Presented by:Group C PCL II 1/12/2014GROUP C;PCL II1.
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Transcript of Presented by:Group C PCL II 1/12/2014GROUP C;PCL II1.
Presented by:Group C
PCL II
04/10/23 GROUP C;PCL II 1
04/10/23 GROUP C;PCL II 2
1. HAKIZIMANA NIYOYITA ADOLPHE UG121136812. HAKORIMANA FIDELE UG121135293. HATEGEKIMANA INNOCENT UG121138234. HAVUGARUREMA LEONARD UG121131635. IGIRANEZA BRAVE UG121134496. IMFURANKUNDA HABIMANA HONORIN UG121129867. INGABIRE DIANE UG12115269 8. INGABIRE PROSPER UG121131839. ISHIMWE ELICIEN UG1211297310. ISHIMWE EPIPHANIE UG1211361011. ISHIMWE MARIE CONSOLATRICE SAGE UG 1211422612. NSANZIMANA Jean de Dieu UG12113945
GROUP MEMBERS
Hepatitis A Virus Introduction
Naked RNA virus Related to enteroviruses, formerly known as
enterovirus 72, now put in its actual family:picornavirus
One stable serotype only Difficult to grow in cell culture: primary marmoset cell
culture and also in vivo in chimpanzees and marmosets .
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Hepatitis A Virus
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Source ofvirus
feces blood/blood-derived
body fluids
blood/blood-derived
body fluids
blood/blood-derived
body fluids
feces
Route oftransmission
fecal-oral percutaneouspermucosal
percutaneouspermucosal
percutaneouspermucosal
fecal-oral
Chronicinfection
no yes yes yes no
Prevention pre/post-exposure
immunization
pre/post-exposure
immunization
blood donorscreening;
risk behaviormodification
pre/post-exposure
immunization;risk behaviormodification
ensure safedrinking
water
Introduction cont’d
A B C D E
HAV biology HAV is one kind of picornavirus and used to be classified as
enterovirus type72, but recently, it is considered to be classified as heparnavirus
Hepatitis A virion is a naked spherical particle, diameter 27nm Consists of a genome of linear, single-stranded RNA, 7.5kb.
The genome may be divided into 3 coding region: P1 region (encoding structural protein), P2 and P3 regions (encoding non-structure protein)
During acute stage of infection, HAV can be found in blood and feces of infected human and primates
Marmoset and chimpanzee are susceptible animals
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HAV STRUCTURE
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HAV on EM
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HAV biology
HAV can not cause cytopathy, replicate within cytoplasma of hepatocytes and via bile are discharged with feces
7 genotypes, 1, 2, 3, 7 types from human body
Only one antigen-antibody system. Anti-HAV IgM is diagnostic evidence of recent infection, IgG is protective antibody.
Resistance of HAV: 56°C, 30 min, usually temperature 1 week, dry feces at 25°C 30 days, fresh water, sea water ,shellfish or soil for several months. 70% alcohol at 25°C , 3 min, 100°C, 5 min and ultraviolet, 1 min
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Close personal contact
(e.g., household contact, sex contact, child day care centers)
Contaminated food, water(e.g., infected food handlers, raw shellfish)
Blood exposure (rare)(e.g., injecting drug use, transfusion)
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Transmission-Epidemiology
EndemicityDisease
RatePeak Age
of InfectionTransmission Patterns
High Low to High
Early childhood
Person to person;outbreaks uncommon
Moderate High Late childhood/
young adults
Person to person;food and waterborne outbreaks
Low Low Young adultsPerson to person;food and waterborne outbreaks
Very low Very low Adults Travelers; outbreaks uncommon
Global Patterns of Hepatitis A Virus
Transmission
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pathogenesis
HAV invade into human body by mouth and cause viremia.
After one week,the HAV reach liver cells replicate within.
Then enter intestine with bile and appear in feces.
