Call Girls Kochi Just Call 9907093804 Top Class Call Girl Service Available
Ā
Hepatitis
1. VIRAL
HEPATITIS
P R E S E N T E D B Y :
ā¢ M E G H N A D A S ( R O L L N O . 4 1 )
ā¢ M E M A S I N G H A ( R O L L N O . 4 2 )
ā¢ N A B A N I T A D E V I ( R O L L N O . 4 3 )
ā¢ N E H E M I A H N A R Z A R Y ( R O L L N O . 4 4 )
MODERATOR : DR. MOUSHUMI BISWAS
Asst. Professor, Community Medicine
Silchar Medical College and Hospital
3. What is Viral Hepatitis?
ā¢ Viral hepatitis is a systemic disease with primary
inflammation of the liver by any one of the heterogeneous
group of hepatotrophic viruses.
ā¢ The most common causes of viral hepatitis are the five
unrelated hepatotrophic viruses Hepatitis A, Hepatitis B,
Hepatitis C, Hepatitis D and Hepatitis E.
ā¢ Other causes of hepatitis include heavy alcohol use,certain
medications, toxins, other infections,autoimmune diseases
and non-alcoholic steatohepatitis (NASH).
Source : https://www.niaid.nih.gov/diseases-
conditions/hepatitis
4. History
ā¢ Around 400 B.C., Greek Physician, Hippocrates recorded
the first documentation of an epidemic jaundice.
ā¢ In 1950s and 1960s Saul Krugman, a NYU researcher
infamously carried out experiments on mentally disabled
students at Willowbrook State School, where hepatitis
infections were highly endemic.
Source : https://pubmed.ncbi.nlm.nih.gov/22892603/
Munson, Ronald (1996). Intervention and Reflection: Basic Issues in
Medical Ethics. pp. 273ā281.pubmed.ncbi.nlm.nih.gov
6. ā¢ Hepatitis B surface antigen was discovered by Baruch
Samuel Blumberg in 1965.
ā¢ In 1970, David Dane first isolated the hepatitis B virion
at Londonās Middlesex Hospital, and named the virion
the 42-nm āDane particleā.
ā¢ HCV was discovered in 1989.
Source : https://www.hepb.org/prevention-and-
diagnosis/vaccination/history-of-hepatitis-b-
vaccine/
9. ā¢ Hepatitis A (formerly known as āinfectiousā hepatitis or epidemic
jaundice) is an acute infectious disease caused by hepatitis A
virus(HAV).
ā¢ It occurs mainly in children and young adults.
ā¢ The disease is benign with complete recovery in 4-6 weeks.
Source: K. Park, 26th e
10. Problem Statement
ā¢ Endemic in most developing countries, with frequent outbursts
of minor or major outbreaks.
ā¢ WHO estimates that about 1.4 million cases occur every year
worldwide.
Areas with high levels of infection
Developing countries with very poor sanitary conditions and
hygienic practices.
Areas with intermediate levels of Infection
Developing countries, countries with transitional economies
etc.
Source: K. Park, 26th e
11. Areas with low levels of infection
Developed countries with good sanitary and hygienic
conditions.
Source: K. Park, 26th e
12. EPIDEMIOLOGICAL FACTORS
a) AGENT: The causative agent, the Hepatitis A virus, is
enterovirus(type 72) of the picornaviridae family. It multiplies
only in hepatocyte. Only one serotype is known.
b) RESISTANCE: The virus is fairly resistant to low pH, heat and
chemicals. Formalin is stated to be an effective disinfectant. The
virus is inactivated by ultra violet rays and by boiling for 5
minutes or autoclaving.
AGENT FACTORS
Source: K. Park, 26th e
13. c) RESERVOIR OF INFECTION: The human cases are the only
reservoir of infection. There is no evidence of a chronic
carrier state.
d) PERIOD OF INFECTIVITY: The risk of transmitting HAV is
greatest from 2 weeks before to 1 week after the onset of
jaundice.
e) INFECTIVE MATERIAL: Mainly manās faeces. Blood, serum
and other fluids are infective during the brief stage of
viraemia.
f) VIRUS EXCRETION: HAV is excreted in the faeces for about
2 weeks before the onset of jaundice and for up to 2 weeks
thereafter.
Source: K. Park, 26th e
14. HOST FACTORS
a) AGE: Infection with HAV is more frequent among
children than in adults. However people from all ages
may be infected if susceptible. In young children,
infections tends to be mild of subclinical; the clinical
severity increases with age.
b) SEX: Both sexes are equally susceptible.
c) IMMUNITY: Immunity after attack probably lasts for life.
