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RUBELLA

Titiek Djannatun
Bagian Mikrobiologi Universitas YARSI

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

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.

Morphology Virus

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

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

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

Viral Pathogenesis

Rubella Pathogenesis

Viral Pathogenesis

Clinical Features
maculopapular rash
lymphadenopathy
fever

arthropathy (up to 60% of cases)

Rash of Rubella

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 Epitel
permukaan tubuh (Kulit, Saluran pernafasan, conjunctiva (Replikasi
fokal)
Simptom awal Malaise, Mild Fever, SoreThroath, Limfadenopati
aurikular posterior dan suboksipital
Rash/Pink makula papular Wajah Badan Ekstremitas (Advancing
dan resolving 3 days

KOMPLIKASI Arthralgia, arthritis, encephalitis Banyak pada dewasa

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

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

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

Congenital Rubella Syndrome

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.

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.

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

DIAGNOSIS, KULTUR, PENCEGAHAN, TERAPI


SPESIMEN Swabtenggorok/nasofaring (3-4 hari setelah
gejala), Urine, cairan tubuh (Bayi)
KULTUR Jaringan kera ( BSC-1, Vero), jaringan kelinci (RK13, 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

Typical Serological Events following acute


rubella infection

Note that in reinfection, IgM is usually absent or only present transiently at a low level

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 Attenuated
Vaccine (MMR)

Live Attenuated
Vaccine (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

MEASLES (RUBEOLA)
Penyebab kematian 1 million anak di negara berkembang
1963/1964 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 medical
care
Infeksius Periode inkubasi, fase prodomal, Skin rash

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

PATOGENESIS
Virus Mukosa saluran pernafasan Sel trachea dan bronchialis
Sistem limfatik (Replikasi) Pembuluh darah (viremia) Kulit dan
beberapa organ
Membentuk Giant cell
Imunitas Ab, CMI
Gejala : Sore throath, batuk kering, sakit kepala, conjunctivitis,
limphadenopati, fever
Awal Lesi oral (Kopliks 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

Measles Pathogenesis

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 hari
Penyakit 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

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 sekunder
Vitamin A Meningkatkan pertahanan mukosa

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

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
death/year worlwide)