The document discusses hepatitis A, a viral infection that causes inflammation of the liver. It begins by describing the epidemiology of hepatitis A, including that it is more common in areas with poor sanitation. It then covers the hepatitis A virus itself, noting it is a small RNA virus transmitted via the fecal-oral route. For prevention, the document recommends measures like handwashing and vaccination.

1. HEPATITIS
RAJALEKSHMY. P. R
DEPT OF SWASTHAVRITTA
AMRITA SCHOOL OF AYURVEDA 1

2. • It is the largest gland of the body.
• Located behind the ribs in the right upper quadrant,
from 5th-12th rib.
• It weighs 1800gms in men and 1400gms in women.
• It is divided into 4 lobes and multiple lobules.
• It is connected to two large blood vessels,
the hepatic artery and the portal vein.
• These blood vessels subdivide into small
capillaries known as liver sinusoids, which
then lead to a lobule.
LIVER: A GLANCE.....
2

3. LOBULE
• The lobules are roughly hexagonal, and consist of plates of
hepatocytes radiating from a central vein.
• The central vein joins to the hepatic vein to carry blood out from
the liver.
• A distinctive component of a lobule is the portal triad, which can
be found running along each of the lobule's corners.
3

4. Portal triad
• Branch of the hepatic artery
• branch of the hepatic portal vein
• Bile duct
4

5. BLOOD SUPPLY
• The hepatic portal vein delivers approximately 75% of the liver's
blood supply, and carries venous blood drained from
the spleen, gastrointestinal tract, and its associated organs.
• The hepatic arteries supply arterial blood to the liver, accounting
for the remaining quarter of its blood flow.
• Blood flows through the liver sinusoids and empties into the
central vein of each lobule.
• Central vein hepatic vein inferior vena cava
5

6. Functions
• Glucose metabolism
• Protein metabolism
• Fat metabolism
• Vitamin and iron storage
• Drug metabolism
• Bile formation
• Bilirubin excretion
6

7. HEPATITIS
• Inflammation of the liver.
• Hepatitis is acute when it lasts less than six months and chronic when it
persists longer.
• Acute hepatitis can be self-limiting can progress to chronic hepatitis, or,
rarely, can cause acute liver failure.
• Chronic hepatitis may have no symptoms, or may progress over time
to fibrosis (scarring of the liver) and cirrhosis (chronic liver failure).
• Cirrhosis of the liver increases the risk of developing hepatocellular
carcinoma.
7

8. CAUSES
Toxins
Certain drugs
Some diseases
Heavy alcohol use
Bacterial and viral infections
8

9. CLASSIFICATION
Viral
Non-viral
Auto immune
Bacterial
Parasitic
9

10. VIRAL HEPATITIS
Viral hepatitis is a systemic disease
with primary inflammation of the
liver by any one of a heterogeneous
group of hepatotropic viruses.
10

11. CONTD…..
•The most common causes of viral hepatitis are the five
unrelated hepatotropic viruses - Hepatitis A, Hepatitis
B, Hepatitis C, Hepatitis D, and Hepatitis E.
•In addition to the nominal hepatitis viruses, other viruses
that can also cause liver inflammation include Herpes
simplex, Cytomegalovirus, Epstein–Barr virus, Yellow
fever or Rubella virus. 11

12. Viral Hepatitis
A
Viral Hepatitis
B
Viral Hepatitis
C
Viral Hepatitis
D
Viral Hepatitis
E
Agent Hepatitis A
virus
(HAV); ssRNA
Hepatitis B
virus (HBV);
dsDNA
Hepatitis C
virus (HCV);
ssRNA
Hepatitis D
virus (HDV);
ssRNA
Hepatitis E
virus (HEV);
ssRNA
Route of
Transmission
Fecal-oral Parenteral,
Vertical,
Sexual.
Parenteral Parenteral Fecal-oral
Age affected Children Any age Adults Any age Young adults
Carrier state Nil Common Present Nil (only with
HBV)
Nil
Incubation
period
10-50 days
(avg. 25-30)
50-180 days
(avg. 60-90)
40-120 days 2-12 weeks 2-9 weeks
Chronic infection No Yes Yes Yes No
Specific Ig and Ig and Nil HBV vaccine Nil
12

