Hepatitis is inflammation of the liver that can be caused by viruses. The document discusses the different types of viral hepatitis (A, B, C, D, E, G), their symptoms, modes of transmission, potential for chronic infection and liver cancer, diagnosis, and treatment options. It provides details on the pathophysiology, incubation periods, and clinical presentations of hepatitis A, B, and C. Prevention methods include vaccination, hygiene practices, and immunoglobulin treatment for certain types.

1. VIRAL HEPATITIS
Dr Snigdha Pattnaik.

2. What Is Hepatitis?
 Hepatitis is a medical condition defined by the inflammation of
the liver and characterized by the presence
of inflammatory cells in the tissue of the organ.
 It can be caused by viruses→ hepatitis A
hepatitis B
hepatitis C
hepatitis D
hepatitis E
hepatitis G
 Hepatitis A & E having no chances of chronicity & liver cancer
while hepatits B, C & D having chances of chronicity & liver
cancer.

3. Table 24.12

4. Sign & symptoms of hepatitis
 DARK URINE
 Abdominal discomfort
 Right upper abdominal pain
 Jaundice
 Fever
 Nausea
 Anorexia
 Diaherrea
 Fatigue
 Hepatomegalin
 Elevated level of bilirubin

5. HEPATITIS TRANSMISSION
A  Close personal contact
 Contaminated food, water
 Blood exposure (rare)
B  Parenteral - IVDA, Health Workers are at increased risk.
 Perinatal - Mothers who are HBeAg positive are much more likely to
transmit to their offspring than those who are not.
C  Percutaneous
 IV drugs
 Transfusion, transplant from infected donor
 Therapeutic (contaminated equipment, unsafe injection practices)
 Occupational (needle stick)
 Per mucosal, Perinatal, Sexual

6. HEPATITIS TRANSMISSION
D  Percutanous-injecting drug use
 Permucosal- sex contact
E • Consumption of faecally contaminated drinking water has given rise to
epidemic cases,
• Ingestion of raw or uncooked shellfish has been the source of sporadic cases
in endemic areas
G  blood and blood products and
 Sexual contact
 IV drug abuse and other parenteral ways of infection,tattooing
 transmission from infected mother to a child during the birth

7. Hepatitis A
 HAV infection is one of the most frequently reported
vaccine preventable diseases.
 HAV does not cause chronic hepatitis and only rarely
causes fulminant hepatitis.
 HAV occurs throughout the world and is endemic in
countries with poor hygiene and sanitation.
Pathophysiology
 The natural history of the infection is divided into three
stages :
 Incubation, Acute hepatitis, and Convalescence

8. Incubation begins after parenteral or oral inoculation
with the virus
HAV replication occurs & antigens are found in
hepatocyte cytoplasm
Largest concentration of viral particles are found in
stool specimens during the 1 to 2 weeks
During the incubation stage, the host is asymptomatic
Acute hepatitis begins with a preicteric phase (before
the onset of jaundice)
acute anicteric hepatitis

9. Hepatocyte destruction to produce significant liver dysfunction
characterized by interruption of bilirubin metabolism and flow
acute icteric hepatitis
Most patients with either acute anicteric or icteric hepatitis go through the
convalescence stage
IgM anti-HAV usually is detectable 5 to 10 days before symptoms appear.
After 2 to 6 months, the IgM antibodies are replaced with IgG antibodies,
which usually persist throughout life and confer immunity to HAV.

10. Transmission
 Faeco oral route.
 Parentral route.
 Sexual route (rare)

11. Diagnosis of HAV
 Acute infection is diagnosed & Past Infection i.e.
immunity is determined by the detection of HAV-IgM &
HAV-IgG in serum by EIA.
 Direct Detection –PCR of faeces.
 Mild elevations of
serum bilirubin
γ –globulin
ALT and AST values (about twice than normal).
Normal values
AST > M:8-46 IU/L, F:7-34 IU/L
ALT > M:9-69 IU/L, F:3-33 IU/L

12. Prevention and containment
 Control of reservoir : proper disinfection of feces and
fomites.
 0.5 % sodium hypochlorite has been recommended.
 Control of transmission :promotion of hygiene, proper
sewage disposal.
 Control of susceptible :IgG 0.02ML/KG.
 VACCINES

13. A single 0.02-mL/kg dose of Ig is adequate for short trips (less than 3
months), but 0.06 mL/kg dose for every 5 months is necessary for
longer visits.

14. HEPATITIS B
 66 % of world population are at risk.
 2 billion people are infected.
 240 million chronic carrier.
 Estimated death 6l per yr from cirrhosis and
hepatocellular carcinoma.
 ACCOUNTS FOR 60-80 % OF Primary liver cancer.
 5-10 % of adult.,90% of 9nfants became carrier.

