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Viral Hepatitis

Hepatitis Viral Families

EPIDEMIOLOGY (Ref. Hari. 18th ed., Pg - 2537)
Hepatitis A – Transmitted by Feco-oral route Q. Occurs more in childrenQ.
Hepatitis B – Transmitted by percutaneous inoculation Q. Sexual intercourse Q and vertical transmission from mother to child. As per WHO report that in Asia there is 20-40% chance of vertical transmission in HBeAg negative mothers. (LQ 2012)
90% of HBeAg positive mother and 10% of anti HBe positive mothers transmit HBV infection to their off spring.
The most infections occur approximately at the time of delivery Q and are not related to breast-feedingQ.
Serum, semen and saliva are most infectious for hepatitis B transmission hepatitis B antigen is present in all body secretions except stools. (LQ 2012)


Important Points

The conditions in which there is increased prevalence of hepatitis B infection are

  1. Down’s syndromeQ
  2. Lepromatous leprosyQ
  3. LeukemiaQ
  4. Hodgkin’s diseaseQ
  5. Polyarteritis nodosaQ
  6. HemodialysisQ
  7. I.V. drug usersQ
Hepatitis C – The mode of transmission are percutaneous, perinatal and sexual intercourse. Most common cause of Blood Transfusion induced hepatitis.
The perinatal and sexual route are seen in co-infection with HIV and high level viremia, the risk being 5%.
Breast feeding does not increase the risk of HCV infection.
Hepatitis D – The modes of transmission are percutaneous sexual and perinatal.
Hepatitis E – The mode of transmission is feco oral routeQ.
PATHOLOGY (Ref. Hari. 18th ed., Pg - 2545) The typical morphologic lesion of all types of viral hepatitis are similar and consist of panlobular infiltration with mononuclear cellsQ, hepatic cell necrosisQ, hyperplasia of Kupffer Q cells and variable degrees of cholestasisQ.
  1. Hepatic cell regeneration is present evident by mitotic figures, multi nucleated cells and rosette Q and pseudo acinar formationQ.
  2. Mononuclear infiltration Q consists of lymphocytes, plasma cells and eosinophils.
  3. Liver cell damage consists of (1) Necrosis of cell (2) Ballooning of cells (3) Acidophilic degeneration (Apoptosis) Q of hepatocytes (councilman bodiesQ).
  4. Bridging necrosis Q indicates more severe lesion.
  5. In hepatitis C, there is relative paucity of inflammation, the presence of fat & bile duct lesionQ.
Extra Edge
Acute Hepatitis
  1. Focal/Centrifugal Necrosis
  2. Ballooning Degeneration
  3. Acidophilic Degeneration of hepatocyte (councilman bodies)
  4. Architecture Changes