13. 13

14. INTRODUCTION
• Hepatitis A refers to liver inflammation caused by infection with the hepatitis
A virus(HAV).
• HAV has been known as infectious jaundice since 1912.
• Acc. To WHO, HAV had many names in the past:
• Epidemic hepatitis
• Epidemic jaundice
• Infectious hepatitis
• Catarrhal jaundice
• HA and type A hepatitis
14

15. HISTORY
• HAV is referred to as one of the oldest diseases known to mankind
by the WHO.
• It was recognized as a separate entity from other types of hepatitis
during world war II.
• It was discovered in1973 by Steven. M. Feinstone as a non
enveloped, spherical, positive stranded RNA virus.
• HAV was an unidentified viral disease prior to this discovery.
15

16. EPIDEMOLOGY
• Globally, symptomatic HAV infections are believed to occur in around 1.5 million
people a year.
• In 2010, acute hepatitis A resulted in 102,000 deaths, which is slightly up from
99,000 in 1990.
• Hepatitis A is much more common in countries with underdeveloped sanitation
systems and, thus, is a risk in most of the world.
• HAV is a common infection in developing nations of Africa, Asia, and Central and South
America. 16

17. 17
INDIA
• Largest outbreak occurred in Delhi in 1955-56, when
more than 40000 people were affected, because of the
contamination of river Yamuna with the sewage.
• Even though, mortality is very low, incapacitation is very
high resulting in great loss of human resource.
• Another epidemic in Delhi in 1970 due to contamination
of Okhla water supply.

18. Areas with high levels of infection
• In developing countries with poor
sanitation and hygiene, children are
infected before age of 10 yrs.
• Symptomatic disease rates are low.
• Outbreaks are rare.
Areas with intermediate levels of infection
• In developing countries, countries with
transitional economies and regions where
sanitary conditions are variable, children escape
infection in childhood.
• Higher susceptibility in old age groups.
• Higher disease rates
• Large outbreaks can occur.
Area with low levels of infection
• In developed countries with good sanitary and hygienic condns:
infection rates are low.
• Disease may occur among adolescents and adults in high risk groups
such as injecting drug users, homo sexual men, people travelling to
areas of high endemicity and in isolated population such as closed
religious community.
18

20. DENSITY OF HEPATITIS A INFECTION
20

21. INTEGRATED DISEASE SURVEILLANCE PROJECT 2010
21

22. 22

23. 23

24. 24

25. HEPATITIS A VIRUS
• Naked RNA virus
• Previously known as enterovirus(type 72).
• One stable serotype only.
• 7 genotypes exist(four human & three simian)
• Difficult to grow in cell culture.
• Human and vertebrates serve as natural hosts.
• Replication in hepatocytes.
25

26. CONTD…..
• Fairly resistant to low pH, heat and chemicals.
• Survives more than 10 weeks in well water.
• Resistant to heat at 60 degree Celsius for 1 hr.
• Not affected by chlorination.
• Formalin-effective disinfectant.
• Virus inactivated by UV rays, boiling(5 mts) or autoclaving.
• Viral particles first demonstrated in liver cells by workers in
Phoenix laboratory in Arizona- hence called phoenix antigen.
26

27. RESERVOIR
•Human reservoir(active clinical case or sub clinical case
or a carrier-healthy/incubatory).
•Subclinical cases and carriers are responsible for the
endemicity of the disease in community.
•No evidence of chronic carrier state.
•Asymptomatic infections are common in children. 27

28. PERIOD OF INFECTIVITY
• Risk of transmitting HAV is greatest from 2 weeks before to 1
week after the onset of jaundice.
• Infectivity falls rapidly with the onset of jaundice.
28

29. INFECTIVE MATERIAL
• Mainly man’s faeces
• Blood, serum and other fluids(during stage of viraemia)
29

30. VIRUS EXCRETION
• HAV is excreted in faeces for about 2 weeks before onset of
jaundice and for upto 2 weeks thereafter.
• Also excreted in urine.
30