Second attacks have been reported in about 5% of the
patients.
Source: K. Park, 26th e
15. ENVIRONMENTAL FACTORS
ā¢ Cases may occur throughout the year. In India the disease
tends to be associated with periods of heavy rainfall.
ā¢ Poor sanitation and overcrowding favour the spread of
infection, giving rise to water-borne and food-borne
epidemics.
Source: K. Park, 26th e
16. INCUBATION PERIOD
ā¢ 10 to 50 days (usually 14-28 days).
ā¢ The length of the incubation period is proportional to
the dose of the virus ingested.
Source: K. Park, 26th e
17. MODES OF TRANSMISSION
a) FAECAL-ORAL ROUTE: This is the major route of
transmission. It may occur direct (person-to-person)
contact or indirectly by way of contaminated food, water or
milk.
b) PARENTERAL ROUTE: Rarely transmitted by parenteral
route. Transmitted by blood and blood products or by skin
penetration through contaminated needles.
c) SEXUAL TRANSMISSION: Transmission may occur mainly
among homosexual men because of oral-anal contact.
Source: K. Park, 26th e
18. SYMPTOMS
ā¢ The large majority of infections are asymptomatic.
ā¢ The cases range from asymptomatic infections to severe
ones.
ā¢ The symptoms can include fever, malaise, loss of
appetite, diarrhoea, nausea, abdominal discomfort,
dark- colored urine and jaundice.
Source: WHO Report on Hepatitis A
20. DIAGNOSIS
ā¢ Demonstration of HAV particles or specific viral antigens in the faeces,
bile and blood using immunoelectron microscopy, ELISA and isolation
methods.
ā¢ Detection of IgM and IgG antibodies using ELISA kits.
ā¢ Biochemical tests : supplements the diagnosis.
a) Alanine aminotransferase(ALT)
b) Bilirubin
c) protein
Source: Microbiology, Dr. CP Baveja 6e
21. Prevention and Containment
a)CONTROL OF RESERVOIR: Complete bed rest and disinfection
of faeces and fomites.
b)CONTROL OF TRANSMISSION: promoting simple measures of
personal and community hygiene, e.g., hand washing before
eating and after toilet; the sanitary disposal of excreta will
prevent contamination of food, water and milk; and
purification of community water supplies.
c)CONTROL OF SUSCEPTIBLE POPULATION:
i) Vaccines: Two types of vaccines are used worldwide
a) Formaldehyde inactivated vaccines: used
commonly worldwide.
Source: K. Park, 26th e
22. ii) Human Immunoglobulin: The duration of protection
is limited to approximately 1-2 months and
3-5 months following administration of IgG at
dose of 0.02 and 0.06ml/kg body weight
respectively. 80-90% effective if given within
14 days after exposure.
b) Live attenuated vaccines ā manufactured in China
and available in several countries.
Source: K. Park, 26th e
24. ā¢ Hepatitis B, formerly known as "serum" hepatitis is an acute systemic
infection with major pathology in the liver, caused by hepatitis B virus
(HBV).
ā¢ HBV infection can be either acute or chronic, and may range from
asymptomatic infection or mild disease, to severe, or rarely fulminant
hepatitis.
ā¢ Acute hepatitis B is usually a self-limiting disease marked by acute
inflammation and hepatocellular necrosis with case fatality of 0.5 to 1 per
cent.
ā¢ Chronic hepatitis B infection encompasses a spectrum of disease and is
defined as persistent HBV infection with or without associated active viral
replication and evidence of hepatocellular injury and inflammation
Parkās Textbook of Preventive and Social Medicine
25. PROBLEM STATEMENT
ā¢ Hepatitis B is endemic throughout the world, especially in tropical and
developing countries and also in some regions of Europe.
ā¢ The HBV infection is a global problem, with 60 per cent of all the world's
population living in areas where there are high levels of infection.
ā¢ Depending on the prevalence of hepatitis B surface antigen, the
geographical areas divided are as follows:
PREVALENCE AREAS
ā„8% HIGH ENDEMIC
5%-7% HIGH INTERMEDIATE
2%-4% LOW INTERMEDIATE
<2% LOW ENDEMIC Parkās Textbook of Preventive and
Social Medicine
26. ā¢ In 2015 the global prevalence of HBV infection in the general population was
estimated at 3.5% with about 257 million persons living with chronic HBV
infection.
