HEPATITIS
A general term that means inflammation of the liver
Inflammation of the liver :
Infection
Exposure to alcohol
Certain medication
Chemical
Poison
Disorder of the immune system
HEPATITIS A
Liver inflammation caused by infection with HAV
Does not cause chronic
It heals completely
Develop lifelong immunity
Tend to occur in epidemic and outbreaks
VIROLOGY
HAV is an unenveloped
Ss RNA virus
Diameter 27 nm
It is not inactivated by ether and stable at -20 C and
low pH
As enterovirus type 72
Picornavirus
PATHOGENESIS
Replicate initially in the enteric mucosa
It can be demonstrated in feces for 10-14 days before
onset of disease
Multiplication in the intestine is followed by a period
of viremia with spread to the liver
Respon to replication in the liver :
Lymphoid cell infiltration
Necrosis of liver parenchimal cells
Proliferation of Kupffer cells
H A. CAUSES
Found in the stool of people with HAV
It is transmitted as fecal-oral
If food or drinking water becomes contaminated with
stool from an infected person
Can also be spread by eating raw or undercooked
shelfish collected from water that has been
contaminated by sewage
Increased Risk
Household contacts of people infected with HAV
International traveles
People who may come in to contact with HAV at
work
Workers in professions :
Health care
Food preparation
Sewage and waste water management
SYMPTOMS
Many people have no symptom
Sometime symptoms are so mild
Older people are more likely to have symptoms
Usually develop between 2-6 weeks after infection
Nausea
Vomitting – severe : dehydration
Diarrhea, especially in children
Low grade fever
Loss of appetite
Cont …
Rash
Tiredness, fatigue
Jaundice
Urine is dark brownish in color
Pain in area of liver
EXAMS and TESTS
Tes for liver function
Increase aminotransferase 1-3 weeks
Test for antibody to HAV
IgM anti-HAV
Large amount of vomiting
electrolytes
TREATMENT
No specific medicines to cure infection with HAV
Except to relieve symptoms
Prevent :
Passive immunization
 Immuneglobulin (ISG) effective when given within 2 W of
expossure
 Is protective if given before or during the incubation period
Active immunization :
 Formalin-killed vaccine are more promising, they have
efficacy in children
IMMUNITY
Antibody to HAV can be detected during early illness
when the virus is still found in feces
Most patients with symptom or signs of acute HA
already have detectable antibody in serum
Early antibody are predominantly IgM which can
detected for several weeks or months
During convalescence : IgG – are immune to
reinfection
Cont…
Sifat virus :
Autoclave
Air mendidih, 5 menit
Oven sterilisasi
Radiasi UV (1 menit)
Formalin
Klorin (10-15 ppm, 30 mnt)
Makanan dipanaskan > 85 C, 1 mnt
HEPATITIS B
Problem kesehatan global
2 milyar terinfeksi VHB
350 juta infeksi kronik
Tanpa interfensi 15-40% berkembang :
Sirosis hati
Karsinoma hepatoseluler
RISIKO KRONISITAS
NEONATUS : 90-95%
BALITA : 30-50%
DEWASA : 5-10% (90% SEMBUH)
VIRUS HEPATITIS B
Non sitopatik
Kerusakan hati :
Respon imun
Sitokin inflamasi
Hepadnaviridae
Ds-DNA dengan 3200 bp
Envelop : HBsAg
Precore/core : HBeAg, HBcAg
Cont …
Masa inkubasi 50-180 hr (rata-rata 2 bl)
Onset penyakit : perlahan
Kenaikan enzim aminotransferase 1-6 bl
Symptoms :
Appetite loss
Fatigue,
Nausea and vomiting
Low-grade fever
Muscle and joint aches
Yellow skin and dark urinee due to jaundice
TRANSMISI
DARAH, CAIRAN TUBUH
Blood transfusion
Contact with blood in health care setting
Had direct contact with blood of an infected person by
touching an open wound or been stuck with a needle
Had unsafe sex with infected person
Received a tatto or acupuncture with contaminated
instruments
Share needles during drug use, unsafe injections
Share personal item (toothbrushes, razor)
Perinatal (from mother to baby at birth)
MARKER SEROLOGIK
HBsAg :
petanda serologik pertama muncul