31. HOST FACTORS
Age
Frequent among children than adults.
People from all ages get infected (if susceptible).
Severity increases with age.
Anicteric : icteric
1:3(adults)
12:1(children)
Sex
Both sex are equally susceptible.
Immunity
Acquired after an infection.
Immunity after attack lasts for life.
Second attack reported in about 5% patients.
31
Pregnancy
VHA during pregnancy carries a high
mortality.
No transplacental transmission

32. ENVIRONMENTAL FACTORS
• Can occur throughout the year
• In India, associated with heavy rainfall.
• Poor sanitation and over crowding favours spread of infection.
32

33. TRANSMISSION
• Faecal oral route
• Direct contact(person to person)
• Indirect- contaminated water, food or milk
• In developed countries, foodborne outbreaks are frequent.
• Eg. Consumption of salads, vegetables and raw or inadequately cooked
shellfish cultivated in sewage polluted water.
33

34. • Parenteral route
• Occur during the stage of viremia
• Rare; mode is of minor importance.
• Eg. By blood or blood products or skin penetration through contaminated
needles
• Sexual transmission
• Occurs in homo sexual men
• Oral anal contact
Unknown
52%
Intl travel
5%
Household/
sexual
25%
Outbreak
3%
Day care
15%
34

35. INCUBATION PERIOD
• 10-50 days( usually 14-28 days).
• Length of incubation period proportional to dose of virus ingested.
35

36. PATHOGENESIS
36

37. •After ingestion, the HAV survives in gastric acid, moves
to the small intestine and reaches the liver via the portal
vein.
•Replicates in hepatocyte cytoplasm.
•Degeneration and necrosis of hepatocytes.
•Affects liver functions- hyperbilirubinaemia-jaundice
•Inflammation of liver-hepatomegaly-pressure effects on
other organs.
37

38. CLINICAL FEATURES
38
Pre-icteric stage
• Sudden onset of fever, chills, fatigue,
malaise, head ache and body ache
• Within a day or two, develops gastro
intestinal symptoms
• High coloured urine, light coloured
stools lasting for about of 3 to 5 days.
Icteric stage
• Onset of jaundice
• With onset of jaundice, fever subsides.
• Sclera looks yellow and skin looks
lemon tinged.
• Nausea and vomiting decreases.
• High coloured urine continues for
several days.
• Jaundice usually reaches maximum by 2
weeks and decreases steadily thereafter.
• Stage lasts for 4 to 6 weeks.

39. 39
Convalescent stage
• After about 6 to 8 weeks, inflammatory
process comes down, there is regeneration
of cells.
• Appetite improves
• Icterus disappears
• Urine and stools become normal
• Stage lasts for 2 to 6 weeks.

40. • Resolves in 98% cases but relapse of symptoms noted in 3-20% cases.
Outcome Children Adults
Sub clinical infection 80-95% 10-25%
Icteric disease 5-20% 75-90%
Complete recovery > 98% > 98%
Chronic disease None None
Mortality rate 0.1% 0.1% 40

41. 0 1 2 3 4 5 6 7 8 9 10 11 12 13
Week
Response
Clinical illness
ALT
IgM IgG
HAV in stool
Infection
Viremia
EVENTS IN HEPATITIS A VIRUS INFECTION
41

42. CONCENTRATION OF HEPATITIS A VIRUS IN VARIOUS BODY FLUIDS
Source: Viral Hepatitis and Liver Disease 1984;9-22
J Infect Dis 1989;160:887-890
Feces
Serum
Saliva
Urine
100 102 104 106 108 1010
BodyFluids
Infectious Doses per mL
42

43. COMPLICATIONS
• Fulminant hepatitis A/acute liver failure is a rare but devastating
complication of HAV infection.
• HAV liver parenchymal cells release of toxins
• The cell then produces new viral components that are released into the bile
capillaries hepatic necrosis.
• The fulminant form of hepatitis occurs when this necrotic process kills so
many liver cells.
• Fulminant hepatic failure can also lead to encephalopathy and cerebral
oedema. 43