ā¢ In 2015, globally, an estimated 887,220 persons died as a result of HBV infection
ā¢ Co-infections with other viral infections occur most frequently in high HBV
endemic areas. About 2. 7 million of the 36. 7 million people infected with HIV
worldwide are co-infected with HBV. Approximately 10%-15% of patients with
chronic HBV infection are co-infected with HCV.
ā¢ HBV infection also causes a significant economic burden in terms of years of life
lost from liver disease.
337,454 due to hepatocellular
carcinoma (HCC)
462,690 due to cirrhosis
Parkās Textbook of Preventive and Social Medicine
27. EPIDEMIOLOGICAL DETERMINANTS OF
HEPATITIS B
AGENT FACTORS
(a) AGENT:
ā¢ HBV is a complex, 42- nm, double- shelled DNA
virus, originally known as the "Dane particle".
ā¢ HBV occurs in three morphological forms in the
serum of a patient:
1) small spherical particles with an average diameter of 22-nm. These
particles are antigenic and stimulate production of surface antibodies.
2) tubules of varying length and diameter
3) Dane particle which corresponds morphologically to hepatitis B virus.
ā¢ Dane particle is considered infectious.
Parkās Textbook of Preventive and Social Medicine
http://googleimages.in
28. A person who is serologically positive for the surface antigen is circulating
all morphological forms, of which 22-nm particles constitute the bulk.
(b) RESERVOIR OF INFECTION:
ā¢ Man is the only reservoir of infection which can be spread either from
carriers or from cases.
(c) INFECTIVE MATERIAL : Contaminated blood is the main source of
infection.
ā¢ Also found in body secretions such as saliva, vaginal secretions and
semen of infected persons.
(d) RESISTANCE :
ā¢ It is capable of surviving for at least 7 days on environmental surfaces.
ā¢ It can be readily destroyed by sodium hypochlorite.
Parkās Textbook of Preventive and Social Medicine
29. (e) PERIOD OF COMMUNICABILITY :
ā¢ During the incubation period (for a month before jaundice) and acute
phase of the disease, or until disappearance of HBsAg and appearance
of surface antibody.
HOST FACTORS
(a) AGE : Age dependent
ā¢ Acute hepatitis B occurs in approximately 1 per cent of perinatal, 10 per
cent of early childhood (1- 5 years of age), and 30 per cent of late (> 5
years age) HBV infections.
ā¢ The development of chronic HBV infection is inversely related to age
and occurs in approximately 80-90 per cent of persons infected
perinatally.
Parkās Textbook of Preventive and Social Medicine
30. (b) HIGH-RISK GROUPS :
ā¢ Surgeons (50 times higher than that in the general population, and is more
than twice that of other physicians.)
ā¢ Other high risk groups comprise recipients of blood transfusions, health
care and laboratory personnel, homosexuals, percutaneous drug abusers,
infants of HBV carrier mothers, recipients of solid organ transplants and
patients who are immunocompromised.
ā¢ Serological screening and vaccination of high-risk groups is highly
recommended.
(c) HEPATITIS B AND HIV INFECTION :
ā¢ 10 per cent of the 40 million people infected with HIV worldwide are
coinfected with HBV.
ā¢ Although HBV infection appears to have a minimal effect on the
progression of HIV. Parkās Textbook of Preventive and Social Medicine
31. (d) HUMORAL AND CELLULAR RESPONSES : Three distinct antigens-
ā¢ a surface antigen, also known as "Australia antigen" (HBsAg)
ā¢ a core antigen ( HBcAg ),
ā¢ an e antigen ( HBeAg ).
They stimulate the production of corresponding antibodies.
These antibodies and their antigens constitute very useful markers of HBV
infection.
MODES OF TRANSMISSION
a) PARENTERAL ROUTE: Hepatitis B is essentially a blood-borne infection.
Transmitted by infected blood and blood products through transfusions,
dialysis, contaminated syringes and needles, pricks of skin, handling of
infected blood. Parkās Textbook of Preventive and Social Medicine
32. b)PERINATAL TRANSMISSION:
ā¢ Most infections appear to occur at birth, as a result of a leak of maternal
blood into the baby's circulation, or ingestion or accidental inoculation of
blood.
C) SEXUAL TRANSMISSION:
ā¢ Various body fluids including saliva, vaginal, menstrual and seminal fluids
have been implicated as vehicles of human transmission.
