hepatitis b disease surveilance :epidemiology:school of public health: university of louisville
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Hepatitis B Disease
Surveillance and Health
Statistics SALWA F RASHID MD, CPH
OCTOBER 2015
Hepatitis B
An infection of the liver caused by HBV
The hepatitis B virus was discovered in 1965 by Dr Baruch Blumberg
Hepadnaviridae family
Small, partially double stranded DNA Virus
Numerous antigenic components
Humans are only known host
May retain infectivity for more than 7 days at room temperature
Blood banks began using the test in 1971 to screen blood donations, risk of hepatitis B infections from a
blood transfusion decreased by 25 percent
Hepatitis B
About 2 billion persons around the world have
been infected with HBV
About 250 million have chronic infections around
the globe
Significant cause of morbidity and mortality
780 000 estimated deaths/year due to
complications. (1)
Hepatitis B
90% of infected adults will recover during the first year of infection
5% of adults will develop chronic hepatitis B infection.
30-50 % of adults with chronic hepatitis B will develop cirrhosis or HCC
Children under 6 years old are at risk of developing chronic hepatitis B when infected with the virus
Hepatitis B
In 2013, 3,050 cases of acute hepatitis B in the United States were reported to the CDC
incidence of reported acute hepatitis B was 1.0 cases per 100,000 population
actual number of new infections is estimated to be approximately tenfold higher.
In Kentucky 2013, 214 cases of acute Hepatitis B infection was reported. With rate of 4.9/100,000 population (2)
Hepatitis B
700,000–1.4 million individuals were estimated to
have chronic hepatitis B in the United States (2)
http://www.cdc.gov/hepatitis/statistics/2013survei
llance/index.htm - tabs-801937-1
Hepatitis B Prevalence/GloballyRegion/Country Source Prevalence Most common age Most common mode of
transmission
Increasing prevalence from north to Southeast Asia, China, Pacific island, sub-Saharan Africa, Alaska
WHO 8% or > Perinatal and earlychildhood
Vertical (mother to child during
birth), horizontal in early
childhood Percutaneous
Mediterranean basin, eastern Europe, central Asia, Japan, Latin and South America, Middle East
WHO 2-7 % Early childhood Percutaneous, sexual
United States and Canada, western Europe, Australia, New Zealand
WHO ≤1 % Adult Sexual, percutaneous
INCIDENCE OF HEPATITIS B
Area Source Year Incidence of acute Hepatitis
B/100,000 population
Rate of chronic
Hepatitis B /100,1000
population
Mortality
#
Mortality
Rate
Globally WHO (3) 780 000
United States CDC (2) 2013 1.0 7.7 1,873 0.52
Kentucky CDC (2) 2013 4.9
Canada Study 1 1998/1999 2.3
Europe Studty 2 2000 1.33(M)
0. 58(F)
Taiwan Study 3 1984
2004
9.8
0.6
Italy StuS 19912010
5.1
0.9
Epidemiology of Hepatitis B and
vaccine effectGeographical area/country Source Year Prevalence Incidence Acute Hep B Mortality # Mortality
Rate
United States CDC
1990 (4)20042013
8.52.11.0
1,873
0.52
Kentucky CDC 2013 0.4
U.S and Canada WHO 2015 <1%
CanadaCanada overallCanada BornInuit population
Immigrants from highly endemic
countries(2)
Study 4 1998/1999
2001 0.5-1%
0.1%
6.9%
7.4%
2.3
Epidemiology of Hepatitis B and
vaccine effectGeographical area/country Source Year Prevalence Incidence Acute Hep B
Europe
Northern Europe (Scandinavian
countries and the United Kingdom
Southern Europe
Study #4
< 0.1%
> 8%
1.33(M) 0. 58 (F)
IranStuStudy
2005 2.6%
Africa
(Gambia & Senegal),
Nigeria
15%
13.6%
14.1%(in
pregnant
women)
Epidemiology of Hepatitis B
and effect of vaccinationEastern Mediterraneancountries of North Africa through the MiddleEast to Pakistan
(Study 5) Egypt
1985
Egypt
2009 and 2010
11.7% (Incidence)
4.2%
(Decreased after immunization)
Incidence
South-East Asia
Bangladesh, Bhutan,North Korea, India,Indonesia, MaldivesMyanmar, Nepal, Sri Lanka,Thailand and Timor-Leste.
Study (4)
2005
India
Thailand1992
Thailand
2004
>5%
2-8%
7. 2
4%(universal vaccine)
IncidenceWestern Pacific
Australia, Brunei Darussalam,
Cambodia, China, Cook Islands, Fiji,
Japan, Kiribati, Lao People’s
Democratic Republic, Malaysia,
Marshall Islands, Nauru, New Zealand,
Niue, Papua New Guinea, Philippines,
Republic of Korea, Samoa, Singapore,
Solomon Islands, Tonga, Tuvalu,
Vanuatu, and Vietnam.