44. DIAGNOSIS
• Demonstration of HAV particles in the faeces, bile or blood.
• HAV is detected in the stool from about 2 weeks prior to the onset of jaundice
and 2 weeks thereafter.
• Anti HAV appears in IgM fraction during acute phase.
• Anti HAV IgM usually declines to non detectable level within 3-6 months.
• Anti HAV IgG appears more slowly and persist for decades.
• Acute infection is diagnosed by the detection of HAV-IgM in serum by
(enzyme immunoassay)EIA.
• Past Infection i.e. immunity is determined by the detection of HAV-IgG by
EIA.
44

45. CONT….
• Detection of Antibody: By ELISA
• Biochemical tests:
• i) Alanine aminotransferase (ALT)
• ii) Bilirubin
• Demonstration of viral particles in the stools by electron
microscopy.
45

46. PREVENTION
Control of reservoir
• Complete bed rest
• Disinfection of
faeces and fomite
Control of transmission
• Promote simple measures of personal and
community hygiene
• Eg. Hand washing before and after toilet
• Sanitary disposal of excreta
• Purification of community water supply
46

47. Control of susceptible population
Passive immunization-human normal immunoglobulin
Prepared from pooled plasma of multiple donors.
Agent/condition Target population Preparation Dose
Hepatitis A Family contacts
Institutional
outbreaks
IG 0.02 ml/kg of body
weight(3.2 mg/kg of
body weight)
Travellers exposed to
unhygienic
conditions in tropical
or developing
countries
IG 0.02-0.05 ml/kg of
body weight(3.2-8.0
mg/kg of body
weight)
Once in 4 months
47

48. VACCINATION
• Formaldehyde inactivated vaccine
• Live attenuated vaccines
Produced in several
countries
World wide used
Manufactured in
China
Available in several
countries
48

49. INACTIVATED VACCINE
• Cell cultured liquid vaccine
• Hepatitis virus of HM-175 strain( F strain) is propagated on
human diploid cells, purified by ultra filtration technique and
inactivated by formaldehyde and adsorbed on aluminium
hydroxide.
• Dose: adults-1 ml; children-0.5ml given IM in deltoid region.
• Licensed for use in children above 12 months of age.
• Interval between the first and second booster dose: 6-12 months
49

50. • Immunity lasts for 15-20 yrs.
• Marketed as HAVRIX.
• Storage temp: 2-8˚ C
• A combination vaccine containing inactivated Hepatitis A and
Hepatitis B vaccine has been licensed since 1966 for children in
several countries.
• Schedule of combined vaccine is 0, 1 and 6 months.
• Combination of hepatitis A and B, hepatitis A and typhoid vaccine
are developed for travellers.
50

51. LIVE VACCINE
• Live attenuated freeze dried vaccine containing H2 strain of hepatitis A virus.
• Single dose of 0.5ml is administered subcutaneously in deltoid region for all
above one year of age.
• Safe, immunogenic with good tolerability
• No booster dose required.
• Storage temp: 2-8˚C.
• Recommended for both pre exposure prophylaxis of high risk individuals and
post exposure prophylaxis.
• Marketed as Biovac-A.
51

52. WHO SHOULD BE VACCINATED?
• All children at age 1 year (i.e., 12–23 months)
• Children and adolescents ages 2–18 who live in states or communities where
routine Hepatitis A vaccination has been implemented because of high
disease incidence
• Persons traveling to or working in countries that have high or intermediate
rates of Hepatitis A.
• Homo sexuals
• Users of illegal injection
• Persons who have occupational risk for infection
• Persons who have chronic liver disease.
52

53. VACCINES IN INDIA
No Brand Name Manufacturers Type
1 Avaxim Aventis Pasteur India Ltd Injection
2 Avaxim 80U Paediatric Aventis Pasteur India Ltd Injection
3 Havrix
Glaxo Smithkline
Pharmaceuticals Ltd.
Injection
4 Havrix (360)
Glaxo Smithkline
Pharmaceuticals Ltd.
Injection
5 Havrix (720)
Glaxo Smithkline
Pharmaceuticals Ltd.
Injection 53

54. THANK YOU
54