rubella rubeola
DESCRIPTION
m mnTRANSCRIPT
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RUBELLA
TITIEK DJANNATUN
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Rubella
History
1881 Rubella accepted as a distinct disease
1941 Associated with congenital disease (Gregg)
1961 Rubella virus first isolated
1967 Serological tests available
1969 Rubella vaccines available
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Characteristics of Rubella
RNA enveloped virus, member of the togavirus family
Spread by respiratory droplets.
In the prevaccination era, 80% of women were already infected by childbearing age.
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Morphology Virus
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RUBELLA (GERMAN MEASLES)
CAMPAK GERMAN/CAMPAK 3 HARIAN demam akut ruam kulit dan limphadenopati auricular posterior dan subooipital pada anak dan remaja
INFEKSI IBU HAMIL abnormalitas pada janin MALFORMASI KONGENITAL, RETARDASI MENTAL
VIRUS : FAMILIA TOGAVIRIDAE
GENUS RUBIVIRUS
SS RNA, BERENVELOPE
HOSPES HANYA MANUSIA
VIRUS TERATOGENIK
INFEKSI ANAK, DEWASA (POSTNATAL)
KONGENITAL
SEKRESI RESPIRASI, URINE
REPLIKASI Pada FASE PRODROMAL (1 MINGGU STLH RUAM KLR)
SUBKLINIK BBRP MINGGU VIRUS TERDETEKSI DI NASOFARING
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PATHOGENESIS OF RUBELLA
SITE OF VIRUS
GROWTH
RESULT COMMENT
RESPIRATORY
TRACT
VIRUS SHEDDING BUT SYMPTOMS
MINIMAL ( MILD SORE THROATH,
CORYZA, COUGH)
PATIENT INFECTIOUS 5 DAYS
BEFORE TO 3 DAYS AFTER
SYMPTOMS
SKIN RASH OFTEN FLEETING, ATYPICAL:
IMMUNOPATHOLOGY INVOLVED (Ag-
Ab COMPLEXES)
LYMPH NODES LYPHADENOPATHY MORE COMMON IN POSTERIOR
TRIANGLE OF NECK OR BEHIND
EAR
JOINTS MILD ARTHRALGIA, ARTHRITIS IMMUNOPATHOLOGY INVOLVED
(CIRCULATING IMMUNE
COMPLEXES)
PLACENTA/FETUS PLACENTITIS, FETAL DAMAGE CONGENITAL RUBELLA
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Viral Pathogenesis
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Rubella Pathogenesis
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Viral Pathogenesis
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Clinical Features
maculopapular rash
lymphadenopathy
fever
arthropathy (up to 60% of cases)
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Rash of Rubella
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GEJALA KLINIS
POST NATAL :
MASA INKUBASI 2-3 MINGGU
Infeksi virus pada mukosa saluran pernafasan atas JAR LIMFOID (replikasi pada limfonodi servikal) Viremia (5-7 hari) RES EPITEL PERMUKAAN TBH (KULIT, SAL NAFAS, CONJUNCTIVA (REPLIKASI FOKAL))
SIMPTOM AWAL MALAISE, MILD FEVER, SORE THROATH, Limfadenopati aurikular posterior dan suboksipital
RASH/PINK MAKULA PAPULAR WAJAH BADAN EKSTREMITAS (ADVANCING & RESOLVING 3 DAYS)
KOMPLIKASI ARTHRALGIA, ARTHRITIS, ENCEPHALITIS BANYAK PADA DEWASA
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GEJALA KLINIS KONGENITAL :
Ibu dapat tanpa gejala viremia infeksi placenta dan janin (IgG ibu tidak dapat melewati placenta) infeksi sel janin (efek teratogenik)
Ibu hamil (3-4 bln pertama) yang terdeteksi virus selalu menyebabkan infeksi janin infeksi virus pada sel janin sebabkan efek teratogenik
Infeksi virus dalam rahim menyebabkan neonatus terinfeksi (kronis). Virus dapat terdeteksi saat bayi lahir padasekresi faring dan berbagai organ, cairan serebrospinal, urin, rectal swab. Ekskresi berlangsung 12-18 bulan setelah kelahiran
Infeksi pada 1ST trimester pertama kematian janin, aborsi spontan, bayi lahir dengan BB rendah
BAYI abnormalitas jantung, lesi okuler, tuli, retardasi fisik/mental, Anemia, Hepatitis, Pneumonia, Corditis, infeksi tulang
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Risks of rubella infection during pregnancy
Preconception minimal risk
0-12 weeks 100% risk of fetus being congenitally infected
resulting in major congenital abnormalities.
Spontaneous abortion occurs in 20% of cases.
13-16 weeks deafness and retinopathy 15%
after 16 weeks normal development, slight risk of deafness
and retinopathy
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Congenital Rubella Syndrome
Classical triad consists of cataracts, heart defects, and sensorineural deafness.
Many other abnormalities had been described and these are divided into
transient, permanent and developmental.
