Torch
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TORCHToksoplasmaOther: Syphilis, Strepto Gr-B, ListeriosisRubellaCytomegalovirus, ChlamydiaHerpes, HIV, HPV, H.ParvovirusB19, HBV, HCV
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SOURCE OF TORCH IN THE BODY: Live in nucleated cell onlyHSV2 (Nerve)HSV1 (Nerve)CMV (Mucosa)Toxoplasma (Muscle)Rubella (Respiratory)
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CLINICAL STAGES OF TORCH INFECTIONSOURCE CASE:Agent:PopulationTransmissionGenerationEXPOSURE TO CONTACT:Intensity and durationCONTACT:Inborn defensesImmune defensesNO INFECTIONINFECTION:Cell mediated immunityHumoral mediated Latency, toleranceNO DISEASEDISEASE:EarlyLate
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MORFOLOGI TORCH (SKEMA)ConoidPole-ringRhoptrienNucleusMitochondriaMicronemenT. GondiiRubellasurface and transmembrane AntigenNucleocapsid andssRNA genomeHerpesviridaeHSV1/2CMVVZVEBV
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THE ANTIBACTERIAL ROLE & EFFECT OF ANTIBODYAntibody to LipotheicFimbriaeCapsulesLipid bilayerM proteinCapsuleToxinAttachmentBacterialproliferationPhagocyteavoidanceHost damageToxicInvasiveBacterial metabolictransportand receptorAntibody neutralize antigenAntibody neutralize spreadingfactors, hyaluronidaseAntibody block/neutralizeXXXXXXXSurvival of 100 bacteria (%)12 hour100
10
1
0.1
0.01Effect Antibody & ComplementNon Ab, non C3b(+) Ab, non C3b(+) Ab, (+) C3b
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IMMUNE SYSTEM IN ACUTE INFLAMMATIONInflammatory mediatorsInjuryAntigen: Viral, Bacteria, Parasite, Fungal, TumorIgM/GIgEMast cellC3a/C5aBradikininFibrinogen2A22B4341B1AHistamine2B22B3Tumor, Rubor, Calor, Dolor, Punctio lesie5TsTcThHageman.FB2B1
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REAKTIFASI TORCH & PENYAKIT PENYERTA LAIN PADA BERBAGAI KADAR CD4 PENDERITA DEFISIENSI IMMUNEIM. 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 = NHL224/ul = Kaposi.S
DEF. LANJUT (CD4
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TRANSMITTY OF TORCHTOXOPLASMARUBELLACMVHSV1/2 (Fecal-oral)Aerosal(In-/direct contact,(Intimate.C)Trans-fuse/plantation)
Salad (oocyst)DropletSexual intercourseSexual.IRaw meat (cyst)
Mother-baby++, labor, lactation+ labor
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SEROPREVALENCE OF IgG/M ANTI-TORCH IN THE MOTHER LIVE IN INDONESIACITYTOKSO (%)RUBELLA CMV (%)HSV2 (%)IgG IgMIgG IgMIgG IgMIgG IgM
Jakarta61,6 16,467,1 1,493,2 2,742,5 12,3Bandung74,5 11,374,5 -94,3 -55,7 16,0Semarang44,0 18,078,0 -99,0 -48,0 20,0Yogyakarta55,4 16,379,4 -98,9 -44,6 28,3Surabaya55,5 18,877,2 1,099,0 -39,6 16,8Denpasar23,0 5,078,0 3,098,0 -56,0 21,0
National52,1 14,276,1 0,997,2 0,448,1 19,2
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SEROPREVALENCE OF IgG ANTI TOKSOPLASMA IN MAMALIA IN INDONESIA GoatCatDogFog (%)(%)(%)(%)Kalimantan61,0---Lampung47,59,0--Sumut23,53,3--Tuban20,6---Gresik20,0---Jakarta-72,775,6-Jabar---51,0Irian---50,0Yogya50--40,0
National20-613-73-40-50
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CMV: Viral excretion from assymptomayic persons NeonatusChildAdult (%) (%) (%)
Urine0,5-2,510-290-2Oral secrete0,5-2,510-290-2Cement - -5-10Cervical secrete - -10-28Milk - -13-27
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MODE OF TORCH INFECTION IN THE FETUS AND NEWBORN Fetus Newborn TransplacentalDuringbirthShortly after birthToksoplasma++--Rubella++--Cytomegalo+++++/MilkHerpes++++
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MOST FREQUENT PHYSICAL SIGNS OF SEVERE CONGENITAL TORCH INFECTIONDEFECTTOKRUBCMVHSV2Apparent 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 TERLIBATBBL Rendah60%Hepatomegali65%Abnormal lipat palmar45%Splenomegali60%Pneumonia15%Ikterik15%Anemia hemolitik13%Kardiovaskuler(MI,Septal,Stenosis,PDA)70%Trombositopenia50%
Mata77%Tuli50%Katarak bilateral30%Retardasi40%Retinopatia25%Protein liquor > 5%Mikroptalmia10%Mikrosefal 2%Opasitas kornea 7%Radioluscent femur,tibia35%Glaukoma 5%
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RELATIONSHIP BETWEEN SEVERITY CONGENITAL TOXOPLASMOSE and TIME OF INFECTION IN THE GRAVIDInfection risk in fetusX 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 INFECTIONInfected FetusSevere (%)Mild/Non-(%)symptom (%)
1st Trimester25 60 402nd Trimester54 30 703th Trimester65 0 100
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SEVERITY OF CONGENITAL DEFECT IN THE FETUS BY TIME OF RUBELA INFECTION IN THE GRAVIDUmur% Janin% JaninKehamilanterinfeksiCacat
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CLINICAL MANIFESTATION OF CMV INFECTIONTISSUECHLIDREN/ADULTAIDS
Eyes-ChorioretinitisLung-PneumoniaGIT-EsophagocolitisNervous systemPolineuromyelitisMeningoencephalisLymphoid systemMILpenia, limfositosisMajor organCarditisHepatitisDiseasesSubclinicSevere, generalized
Re-/1st INFECTIONREACTIVATIONTransfusionOld ageContactHydraemiaAIDS/TransplantationChronic diseases
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METHODS FOR TORCH DETECTIONToxoRubCMVHSV1/2HA 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 SENSITIVITYMicroscope105/mlPCR1/mlCulture 104/ml1,2,3,4 Serologic 10,4,3,2,1/ml1 Particle MO Detection4 Antigen Detection4 IgM anti MO Detection4x5=20 IgG antiMO Detection4x5x4=80 IgG EIAanti MO Detection2n PCR gene
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KINETICK OF SEROLOGIC MARKER IN TORCH INFECTION.0.3.6.12.24 MonthsIgE anti-TORCHIgAIgMIgGIgG high avidityIgG low avidity1st Infection