This document discusses hepatitis and its prevention. It begins with an introduction and history of hepatitis, noting its identification as an infectious disease in the 8th century. It then classifies and describes the features, symptoms, transmission, investigation and management of the main types of hepatitis - A, B, C, D and E. For hepatitis A, it outlines the faecal-oral transmission, RNA nature, incubation period and high risk countries. Prevention methods like vaccination and immune serum globulin are discussed. Hepatitis B pathogenesis, markers, diagnosis, vaccination and post-exposure prophylaxis are explained in detail. Guidelines for workplace safety practices are also provided.

1. HEPATITIS AND ITS PROPHYLAXIS
DR.NITI SARAWGI (pg)
DEPARTMENT OF OMFS

2. CONTENTS
• INTRODUCTION
• HISTORY
• CLASSIFICATION
 Hepatitis A
Features , Symptoms , Investigation , Management
 Hepatitis B
Features , Pathogenesis , Symptoms , causes ,
Investigation ,Prevention , Management .
 Hepatitis C
Features , Symptoms , Investigation , Management
 Hepatitis D
Features , Symptoms , Investigation , Management
 Hepatitis E

3. HEPATITIS = inflammation of liver

4. History
The manifestations of liver diseases found to be infectious in 8th century. By
1885, hepatitis was found to be transmittable through blood transfusions and
syringes during the wars of the 17th-19th centuries.
In 1947, Mac Callum classified viral hepatitis into two types: Viral Hepatitis A
and Viral Hepatitis B. In 1965,Baruch Blumberg, discovered the Australia
antigen(later known to be Hepatitis B surface antigen, or HBsAg) in the
blood.
Later in 1968, Prince and Okochi isolated the Australia antigen in hepatitis B
patients, and from this information, the first vaccine for hepatitis B was
produced in 1981 and licensed as “Heptavax”

5. HEPATITIS - causes
ACUTE:
Viral hepatitis
Non-viral infection
Alcohol
Toxins
Drugs
Ischemic hepatits
Autoimmune
CHRONIC:
Viral hepatitis
Alcohol
Drugs
Autoimmune
Heredity

6. HEPATITIS - symptoms
ACUTE:
Muscle and join ache
Fever
Nausea or vomiting
Loss of apetite
Abdominal pain
Dark urine
Jaundice
CHRONIC:
tiredness, weakness
Weight loss
Peripheral oedema
Ascites

7. Hepatitis viruses

8. Hepatitis A
• Transmission : faecal-oral
• Nucleic acid : RNA
• Incubation : 2-4weeks
• Size :27 nm
• High-risk countries:
Eastern Europe, Africa, Asia, South America

9. Hepatitis A
Hepatitis A signs and symptoms
• Fatigue
• Nausea and vomiting
• Abdominal pain or discomfort
• Clay-colored bowel movements
• Loss of appetite
• Low-grade fever
• Dark urine
• Joint pain
• Yellowing of the skin and eyes (jaundice)

10. TRANSMISSION
The hepatitis A virus is transmitted primarily by the
faecal-oral route
Waterborne outbreaks

11. Anti-HAV is important for diagnosis.
IgM type indicating a primary
immune response.
IgG type used as a marker of previous
infection.
INVESTIGATION

12. Hepatitis A Serology

13. LIVER FUNCTION TEST
• Information about the state of a patient's
liver
• These tests include:
• albumin
• bilirubin (direct and indirect)
• Liver transaminases (AST or SGOT and
ALT or SGPT)

14. •ALBUMIN:
• It is the main constituent of total protein.
• Normal range: 3.5-5 g/dl
• Increased: dehydration
• Decreased: chronic liver disease, cirrhosis
•ALKALINE PHOSPHATASE:
• Normal range: 30-115 U/L
• Enzyme in the cells lining the biliary ducts of the liver.
• ALP levels increased in: large bile duct obstruction,
intrahepatic cholestasis, or infiltrative diseases of the liver.
• In the third trimester of pregnancy, ALP is about two to
three times higher
• ↓- hypothyroidism, malnutrition.