ā¢ Particularly male homosexuals, are at very high risk of infection with
hepatitis B.
d) OTHER ROUTES:
ā¢ Transmission from child-to- child, often called horizontal transmission, is
responsible for a majority of HBV infections and carriers in parts of the
world other than Asia.
Parkās Textbook of Preventive and Social Medicine
34. INCUBATION PERIOD
30 to 180 days, i.e 1-6 months (average is about 75 days).
CLINICAL PICTURE
ā¢ The symptoms and manifestations of hepatitis B are similar to those of
other types of viral hepatitis.
ā¢ The picture is complicated by the carrier state and by chronic liver
disease, which may follow the infection.
ā¢ Longitudinal studies of untreated persons with CHB show 8-20 per cent
cumulation risk of developing cirrhosis over 5 years.
ā¢ In those with cirrhosis, there is an approximately 20 per cent annual risk
of hepatic decompensation and the annual incidence of hepatic B related
HCC is high, ranging from 1 to 5 per cent.
Parkās Textbook of Preventive and Social Medicine
35. CHB
INACTIVE
NO SIGNIFICANT LIVER DISEASE
PROGRESSIVE LIVER
FIBROSIS
(Untreated person)
CIRRHOSIS
(Hepatic decompensation)
HCC
āŖOutcome of chronic HBV infectionParkās Textbook of Preventive and Social
Medicine
36. DIAGNOSIS
ā¢ Antigen markers: HBsAg, HBcAg, HBeAg
ā¢ Antibody markers: Anti-HBs, Anti- HBe, Anti- HBc
Detects the presence of either antigens or antibodies, typically in serum or
plasma but also in capillary blood and oral fluid. These include:
1. Rapid diagnostic test (RDTs)
2. Laboratory-based immunoassays. e.g. ELISA, enzyme immunoassays
(EIAs), chemiluminescence immunoassays (CLIAs), and
electrochemiluminescence immunoassays (ECLs).
ā¢ Molecular markers: HBV DNA
Detected by PCR
ā¢ Non specific markers: Elevated liver enzymes and serum bilirubin.
Parkās Textbook of Preventive and Social Medicine
Essentials of Medical microbiology
38. HBsAg Anti-HBs Anti-HBc HBeAg Anti-HBe Interpretation
+ - IgM + - Acute hepatitis B
+ - IgG + - Chronic hepatitis B with active viral replication
+ - IgG - + Chronic hepatitis B with low viral replication
+ + IgG + or - + or - Chronic hepatitis B with heterotypic anti-HBs
- - IgM + or - - Acute hepatitis
- + IgG - + or - Recovery from hepatitis B (immunity)
- + _ - - Vaccination (immunity)
- - IgG - - False positive, less commonly, infection in remote
past
Parkās Textbook of Preventive and Social Medicine
39. CHRONIC HEPATITIS B INFECTION
ā¢ Chronic HBV infection is defined as persistence of hepatitis B surface
antigen (HBsAg) for six months or more after acute infection with HBV.
ā¢ Worldwide, there are an estimated 257 million people living with chronic
HBV infection and 110 million persons are HCV-antibody positive, and 80
million have chronic viraemic HCV infection.
Parkās Textbook of Preventive and Social Medicine
43. HEPATITIS B VACCINE
ā¢ In 1981, first Hepatitis vaccine was approved.
ā¢ In 1986, recombinant Hepatitis B vaccine was introduced.
ā¢ Active substance in this recombinant vaccine is HBsAg .
ā¢ Now-a-days, plasma derived Hepatitis B vaccine is used.
ā¢ Hepatitis B vaccine is available as Monovalent formulation , or in Fixed
combination with other vaccines.
ā¢ Hepatitis B vaccine does not interfere with immune response of any other
vaccine and vice versa.
ā¢ At birth , only Monovalent Hepatitis B vaccine should be used .
ā¢ Birth dose of Hepatitis B vaccine can be safely given with BCG vaccine at
different sites .