Clinical and Epidemiologic Features of Viral Hepatitis (Ref. Hari. 18th ed., page - 2546, Table 304.2)
Incubation (days) 15–45, mean 30 30–180, mean 60–90 15–160, mean 50 30–180, mean 60–90 14–60, mean 40
Onset Acute Insidious or acute Insidious Insidious or acute Acute
Age preference Children, young adults Young adults (sexual and percutaneous), babies, toddlers Any age, but more common in adults Any age (similar to HBV) Young adults (20–40 years)
Fecal-oral +++ +++
Percutaneous Unusual +++ +++ +++
Perinatal +++ ± +
Sexual ± ++ ± ++
Severity Mild Occasionally severe Moderate Occasionally severe Mild
Fulminant 0.1% 0.1–1% 0.1% 5–20% 1–2%
Progression to chronicity None Occasional (1–10%) (90% of neonates) Common (85%) Common None
Carrier None 0.1–30% 1.5–3.2% Variable None
Cancer None + (neonatal infection) + ± None
Prognosis Excellent Worse with age, debility Moderate Acute, good
Chronic, poor
Prophylaxis IG
Inactivated vaccine
Recombinant vaccine
None HBV vaccine (none for HBV carriers) Vaccine
Therapy None Interferon
Pegylated interferon
Pegylated interferon plus ribavirin Interferon ± None
Clinical features:
Fatigue is the most common symptoms
  1. Anorexia, nausea, vomiting, fatigue, jaundice, myalgia, headache, photophobia, pharyngitis, cough, coryza.
  2. Serum sickness like syndrome occur in hepatitis B leading to urticarial rash, angioedema, high grade fever and arthritis.
  3. Pain Right upper abdomen due to enlargement of liver.
  4. Splenomegaly and cervical lymphadenopathy are seen in upto 20% cases.
  5. Spider angioma appear during icteric phase and disappear during convalescence.
Laboratory features:
  1. ALT and AST rise, both > 500 IU/L, ALT > AST, ALP ↑ but < 3 times of normal - (normal ALP 30–120 IU/L)
  2. Serum bilirubin rise, and jaundice is usually visible in the sclera when serum bilirubin level are > 2.5 mg/dl.
  3. Prolonged PT is associated with poor prognosis.Q
  4. Hypoglycemia due to nausea, vomiting, inadequate intake and poor hepatic glycogen reserves.
  5. Microscopic hematuria and proteinuria especially in hepatitis B.Q
  6. Elevation of gamma globulin. IgM level is elevated more characteristically during acute hepatis A.Q
  7. False positive RA factor and ANA.
  8. Antibodies to liver kidney microsomes (LKM) in hepatitis C and D.Q
Extra Edge
Hepatitis B may be spread from infected mothers to their babies at birth ('vertical' transmission).
  1. The rate of transmission of hepatitis B from mother to newborn is very high, and almost all infected infants will develop chronic hepatitis B.
  2. Transmission can be significantly reduced through immunoprophylaxis.
  3. This risk is as high as 90% if the mother is also positive for HBeAg. Symptoms usually begin 6 weeks to 6 months after exposure to the virus (average 2 months). Hepatitis has age dependent prognosis.
  4. Children are less likely than adults to clear the infection. More than 95% of people who become infected as adults or older children will stage a full recovery and develop protective immunity to the virus.
  5. However, this drops to 30% for younger children, and only 5% of newborns that acquire the infection from their mother at birth will clear the infection.
Window period = Disappearance of HBs antigen & appearance of HBs Ab
Sexual B >>> C (Rare) (Ref. Hari. 18th ed., Pg-2546)
Vertical B >>> C (uncommon)
Chronicity C >>> B
Tattooing B = C
Progression to cirrhosis is faster in hepatitis B as compare to Hep C.
But HCC occurrence is more in Hep C as compare to Hep B. This is the reason why Hep C is the most common cause for liver transplantation in the world.


Important Points

Hepatitis A

  1. IgM anti HAV during acute illness.Q
  2. IgG anti HAV for previous Q infection.
  3. HAV is present in the liver, stool, blood during late incubation and early preicteric phase.
  4. HAV disappears when jaundice appearsQ

Hepatitis B:


Sequence of appearance of Virological Marka

  1. The first virological marker detectable in serum is HBsAg.
  2. HBeAg appear concurrently or shortly after HBsAg, along with HBV DNA.
  3. Next to appear is anti HBc IgM antibodies Q, 1-2 weeks after appearance of HBsAg. (HBcAg is not present in blood)
  4. Anti HBe antibody
  5. Anti HBs antibody


Extra Edge
Important Points: there is a gap of several weeks between the disappearance of HBsAg and the appearance of anti HBs. This is known as window periodQ. In this period IgM anti HBc represent the serological evidence of HBV infection. (LQ 2012)


Serology of Hepatitis B
  HBsAg Anti HBsAb HBe Ag Anti HBeAb Anti HBcAb
Acute HBV (with high infectivity) + - +   IgM
Acute HBV with low infectivity) + - - + IgM
Chronic HBV (High infectivity) + - +   IgG
Chronic HBV (low infectivity) + - - + IgG


Extra Edge
  1. HBs Ag would be positive even in chronic infection and hence cannot be used to establish a diagnosis of acute Hepatitis B infection.
  2. HBsAg → Present in acute infection, chronic infection and carrier state.
  3. HBeAg = Active, infective disease
  4. HBs Ab = Its presence is safe for blood transfusion.