15. • BILIRUBIN:
• asses liver function
• Evaluates diseases concerning with production,
uptake, storage, metabolism, excretion of bilirubin
• Total bilirubin: 0.1 – 1 mg/dl
• Direct bilirubin: 0.1-0.4 mg/ dl
• ↑ total bilirubin-: acute and chronic hepatitis,
cirrhosis, biliary tract obstruction, hemolysis
• ↑ direct (conjugated)-: obstructive liver disease,
hepatitis
• ↑ indirect ( unconjugated) -: hemolytic anemia,
hepatocellular liver disease

16. • ASPARTATE AMINOTRANSFERASE (AST/SGOT):
• Enzyme associated with liver parenchymal cells.
• Normal range: 5- 25 U/L
• ↑- liver disease
• ALANINE AMINOTRANSFERASE (ALT/SGPT):
• normal range: 5-30 U/L
• ↑- liver disease (more specific than AST), pancreatitis,
biliary obstruction

17. Prevention
• Hygienic Measures
• Passive Immunization
( gives <3 months immunity to those at risk)
• Active Immunization
• Hepatitis A Vaccine
Four hepatitis A monovalent vaccines are currently available
(Haverix, Vaqta, Avaxim and Epaxal), prepared from different
strains of the hepatitis A virus; all are grown on human diploid cells .

18. Management
Immediate protection can be provided by immune
serum globulin. If this is given soon after exposure to the
virus.
The protective effect of immune serum globulin is
attributed to its anti HAV content.
CHRONIC LIVER DISEASE DOES NOT OCCUR!

19. Hepatitis B

20. Hepatitis B:
ACUTE CHRONIC- 5-10%
(infection >6months)
• Every year 1 to 2 million people die due to an
infection by this virus
complications of chronic hepatitis

21. • Transmission: blood and body fluids.
• Incubation: 1-6 months
• Hepatitis B virus primarily interferes with functions of the
liver by replicating in liver cells
• During HBV infection, the host immune response causes
both hepatocellular damage and viral clearance

22. • HBV not only transmitted through percutaneous
exposure , but also can be transmitted through surface
contact with dried blood or other potentially
infectious materials.
• HBV infections that occur in workers with no
history of exposure or occupational percutaneous
injury might have resulted from direct or indirect
blood or body fluid exposures that inoculated HBV
into cutaneous scratches, abrasions, burns, or other
lesions, or on mucosal surfaces

23. HEPATITIS B VIRUS:

24. HOW THE VIRUS REPRODUCES ??

28. HEPATITIS B MARKERS:
 HBsAg: Present in acute or chronic infection.
 HBsAb: Present in recovery or immunization
 Anti -HB Core: May be “Total” (IgG&IgM) or
IgM. Lifelong marker of past and active infection
in either acute or chronic.
 HBeAg: Acute infection, and extremely infectious.

29. Diagnosis:
 HBsAg N.
 HBcAB (TOTAL) N.
 HBsAB N.
 HAV-IGM N.
 HCV N.
 NO evidence of viral hepatitis .

30.  HBsAG N.
 HBcAB (TOTAL) P.
 HBsAB P.
 HAV-IGM N.
 HCV N.
 PAST INFECTION.

31.  HBsAg N.
 HBcAB (total) N.
 HBsAB P.
 HAV-IGM N.
 HCV N.
 IMMUNIZATION.

32.  HBsAg P.
 HBcAB (Total) P.
 HBsAB N.
 HAV-IGM N.
 HCV N.
MAY BE ACUTE OR CHRONIC.
 Hep. B Core IgM to clarify.
 The IgM will be positive , If Acute.

33.  HBsAG P.
 HBcAB (total) P.
 HBsAB P.
 HAV-IGM N.
 HCV N.
 Past infection with recovery, and then re-infection that
has become chronic, this is very rare but does happen.

34.  HBsAg P.
 HBcAB (TOTAL) P.
 HBsAB N.
 HAV-IGM P.
 HCV P.
 Co infection with HBV, HAV, and HCV

35. What are the clinical symptoms of
Hepatitis B??

36. Causes of Hepatitis B

37. How will I keep from becoming infected
with HBV at work??
 The primary measure for prevention
of hepatitis B is immunization.
 Hepatitis B can be prevented using
either pre-exposure prophylaxis with
hepatitis vaccine or post-exposure
prophylaxis with hepatitis B immune
globulin and hepatitis vaccine.