15.  Type 1 : Nepal ,Srilanka HBsAg carrier rate is 0.9-1%
 Type 2 :Bhutan, India,Indonesia and Maldives 5-7 %
 Type 3:Bangladesh,korea Myanmar and Thailand-9-
12%.
 India : HBsAg IN hospital staff is 10.87 %
 Voluntary blood donor 6 %
 Multiple transfused pt 18-30%

16. HEPATITIS B
Dane Particle,Spherical particles and tubules.

17.  Reservoir :man.carrier state presence of
HBsAg for more than 6 months.
 Infective material : contaminated blood and
body fluids.
 Resistance : 7 days in enviromenta surfaces.
Destroyed by sodium hypochlorite and heat
sterilization.
 Communicability :several months,until the
dissapearance of HBsAg and appearance of
surface antigen.

18. HOST FACTORS
 AGE :outcome is inversely propotional to age of
infection.
 Fulminant hepatitis is seen if the person is infected in
early childhood.
 Mortality is about 90 % from chronic HBv infection
due to fulminant hepatitis.
 Risk groups : Surgeons,homosexuals,repeated blood
transfusion,iv drug Users.
 10 % OF hiv PT ARE CO INFECTED WITH hbV.

19. • HBV is a leading cause of chronic hepatitis,
cirrhosis, and hepatocellular carcinoma.
Pathophysiology:
HBV
↓invade into
Human body
↓by
Skin & mucosa
↓via
Blood flow
↓enter into organs like
Liver, pancreas, bileduct, vessels,
WBC, bone marrow, glomerular
basement membrans.
HBcAg,HBsAg,HBeAg and
HLA-Ⅰ
↓appear on
infected liver cells.
↓ recognized by
CTL simultaneously
↓lead to
cytolysis of liver cells

20. Acute hepatitis B infection
3-5% of adult
acquired infections
Liver failure
Hepatocellular
carcinoma
Chronic HBV infection
95% of infant
acquired infections
Chronic hepatitis
Cirrhosis
Liver transplantDeath Death
12-25% in 5 years
20-23% in 5 years6-15% in 5 years
Possible Outcomes of HBV Infection

21. Diagnosis of HBV
 HBsAg
 HBsAb
 anti-HBcIgM
 anti-HBcIgG
 HBeAg
 Anti-Hbe
 HBV-DNA
 used as a general marker of infection.
 used to document recovery and/or immunity to HBV
infection.
 marker of acute infection.
 past or chronic infection.
 indicates active replication of virus and therefore
infectiveness.
 virus no longer replicating. However, the patient can
still be positive for HBsAg which is made by
integrated HBV
 indicates active replication of virus, more accurate
than HBeAg especially in cases of escape mutants.
Used mainly for monitoring response to therapy

22. HOST FACTORS
 AGE :outcome is inversely propotional to age of
infection.
 Fulminant hepatitis is seen if the person is infected in
early childhood.
 Mortality is about 90 % from chronic HBv infection
due to fulminant hepatitis.
 Risk groups : Surgeons,homosexuals,repeated blood
transfusion,iv drug Users.
 10 % OF hiv PT ARE CO INFECTED WITH hbV.

23. Modes of Transmission
 Parenteral route :
 Perinatal transmission : anicteric ,detected by
appearance of surfaceantigen between 60-120 daysafter
birth.
 Sexual transmission.
 Other : horizontal transmission.
 INCUBATION PERIOD : 30- 180 days.

24.  Preicteric period
 In HA, HE, the onset is abrupt with fever;
but HB, HC, the onset is insidious.
 The initial symptoms: loss of appetite,
nausea, vomiting lassitude, abdominal
pain and diarrhea.
 The end of the period, the urine darkens.
A few patients, especial children, fever,
headache, upper respiratory tract
symptome are main manifestations
 The duration of this period varies from 1-
21 days, average 5-7 days

25.  Icteric period
 The urine deepens continuously and
jaundice appears on the skin and sclera
within 2 weeks
 Subjective symptoms is abate
 Pruritus may appear about 1 week
 Liver palpable 7%, spleen palpable 20%
 The period lasts 2-6 weeks

26.  Convalscent period
 The jaundice disappear gradually, symptoms abate or disappear
 Liver and spleen retract, liver function return to normal
 The period lasts 2 weeks to 4 months, average 1 month
 About 10% of HB and 50% of HC will become chronic hepatitis
 Acute hepatitis D:
 Co-infection with HBV
 Super-infection with HBV
 Acute hepatitis E is similar to acute hepatitis A, but cholestasis
is obvious and symptoms and signs is severe.
 If women with pregnancy suffer from the HE－－fulminant
hepatitis
 If HB super-infect HEV or HCV－－fulminant hepatitis

