mikro 1 - rubella rubeola

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RUBELLA Titiek Djannatun Bagian Mikrobiologi Universitas YARSI

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Rubella Rubeola

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Page 1: 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)