38. What is hepatitis B vaccine?
 Hepatitis B vaccine has been available since 1982.
 Made with recombinant DNA technology, and contain
protein portions of HBV.
 The vaccine administrated IM
 usually given on schedule of 0,1,6 months

39. Dosage:

40. Who should be vaccinated?
 Everyone 18 years of age and younger
 over 18 years of age who are at risk for HBV
infection, which include :
 drug users
 person at occupational risk of infection
 hemodialysis patients
 household and sex contacts of persons with chronic HBV
infection

41. Post exposure Prophylaxis for
Hepatitis B
 For an infant with perinatal exposure to an
HBsAg-positive and HBeAg-positive mother, a regimen
combining one dose of HBIG at birth with the hepatitis B
vaccine series started soon after birth is 85%-95% effective
in preventing development of the HBV carrier state .

42. • For percutaneous (needlestick, laceration, or bite)
or permucosal (ocular or mucous-membrane) exposure to blood,
the decision to provide prophylaxis must include consideration of
several factors,
• a) whether the source of the blood is available.
• b) the HBsAg status of the source.
• c) the hepatitis B vaccination and vaccine-response status of
the exposed person

43. • For perrcutaneous exposure,. A regimen of two doses
of HBIG, one given after exposure and one a month later, is
about 75% effective in preventing hepatitis B in this setting . For
sexual exposure to a person with acute hepatitis B, a single dose of
HBIG is 75% effective if administered within 2 weeks of last
sexual exposure .

44. • Exposed person has not been vaccinated or has not
completed vaccination. Hepatitis B vaccination should be
initiated. A single dose of HBIG (0.06 mL/kg) should be
administered as soon as possible after exposure and within 24
hours, if possible. The first dose of hepatitis B vaccine should
be administered intramuscularly at a separate site
• If the exposed person has begin but has not completed
vaccination, one dose of HBIG should be administered
immediately and vaccination should be completed as scheduled

45. Exposed person has already been vaccinated against
hepatitis B, and anti-HBs response status is known.
(a) If the anti-HBs level is adequate, no treatment is
necessary.
(b) If the anti-HBs level is inadequate, a booster dose of
hepatitis B vaccine should be administered.

46. Specific Practices To Be
Utilized in workplace!!!!!!!!!!!!
 How to dispose of small amount of regulated
waste and remove gloves:

49. How to dispose a larger amounts of
regulated waste:
 Before removing disposable gloves, gather all
contaminated materials together and put them
in a biohazard (red) bag.
 Make sure the bag intact and that there is no
danger of leaking.
 Strip off disposable gloves, drop them into the
red bag, close the bag by handling only the
clean outside surfaces ,do not throw the
biohazard bag into the regular trash.
 Wash hands with soap and water ,make
arrangements to properly dispose of the
biohazard bag.

50. MANAGEMENT

51. Management Guidelines
- Simple non –invasive tests to assess which stage of liver
disease is the patient in
- -prioritizing those with liver cirrhosis – advanced liver disease
- -the use of two safe and highly effective medicines –tenofovir
or entecavir for treatment of chronic hepatitis
- -regular monitoring to assess the presence of liver cancer of if
the treatment is working and whether it can be stopped.

52. • Interferon-alfa
It acts by augmenting a native immune response
 It is contraindicated in the presence of cirrhosis as it may
cause a rise in serum transaminases and precipitate liver failure.
 side effects are common include fatigue, depression ,irritability
,bone marrow suppression and thyroid disease.
• Lamivudine
It is a nucleoside analogue which inhibit DNA polymerase and
suppresses HBV-DNA level
Usual Adult Dose for Chronic Hepatitis B-
100 mg orally every 24 hours