27. Treatment of HBV
 Interferon -
 alpha-interferon 2b (original)
 alpha-interferon 2a (newer, claims to be more efficacious and
efficient)
 Lamivudine – 100mg/day. a nucleoside analogue reverse
transcriptase inhibitor. Well tolerated but problem is the rapid
emergence of drug resistance.
 Adefovir –10mg/day. less likely to develop resistance than
Lamivudine and may be used to treat Lamivudine resistance HBV.
However more expensive and toxic
 Entecavir –0.5mg/day. most powerful antiviral.
 Successful response to treatment will result in the disappearance of
HBsAg, HBV-DNA.

28. Cont..
 Hepatitis B Immunoglobulin –HBIg is particular effective within
48 hours of the incident.
 Hepatitis B immune globulin (HBIG) is produced from plasma that
contains high titers of antibody against HBsAg. It is used to provide
passive immunity against hepatitis B infection.
 HBIG (0.06 mL/kg for adults and children) should be administered
by IM injection.
 Newborns of hepatitis B surface antigen positive mothers should
receive HBIG 0.5 mL IM within 12 hours of birth.
 The most common adverse reactions of HBIG are local pain,
swelling, and erythema at the injection site. Allergic reactions, body
and joint pain, muscle cramps, malaise, and fever have also been
reported.

30. Hepatitis C
 Hepatitis C virus also known as Non A or Non B virus found
while doing experiments on Chimpanzees.
 HCV has been classified into a total of six genotypes (type 1
to 6) on the basis of phylogenetic analysis.
 Genotype 1 and 4 has a poorer prognosis and response to
interferon therapy.
 In chronic HVC CD4+T & CD8+T cells have been identified.
Due to HCV.
↓
hepatocytic injury
↓
Produce antiviral cytokines
↓by
T-lymphocytes

31. Pathophysiology
 The incubation period for HCV hepatitis ranges from 2 to 26 weeks,
with a mean of 6 to 12 weeks.
HCV enters in hepatocytes
Uncoats virus and release genome for replication
Viral genome work as templete for translation of polyprotein
Non structural protein form complex with genome and formation of
positive strand
RNA interact with envelope and core the protein
New virus synthesized

32. Diagnosis of HCV
 HCV antibody -Not useful in the acute phase as it takes at
least 4 weeks after infection before antibody appears.
 HCV-RNA - various techniques are available e.g. PCR and
branched DNA. May be used to diagnose HCV infection
in the acute phase. However, its main use is in monitoring
the response to antiviral therapy.
 HCV-antigen - an EIA for HCV antigen is available. It is
used in the same capacity as HCV-RNA tests but is much
easier to carry out.
 ELISA test results to be confirmed with Immunoblotting
assay.

33. Clinical Outcome of Hepatitis C Infection
Acute
Infection
Fulminant
<1%
Asymptomatic,
anicteric
70-80%
Symptomatic,
icteric
20-30%
Chronic infection
70-85%
Death
CompleteRecovery
15-30%
Mild hepatitis
30-50%
Chronic hepatitis
moresevere
20-50%*
Cirrhosis,
irreversible
10-20%*
Hepatocellular
carcinoma
5-10%*
Death

34. Treatment of HCV
 Interferon - may be considered for patients with
chronic active hepatitis. The response rate is around
50% but 50% of responders will relapse upon
withdrawal of treatment.
 Ribavirin -Dose is 800ml/kg. Recent studies suggest
that a combination of interferon and ribavirin is more
effective than interferon alone.
 No vaccine is available for HCV infection.

35. Drug Brand
name
Dose Action A/E Other
Lamivudine Hepavud 100
mg/d
Supressed
HBV DNA
Transient ALT
elevation
Resistance is
produced
Adefovir Adesera 10
mg/d
Supressed
HBV DNA
Headache
Abdominal pain,
nephrotoxicity
Effective in
lamivudine
resistant
Entecavir Baraclude 0.5
mg/d
Supressed
HBV DNA
Lung adenomas Lamivudine
resistant
1.0 mg/d
Ribavirin Cap
Rebetol
800
mg/d
Inhibit DNA
& RNA
viruse
Insomnia,
depression,
rash, pruritus
Use in hep B
& hep C

36. Prevention
 Primary screening :blood and blood products
Secondar and tertiary prevention : education and
councelling,immunization against A AND B,Early
diagnosis and treatment of liver disease.

37. Hepatitis D
 Hepatitis D is caused by the virus HDV. One can
only get hepatitis D , already infected with hepatitis
B.
 HDV is caused by direct cytopathic effect on
hepatocytes.

