MIKRO 1 - Rubella Rubeola
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RUBELLA
Titiek Djannatun
Bagian Mikrobiologi Universitas YARSI
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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 available1969 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 womenwere 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 sub ocipital 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 (Post natal)
kongenital
Sekresi Respirasi, urine
Replikasi Pada fase Prodomal (1 minggu setelah ruam keluar)
Subklinik Beberapa 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-AbComplexes)
Lymph nodes Lymphadenopathy 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 Jaringan limfoid(replikasi pada limfonodi servikal) Viremia (5-7 hari) RES Epitelpermukaan tubuh (Kulit, Saluran pernafasan, conjunctiva (Replikasifokal)
Simptom awal Malaise, Mild Fever, SoreThroath, Limfadenopatiaurikular posterior dan suboksipital
Rash/Pink makula papular Wajah Badan Ekstremitas (Advancing
dan 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 ibutidak dapat melewati placenta) infeksi sel janin (efek teratogenik)
Ibu hamil (3-4 bln pertama) yang terdeteksi virus selalu menyebabkaninfeksi 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 berbagaiorgan, cairan serebrospinal, urin, rectal swab. Ekskresi berlangsung 12-18bulan 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 deafnessand 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, ventricularseptal 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 partof the MMR regimen in the USA, UK and a number ofother countries.
• Some countries such as the Czech Republic continue toselectively vaccinate schoolgirls before they reachchildbearing 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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DIAGNOSIS, 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 Alutination 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
?
Virulence factors Syncytium formation,
ability to suppress CMI
In fetuses : Inhibition
of mitosis, Induction
of apoptosis, and
damage to vascular
endothelium
- Ability to remain
latent
Culture/ Diagnosis ELISA for IgM,
Acute/Convalescent
IgG
Acute IgM,
Acute/Convalescent
IgG
Usually diagnosis
clinically
Usually diagnosis
clinically
Prevention Live AttenuatedVaccine (MMR)
Live AttenuatedVaccine (MMR)
- -
Treatment No antivirals, Vitamin A,
Ab for secondary
bacterial Infections
- - -
Distinguishing
feature of the
rashes
Star on head, spreads
to whole body, last over
a week
Mildeer red rash,
Lasts Approximately
3 days
‘Slaped-Face’ Rash
first, spread to limbs
and 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 berkembang1963/1964 Tersedia vaksin MMR
Virus : Familia Paramyxovirus
Genus Morbilli virus
ss RNA
Tidak ada hewan reservoar
Bahan Pemeriksaan Darah (Hari ke 3 setelah onset), saliva,
Virus tidak dapat dikultur
Transmisi Droplets
Epidemik Padat, imunitas rendah, malnutrisi, tidak tersedia medicalcare
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
Koplik’s spot
• Manifestasi selanjutnya pada kulit
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PATOGENESIS
Virus Mukosa saluran pernafasan Sel trachea dan bronchialis
Sistem limfatik (Replikasi) Pembuluh darah (viremia) Kulit danbeberapa organ
Membentuk Giant cell
Imunitas Ab, CMI
Gejala : Sore throath, batuk kering, sakit kepala, conjunctivitis,
limphadenopati, fever
Awal Lesi oral (Koplik’s spot) Maculapapular exanthum (Ulcerasi
putih kebiruan, kecil pada mukosa buccal berlawanan dengan geraham
bawah, berisi Giant cell dan antigen virus Erupsi pada kepala
Menyebar ke badan dan ekstremitas
Anak Leryngitis, Bronchopneumonia, Infeksi sekunder bakteri (H.
influenzae, S. pneumoniae) sebabkan infeksi telinga dan sinus
Anak dengan leukemia Pneumonia
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Measles Pathogenesis
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PATOGENESIS
Fase prodomal (2-4 hari) Virus terdapat di air mata, sekresi hidung,tenggorok, urin, darah
Ruam kulit Hari ke 14 Interaksi sel T dengan sel terinfeksi virus
pada pembuluh darah kecil 1 Minggu (Pada pasien CMI rusak ruam
tidak timbul) viremia demam turun
Masa inkubasi 9-11 hariPenyakit berlangsung 7-11 hari
Prodomal : 2-4 hari
Fase erupsi : 5-7 hari
Komplikasi serius SSPE (Subacute Sclerosis Panencephalitis)
Degenerasi neurologis Cortex cerebri, batang otak, white matter)
Ibu hamil Keguguran, Bayi dengan berat badan rendah
Kerusakan otak Epilepsi
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KULTUR, DIAGNOSIS, PENCEGAHAN & TERAPI
ELISA IgM (Current infection)
Hari ke 14 Titer IgG meningkat
Preventif vaksinasi MMR (Measles, MUMPS, Rubella)
pada anak umur 12-15 bulan, booster sebelum masuk
sekolah Proteksi selama 20 tahun
Vaksin tidak untuk ibu hamil
Terapi : Obat-obat untuk hilangkan gejala
Antibiotik Cegah infeksi sekunderVitamin A Meningkatkan pertahanan mukosa
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CLINICAL IMPACT OF MEASLES
SITE OF VIRUS GROWTH 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 Koplik’s 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
death/year worlwide)