53. • Adefovir
• It reduces HBV-DNA level, enhances the frequency of HBeAg
seroconvertion and leads to histological improvement ,but is
contraindicated in renal failure.
• Relapse occurs on stopping treatment.
•Entecavior
These drugs are more effective than lamivudine and
adefovir in reducing viral load in HBeAg – positive and HBeAg negative
chronic hepatitis

54. • Liver Transplantation

55. FACTS:

56. Hepatitis C

57. Hepatitis C
ACUTE CHRONIC 50-80%
first 6 months after infection more than 6 months
60-70% asymptomatic often asymptomatic
most patients develop chronic 1/3 progress to cirrhosis in 20y
HCV
• Infects 3-4 million people per year

58. • Transmission: blood esp blood transfusion
• Incubation: 2weeks - 6months
• No vaccine!
• 35% of patients infected with HIV are also infected with
hepatitis C virus

60. Investigation
Serology:
 The HCV protein contains several antigens that give rise to
antibodies in an infected person and these are used in diagnosis
 It may take 6-12 weeks for antibodies to appear in the blood.
Liver Histology:
 Serum transaminase levels in hepatitis c are a poor predictor of
degree of liver fibrosis and so a liver biopsy is often required to stage
the degree of liver damage
LFT
 LFT may be normal or slow fluctuating serum transaminase
between 50 and 200 V/L. Jaundice is rare and only usually appears in
end-stage cirrhosis.

61. Management
• The treatment of choice is pegylated alpha interferon given
weekly subcutaneously , together with oral ribavirin, a synthetic
nucleotide analogue.
• The main side effect of ribavirin is hemolytic anemia.
• Side effect of interferon are insignificant.

62. Hepatitis D

63. Hepatitis D
• Subviral satellite because it can propagate only in the
presence of hepatitis B
coinfection superinfection
• Transmission: parenteral (intravenous drug use mostly)
• Nucleic acid : RNA
• Incubation : 30-60 days
• > 60% develop cirrhosis

64. Investigation
HDV contains a single antigen to which infected individuals
make an antibody(anti-HDV).Delta antigen appears in the
blood only transistently and in practice diagnosis depends on
detecting anti-HDV
Management
Effective management of hepatitis B virus effectively
prevents hepatitis D

65. Hepatitis E

66. • HEV is a single-stranded RNA calcivirus
• It is spread mainly through fecal
contamination of water supplies or food; person-
to-person transmission is uncommon.

69. • Mortality rates are generally low, for hepatitis E is a "self-
limiting" disease, in that it usually goes away by itself and
the patient recovers
• It does not cause chronic liver disease.
• Pregnant women, especially those in the third trimester,
suffer an elevated mortality rate from the disease of
around 20%

70. Signs $ Symptoms
• After a prodromal phase symptoms lasting for days to weeks
follow.
• Symptoms include jaundice, fatigue and nausea
• Symptomatic phase coincides with elevated hepatic
aminotransferase levels.
• Virus detectable in stool and blood serum.

71. Prevention and Management
•vaccine HEV 239,
Treatment of acute HEV infection
Hepatitis E treated with ribavirin for 21days. Although ribavirin
therapy is contraindicated in pregnancy owing to teratogenicity.
The risks of untreated HEV to the mother and fetus are high.

72. Treatment of chronic HEV infection
• Ribavirin monotherapy (600–1000 mg/day) for at
least 3 months seems to be the first treatment option for
patients with chronic hepatitis E who are not able to clear
HEV after immunosuppression is reduced

73. Hepatitis F

74. Hepatitis G

76. Hepatitis TT

77. • In 1997, a novel DNA virus was isolated from the serum of
a patient with post-transfusion hepatitis of unknown
etiology in Japan
• TTV is a nonenveloped, single-stranded and circular DNA
virus, and its entire sequence of ~3.9 kb has been
determined.

78. TRANSMISSION
• Recent reports indicate that TTV can be transmitted via
blood/blood products
• In another study, a high rate of cervical carriage (66%) of TTV
DNA was found by PCR, which suggests that perinatal and
sexual transmission is possible.

79. CONCLUSION

80. References
Harrison's Principles of Internal Medicine
Davidson's Principles and Practice of Medicine, 21st Edition
Ananthanarayan .Text book of Microbiology
Internet source