38. Pathophysiology
Delta hepatitis arises in two ways :(1) coinfection and (2) superinfection
In first case, HBV infection become established before HBsAg is available for
the development of complete HDV virions
coinfected persons can clear the viruses and recover completely
Fulminant hepatitis, and rarely chronic hepatitis, may occur
In superinfected individuals in most cases, there is an acceleration of hepatitis,
most often to leads chronic hepatitis
carrier may have been previously asymptomatic ("healthy") or may have
underlying chronic hepatitis

39. 39

40.  DIAGNOSIS :
Following HBV-HDV co-infection both IgM
anti-HDV and IgG anti-HDV are detectable in
the serum.
Following HBV-HDV super infection, chronic
HDV infection with detectable HDAg usually
occurs. Both IgM anti-HDV and IgG anti-HDV
remain detectable.

41. Treatment
 Alpha-interferon (IFN) effective therapy for hepatitis D.
 Dose of IFN : 9 million units (MU) three times a weekly.
 Besides IFN, other drugs such as, acyclovir, ribavirin have been helpful.
 Pegylated-IFN could represent a reasonable therapeutic option in the
chronic hepatitis D.
 Liver transplantation provides a valid option for end-stage HDV liver
disease.
 Hepatitis D infection can also be prevented by hepatitis B vaccine.

42. Hepatitis E
• It is caused by the
virus HEV.
• Replicative virus has
been found in
the→small intestine
colon
lymph nodes
liver of
experimentally
infected pigs. It causes
swelling of the liver, but
no long-term damage. It is
Calicivirus.

43. Diagnosis of HEV
• Acute hepatitis E is diagnosed when the presence
of IgM & IgG anti-HEV is detected.
• Immunofluorescent antibody blocking assays to
detect antibody to HEV antigen in serum and liver.
• Immune electron microscopy to visualize viral
particles in faeces.
• HEV RNA can be detected in acute phase faeces
by PCR.

44. Treatment
 Pegylated α-interferon can effectively treat chronic HEV
infection.
 Ribavirin was given at 600-800 mg/day in 2 separate
doses.
 Ribavirin inhibits the replication of HEV.
 After three months therapy of ribavirin HEV RNA may
undetectable in serum.
 Anemia was the main side effect caused by ribavirin
therapy.

45. HEPATITIS G
• HGV is RNA virus and is similar to HCV but only has 25 amino
acids.
• A 34 year-old surgeon name G. Barker, who fell ill in 1966 with a
non-A non-B hepatitis which at the time was thought to have been
caused by a new, infectious hepatic virus. In 1995-96 the virus was
identified as a distinct virus different from other human hepatitis
viruses (A, B, C, D, E) and was named “GB agent” after the surgeon
& then known as HGV.
• Three genotypes of this virus were identified by investigators and
termed GB-A, GB-B and GB-C. GB-A and GB-B are likely tamarin
viruses; GB-C can infect humans.
• It can be diagnosed only by detecting its RNA in the serum by
polymerase chain reaction.

46. Cont…
 HGV is a distinct from the other hepatitis viruses.
 It is found in blood donor, patients on heamodialysis and as a
coinfection with HIV.
 HGV is cleared from plasma in majority of people.
 Small percentage of cases have chronic HGV infection who do
not develop hepatitis in also their blood is not infected with
this virus.
 This type of patients daignosed by screening of HGV-RNA in
patients serum.

47. HEPATITIS PREVENTION
A  Vaccination
 Maintain good hygienic condition
B  Vaccination
 Never share drug equipment, i.e. needles, syringes
 Never share tooth brushes/razors or any personal hygiene articles that have blood on them (even
tiny amounts)
 Always make sure new & sterilized equipment is being used for tattooing & piercing
 Make sure ink for tattooing is not being shared
C  No vaccine is available.
 Current recommendations for prevention of HCV include universal precautions for the prevention
of blood-borne infections and anti-HCV screening of blood, organ, and tissue donors.
 Programs that focus on reducing HIV transmission are also likely to decrease transmission of HCV
in high-risk groups.
D  There is no vaccine for Hepatitis D, but it can be prevented in persons who are not already HBV-
infected by giving Hepatitis B vaccine
E  The only way to prevent the disease is to reduce the risk of exposure to the virus.
 Reducing risk of exposure means avoiding tap water when traveling internationally and practicing
good hygiene and sanitation.
 Avoid drinking water (and beverages with ice) of unknown purity and uncooked fruit/vegetables
G  No vaccine available
 Use of disposable syringes and avoiding contaminated needles for ear piercing and tattooing are
also effective measures.