTED CNS INFECTION
(Meningitis, Meningoencephalitis)
 SUSPECTED INTRACRANIAL
BLEEDING
 SUSPECTED MULTIPLE
SCLEROSIS
KONTRA INDIKASI
 SUSPECTED RAISED
INTRACRANIAL PRESSURE
 HEADACHE
 UNCONSCIOUSNESS
 LOCAL SEPSIS
 SUSPECTED SPINAL CORD
COMPRESSION
 NECK STIFFNESS

85. Viral Infection
 Peningkatan jumlah sel
(lymphocytes atau
monocytes)
 Sel mononuklear 10-
1000/mm3
 Protein sedikit meningkat
 Glukosa normal
Bacterial Infection
 Lymphocytic pleocytosis
 Sel PMN predominan (50-
4000/mm3)
 Protein meningkat
 Kadar glukosa kurang 2/3
glukosa darah

86. Parameter Bacterial Viral Neoplastic Fungal
OP (< 170 mm
CSF)
> 30 mm 200 mm 200 mm 300 mm
WBC ( < 5
mononuklear)
> 1000 / L < 1000 / L < 5000 / L < 5000 / L
% PMNS (O) > 80 % 1 – 5 % 1 – 50 % 1 – 50 %
Glukosa ( > 40
mg/dL)
< 40 mg / dL > 40 mg / dL < 40 mg / dL < 40 mg / dL
Protein ( < 50
mg/ dL)
> 200 mg/ dL < 200 mg / dL > 200 mg / dL > 200 mg /
dL
Gram stain (-) (+) (-) (-) (-)
Cytology (-) (-) (-) (+) (+)
Greenlee , 1990

87. Profile Of CSF in Acute Meningitis and Encephalitis
Investigation Reference
Range
Meningitis
Bacterial
Meningitis
Viral
Encephalitis
Opening pressure < 30 mmH2) Raised Normal Increased
Total WBC count < 5 x 10 6/L Greatly
increased
Moderately
increased
Moderately
increased
WBC Differential Lymphocytes (60%-
70%), monocytes
(30%-50%), no
neutrophil or red
blood cell
Neutrophils
predominant
Lymphocytes
predominant
Lymphocytes
predominant
[Glucose] 28-44 mmol/L Decreased Normal Normal
CSF: serum
glucose Ratio
>60% Decreased
34/109
Normal Normal
[Protein] <0,45g/L Increased Normal or slightly
increased
Normal or slightly
increased
Berkley, 2003

91. MENINGITIS - MENINGOENSEFALITIS

92. Current causes of community-acquired bacterial meningitis
in children and adults in the United States and Canada
Bacterium Causative organism
(% of cases)
Incidence (per
100,000 population)
Case-
fatality rate
(%)
Streptococcus
pneumoniae
30-50 0.6-1.2 19-46
Neisseria
meningitidis
15-40 0.5-1 3-17
Haemophilus
influenzae
2-7 <1 3-11
Listeria
monocytogene
s
1-3 0.1-0.2 15-40
Other
bacteria*
<5 Not available Not available
*Including streptococci, staphylococci, aerobic gram-negative bacilli, and
anaerobic organisms.
Black, 2001

93. Age
group
Common bacterial pathogens Empiric
Regimens
0-1 month S. agalactiae, E. coli, K. pneumoniae, L.
monocytogenes
ampicillin +
cefotaxime
1-3 months S. agalactiae, E. coli, L..monocytogenes,
S.pneumoniae, N. meningitidis, H. influenzae
ampicillin +
ceftriaxone
3 mo-18 yrs N. meningitidis, S. pneumoniae,
H. influenzae
ceftriaxone +
vancomycin
18-50 years S. pneumoniae, N. meningitidis ceftriaxone +
vancomycin
> 50 years S. pneumoniae, N. meningitidis,
L. monocytogenes,aerobic gram-negative
bacilli
ampicillin +
ceftriaxone
neurosurger
y patients
P. aeruginosa, coagulase-negative
staphylococci Black, 2001

