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S3 L17 Hepatitis Virus

S3 L17 Hepatitis Virus

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Published by 2013SecB
Nina Ian John “G” Rachel Mark Jocelle Edo Gienah Jho Kath Aynz Je Glad Nickie Ricobear Teacher Dadang Niňa Arlene Vivs Paul F. Rico F. Ren Mai Revs Mavis Jepay Yana Mayi Serge Hung Tope Ag Bien

S3 L17: Hepatitis A-E Viruses by Dra. Madrid
TYPES OF HEPATITIS Hepatitis Virus Family Genome Antigens Antibodies Source of Virus Spread Route of Transmission Chronic Infection Prevention A HAV Picornavirus ssRNA HAV-Ag Anti-HAV Feces Fecal-Oral Fecal-Oral No Pre/Post exposure immunization B HBV Hepadnav
Nina Ian John “G” Rachel Mark Jocelle Edo Gienah Jho Kath Aynz Je Glad Nickie Ricobear Teacher Dadang Niňa Arlene Vivs Paul F. Rico F. Ren Mai Revs Mavis Jepay Yana Mayi Serge Hung Tope Ag Bien

S3 L17: Hepatitis A-E Viruses by Dra. Madrid
TYPES OF HEPATITIS Hepatitis Virus Family Genome Antigens Antibodies Source of Virus Spread Route of Transmission Chronic Infection Prevention A HAV Picornavirus ssRNA HAV-Ag Anti-HAV Feces Fecal-Oral Fecal-Oral No Pre/Post exposure immunization B HBV Hepadnav

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Published by: 2013SecB on Dec 12, 2010
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S3 L17: Hepatitis A-E Viruses
by Dra. Madrid 
DDDeeeccceeemmmbbbeeerrr111,,,222000111000 
TYPES OF HEPATITIS
 
Hepatitis A B C D EVirus
HAV HBV HCV HDV HEV
Family
Picornavirus Hepadnavirus Flavivirus Satellite Calicivirus
Genome
ssRNA dsDNA ssRNA ssRNA ssRNA
Antigens
HAV-Ag HBsAgHBeAgHBcAgHCV-Ag HDV-Ag HEV-Ag
Antibodies
 Anti-HAV Anti-HBs Anti-HBc Anti-HBe Anti-HCV Anti-HDV Anti-HEV
Source of Virus
Feces Blood / Blood-derived bodyfluidsBlood / Blood-derived bodyfluidsBlood / Blood-derived bodyfluidsFeces
Spread
Fecal-Oral ParenteralSexualPerinatalParenteral?SexualParenteral?SexualFecal-Oral
Route of Transmission
Fecal-Oral PercutaneousPermucosalPercutaneousPermucosalPercutaneousPermucosalFecal-Oral
Chronic Infection
No Yes Yes Yes No
Prevention
Pre/Post exposureimmunizationPre/Post exposureimmunizationBlood donor screening;Risk behavior modificationPre/Post exposureimmunization;Risk behavior modificationEnsure safe drinkingwater 
HEPATITIS AClinical Features
Incubation Period
o
 
 Average: 30 days
o
 
Range: 15-50 daysJaundice by age group
o
 
<6yrs (10%)
o
 
6-14 yrs (40-50%)
o
 
>14 yrs (70-80%)Complications
o
 
Fulminant Hepatitis
o
 
Cholestatic Hepatitis
o
 
Relapsing HepatitisChronic Sequelae: None
CONCENTRATION OF HEPATITIS A VIRUS IN VARIOUS BODY FLUIDSEVENTS IN HEPATITIS A INFECTION (CDC)
 As the immune system responds to the infection, the amount of virus in theblood (viremia) and in the stool (HAV in stool) disappears. The liver enzyme, ALT goes up at the beginning of the infection, but decreases to normal at about8 weeks. IgM shows acute infection and IgG is positive long
 –
term.
Virus Transmission
Close personal contact
 
o
 
household contact
 
o
 
sex contact
 
o
 
child day care centers
 
Contaminated food and water 
 
o
 
infected food handlers
 
o
 
raw shellfish
 
Blood exposure (rare)
 
o
 
injecting drug use
 
o
 
transfusion
 
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Laboratory Diagnosis
 Acute infection: dectection of HAV-IgM in serum by EIA
 
Past Infection: immunity is determined by the detection of HAV-IgGby EIA
 Vaccination Strategies: Epidemiologic Considerations
Many cases occur in community-wide outbreaks
 
o
 
No risk factor identified for most cases
 
o
 
Highest attack rates in 5-14 years old
 
o
 
Children serve as reservoir of infection
 
Persons at increased risk of infection
 
o
 
Travelers
 
o
 
Homosexual men
 
o
 
Injecting drug users
 Hepatitis A Prevention-Immune Globulin
Pre-exposure
o
 
Travelers to intermediate and high HAV-endemic regions
 
Post-exposure (w/in 14 days)
o
 
Routine
 
 
Household and other intimate contacts
 
o
 
Selected situations
 
 
Institutions: day care centers
 
 
Common source exposure: food prepared byinfected food handler 
 HEPATITIS BClinical Features
Incubation Period
o
 
 Average: 60-90 days
o
 
Range: 45-180 daysClinical Illness (jaundice):
o
 
<5yrs (<10%)
o
 
5 yrs (30-50%)
o
 
>5 yrs (70-80%) Acute Case-fatality rate: 0.5-1%Chronic Infection
o
 
<5yrs (30-90%)
o
 
5yrs (2-10%)Premature mortality from chronic liver disease: 15-25%
PREVALENCESpectrum of Chronic Hepatitis B Disease
Chronic Persistent Hepatitis: asymptomatic
 