Study#4non-Aboriginal populations of
Australia and New Zealand
The Northern and Central Asian
small South Pacific island nations
China 1992
2002(small surcharge)
2005 (no charge)
2009
0.1%
7 and 12
30
9.8(parents had to
pay for vaccines)
7.2(children <1%)
Refugees resettled in Kentucky
Refugees resettled in Kentucky
October 2012-2015 Refugees who went to a
clinic in Jefferson County
October 2012-2015 Refugees who went to
a clinic in Jefferson County
Methods of transmission
The virus is blood born transmitted by:
Exposure to infectious blood or body fluids
Vertical transmission during birth
Injected drug use
Sexual contact
Blood transfusion
Dialysis
Tattooing
Acupuncture
Health care workers
House hold contact with skin or mucosal abrasion who come in contact with infectious fluid
Diagnosis
Signs and symptoms
Acute infection
(Acute viral Hepatitis)
Malaise, Nausea and vomiting, fever, general aches, abdominal pain, dark
color urine, and
Either a) Jaundice or b) Elevated ALT>100 IU/L
• Laboratory Criteria
- HBsAg positive Immunoglobulin M (IgM)
- antibody to hepatitis B core antigen (IgM anti-HBc) positive (if done
- patient not known to have chronic hepatitis B
Hepatitis B
Symptoms last for few weeks and then the infection clears leaving
the person with natural immunity (due to infection) A few people may
have more severe liver disease
Diagnosis
• The likelihood of developing symptoms of acute
hepatitis is age dependent:
90% of infected adults will recover during the
first year of infection
Diagnosis
(fulminant hepatic failure)
sever form and may result in death
develops in 1% of cases *
(Asymptomatic infection)
May go unrecognized
Diagnosis
Chronic infection
presence of HBsAg in serum for at least 6 months or the presence of
HBsAg and the absence of anti-HBc immunoglobulin M (IgM). *
(asymptomatic)
(chronic hepatitis), persons with chronic hepatitis can be a source of
spreading the infection
chronic inflammation of the liver can lead to cirrhosis which in turn
leads to liver cancer (Hepatocellular carcinoma)
Alcohol use should be avoided in patients with chronic hepatitis B
infection as it will increase there risk for both ( Liver cirrhosis and
caner)(14) hepatocellular carcinomas.
Diagnosis
The risk of developing chronic infection is
inversely associated with age
>90% of infants infected at birth or in their first
year of life
25% to 50% of children ages 1 to 5 years
5% to 10% of older children and adults
Diagnosis
Laboratory tests:
LFT: increased ALT, AST (transaminitis)
Serum Assays:
HBsAg: marker of infection
HBsAb: marker of immunity or recovery
Diagnosis/Laboratory tests
Anti-HBc-IgM: marker for acute infection
Anti-HBc-IgG: marker for chronic infection
HBeAg: active replication
Anti-Hbe: inactive replication
Diagnosis/Laboratory tests
HBV-DNA: active replication (more accurate),
detected by PCR test, (viral load), to determine
infection status and to follow up response for
treatment.
Hepatitis B
Early during the infection the HBs-Ag can be undetectable (Window*)
and the only think that appears is anti-HBc IgM
after HBsAg appears, HBeAg will appear which is associated with
high replication rates and increased infectivity
When HBe-Ag is cleared, and anti-HBe levels increase, there will a
fast decrease in viral replication
Window period is the time between clearance of Hbs-Ag and the
appearance of anti-HBs and anti-HBc IgG
Persons who are able to clear the infection will have undetectable
HBsAg, and positive IgG to HBs-Ag and HBc-Ag.
Hepatitis B
Persons in whom HBsAg stay reactive for six months or more are
known as hepatitis B carriers
They can have chronic hepatitis which is shown by elevated liver
enzymes most commonly (ALT) due to inflammation of the liver
which occurs in the immune clearance phase of the chronic infection.
Carriers with HBeAg negative, especially persons who are infected
during adulthood have minimal replication and therefore they are at
lower risk of developing liver cirrhosis and cancer or infecting others
Prevention The hepatitis B vaccine is the mainstay of hepatitis B prevention.
Vaccine is given within 24 hours of birth.
Immunologic memory develops following vaccination
Antibody level declines following successful vaccination
Anamnestic response upon exposure (antibody level increases quickly)
excellent record of safety and effectiveness
first hepatitis B vaccine, was initially a heat-treated form of the virus.
In 1981, the FDA approved a more sophisticated plasma-derived hepatitis B vaccine for human use. This “inactivated” type of vaccine
The use of this vaccine was discontinued in 1990 and it is no longer available in the U.S.
Current Recombinant Hepatitis B Vaccines
In 1986, research resulted in a second generation of genetically engineered (or DNA recombinant) hepatitis B vaccines.
Prevention
Since 1982, over 1 billion doses of hepatitis B vaccine
have been given globally.