Park Ņs Textbook of Preventive and Social medicine
https://en.m.Wikipedia.org/wiki/Hepatitis_B_vaccine
45. RECOMMENDED FOR
ā¢ All infants
ā¢ Unvaccinated children under 19 yrs
ā¢ Unvaccinated adults more than 19 yrs
ā¢ HIGH RISK PERSONS
a. High risk sexual behaviour
b. multiple partners
c. Household contacts of HBsAg positive persons
d. Injecting drug users
e. Require blood or blood products
f. Recipients of solid organ transplantation
g. Occupational risk of HBV infection
h. International travellers to HBV endemic countries
i. Health care and public safety personnel Park Ņs Textbook of Preventive and Social medicine
https://www.cdc.gov/hepatitis/hbv/hbvfaq.htm
46. ROUTE OF ADMINISTRATION
ā¢ Intramuscular , over deltoid muscle
ā¢ In infants and under 2 yrs , anterolateral aspect of thigh is preferred
DOSAGE
ā¢ 10-20 mcg/dose
ā¢ Children below 10 yrs , half of the dose is given
SCHEDULE
ā¢ Recommended schedule for adults : Three doses , given at 0 ,1 and 6
months
ā¢ Under NIS : given at 6 , 10 , 14 wks . Additional birth dose is given
Park Ņs Textbook of Preventive and Social medicine
Essentials of Medical Microbiology , Apurba S Sastry
48. ā¢ Birth dose should be given within 24 hrs of the birth .
ā¢ Infants born prematurely and of low weight, birth dose should not be
counted and 3 additional doses should be given .
ā¢ At any age ,interruption of vaccination schedule does not require
restarting of the vaccine , the missed dose should be given as soon as
possible.
ā¢ Minimum recommended interval between doses is four weeks as
longer dose intervals may increase the final anti-HBs titres but not the
sero-conversion rate .
Park Ņs Textbook of Preventive and Social medicine
49. STORAGE
ā¢ Stored at 2-8 ÖÆC
ā¢ Freezing must be avoided
CONTRAINDICATION
ā¢ Individuals with the history of allergic reaction to any of the vaccine
components.
Park Ņs Textbook of Preventive and Social medicine
50. PROTECTIVE ANTIBODY LEVELS
ā¢ Complete vaccine series induces protective antibody levels in more
than 95% of infants , children and young adults .
ā¢ After 40 yrs of age, protection following the primary vaccination
series drops below 90% .
ā¢ By 60 yrs, protective antibody levels are achieved only in 65-75% .
ā¢ Duration of protection is at least 30 yrs.
ā¢ Immunosuppressive illness are associated with reduced
immunogenicity of the vaccine .
Park Ņs Textbook of Preventive and Social medicine
Essentials of Medical Microbiology , Apurba S Sastry
51. PENTAVALENT VACCINE
ā¢ Combined vaccine provides protection against ā Diphtheria , Pertussis,
Tetanus, Hepatitis B and Hib
ā¢ Additional birth dose of Hepatitis B vaccine and booster dose of DPT are
given separately
ā¢ 0.5 ml given at 6, 10 and 14 wks , intramuscularly, in anterolateral aspect of
mid-thigh using auto-disabled syringe
ā¢ As per NIS schedule , this vaccine should be started for any child more than
6 wks and can be given up to 1 yr of age .
ā¢ It is in liquid form, freeze sensitive, stored and transported at 2-8 degree
Celsius
Park Ņs Textbook of Preventive and Social medicine
http://vbch.nic.in
53. HEPATITIS B IMMUNOGLOBULIN (HBIG)
ā¢ For immediate protection, those exposed to HBsAg positive blood -
a) Surgeons, nurses or laboratory workers
b) Newborn infants of carrier mothers
c) Sexual contacts of acute Hepatitis B patients
d) Recipients of liver transplantation
ā¢ Should be given within 6 hrs
ā¢ Two doses ā 0.05-0.07 ml/kg of body weight, should be given 30 days apart
ā¢ Administered intramuscularly in the anterolateral thigh in infants and in deltoid in
adult .
ā¢ short term passive protection , lasts 3 months
Park Ņs Textbook of Preventive and Social medicine
https://www.cdc.gov
55. PASSIVE- ACTIVE IMMUNIZATION
ā¢ Simultaneous administration of Hepatitis B vaccine and HBIG is more
efficacious
ā¢ Ideal for prophylaxis of accidental exposure to blood containing
Hepatitis B virus and for prevention of carrier state in the new born
babies of carrier mothers or HBV infected mothers
ā¢ HBIG should be given within 24 hrs and Hepatitis B vaccine should be
given within 7 days .
Park Ņs Textbook of Preventive and Social medicine
56. OTHER MEASURES
ā¢ All blood donors should be screened for HBV infection
ā¢ Health workers should be alerted
ā¢ Adequate sterilization of instruments and practice of simple hygienic measures
ā¢ Carriers should be told not to share personal items , use barrier methods of
contraception , and should not donate blood
ā¢ High risk groups should be screened for HBsAg and should be offered vaccination
ā¢ Screening of blood bags , semen and organ donors .