Chronic Active Hepatitis: symptomatic exacerbations of hepatitis
 
Cirrhosis of Liver Hepatocellular carcinoma
DISEASE PROGRESSIONGlobal Patterns of Chronic HBV Infection
High (>8%): 45% of global population
 
o
 
Lifetime risk of infection >60%
 
o
 
Early childhood infections common
 
Intermediate (2-7%): 43% of global population
 
o
 
Lifetime risk of infection 20-60%
 
o
 
Infections occur in all age groups
 
Low (<2%): 12% of global population
 
o
 
Lifetime risk of infection <20%
 
o
 
Most infections occur in adult risk groups
 
CONCENTRATION OF HEPATITIS B VIRUS IN VARIOUS BODY FLUIDS
High
 
Moderate
 
Low/Not Detectable
 
Blood
 
Serum
 
Wound exudates
 
Semen
 
Vaginal fluid
 
Saliva
 
Urine
 
Feces
 
Sweat
 
Tears
 
Breastmilk
 
Modes of Transmission
Sexual: sex workers and homosexuals are particular at risk
 
Parenteral: IVDA, health workers are at increased risk
 
Perinatal: main means of transmission in high prevalencepopulations. Mothers who are HBeAg positive are much more likelyto transmit to their offspring than those who are not
 Diagnosis
 A battery of serological tests are used for the diagnosis of acute andchronic hepatitis B infection
HbsAg
: used as general marker of infection
 HbsAb
: used to document recovery and/or immunity to HBVinfection
 Anti-HBc IgM
: marker of acute infection
 Anti-HBc IgG
: past or chronic infection
 HbeAg
: indicates active replication of virus and thereforeinfectiveness
 Anti-Hbe
: virus no longer replicating. However, the patient can stillbe (+) for HBsAg w/c is made by integrated HBV
 
GLOBAL PATTERNS OF HEPATITIS A VIRUS TRANSMISSIONEndemicity DiseaseRatePeak Age of InfectionTransmnsission Patterns
High Low toHigh
 
Early Childhood
 
Person to person;Outbreaks uncommon
 
Moderate High
 
Late Childhood/Young Adults
 
Person to person; Foodand waterborne outbreaks
 
Low Low
 
Young Adults
 
Person to person; Foodand waterborne outbreaks
 
Very Low Very Low
 
 Adults
 
Travelers; Outbreaksuncommon
 
 
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HBV-DNA:
indicates active replication of virus, more accurate thatHbeAg especially in cases of escape mutants. Used mainly for monitoring response to therapy
 TreatmentInterferon
o
 
for HBeAg +ve carriers wit chronic active hepatitis
 
o
 
response rate is 30-40%
 Lamivudine
o
 
a nucleoside analogue reverse transcriptase inhibitor 
 
o
 
Well tolerated,most patiens will respond favorably
 
o
 
Tendency to relapse on cessation of treatment
 
o
 
Rapid emergence of drug resistance
 
*Successful response to treatment will result in the disappearance of HBsAg, HBV-DNA and seroconversion to HbeAg
PreventionVaccination
o
 
Highly effective recombinant vaccines are now available
 
o
 
given to those who are at increased risk of HBV infectionsuch as health care workers
 
o
 
given routinely to neonates as universal vaccination inmany countries
 
Hepatitis B Immunoglobulin (HBIG)
o
 
Protect persons exposed to hepatitis B
 
o
 
efficacious w/in 48 hrs of the incident
 
o
 
given to neonates who are at increased risk for contracting hepatitis B (i.e. whose mother are HBsAg(+)and HBeAg (+))
 
Other measures
 
o
 
screening of blood donors
 
o
 
blood and body fluid precautions
 HEPATITIS CClinical Features
Incubation Period
o
 
 Average: 6-7weeks
o
 
Range: 2-26 weeksClinical Illness (jaundice): 30-40% (20-30%)Chronic Hepatitis: 70%Persistent Infection: 85-100%Immunity: No protective antibody response identified
 Chronic Hepatitis C Infection
The spectrum is essentially the same as chronic hepatitis B infection
 
 All the manifestations of chronic hepatitis B infection may be seen,though with a lower frequency
 
i.e. chronic persistent hepatitis, chronic active hepatitis, andhepatocellular carcinoma
 Risk Factors Associated with Transmission of HCV
Transfusion or transplant from infected donor 
 
Injecting drug use
 
Hemodialysis (yrs on treatment)
 
 Accidental injuries with needles/sharps
 
Sexual/household exposure to anti-HCV-positive contact
 
Multiple sexual partners
 
Born to HCV- infected mother 
 DISEASE PROGRESSIONLaboratory DiagnosisHCV antibody
o
 
generally used to diagnosis to hepatitis C infection
 
o
 
not useful in acute phase as it takes at least 4 weeksonbefore antibody appears
 HCV-RNA
o
 
techniques include PCR and branched DNA
 
o
 
maybe used to diagnose HCV infection in the acutephase
 
o
 
main use is in monitoring the response to antiviraltherapy
 HCV-antigen
o
 
an EIA for HCV antigen is available
 
o
 
used in the same capacity as HCV-RNA tests but ismuch easier to carry out
 
DIAGNOSTIC TESTSSpecifications Diagnostic Test Type
 
Serologic
 
Virologic
Mode of detection Antibodies VirusSensitivity > 95% > 98%Specificity Variable > 98%Detection Post-exposure 2-6 mos 2-6 wksUse Screening Confirmation

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