Transient low birth weight, hepatosplenomegaly, thrombocytopenic purpura bone lesions, meningoencephalitis, hepatitis, haemolytic anemia
pneumonitis, lymphadenopathy
Permanent Sensorineural deafness, Heart Defects (peripheral pulmonary stenosis,
pulmonary valvular stenosis, patent ductus arteriosus, ventricular septal defect) Eye Defects (retinopathy, cataract, microopthalmia, glaucoma, severe myopia) Other Defects (microcephaly, diabetes mellitis, thyroid disorders, dermatoglyptic abnormalities
Developmental Sensorineural deafness, Mental retardation, Diabetes Mellitus, thyroid disorder
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Congenital Rubella Syndrome
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Prevention (1)
Antenatal screening
All pregnant women attending antenatal clinics are tested for immune status against rubella.
Non-immune women are offered rubella vaccination in the immediate post partum period.
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Prevention (2)
Since 1968, a highly effective live attenuated vaccine has been available with 95% efficacy
Universal vaccination is now offered to all infants as part of the MMR regimen in the USA, UK and a number of other countries.
Some countries such as the Czech Republic continue to selectively vaccinate schoolgirls before they reach childbearing age.
Both universal and selective vaccination policies will work provided that the coverage is high enough.
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Laboratory Diagnosis
Diagnosis of acute infection
Rising titres of antibody (mainly IgG) - HAI, EIA
Presence of rubella-specific IgM - EIA
Immune Status Screen
HAI is too insensitive for immune status screening
SRH, EIA and latex agglutination are routinely used
15 IU/ml is regarded as the cut-off for immunity
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DIAGNOSA, KULTUR, PENCEGAHAN, TERAPI
SPESIMEN Swabtenggorok/nasofaring (3-4 hari setelah gejala), Urine, cairan tubuh (BAYI)
KULTUR Jaringan kera ( BSC-1, VERO), jaringan kelinci (RK-13, SIRC), jaringan ginjal kera hijau CPE immunofluorescein (3-4 hari pasca inokulasi)
SEROLOGI HI, ELISA, LATEX AGLUTINATION IgM (terdeteksi 2 minggu setelah muncul ruam, menetap kurang dari 6 minggu) IgG (kekebalan seumur hidup)
PENCEGAHAN Vaksin MMR
TERAPI Penyakit ringan Sembuh sendiri Tidak ada terapi khusus
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Typical Serological Events following acute rubella infection
Note that in reinfection, IgM is usually absent or only present transiently at a low level
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MACULOPAPULAR RASH DISEASES
DISEASE MEASLES RUBELLA FIFTH DISEASE ROSEOLA
CAUSATIVE
ORGANISM(S)
Measles virus (Rubeola) Rubella virus Parvovirus B 19 Human Herpesvirus 6 or
7
MOST COMMON
MODES OF
TRANSMISSION
DROPLETS CONTACT DROPLETS CONTACT
DROPLETS CONTACT,
DIRECT CONTACT
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VIRULENCE FACTORS SYNCYTIUM
FORMATION, ABILITY
TO SUPPRESS CMI
IN FETUSES :
INHIBITION OF
MITOSIS, INDUCTION
OF APOPTOSIS, &
DAMAGE TO
VASCULAR
ENDOTHELIUM
- ABILITY TO REMAIN
LATENT
CULTURE/ DIAGNOSIS
ELISA FOR IgM,
ACUTE/CONVALESCEN
T IgG
ACUTE IgM,
ACUTE/CONVALESCEN
T IgG
USUALLY DIAGNOSIS
CLINICALLY
USUALLY DIAGNOSIS
CLINICALLY
PREVENTION LIVE ATTENUATED
VACCINE (MMR)
LIVE ATTENUATED
VACCINE (MMR)
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TREATMENT
NO ANTIVIRALS, VIT A,
AB FOR SECONDARY
BACTERIAL
INFECTIONS
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DISTINGUISHING
FEATURE OF THE
RASHES
