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TORCH T oksoplasma O ther: Syphilis, Strepto Gr-B, Listeriosis R ubella C ytomegalovirus, Chlamydia H erpes, HIV, HPV, H.Parvovirus B19, HBV, HCV

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TORCH

• T oksoplasma• O ther: Syphilis, Strepto Gr-B, Listeriosis• R ubella• C ytomegalovirus, Chlamydia• H erpes, HIV, HPV, H.Parvovirus B19, HBV,

HCV

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SOURCE OF TORCH IN THE BODY: Live in nucleated cell only

HSV2 (Nerve)

HSV1 (Nerve)

CMV (Mucosa)

Toxoplasma (Muscle)

Rubella (Respiratory)

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CLINICAL STAGES OF TORCH INFECTION

SOURCE CASE:Agent:PopulationTransmissionGeneration

EXPOSURE TO CONTACT:Intensity and duration

CONTACT:Inborn defensesImmune defenses

NO INFECTION INFECTION:Cell mediated immunityHumoral mediated “Latency, tolerance

NO DISEASE DISEASE:EarlyLate

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MORFOLOGI TORCH (SKEMA)

ConoidPole-ring

Rhoptrien

Nucleus

Mitochondria

Micronemen

T. Gondii Rubella

surface and transmembrane Antigen

Nucleocapsid andssRNA genome

Herpesviridae

HSV1/2

CMV

VZV

EBV

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THE ANTIBACTERIAL ROLE & EFFECT OF ANTIBODY

Antibody to

LipotheicFimbriaeCapsules

Lipid bilayer

M proteinCapsule

Toxin

Attachment

Bacterialproliferation

Phagocyteavoidance

Host damage

Toxic

Invasive

Bacterial metabolictransportand receptor

Antibody neutralize antigen

Antibody neutralize spreadingfactors, hyaluronidase

Antibody block/neutralize

X

X

X

X

X

X

X

Survival of 100 bacteria (%)

1 2 hour

100

10

1

0.1

0.01

Effect Antibody & Complement

Non Ab, non C3b(+) Ab, non C3b(+) Ab, (+) C3b

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IMMUNE SYSTEM IN ACUTE INFLAMMATION

Inflammatory mediators

Injury

Antigen: Viral, Bacteria, Parasite, Fungal, Tumor

IgM/G IgE

Mast cell C3a/C5a

BradikininFibrinogen

2A2

2B43

4

1B 1A

Histamine

2B2

2B3

Tumor, Rubor, Calor, Dolor, Punctio lesie5

Ts Tc

Th

Hageman.F

B

2B1

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REAKTIFASI TORCH & PENYAKIT PENYERTA LAIN PADA BERBAGAI KADAR CD4 PENDERITA

DEFISIENSI IMMUNE

• IM. NORMAL (CD4>750/UL) M.nucleosis : 4L+Mioatralgia

• DEF. DINI (CD4>500/UL, LOW-RISK, OPPORTUNITY): Autoimun.D: Ruam kulit, ITP, S.Sjogren, Guillain-Bare, Polio, Demielinisasi syaraf perifer, M.Ensefalitis, Low Re-activation TB/TORCH

• DEF.MENENGAH (CD4=200-500/UL, MIDLE OPPORTUN)

• Diare, BBturun, Lnnpatia, fever Infeksi ringan-Keganasan: 395/ul = TBC; 275/ul = HZV,HSV, K.oral, HL 240/ul = NHL

• 224/ul = Kaposi.S

• DEF. LANJUT (CD4<200/UL, AIDS-OPPORTUNISTIK) : 122/ul = P.Karinii 98/ul = Kompleks M.Avium 93/ul = E’is Toksoplasma 73/ul = M’is Kriptokokus 29/ul = Retinitis CMV

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TRANSMITTY OF TORCH

TOXOPLASMA RUBELLA CMV HSV1/2 (Fecal-oral) Aerosal (In-/direct contact, (Intimate.C)

Trans-fuse/plantation)

Salad (oocyst) Droplet Sexual intercourse Sexual.IRaw meat (cyst)

Mother-baby + +, labor, lactation + labor

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SEROPREVALENCE OF IgG/M ANTI-TORCH IN THE MOTHER LIVE IN INDONESIA

CITY TOKSO (%) RUBELLA CMV (%) HSV2 (%)IgG IgM IgG IgM IgG IgM IgG IgM

Jakarta 61,6 16,4 67,1 1,4 93,2 2,7 42,5 12,3Bandung 74,5 11,3 74,5 - 94,3 - 55,7 16,0Semarang 44,0 18,0 78,0 - 99,0 - 48,0 20,0Yogyakarta 55,4 16,3 79,4 - 98,9 - 44,6 28,3Surabaya 55,5 18,8 77,2 1,0 99,0 - 39,6 16,8Denpasar 23,0 5,0 78,0 3,0 98,0 - 56,0 21,0

National 52,1 14,2 76,1 0,9 97,2 0,4 48,1 19,2

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SEROPREVALENCE OF IgG ANTI TOKSOPLASMA IN MAMALIA IN INDONESIA

• Goat Cat Dog Fog

• (%) (%) (%) (%)