Vaccination decreased the rate of chronic infection to
less than 1% in countries known to have increased rates
prior to the vaccine (8-15%)
As of 2013, 183 Member States vaccinate infants against
hepatitis B as part of their vaccination schedules and 81%
of children received the hepatitis B vaccine
Prevention
IMPACT OF PREVENTION OF TRANSMISSION
Prevention strategies
Primary prevention of new infections (vaccines and post-exposure
prophylaxis)
Secondary prevention of HBV transmission by appropriate sexual and
sanitary practices.
Tertiary prevention of the pathological consequences of chronic HBV by
anti-viral treatment.
The risk of progression from acute to chronic infection is inversely
proportional to the age of infection.
90% of infants who acquire HBV infection from their mothers at birth
become chronically infected, whereas in adults
5% of acute HBV cases remain chronically infected
Who should get the vaccine?
Everyone 18 years of age and younger
Adults over 18 who are at risk
Who should get the vaccine?
Household contacts of persons with chronic HBV infection
Sex contacts of infected people
Persons with multiple sexual partners
Homosexual men
Injected drugs users
Health care workers who might be exposed to blood or body
fluids
Patients on Hemodialysis
Persons who need 3 doses
Infant whose mother is infected with HBV:
First Dose: within 12 hours of birth
Second Dose: 1 - 2 months of age
Third Dose: 6 months of age
Persons who need 3 doses
Infant whose mother is NOT infected with HBV:
First Dose: between birth – 2 months of age
Second Dose: 1 - 4 months of age (at least 1 month
after first dose)
Third Dose: 6 - 18 months of age (at least 2 months
after the second dose)
Hepatitis B Vaccine/Adult Schedule
Usual Minimum
Dose Interval Interval
Dose 1
Dose 2 1 month 4 weeks
Dose 3 4-6 months 8 weeks*
*third dose must be separated from first dose by at least 16 weeks
Treatment
Key recommendations:
Identifying who needs the treatment by non-invasive test
to know the stage of the liver disease.the use of a few
simple non-invasive tests to assess the stage of liver
disease
prioritizing treatment for those with cirrhosis
Use tenofovir or entecavir, for the treatment of chronic
hepatitis B; which are known to be effective and safe
regular monitoring by lab tests for early detection of liver
cancer, and to follow up response to treatment.
Bibliography (1) World Health Organization (WHO). Hepatitis B - Updated July 2015.
http://www.who.int/mediacentre/factsheets/fs204/en/
(2) Surveillance for Viral Hepatitis – United States, 2013 (Centers for Disease Control and Prevention)
http://www.cdc.gov/hepatitis/statistics/2013surveillance/index.htm#tabs-801937-1
3) World Health Organization (WHO). Hepatitis B - Updated July 2015
http://www.who.int/csr/disease/hepatitis/whocdscsrlyo20022/en/index1.html#world
4) Centers for Disease Control and Prevention (CDC). Web.
http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5251a3.htm
5) Hepatitis B (WHO)
http://www.who.int/mediacentre/factsheets/fs204/en/
(6)Hollinger FB, Liang TJ. Hepatitis B Virus. In: Knipe DM et al., eds. Fields Virology, 4th ed. Philadelphia, Lippincott Williams & Wilkins, 2001:2971-3036.
(7) Guidotti LG et al. Hepatitis B virus nucleocapsid particles do not cross the hepatocyte nuclear membrane in transgenic mice. Journal of Virology, 1994, 68:5469-5475.
(8) Mahoney FJ. "Update on Diagnosis, Management, and Prevention of Hepatitis B Virus Infection." Clinical Microbiology Reviews 12.2 (1999): 351-66. (9) McMahon BJ, et al. "Acute Hepatitis B Virus Infection: Relation of Age to the Clinical Expression of Disease and Subsequent Development of the Carrier State." The Journal of Infectious Diseases151.4 (1985): 599-603.
(10) Centers for Disease Control and Prevention(CDC). Hepatitis B VIS. Page last updated: June 18, 2013. http://www.cdc.gov/vaccines/hcp/vis/vis-statements/hep-b.html
(11)"Hepatitis B Vaccine History." Hepatitis B Foundation: Vaccine History. Web.
http://www.hepb.org/professionals/hepatitis_b_vaccine.htm
Bibliography
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Journal of Infectious Diseases. 2001;12(6):345-350. Magdzik, Wiesław. "Hepatitis B
Epidemiology in Study 2: Poland, Central and Eastern Europe and the Newly Independent
States." Vaccine 18 (2000)
Study 3: Romano L., Paladini S., and Zanetti AR. "Twenty Years of Universal Vaccination
against Hepatitis B in Italy: Achievements and Challenges." Journal of Public Health
Research 1.2 (2012): 126-9.
Study 4: Papastergiou, Vasilios, et al. "Global Epidemiology of Hepatitis B Virus (HBV)
Infection." Current Hepatology Reports 14.3 (2015)
Study 5: Shalaby S, Kabbash IA, El Saleet G, et al. Hepatitis B and C viral infection:
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