Hepatitis A + B

Preparation by : Ubayda M. Alastal

Presented to : Dr. Fouad A. Issawi

Outline :
 History & Introduction
 Magnitude of problem
 Agent factors
 Host factors
 Environmental factors
 Modes of transmission & portal of entry
 Pathology
 Clinical features
 Complications
 Treatment
 Prevention & immunization
Hepatitis A virus
History

 Itwas discovered in 1973 by Steven feinstone as

a non enveloped spherical RNA virus

 HAV was unidentified viral disease prior to this

discovery
Magnitude of problem & Epidemiology
 Worldwide, HAV occurs in sporadic cases or in
epidemics. In developing countries,it is closely
associated with poor sanitation. It largely affects
children .
 In developed countries, Hepatitis A is uncommon where
sanitation is good and vaccination to
high-risk groups is available.
n Palestine, the reported incidence rate of hepatitis A is
about 108 per 100.000 annually throughout the last
years.
Prevalence of antibody to hepatitis A virus, 2013
Source: CDC YellowBook
 Agent factors

 Hepatitis A Virus is a member of picornaviridae family. It is a

spherical, nonenveloped RNA virus
 reservoir of infection : human is only reservoir
 Infective material : any food that contaminated
with virus by feco-oral route
Period of communicability: 1-2 weeks before symptoms
to one week after onset of jaundice
 Host factors

 Humans are the only natural host

 most children (90%) have been infected with the hepatitis A
virus before the age of 10 years 
 M=F
 In children aged <6 years, 70% of infections are asymptomatic
 Among older children and adults, infection is typically
symptomatic
 Environmental factors

 poor sanitation;
 lack of safe water;
 living in a household with an infected person;
 travelling
to areas of high endemicity without being
immunized.
 Modes of transmission & portal of entry

 The hepatitis A virus is transmitted primarily by the faecal-

oral route; that is when an uninfected person ingests food or
water that has been contaminated with the faeces of an
infected person.
 In families, this may happen though dirty hands when an
infected person prepares food for family members
Pathology
Clinical features
 Complications

 Fulminating hepatitis as complications occur in approximately

(0.4%) of cases that require hospital admission

 Fulminatinghepatitis is particularly common in patients with

chronic HCV infection

 Mortality is approximately (0.2%) and common in elderly, i.e.

severity increase with age
 Treatment

 There is no specific treatment for hepatitis A virus infection.

 Treatment and management of HAV infection is supportive
 For Mild/ moderate cases, (80%) of cases manage can be
managed as an outpatient emphasizing rest and oral
hydration.
 Sever attack with vomiting, dehydration and signs of hepatic
decompensation require admission to the hospital.
 Prevention & immunization

 Improved sanitation, food safety and immunization are the

most effective ways to combat hepatitis A.

 Passiveimmunization with human immunoglobulin is not

recommended in our country. Active immunization: HAV
vaccination is available in the world, but it is not
recommended for our country due to high endemicity of our
area.
Hepatitis B virus
History
 The hepatitis B virus was discovered in 1965
by Dr. Baruch Blumberg who won the Nobel Prize for
his discovery.
Dr. Blumberg who was studying haemophilia, found an
antibody two patients which reacted against an
antigen from an Australian Aborigine. Later the
antigen was found in patients with serum type
hepatitis and was initially designated "Australian
Antigen". Subsequent study has shown the Australia
Antigen to be the hepatitis B surface antigen
Magnitude of problem & Epidemiology
• 2 billion people have been infected (1 out of 3 people).

• 350 million people are chronically infected.

• 10-30 million will become infected each year.

• An estimated 1 million people die each year from hepatitis B

and its complications.

• Approximately 2 people die each minute from hepatitis B.

• The virus causes 60-80% of all primary liver cancer.

Source-(WHO, hepb.org)
Source: http://www.wikidoc.org/index.php/Hepatitis_B_virus
 Agent factors
• Virus of the hepadnaviridae family.
• It replicates within infected liver cells.
• The outer protein collectively known as HBs or surface protein (surface coat).
• Inner to outer coat surrounds an inner protein shell composed of HBc (core particle or
capsid)
• Core particle surrounds viral DNA and the DNA polymerase enzyme.
 Agent factors
RESERVOIR OF INFECTION
 Human is the only reservoir of infection.
 Spread from a case or carrier.
 Cases may range from inapparent to symptomatic cases.