HBs Ag Anti HBs Ab
Indicates that the person is infected with the virus. The infection may manifest as ‘disease’ either acute or chronic, or be just present as in carrier state.
HBs Ag thus indicated as possible:
i. Acute disease
ii. Chronic disease
iii. Carrier state
With the development of antibody to HBs Ab i.e. Anti HBs Ab, the HBs antigen disappears from the serum.
Anti HBs Ag indicates good immunity.
Anti HBs Ag indicates protection against Hep B
HBC Ag Anti HBc Ab
It is a hidden component of the viral score and is not detectable at all Develop early in the course of disease
It is the first antibody to appear after an acute infection and persists in serum even during the recovery phase
- When acute antibody is of IgM type
- When chronic antibody is of IgG type
HBe Ag Anti HBe Ab
Denotes high infectivity and active disease Denotes low infectivity
DNA polymerase
  1. It is a marker for active viral replication.
  2. It is usually associated with Acute viral hepatitis B when there is active viral replication and hence
  3. DNA polymerase is often present in acute Hepatitis B infection, its presence suggests active virus replication (like HBeAg, HBV DNA) and it is not be used as a laboratory marker for acute hepatitis B infection.
Markers for HBV Replication
  1. Qualitative Markers:- HBe Ag is a qualitative marker for HBV replication
  2. Quantitative Markers
    1. HBV DNA is a quantitative definitive marker for HBV replication
    2. DNA polymerase is a definitive marker for HBV replication
Genomic structure of Hepatitis B
‘S’ Gene ‘C’ Gene ‘P’ Gene ‘X’ Gene
Codes for the envelope protein, HBs Ag Codes for two nucleocapsid protein.
a. HBc Ag: the intracellular core protein
b. HBe Ag: A soluble non particulate nucleocapsid protein.
Codes for DNA polymerase
This DNA polymerase has two activities:
a. DNA dependent DNA polymerase
b. RNA dependent Reverse Transcriptase
Codes for HBx Ag.
It is a small non particulate protein, that can transactivate the transcription of cellular and viral gene.
Hepatitis E
  1. It is transmitted by feco oral route.
  2. Most common cause of epidemic of hepatitis in India is Hepatitis E
  3. Most common cause of epidemic of hepatitis in India in Children is Hepatitis A
  4. Hepatitis E: Both IgM anti HEV and IgG HEV can be detected.
Hepatitis G (PNQ)
  1. HGV a flavivirus, percutaneously transmitted and associated with chronic viremia lasting at least 10 years.
  2. HGV detected in 1.5% of blood donors, 50% of injections drugs users, 30% of hemodialysis patients, 20% of hemophiliacs, and 15% of patients with chronic hepatitis B or C,
  3. It does not appear to cause important liver disease or affect the response of patients with chronic hepatitis B or C to antiviral therapy.
  4. HGV coinfection may improve survival in patients with HIV infection and reduce the degree of fibrosis in patients with HCV-HIV coinfection.
Hepatitis A
Passive immunization – human immunoglobulins Q prepared from pooled plasma of healthy donors.
Hepatitis B:
Active immunization – for pre exposure prophylaxis in:
  1. Health workers exposed to blood
  2. Hemodialysis patients and staff
  3. I.V. drug users
  4. Hemophiliacs
  5. Contacts of HBsAg carriers
  6. Homosexual individuals.
Dose: 3 I/M inj at 0, 1 & 6 months.Q


Extra Edge Pregnancy is not a contraindication to vaccination.Q

Post exposure prophylaxis:
  1. Perinatal exposure – single dose of HBIG(0.5 ml) followed by 3 doses of vaccine starts within 12 hrs of life.
  2. Needle stick injury – single dose of HBIG(0.06ml/kg) within 6 hr followed by 3 doses of vaccine within 1 week.
  3. Sexual contact – single dose of HBIG(0.06 ml/kg) within 2 weeks followed by 3 doses of vaccine.

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