ā¢ Following safe sex practices
ā¢ Health education
Park Ņs Textbook of Preventive and Social medicine
Essentials of Medical Microbiology , Apurba S Sastry
58. INFECTIONS WITH HBV AND HCV EVOLVE IN THREE
PHASES
a) New infections ( asymptomatic / symptomatic in the form of acute hepatitis )
b) Chronic hepatitis ( asymptomatic )
c) Sequelae ( cirrhosis and HCC ) that lead to morbidity and mortality
Park Ņs Textbook of Preventive and Social medicine
59. 1. SURVEILLANCE FOR ACUTE
HEPATITIS THAT REFLECTS NEW
INFECTIONS
2. SURVEILLANCE FOR CHRONIC ,
PREVALENT HEPATITIS
3. SURVEILLANCE FOR SEQUELAE
ACTIVITIES ā¢ Syndromic surveillance in the
general population
ā¢ Event based surveillance
ā¢ Enhanced case reporting
ā¢ Regular biomarker surveys ā¢ Combination of data from
death certificates, and testing
of patients with cirrhosis and
HCC for HBV and HCV infection
POPULATION UNDER
SURVEILLANCE
ā¢ Persons presenting with acute
hepatitis to health care facilities
ā¢ Persons without acute
symptoms tested during
population surveys
ā¢ Persons diagnosed with
cirrhosis and HCC
USUAL IMPLEMENTER ā¢ Communicable disease
surveillance
ā¢ Hepatitis programme
ā¢ Hepatitis programme in
coordination with other actors
implementing biomarker
surveys
ā¢ Vital registration
ā¢ Sentinel sites caring for
patients with cirrhosis and HCC
ā¢ Cancer registries
CASE DEFINITIONS TO USE ā¢ Presumptive cases of acute
hepatitis
ā¢ Confirmed case of acute hepatitis
ā¢ Chronic HBV and HCV infection
ā¢ Serological evidence of past or
present HCV infection
ā¢ Cases of cirrhosis and HCC
ā¢ Chronic HBV and HCV infection
OBJECTIVE OF THE
SURVEILLANCE ACTIVITY
ā¢ Detect outbreaks
ā¢ Describe trends in type specific
acute hepatitis and identify risk
factors
ā¢ Estimate the prevalence of
infections
ā¢ Model incidence trends
ā¢ Estimate mortality from HBV
or HCV associated HCC and
cirrhosis
61. ā¢ In May 2016 , the World Health Assembly adopted the first ā Global
Health Sector Strategy on Viral Hepatitis, 2016-2021
ā¢ Highlights the critical role of Universal Health Coverage
ā¢ Vision of eliminating viral hepatitis as public health problem
ā¢ Target of reducing new cases of chronic HBV and HCV infections by
90%
ā¢ Target of reducing deaths due to viral hepatitis by 65%
ā¢ Focuses on HBV and HCV
Park Ņs Textbook of Preventive and Social medicine
62. KEY INTERVENTIONS
ā¢ PREVENTION INTERVENTIONS
a. Three dose Hepatitis B vaccine for infants
b. Prevention of HBV mother to child transmission using Hepatitis B
birth dose or others
c. Blood safety and injection safety
d. Harm reduction for persons who use drugs
ā¢ TREATMENT INTERVENTIONS
a. Diagnosis of HBV and HCV
b. Treatment of HBV and HCV
Park Ņs Textbook of Preventive and Social medicine
64. ā¢ Hepatitis C , also known as post transfusion hepatitis, is a contagious
liver disease that results from infection with the hepatitis C virus.
ā¢ The virus can cause both acute and chronic hepatitis , ranging in severity
from a mild illness to a serious, lifelong illness including liver cirrhosis
and cancer.
ā¢ It is among the most common virus that infect the liver .
Parkās textbook of Preventive and
social medicine,26th edition
65. PROBLEM STATEMENT
ā¢ Hepatitis is prevalent in all WHO regions.
ā¢ The highest burden of the disease is in the Eastern Mediterranean
Region and European Region, with 12 million people chronically infected
in each region.
ā¢ Globally, an estimated 58 million people have chronic hepatitis C virus
infection, with about 1.5 million new infections per year.
ā¢ WHO estimated that in 2019, approximately 2,90,000 people died from
hepatitis C, mostly from cirrhosis and hepatocellular carcinoma.