95.  Kongenital : Ibu hamil  infeksi : ookista
(feses kucing)  plasenta  bayi.
 Akuisita (droplet binatang piaraan) : makan
daging belum masak (dengan kista) 
kontak feses kucing (dengan kista)  usus
 darah  meningen  otak (destruksi).
Etiologi : Toxoplasma gondii

96. Kongenital (infeksi pasif) :
 Demam, kejang dan rash
 Hepatosplenomegali
 Chorioretinitis
 Hidrosefalus / mikrosefalus
 Kalsifikasi otak
 Retardasi mental
Manifestasi klinik
Akuisita  sama dengan meningoensefalitis kadang-kadang
tanpa panas.
 Toxoplasma gondii di LCS
 Biopsi otot
 Limfonodi
 Serologis : tes antibody fluid rescent indirect (+)
 Sabin feldman dye test titer 1 : 512 atau lebih
Diagnosis

97. Hari I  Sulfadiazine : 4 gr
Pirimetamine : 100 – 200 mgr
Hari II sampai 4 minggu  Sulfadiazine : 2-6 mg/hari
Pirimetamine 25 mg/hari
Fansidar (sulfadiazine + pirimetamine)
Hari I : 4 tablet
Hari II sampai 3 minggu : 1 tablet
Spiramisin (untuk ibu hamil)
Leucovorin + asam folat : 2 – 10 mg/hr (selama 4 mgg)

98. Sifilis, cryptococcus dan tuberculosis.
Meningitis sifilitik : - simtomatik
- asimtomatik.
Meningitis Tb : - basil Tb sering tak tampak  cat.
- Kultur Tb  lama (beberapa minggu)
- Serologis IgG Tb (+)  sensitivitas 70%.
Cryptococcus : jumlahnya turun dalam cat.
Lekemia (meningitis lekemia)  LCS :
 sel limfoblas / mieloblas (+)
 Stadium akhir : sel limfoblas / mieloblas beribu-ribu.
Misalnya :
sinusitis paranasal/mastoiditis, abses otak  LCS : sel
mononukleus predominan, glukosa normal dan organisme
tidak ada
Infeksi bakteri yang terletak dekat mening
Infeksi meningeal spesifik/parainfeksiosa  organisme tdk mungkin diisolir.
Invasi neoplasma (limfoma/karsinoma)

99.  Demam
 Nyeri kepala hebat
 Kejang umum
 Gangguan kesadaran
 Kaku kuduk
 Brudzinky (+)
 Tanda Kernig (+)
 Mungkin terdapat bercak
merah (Neisseria)
Gejala klinik pada dewasa
dan anak lebih 5 tahun
 Nyeri kepala  tak tahu
 Kaku kuduk  mungkin tak ada
 Demam dan kejang
 Ngantuk
 Mudah terangsang
 Fontanella cembung.
Gejala klinik pada
anak-anak dan bayi

101. • Konsep Fisiologik
• Kemungkinan komponen anatomi
 Dinding Kapiler
 Membrana Pialgial dan ruang Virchow - Robin
 Prosesus sel-sel Glia
Adalah suatu mekanisme pertahanan agar bahan-bahan
berbahaya tidak mudah begitu saja masuk kedalam cairan otak
( termasuk disini juga obat-obatan )

102. Definition:
A barrier made up of neuroglia and
capillary walls which limits the movement
of substances in the bloodstream into the
brain

103. The arachnoid membrane
Choroid plexus epithelium
Cerebral microvascular endothelium (
disorder in this level result separation
intercellular tight junctions, increased
pinocytosis)

105. HERPES SIMPLEX VIRUSES
Herpes simplex viruses account for approximately 10%
to 20% of viral encephalitides in the United States of
which HSV-1causes approximately 95% of cases in
patients beyond the neonatal period approximately one
third of cases caused by primary HSV-1 infection and two
thirds by viral reactivation,HSV-1infection of the central
nervous system (CNS) have a better neurologic outcome
than those infected with HSV-2In the past, the most
specific means for the diagnosis of HSE was brainbiopsy
[1]. However, polymerase chain reaction (PCR) of CSF is
highly sensitive and specific for the diagnosis of HSE
(91% and 92%, respectively, in one study inpatients with
biopsy-proven disease)
Juliana Cepelowicz, MD,Allan R. Tunkel, MD, PhD, Viral Encephalitis