• Kalimantan 61,0 - - -

• Lampung 47,5 9,0 - -

• Sumut 23,5 3,3 - -

• Tuban 20,6 - - -

• Gresik 20,0 - - -

• Jakarta - 72,7 75,6 -

• Jabar - - - 51,0

• Irian - - - 50,0

• Yogya 50 - - 40,0

• National 20-61 3-73 - 40-50

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CMV: Viral excretion from assymptomayic persons

• Neonatus Child Adult• (%) (%) (%)

• Urine 0,5-2,5 10-29 0-2• Oral secrete 0,5-2,5 10-29 0-2• Cement - - 5-10• Cervical secrete - - 10-

28• Milk - - 13-27

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MODE OF TORCH INFECTION IN THE FETUS AND NEWBORN

• Fetus Newborn• Transplacental During birth Shortly after

birth

• Toksoplasma ++ - -

• Rubella ++ - -

• Cytomegalo + ++ ++/Milk

• Herpes + ++ +

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MOST FREQUENT PHYSICAL SIGNS OF SEVERE CONGENITAL TORCH INFECTION

DEFECT TOK RUB CMV HSV2Apparent at birthMicrocephaly + + + +Intracranial calcification + - + -Pneumonitis + + + +Hepatosplenomegaly, Icteric + + + +Trombocytopenia, Petechial, + + + +Purpura, HaemorraghesChoroidoretinitis + + + -Cataracts + + - -Glaucoma - + - -Patent ductus arteriosus/PDA - + - -Bone defect +Skin vesicles - - - +Apparaent months/years after birthSensorineural deafness, Mental.R + + + -Diabetes Mellitus - + - -

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FREQUENCY ORGAN YANG TERLIBAT

BBL Rendah 60% Hepatomegali 65%Abnormal lipat palmar 45% Splenomegali 60%Pneumonia 15% Ikterik 15%

Anemia hemolitik 13%Kardiovaskuler(MI,Septal,Stenosis,PDA) 70% Trombositopenia 50%

Mata 77% Tuli 50%Katarak bilateral 30% Retardasi 40%Retinopatia 25% Protein liquor > 5%Mikroptalmia 10% Mikrosefal 2%Opasitas kornea 7% Radioluscent femur,tibia 35%Glaukoma 5%

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RELATIONSHIP BETWEEN SEVERITY CONGENITAL TOXOPLASMOSE and TIME OF INFECTION IN THE GRAVID

Infection risk in fetus X Severity of congenital defect in fetus

A. Increase of trimester in the gravid , increase the risk of fetus to infectedB. More early infection in the fetus, more severe congenital defect in the fetus

TOKSOPLASMOSETIME OF INFECTION Infected Fetus Severe (%) Mild/Non-

(%) symptom (%)

1st Trimester 25 60 402nd Trimester 54 30 703th Trimester 65 0 100

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SEVERITY OF CONGENITAL DEFECT IN THE FETUS BY TIME OF RUBELA INFECTION IN THE GRAVID

Umur % Janin % JaninKehamilan terinfeksi Cacat

<11W 90 9011-12W 67 3313-14W 67 1115-16W 47 2417-18W 39 Fetal.D19-22W 34 and23-26W 25 Sequele27-28W 12 -7 Bulan 35 -8 Bulan 60 -9 Bulan 100 -

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CLINICAL MANIFESTATION OF CMV INFECTION

TISSUE CHLIDREN/ADULT AIDS

Eyes - ChorioretinitisLung - PneumoniaGIT - EsophagocolitisNervous system Polineuromyelitis MeningoencephalisLymphoid system MI Lpenia, limfositosisMajor organ Carditis HepatitisDiseases Subclinic Severe, generalized

Re-/1st INFECTION REACTIVATIONTransfusion Old ageContact Hydraemia

AIDS/TransplantationChronic diseases

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METHODS FOR TORCH DETECTION

Toxo Rub CMV HSV1/2HA inhibition/HAI, Passive HA - + - -Latex agglutination - + - -Neutralization test - + - -Fluorescent immuno assay/FIA - + - -Anticomplement IFA - + - -

Sabin-feldman dye test + - - -Indirect HA assay/IHA + - + -Complemen fixation/CF + - + +

Indirect fluorescent assay/IFA + - - -RIA, EIA + + + +EIA capture, ISAGA + + - -

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BASIC TO TORCH DETECTION BY SENSITIVITY

Microscope105/mlPCR1/ml Culture 104/ml 1,2,3,4 Serologic 10,4,3,2,1/ml

1 Particle MO Detection

4 Antigen Detection

4 IgM anti MO Detection

4x5=20 IgG antiMO Detection

4x5x4=80 IgG EIAanti MO Detection

2n PCR gene

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KINETICK OF SEROLOGIC MARKER IN TORCH INFECTION

.0 .3 .6 .12 .24 Months

IgE anti-TORCH

IgA

IgM

IgG IgG high avidity

IgG low avidity

1st Infection

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PREVALENCE OF TOXOPLASMA AMONG PREGNANT WOMEN FROM DIFFERENT PARTS OF THE WORLD

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TORCH PRENATAL/MARITAL CARE PLUS

Jan

R

Feb

R

Mar

R

Apr

R

Mei

R

JunS

R

Jul

R

AgtS

R

Sep

R

OktS

R

Nov

R

DesS

R

Ket

G/MTox

G/MRub

G/Mcmv

G/MHsv

G/MAca

Ket