ā¢ In India, Hepatitis C virus type 3 is most prevalent.
https://www.who.int
Global hepatitis report 2020
66. EPIDEMIOLOGICAL DETERMINANTS
ā¢ Agent factors
a) Agent: The causative agent, the hepatitis C virus , a flavivirus , genus
Hepacivirus , is a 50-60 nm virus with a linear single stranded RNA genome,
enclosed within a core and surrounded by an envelope carrying glycoprotein
spikes.
b) Reservoir: Humans
c) Source of infection: A case.
d) Period of communicability: 1 week before the onset of symptoms.
ā¢ Host factors
a) Age : Adults
b) Risk factors: people who received blood products or organs ,injecting drug
users. Parkās textbook of preventive and social medicine,26th edition
67.
68. TRANSMISSION
ā¢ Exposure to infectious blood (most common)
a) Receipt of contaminated blood transfusions and organ transplants.
b) Injections with contaminated syringes.
c) Injection drug use and d) being born to hep B infected mother.
ā¢ Sexual contact with an infected person (less common)
NOT SPREAD THROUGH: breast milk, food or water , casual contact such as hugging ,
kissing and sharing food or drinks with an infected person.
Parkās Textbook of preventive and social
medicine,26th edition
69. INCUBATION PERIOD: 2 weeks to 6 months
SYMPTOMS
ā¢ Approximately 80% are asymptomatic.
ā¢ Fever, fatigue, decreased appetite, nausea , vomiting ,abdominal pain, dark urine
,grey colored feces, joint pain and jaundice.
ā¢ HCV
15-45%(self limiting) 55-85%(chronicity)
15-30%(progressive) 70-80%(persistent)
cirrhosis HCC (5-6%)
Parkās textbook of preventive and
social medicine,26th edition
71. PREVENTION
ā¢ Primary prevention
1) Hand hygiene : surgical hand preparation, hand washing.
2) Safe and appropriate use of health care injections.
3) Comprehensive harm reduction services to injection drug users.
4) Testing of donated blood for hepatitis B and C.
5) Promotion of correct and consistent use of condoms.
Parkās textbook of preventive and
social medicine,26th edition
72. ā¢ Secondary and Tertiary prevention
For people infected with hepatitis C virus ,WHO recommends:
1) Education and counselling on options for treatment
2) Immunization with hepatitis A and B vaccine to prevent coinfection.
3) Early and appropriate medical management.
4) Regular monitoring for early diagnosis of chronicity.
As of now, there is no effective vaccine against hepatitis C so prevention
depends on reducing the risk of exposure to the virus in health care settings
and in higher risk populations.
Parkās textbook of preventive and social
medicine ,26th edition
73. DIAGNOSIS
ā¢ The presence of antibodies against the hepatitis C virus indicates
that a person is or has been infected.
ā¢ Anti HCV ā appears after infection ; disappears after recovery
:persists in chronic hepatitis C.
ā¢ The hepatitis C virus recombinant immunoblot assay (RIBA) and
hepatitis C virus RNA testing are used to confirm the diagnosis.
ā¢ HCV-RNA ā after exposure becomes detectable in the serum after
7-14 days , followed by amino-transferase elevation and later (after
4-10 weeks) by presence of antibodies.
Davidsonās principles and practice of medicine
74. CHRONIC HEPATITIS C
ā¢ Chronicity is the hallmark of HCV infection
ā¢ Worldwide an estimated 80 million people have chronic viraemic HCV
infection.
ā¢ A number of factors like alcohol consumption, coinfection with HIV or HBV
and older age at the time of infection can accelerate progression to
advanced liver disease.
ā¢ Fatigue is the most common symptom. Jaundice is rare.
ā¢ Prominent extrahepatic features-mostly in the form of autoimmune and
lymphoproliferative states.
Davidsonās principles and practice of
medicine ,23rd edition
75. THE WHO ā5Csā
The WHO 5Cs are principles that apply to all models of hepatitis testing and in all settings :
Consent
Confidentiality
Correct test results
Counselling
Connection
(linkage to prevention , treatment and care services)
This means hepatitis testing for diagnosis must always be voluntary and consent for testing
informed by pre-test information.
Parkās textbook of preventive and social
medicine,26th edition
76. Summary algorithm for diagnosis and treatment of chronic HCV
infection.