106. VARICELLA-ZOSTER VIRUS
The most common extracutaneous site of
involvement in children with varicella is the CNS.It is
estimated that0.1% to 0.75% of children with
varicella develop encephalitis,as direct involvement
of brain parenchyma or as an autoimmune-mediated
postinfectious,The pathogenesis of varicella
encephalitis includes small vessel vasculopathy with
ischemia and demyelination, medium and large
artery hemorrhage or ischemia, and periventricular
inflammation,The most common neurologic
abnormality associatedwith VZV is cerebellar ataxia
Juliana Cepelowicz, MD,Allan R. Tunkel, MD, PhD, Viral Encephalitis

107. Encephalitis can be a consequence of
cytomegalovirus (CMV) infection of brain
parenchyma in immunosupressed patients,
particularly in patients infected with HIV who have
CMV disease outside the CNS, Two forms of
CMV encephalitis : One form is very similar to
HIV encephalopathy, in which patients have
mental status changes, confusion,disorientation,
progressive apathy, and dementia; thesepatients
differ clinically by the relative acute onset of CMV
encephalitis ,the other is cranial nerve palsy
,nistagmus ,ataxia,ventriculomegaly
CYTOMEGALOVIRUS
Juliana Cepelowicz, MD,Allan R. Tunkel, MD, PhD, Viral Encephalitis

108. The enteroviruses cause a wide spectrum of human
disease, from mild nonspecific fever to aseptic
meningitis and encephalitis,There are almost 70
serotypes of enteroviruses that cause disease; the
newly numbered enteroviruses 70 and 71 have been
reported to commonly cause CNS The clinical
syndrome of enteroviral encephalitis ranges from mild
mental status changes to frank coma; focal findings
may mimic those seen in HSE. A unique form of
brainstem encephalitis,rhombencephalitis
(characterized by myoclonus, tremors,ataxia, and
cranial nerve involvement) has been associated with
enterovirus
ENTEROVIRUSES
Juliana Cepelowicz, MD,Allan R. Tunkel, MD, PhD, Viral Encephalitis

109. Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town
Cytomegalovirus

110. Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town
Herpes simplex virus

111. Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town
Herpesvirus

112. Herpes simplex virus
Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town

113. Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town
Human Imunodeficiency Virus

114. Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town
Adenovirus

115. Human Cytomegalovirus
Image Courtesy of Linda Stannard, of the Department of Medical Microbiology, University of Cape Town

117. Sistem Imun

118. Respon imun terhadap antigen

119. Konjungtiva
Mukosa
Kulit
Rusak Darah
Limfa
Aksi Kuman + Reaksi Tubuh
Runtuhan kuman +Unsur-
unsur tubuh (TOKSIN)
Toksemia
 Prodroma :
Demam, malaise
Anoreksia
Tubuh menang
Tubuh kalah
Sawar Otak Darah (Septikemia)
Kuman

120. INFEKSI TAK MELALUI SAWAR OTAK
Infeksi pada arteri Cairan Serebospinal (SS) Piameter
Jaringan otak
Infeksi langsung
Traumatik : Luka ==> infeksi (infeksi sekitar
kepala otak
Non Traumatik : Mastoiditis ==> Otak
Saraf -saraf Tepi
Otak
Infeksi langsung cairan SS Otak

121. Temperature 0 Centigrade 0 Faranheat
Normal 36.6 - 37.20 C 98 - 990 F
Pyrexia >37.20 C >99
0 F
Hyperpyrexia >41.60 C >1070 F
Subnormal <36.60 C <980 F
Hypothermia <350 C <950 F
Body temperature: The normal and the abnormal
Rationalmedicine, 2002

123. Viral infections in AIDS
•HSV
–Chronic mucocutaneous
infection (oral & anogenital)
–Treatement: acyclovir
•VZV
–shingles
•CMV
–Sites
•retinitis
•encephalitis
•hepatitis
•pneumonia
–Treatment: ganciclovir
–Paradoxical worsening of retinitis
after HAART
•HHV8
–Kaposi’s sarcoma