It’s believed that damage of liver cells maybe caused by immune response.HAV does not cause cytopathy
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After HAV replicating and discharging, liver cells damage begin
Animal experiment proved that immune complex may attend the pathogenesis of HA:
activated T cell secrete γ-INF that promote the representation of HLA- antigen on the liver Ⅰcells, CTL(cytotoxic T lympocyte)may kill the target cell infected with HAV
Step 1:HAV attaches to the basilar surface of the hepatocyte. (HAV demonstrates hepatotropism)The virion binds with its specific glycoprotein receptor.The capsule is internalized through the host cell membrane via clathrin-mediated endocytosis.
Step 2:The viral genomic RNA is released into the host cell.
Step 4: Reverse transcription of the ssRNA strand occurs.
Steps 3,5: The reverse transcribed dsRNA is translated into viral proteins. The proteins are then assembled and packaged into vesicles.
Step 6:The vesicles are released at the apical surface of hepatocyte
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REPLICATION CYCLE OF HAV
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Clinical presentation Prodrome(EARLY STAGE)
patients may have mild flulike symptoms of anorexia, nausea and vomiting, fatigue, malaise, low-grade fever (usually < 39.5°C), myalgia, and mild headache
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Icteric phase
In the icteric phase, dark urine appears first (bilirubinuria).
Pale stool soon follows, although this is not universal.
Jaundice occurs in most (70-85%) adults with acute HAV infection;
The degree of icterus also increases with age.
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Relapsing hepatitis A Relapsing hepatitis A is an uncommon
sequela of acute infection, is more common in elderly persons
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Incubation period: Average 30 days
Range 15-50 days
Jaundice by <6 yrs, <10%age group: 6-14 yrs, 40%-50%
>14 yrs, 70%-80%
Complications: Fulminant hepatitis
Cholestatic hepatitis
Relapsing hepatitis
Chronic sequelae: None04/10/23 GROUP C;PCL II 21
Laboratory Diagnosis
Acute infection is diagnosed by the detection of HAV-IgM in serum by EIA.
Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA.
Cell culture – difficult and take up to 4 weeks, not routinely performed
Direct Detection – EM, PCR technique. It can detect illness earlier than serology but rarely performed.
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FecalHAV
Symptoms
0 1 2 3 4 5 6 12
24
Hepatitis A Infection
Total anti-HAV
Titre
ALT
IgM anti-HAV
Months after exposure
Typical Serological Course
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prevention
Control of source of infection Cut off the route of transmission Protection of susceptible population
Active immunityPassive immunity
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Many cases occur in community-wide outbreaks no risk factor identified for most cases highest attack rates in 5-14 year olds children serve as reservoir of infection
Persons at increased risk of infectiontravelershomosexual meninjecting drug users
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Hepatitis A Vaccination Strategies
Epidemiologic Considerations
Pre-exposuretravelers to intermediate and high
HAV-endemic regions
Post-exposure (within 14 days)Routinehousehold and other intimate contactsSelected situationsinstitutions (e.g., day care centers)common source exposure (e.g., food prepared by
infected food handler)
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Prevention - Immune Globulin
Vaccine Age(years) Dose* Volume(mL)Two-does
schedule(mos)†
HAVRIX§1-18 720 (EL.U.) 0.5 0, 6–12
>18 1,440 (EL.U.) 1.0 0, 6–12
VAQTA¶1-18 25 (U) 0.5 0, 6–18
>18 50 (U) 1.0 0, 6–18
* EL.U. = enzyme-linked immunosorbent assay (ELISA) units. U = units.
† 0 months represents the timing of the initial dose; subsequent numbers represent the months after the initial dose.§ Hepatitis A vaccine, inactivated, GlaxoSmithKline Biologicals. This vaccine also is licensed for a 3-dose series in children aged 1–18 years, with 360 EL.U., 0.5-mL doses at 0, 1, and 6–12 months.r ¶ Hepatitis A vaccine, inactivated, Merck & Co., Inc
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REFERENCES:
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Clinical microbiology made ridiculously simple www.pubmed.com
GOD BLESS YOU ALL!!!!!!!!!!!!!
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