STAR ON HEAD,
SPREADS TO WHOLE
BODY, LAST OVER A
WEEK
MILDEER RED RASH,
LASTS
APPROXIMATELY 3
DAYS
SLAPPED-FACE RASH FIRST, SPREAD TO
LIMBS & TRUNK, TENDS
TO BE CONFLUEENT
RATHER THAN DISTINCT
BUMPS
HIGH FEVER
PRECEDES RASH
STAGE RASH NOT ALWAYS PRESENT
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MEASLES (RUBEOLA)
PENYEBAB KEMATIAN 1 MILLION ANAK DI NEGARA BERKEMBANG
1963/1964 TERSEDIA VAKSIN MMR
VIRUS : FAMILIA PARAMYXOVIRUS
GENUS MORBILLIVIRUS
SS RNA
TIDAK ADA HEWAN RESERVOAR
BAHAN PEMERIKSAAN DARAH (HARI KE 3 STLH ONSET), SALIVA
VIRUS TIDAK BISA DIKULTUR
TRANSMISI DROPLETS
EPIDEMIK PADAT, IMUNITAS RENDAH, MALNUTRISI, TIDAK TERSEDIA MEDICAL CARE
INFEKSIUS PERIODE INKUBASI, FASE PRODOMAL, SKIN RASH
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Pathogenesis Measles/Rubeolla
Virus via blood vessel body (sel epitel permukaan yang pertama adalah sel epitel saluran pernapasan)
Manifestasi awal pada mukosa Kopliks spot
Manifestasi selanjutnya pada kulit
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PATOGENESA
VIRUS MUKOSA SAL PERNAFASAN SEL TRACHEA & BRONCHIALIS SISTEM LIMFATIK (REPLIKASI) PEMBULUH DARAH (VIREMIA) KULIT & BBRP ORGAN
MEMBENTUK GIANT CELL
IMUNITAS AB, CMI
GEJALA : SORE THROATH, BATUK KERING, SAKIT KEPALA, CONJUNCTIVITIS, LIMPHADENOPATI, FEVER
AWAL LESI ORAL (KOPLIKS SPOT) MACULOPAPULAR EXANTHUM (ULCERASI PTH KEBIRUAN, KCL PD MUKOSA BUCCAL BLAWANAN DG GERAHAM BWH, BERISI GIANT CELL & AG VIRUS ERUPSI PADA KEPALA MENYEBAR KE BADAN & EKSTREMITAS
ANAK LARYNGITIS, BRONCHOPNEUMONIA, INFEKSI SEKUNDER BAKTERI (H. influenzae, S. pneumoniae) SBBK INF TELINGA & SINUS
ANAK DG LEUKEMIA PNEUMONIA
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Measles Pathogenesis
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PATOGENESA
FASE PRODROMAL (2-4 HARI) VIRUS TERDPT DI AIR MATA, SEKRESI HIDUNG, TENGGOROK, URINE, DARAH
RUAM KULIT HARI KE 14 INTERAKSI SEL T DG SEL TERINFEKSI VIRUS PADA PEMBULUH DARAH KECIL 1 MINGGU (PADA PASIEN CMI RUSAK RUAM TIDAK TIMBUL) VIREMIA DEMAM TURUN
MASA INKUBASI 9-11 HARI
PENYAKIT BERLANGSUNG 7-11 HARI PRODROMAL : 2-4 HARI, FASE ERUPSI : 5-7 HARI
KOMPLIKASI SERIUS SSPE (SUBACUTE SCLEROSIS PENENCEPHALITIS)
DEG NEUROLOGIS CORTEX CEREBRI, BATANG OTAK, WHITE MATTER)
IBU HAMIL KEGUGURAN, BAYI DENGAN BB RENDAH
KERUSAKAN OTAK EPILEPSI
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KULTUR, DIAGNOSA, PENCEGAHAN & TERAPI
ELISA IgM (CURRENT INFECTION)
HARI KE 14 TITER IgG MENINGKAT
PREVENTIF VAKSINASI MMR (MEASLES, MUMPS, RUBELLA) PD ANAK UMUR 12-15 BLN, BOOSTER SBLM MSK SEKOLAH PROTEKSI SELAMA 20 TAHUN
VAKSIN TIDAK UNTUK IBU HAMIL
TERAPI : OBAT- OBAT UNTUK HILANGKAN GEJALA
ANTIBIOTIK CEGAH INFEKSI SEKUNDER
VIT A MENINGKATKAN PERTAHANAN MUKOSA
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CLINICAL IMPACT OF MEASLES
SITE OF VIRUS
GROWTH
WELL-NOURISHED
CHILD,GOOD MEDICAL CARE
MALNOURISHED
CHILD,GOOD MEDICAL
CARE
LUNG TEMPORARY RESPIRATORY ILNESS LIFE-THREATENING PNEUMONIA
EAR OTITIS MEDIA QUITE COMMON OTITIS MEDIA MORE COMMON, MORE
SEVERE
ORAL MUCOSA KOPLIKS SPOT SEVERE ULCERATING LESSIONS
CONJUNCTIVA CONJUNCTIVITIS SEVERE CORNEAL LESSIONS,
SECONDARY BACTERIAL INFECTION,
BLINDNESS MAY RESULT
SKIN MACULAPAPULAR RASH HEMORRHAGIC RASHES MAY OCCUR
(BLACK MEASLES)
INTESTINAL TRACT NO LESIONS DIARRHAE-EXACERBATES
MALNUTRITION, HALT GROWTH,
IMPAIRS RECOVERY
URINARY TRACT VIRUS DETECTABLE IN URINE NO KNOWN COMPLICATIONS
OVERALL IMPACT SERIOUS DISEASE IN A SMALL
PROPORTION OF THOSE INFECTED
MAJOR CAUSED OF DEATH IN
CHILDHOOD (ESTIMATED ONE
MILLION DEATHS/YEAR WORLDWIDE)