Terdeteksi 1-12 W pascainfeksi
Mendahului gejala klinik
Persisten > 6 bl : infeksi kronik
Anti-HBs :
Marker sembuh infeksi VHB
Persist lifelong
MARKER SEROLOGIK
HBeAg :
Marker risiko penularan
Replikasi virus
Muncul 3-6 W pascainfeksi
Anti-HBe :
Remisi penyakit
MARKER SEROLOGIK
Anti-HBc :
IgM anti-HBc dengan HBsAg : marker infeksi akut virus
hepatitis B
IgG anti-HBc dengan HBsAg : penderita kronik VHB
PREVENTION
VAKSINASI :
Bayi dari ibu HBsAg imunisasi dalam 12 jam stl lahir
People who are at high risk : health care workers
Protection at least 20 years and should be lifelong
UJI SARING DARAH
Avoid sexual contact with person who has acute or
chronic hepatitis B :
Using condoms consistently and properly
TREATMENT
There is no specific treatment for acute hepatitis B
Replacement of fluids
Adequate nutritional balance
Chronic hepatitis B :
Interferon
Anti-viral agent : lamivudin, adefovir
Patients with cirrhosis : liver transplants
HEPATITIS C
Usually becomes chronic (up to 85%)
Chronic infection with HCV : liver failure
First enters the body, usually are no symptoms
Most common 40-60 years of age
Risk factor for liver cancer
VIROLOGY
RNA virus
A member of flaviviridae
Outer coat : envelope contain enzyme and protein
that allow the virus to reproduce within the cells of
the liver
There are 6 different strain (genotypes)
Genotyping is important to guide treatment
Genetic diversity is one reason : difficult to develop
an effective vaccine
Liver Damage ?
Presence of HCV : trigger the human immune system
cause inflammation
Prolong inflammation may cause scarring : cirrhosis
The liver to perform its normal function : liver failure
TRANSMISSION
Needles shared
Needle-sticks in health care workers (average risk 1.8
– 10.0 %)
< 1992 --- acquired the infection from transfusions of
blood
HCV also can be passed from mother to unborn child
(4%)
Sexual intercourse
Instruments or sharp tool have been reused
Prevent of Transmission
Avoiding needle sharing
Safe needle-usage
Person with SMP should use barrier precaution
Screening test for blood products
Not share razors or tootbrushes with others
SYMPTOMS
75 % people have no symptoms when the first
acquired HCV infection
25 % may complaint fatigue, loss of appetite, muscle
aches or fever
Jaundice is rare at this early stage of infection
As cirrhosis develop, symptoms increase and
include :
Weakness
Loss of appetite
Weight loss
Breast enlargement in men
Cont …
A rash on the palms
Difficulty with the clotting of blood
Spider-like blood vessel on the skin
RISK FACTOR FOR SEVERAL DISEASE
Drinking alcohol
 Acquiring other HV
Diagnostic Tests for HCV
Antibody to HCV using ELISA, confirm with
Recombinant Immunoblot Assay (RIBA)
Molecular test for HCV RNA is useful in determining
whether or not a patient has circulating virus in the
blood (viremia)
RNA testing is more sensitive
HCV RNA becomes detectable 1-3 weeks after exposure
Helpful to assess a patients virologic response to
treatment antiviral therapy
Receive antiviral ?
HCV infection and persistent elevation ALT
High levels of HCV RNA in the blood
HCV infection and evidence of fibrosis on liver biopsy
HCV infection and evidence of at least moderate
inflammation and necrosis on liver biopsy
PENCEGAHAN
Tidak ada vaksin
Ditujukan kepada :
Transfusi darah
Pengendalian infeksi pd pelayanan kes
Pekerja sek komersial
Hepatitis D
Terdeteksi antigen delta dan antibodi pada beberapa
infeksi HBV
HDV membutuhkn selubung HBsAg untuk transmisi
Sering dihubungkan dg hepatitis berat pada pasien
HBsAg positif
Vaksinasi HBV tidak melindungi pembawa HBsAg
dar superinfeksi HDV
Hepatitis E
Virus RNA untai tunggal
Ditemukan di New Delhi 1955 pada kontaminasi
suplai air minum
Ditularkan fekal-oral (NANB )
Tidak pernah menjadi kronik
Tidak bersifat onkogenik
Stabil panas
Virus hepatitis 1

Virus hepatitis 1

  • 2.