INFECTIVE MATERIAL
 Contaminated blood is the main source of infection.
 Other sources include- saliva, vaginal secretions and semen of
infected persons.
PERIOD OF COMMUNICABILITY
 Virus present in the blood during incubation period and the acute phase
of disease.
 Communicability is usually several months or until disappearance of
HBsAg or the appearance of surface antibody.
 Host factors
AGE
 HBV infection are age dependent
 Occurs in
 1% of perinatal
 10% of early childhood (1-5yrs of age)
 30% of late childhood (>5yrs of age)
 Development of chronic hepatitis B is inversely proportional to age
 80-90% infected perinatally. 100
90

C a rrie r ris k (% )
 30% in early childhood. 80
70
60
 5% in 6yrs of age. 50
40
30
20
10
0
Birth 1-6 mo 7-12 mo 1-4 yrs 5+ yrs
Age of infection

 Females are more likely than males to produce anti-HBs

 Environmental factors
HIGH RISK GROUPS
 Infection in surgeons are 50 times greater than in general population
and twice that of other physicians.
 Other risk group includes
 Recipients of blood transfusion
 Health care and lab personnel
 Homosexuals, prostitutes, percutaneous drug abusers
 Infants of HBV positive mothers
 Solid organ transplants and immunocompromised persons.
 Serological screening and vaccination of high risk groups are
recommended
 Modes of transmission & portal of entry
 1) Parenteral transmission
Needle stick
injury Household
contacts

 2) Sexual transmission

 3) Vertical transmission
Pathology
infiltration of lymphocytes into the
parenchyma of the liver, spotty of necrosis, fibrosis
leading to cirrhosis, and finally the development of
primary hepatocellular carcinoma.
Acute hepatitis B can range from subclinical disease to
fulminant hepatic failure in about 2% of cases
 Clinical features
 Acute (short-term) illness:
 loss of appetite
 tiredness

 pain in muscles, joints, and stomach

 Diarrhoea and vomiting
 jaundice (yellow skin or eyes)

 Chronic (long-term) infection:

 liver damage (cirrhosis)
 liver cancer
 death
 Complications

 Fulminant hepatitis
 Cirrhosis
 Hepatocellular carcinoma
 Death
 Treatment
 Currently, there is no treatment available for acute hepatitis B.
Symptomatic treatment of nausea, anorexia, vomiting, and other
symptoms may be indicated.
There are 3 main classes of treatment:
 Antiviral: interfering with viral replication.
 Immune modulators: aimed at helping the human immune system to
mountna defense against the virus.
 Alpha-interferon were the first drugs for the treatment of chronic
hepatitis B.
I
t is recommended for individuals who have "replicative disease" (HBeAg
positive).
 Prevention & immunization

HEPATITIS VACCINE
 Recombinant hepatitis B vaccine
 Hepatitis vaccine available in monovalent or in fixed
combination with other vaccines including DPT, Hib,
Hepatitis A.
 At birth only monovalent vaccine is used.
 Prevention & immunization

 Dose
 In adults 10-20 μgm initially and repeat on 1 st and 6th month.
 In children under 10yrs ½ adult dose at same time intervals.
 For greater reliability of absorption the deltoid muscle is preferred.
 For infant and children under 2yrs of age, anterolateral aspect of thigh is used for vaccination.
 Hepatitis vaccine does not interfere with immune response of any other vaccines.
Prevention & immunization
No. of Site of
Item Dose Age
Doses injection

BCG 1 0.05ml Intradermal At birth        

HB 1 0.5ml IM At birth        

IPV 2 0.5ml SC 1st. month 2nd. month      

Penta 3 0.5ml IM 2nd. month 4th. month 6th. month    

18th. 6th.
bOPV 5 2drops Oral 2nd. month 4th. month 6th. month
month year

PCV 3 0.5ml IM 2nd. month 4th. month 12th. month    

Rota 2 1.5ml Oral 2nd. month 4th. month      

MMR 2 0.5ml SC 12th. month 18th. month      

DTP 1 0.5ml IM 18th. month        

DT 1 0.5ml IM 6th. year        

Td 1 0.5ml IM 15th. year        

 Prevention & immunization

 Group at high risk of contracting HBV infection

 Person with high risk sexual behaviour, partners, and house hold contact with
HBsAg +ve individuals.
 Injecting drug users
 Who requires frequent blood or blood products
 Recipient of solid organ transplantation
 Occupational risk of HBV infection.
 International travellers to HBV endemic countries.
? Any Questions
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