1) Serological testing
Anti-HCV antibody
(Single RDT or lab based immunoassay)
Anti HCV + Anti HCV ā
Current or past HCV infection No HCV Infection
2) Confirmation
HCV RNA Nucleic acid test
viremic HCV No current viremic HCV Parkās textbook of preventive and social
medicine,26th edition
77. 3)Treatment assessment
( Viremic HCV infection)
Assessment of stage of liver disease
(non-invasive tests and clinical criteria)
Select DAA(Direct Acting Antiviral ) regimen
Prioritize treatment if:
increased risk of death
evidence of end organ
damage.
Parkās textbook of preventive and social
medicine,26th edition
79. FOR ACUTE CASES:
1)Rest:
ā¢ During the acute symptomatic period, complete rest .
ā¢ In high risk patients(>50 years, pregnant or having major diseases) rest is
continued till signs and symptoms have disappeared and LFT have returned to
normal.
2)Diet:
ā¢ Nutritious general diet of 2000-3000 kcal/day . In the initial good diet is not
tolerated, light diet, fruit drinks and glucose is given.
ā¢ Encourage good protein intake.
ā¢ If vomiting is severe, iv fluids are given.
Davidsonās principles and practice of
medicine,23rd edition
80. 3)Drugs
ā¢ Drugs should be avoided if possible (especially sedatives and hypnotics)
ā¢ Alcohol to be avoided for the next 6 months.
ā¢ Oral contraceptives can be resumed after clinical and biochemical
recovery.
4)Antiviral drugs
ā¢ Some evidence suggests efficacy of Interferon alpha in patients with acute
hepatitis C infection in reducing the rate of chronicity.
Davidsonās principles and practice of
medicine ,23rd edition
81. FOR CHRONIC CASES:
A)CHRONIC HEPATITIS B
ā¢ Two different types of drug are used to treat hepatitis B:
1)Directly acting nucleoside/nucleotide analogues (mainstay of therapy)
- these act by inhibiting the reverse transcription of pre-genomic RNA to HBV
DNA by HBV DNA polymerase.
ā¢ Lamivudine- although effective, long term therapy is often complicated by
the development of viral resistance.
ā¢ Entecavir and tenofovir- Monotherapy is more effective than lamivudine .
2) Interferon āalpha
ā¢ This is most effective in patients with a low viral load by augmenting a
native immune response
Davidsonās principles and practice of
medicine ,23rd edition
82. B)CHRONIC HEPATITIS C
ā¢ Until 2011, the treatment of choice was dual therapy with Pegylated
interferon alpha (given as a weekly subcutaneous injection )together with
oral Ribavarin ,a synthetic nucleotide analogue.
disadvantage: treatment was long āupto 12 months for genotype 1
ribavirin induces hemolytic anemia and is teratogenic
interferon alpha induces influenza-like symptoms.
ā¢ Since 2011, new classes of direct-acting antiviral agents (DAAs) have been
developed.
protease inhibitor(PIs ): Telaprevir, Simeprevir
Nucleoside polymerase inhibitors( NPIs): Sofosbuvir
Non nucleoside polymerase inhibitors( NNPIs): Daclatasvir
Davidsonās principles and practice of
medicine ,23rd edition
83. ā¢ These compounds are targeted to specific steps in the hepatitis C viral life
cycle to disrupt viral replication
ā¢ Initially DAAs were added to interferon/ribavirin based regimens , however
āInterferon-freeā regimens are preferred nowadays.
ā¢ Sofosbuvir + velpatasvir (achieves 99% SVR and is pan-genotypic).
ā¢ Advantage- more efficacious ;well tolerated.
ā¢ Liver transplantation should be considered when complications of cirrhosis
occur.
Davidsonās principles and practice of
medicine ,23rd edition
84. REFERENCES
ā¢ Park Ņs Textbook of Preventive and Social Medicine, K. Park , 26th edition
ā¢ Essentials of Medical Microbiology, Apurba Sankar Sastry and Sandhya Bhat K , 2nd
edition
ā¢ Textbook of Microbiology, Dr. C P Bavega, 6th edition
ā¢ Davidson Ņs Principles and Practice of Medicine, International Edition, 23rd edition
ā¢ https://en.m.Wikipedia.org/wiki/Hepatitis_B_vaccine
ā¢ https://www,cdc,gov/hepatitis/hbv/hbvfaq.htm
ā¢ https://www.cdc.gov
ā¢ https://vbch.nic.in
ā¢ http://googleimages.in
ā¢ https://WHO.int , Global Hepatitis report 2020