    HEPATITIS A general termthat means inflammation of the liver Inflammation of the liver : Infection Exposure to alcohol Certain medication Chemical Poison Disorder of the immune system
  • 3.
    HEPATITIS A Liver inflammationcaused by infection with HAV Does not cause chronic It heals completely Develop lifelong immunity Tend to occur in epidemic and outbreaks
  • 4.
    VIROLOGY HAV is anunenveloped Ss RNA virus Diameter 27 nm It is not inactivated by ether and stable at -20 C and low pH As enterovirus type 72 Picornavirus
  • 5.
    PATHOGENESIS Replicate initially inthe enteric mucosa It can be demonstrated in feces for 10-14 days before onset of disease Multiplication in the intestine is followed by a period of viremia with spread to the liver Respon to replication in the liver : Lymphoid cell infiltration Necrosis of liver parenchimal cells Proliferation of Kupffer cells
  • 6.
    H A. CAUSES Foundin the stool of people with HAV It is transmitted as fecal-oral If food or drinking water becomes contaminated with stool from an infected person Can also be spread by eating raw or undercooked shelfish collected from water that has been contaminated by sewage
  • 7.
    Increased Risk Household contactsof people infected with HAV International traveles People who may come in to contact with HAV at work Workers in professions : Health care Food preparation Sewage and waste water management
  • 8.
    SYMPTOMS Many people haveno symptom Sometime symptoms are so mild Older people are more likely to have symptoms Usually develop between 2-6 weeks after infection Nausea Vomitting – severe : dehydration Diarrhea, especially in children Low grade fever Loss of appetite
  • 9.
    Cont … Rash Tiredness, fatigue Jaundice Urineis dark brownish in color Pain in area of liver
  • 10.
    EXAMS and TESTS Tesfor liver function Increase aminotransferase 1-3 weeks Test for antibody to HAV IgM anti-HAV Large amount of vomiting electrolytes
  • 11.
    TREATMENT No specific medicinesto cure infection with HAV Except to relieve symptoms Prevent : Passive immunization  Immuneglobulin (ISG) effective when given within 2 W of expossure  Is protective if given before or during the incubation period Active immunization :  Formalin-killed vaccine are more promising, they have efficacy in children
  • 12.
    IMMUNITY Antibody to HAVcan be detected during early illness when the virus is still found in feces Most patients with symptom or signs of acute HA already have detectable antibody in serum Early antibody are predominantly IgM which can detected for several weeks or months During convalescence : IgG – are immune to reinfection
  • 13.
    Cont… Sifat virus : Autoclave Airmendidih, 5 menit Oven sterilisasi Radiasi UV (1 menit) Formalin Klorin (10-15 ppm, 30 mnt) Makanan dipanaskan > 85 C, 1 mnt
  • 14.
    HEPATITIS B Problem kesehatanglobal 2 milyar terinfeksi VHB 350 juta infeksi kronik Tanpa interfensi 15-40% berkembang : Sirosis hati Karsinoma hepatoseluler
  • 15.
    RISIKO KRONISITAS NEONATUS :90-95% BALITA : 30-50% DEWASA : 5-10% (90% SEMBUH)
  • 16.
    VIRUS HEPATITIS B Nonsitopatik Kerusakan hati : Respon imun Sitokin inflamasi Hepadnaviridae Ds-DNA dengan 3200 bp Envelop : HBsAg Precore/core : HBeAg, HBcAg
  • 19.
    Cont … Masa inkubasi50-180 hr (rata-rata 2 bl) Onset penyakit : perlahan Kenaikan enzim aminotransferase 1-6 bl Symptoms : Appetite loss Fatigue, Nausea and vomiting Low-grade fever Muscle and joint aches Yellow skin and dark urinee due to jaundice
  • 20.
    TRANSMISI DARAH, CAIRAN TUBUH Bloodtransfusion Contact with blood in health care setting Had direct contact with blood of an infected person by touching an open wound or been stuck with a needle Had unsafe sex with infected person Received a tatto or acupuncture with contaminated instruments Share needles during drug use, unsafe injections Share personal item (toothbrushes, razor) Perinatal (from mother to baby at birth)
  • 21.
    MARKER SEROLOGIK HBsAg : petandaserologik pertama muncul Terdeteksi 1-12 W pascainfeksi Mendahului gejala klinik Persisten > 6 bl : infeksi kronik Anti-HBs : Marker sembuh infeksi VHB Persist lifelong
  • 22.
    MARKER SEROLOGIK HBeAg : Markerrisiko penularan Replikasi virus Muncul 3-6 W pascainfeksi Anti-HBe : Remisi penyakit
  • 23.
    MARKER SEROLOGIK Anti-HBc : IgManti-HBc dengan HBsAg : marker infeksi akut virus hepatitis B IgG anti-HBc dengan HBsAg : penderita kronik VHB
  • 26.
    PREVENTION VAKSINASI : Bayi dariibu HBsAg imunisasi dalam 12 jam stl lahir People who are at high risk : health care workers Protection at least 20 years and should be lifelong UJI SARING DARAH Avoid sexual contact with person who has acute or chronic hepatitis B : Using condoms consistently and properly
  • 27.
    TREATMENT There is nospecific treatment for acute hepatitis B Replacement of fluids Adequate nutritional balance Chronic hepatitis B : Interferon Anti-viral agent : lamivudin, adefovir Patients with cirrhosis : liver transplants
  • 28.
    HEPATITIS C Usually becomeschronic (up to 85%) Chronic infection with HCV : liver failure First enters the body, usually are no symptoms Most common 40-60 years of age Risk factor for liver cancer
  • 29.
    VIROLOGY RNA virus A memberof flaviviridae Outer coat : envelope contain enzyme and protein that allow the virus to reproduce within the cells of the liver There are 6 different strain (genotypes) Genotyping is important to guide treatment Genetic diversity is one reason : difficult to develop an effective vaccine
  • 30.
    Liver Damage ? Presenceof HCV : trigger the human immune system cause inflammation Prolong inflammation may cause scarring : cirrhosis The liver to perform its normal function : liver failure
  • 34.
    TRANSMISSION Needles shared Needle-sticks inhealth care workers (average risk 1.8 – 10.0 %) < 1992 --- acquired the infection from transfusions of blood HCV also can be passed from mother to unborn child (4%) Sexual intercourse Instruments or sharp tool have been reused
  • 35.
    Prevent of Transmission Avoidingneedle sharing Safe needle-usage Person with SMP should use barrier precaution Screening test for blood products Not share razors or tootbrushes with others
  • 36.
    SYMPTOMS 75 % peoplehave no symptoms when the first acquired HCV infection 25 % may complaint fatigue, loss of appetite, muscle aches or fever Jaundice is rare at this early stage of infection As cirrhosis develop, symptoms increase and include : Weakness Loss of appetite Weight loss Breast enlargement in men
  • 37.
    Cont … A rashon the palms Difficulty with the clotting of blood Spider-like blood vessel on the skin RISK FACTOR FOR SEVERAL DISEASE Drinking alcohol  Acquiring other HV
  • 38.
    Diagnostic Tests forHCV Antibody to HCV using ELISA, confirm with Recombinant Immunoblot Assay (RIBA) Molecular test for HCV RNA is useful in determining whether or not a patient has circulating virus in the blood (viremia) RNA testing is more sensitive HCV RNA becomes detectable 1-3 weeks after exposure Helpful to assess a patients virologic response to treatment antiviral therapy
  • 39.
    Receive antiviral ? HCVinfection and persistent elevation ALT High levels of HCV RNA in the blood HCV infection and evidence of fibrosis on liver biopsy HCV infection and evidence of at least moderate inflammation and necrosis on liver biopsy
  • 41.
    PENCEGAHAN Tidak ada vaksin Ditujukankepada : Transfusi darah Pengendalian infeksi pd pelayanan kes Pekerja sek komersial
  • 42.
    Hepatitis D Terdeteksi antigendelta dan antibodi pada beberapa infeksi HBV HDV membutuhkn selubung HBsAg untuk transmisi Sering dihubungkan dg hepatitis berat pada pasien HBsAg positif Vaksinasi HBV tidak melindungi pembawa HBsAg dar superinfeksi HDV
  • 43.
    Hepatitis E Virus RNAuntai tunggal Ditemukan di New Delhi 1955 pada kontaminasi suplai air minum Ditularkan fekal-oral (NANB ) Tidak pernah menjadi kronik Tidak bersifat onkogenik Stabil panas