Tufts OpenCourseware
Author: Kanchan Ganda, M.D.
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1. Viral Hepatitis

Five distinct types of viral hepatitis are commonly seen: hepatitis A, B, C, D and E. Viral hepatitis is an inflammation of the liver caused by (a) poor sanitation (hepatitis A or E, also called infectious hepatitis) or (b) via infected serum/blood transmission (hepatitis B, C, or D, also called serum hepatitis).

1.1. Infectious Hepatitis - HAV (Hepatitis A Virus) and HEV (Hepatitis E Virus)

  • Hepatitis A and E are acute in onset, transmitted via contaminated food or water (“oral-fecal” transmission), and commonly associated with jaundice in 70% of the cases.
  • Hepatitis A has an incubation period of two to six weeks; Hepatitis E two to nine weeks.
  • Hepatitis A is universal in occurrence; hepatitis E is prevalent in Asia, China and Mexico only.
  • HAV and HEV both have endemic outbreaks.

The entire symptomatic period is short lasting (2-3 weeks in most cases). The following symptoms occur: high fever, tiredness, weakness, fatigue, nausea, vomiting, diarrhea, flu-like symptoms. Yellowing of the eyes and skin occurs in 70% of cases. This is Jaundice (Icteris). Jaundice occurs when billirubin levels are very high in the blood. The onset of jaundice heralds the start of the recovery process. Once the patient has become non-icteric and symptom-free, the patient has fully recovered.

To confirm the diagnosis of HAV or HEV, the patient’s blood is tested for the antibodies against the respective viruses. For HAV, the blood is tested for Anti-HAV. For HEV, the blood is tested for Anti-HEV. If the antibody test is positive, the lab determines if the antibody is of the IgM or IgG variety. The Anti-HAV IgM variety is a marker of infection. The Anti-HAV IgG variety is a marker of recovery and confers lifelong immunity to the patient. The Anti-HEV IgM variety is a marker of infection. The Anti-HEV IgG variety is a marker of recovery. This may be associated with a lifelong community.

1.2. Serum Hepatitis - HBV, HCV, and HDV

Hepatitis B, C and D are transmitted via contact with contaminated blood. Hep B and Hep D are also transmitted through sexual contact. With Hepatitis C, transmission by sexual contact does occur but the incidence is low, only about 10%. Hepatitis D, or delta hepatitis, is seen commonly in IV drug users. Hepatitis D is a virus with parasitic tendencies and always needs the presence of Hepatitis B to cause infection in the patient. So Hep D occurs along with a new Hep B infection or it can occur in a patient who is chronically infected with Hepatitis B, a chronic carrier.

Bloodborne hepatitis are insidious (slow and gradual) in onset. Typically, the patient is symptomatic for a few weeks to a few months. The patients frequently complain of tiredness, weakness, fatigue, generalized malaise, loss of stamina, run down feeling, anorexia, aversion to smoking, weight loss, joint pains (arthralgia), skin rashes, dark-colored urine, and occasionally, jaundice (in 30–40% of cases).

1.3. Hepatitis B (HBV)

Hepatitis B has an incubation period of two to six months. This is a DNA virus. It is a 22 nm diameter particle and has three distinct Ag-Ab (antigen-antibody) systems.

  • HBsAg (surface antigen) gives rise to the Anti-HBs (surface antibody).
  • HBeAg (“e” antigen) gives rise to the Anti-Hbe (E antibody).
  • HBcAg (“core” antigen) gives rise to the Anti-HBc (core antibody).
  • HBsAg (refer to the graph in figure at the end of information on Hepatitis B) is the first marker of infection to appear in the blood when the patient gets infected.

Routinely, in most adults who get infected, the patient sheds the HBsAg completely by about five months from the start of infection. It is only after the patient has completely shed the HBsAg that the patient develops Anti-HBs.

  • Anti-HBs will stay in the blood for 15-20 years.
  • Anti-HBs is a marker of immunity.
  • HBeAg is a marker of infection, indicative of viral replication.
  • HBeAg appears in the blood a short time after HBsAg and routinely disappears from the blood a short while before the disappearance of HBsAg from the blood.
  • The patient is highly infectious when the blood is positive for both HBsAg and HBeAg.
  • Anti-HBe occurs after HBeAg has been shed and it is a marker of decreased infectivity.
  • HBcAg does not appear in the blood. It is found in the infected liver cells only and there is no blood test for HBcAg.
  • Anti-HBc does appear in the blood and can be detected a short time after the appearance of HBsAg in the blood.
  • For the first 6 months of the infection, anti-HBc is an IgM antibody ( Anti-HBc [IgM] ).
  • Beyond 6 months from the start of infection, it is an IgG antibody ( Anti-HBc [IgG] ).
  • The Anti-HBc also persists in the blood for 15-20 years. Presence of Anti-HBc [IgM] is a marker of infection. Anti-HBc [IgG] when associated with the presence of Anti-HBs is a marker of immunity.

Note: When a patient’s blood shows the presence of Anti-HBc, it confirms an exposure to a natural infection. Anti-HBc does not occur with immunization against Hep B , which is an acquired immunity.

1.3.1. The Hepatitis B Carrier Patient

In most adult cases, HBsAg is shed prior to 6 months from the start of the infection. If the patient continues to harbor HBsAg beyond the 6 month period, the patient is listed as a chronic carrier. A carrier patient is not immune. Immunity develops only after HBsAg has been completely shed from the patient and Anti-HBs production occurs.

  • A carrier patient may also continue to harbor HBeAg in the blood, when HBeAg does not follow its normal cyclical pattern.
  • Presence of HBeAg is a marker of very high infectivity in a carrier, as it denotes active viral replication. Incidence of occurrence of carrier state is 5-10% in adults and 85% in children. Once a carrier is invariably always a carrier.
  • Immunity gained by a natural infection lasts for about 15-20 years. Immunity gained by immunization lasts for about seven years. If the titer is low, a booster dose is given to enhance the immunity.

1.4. Hepatitis C

Hepatitis C is formerly known as “Non-A, Non-B” Hepatitis. It is the worst kind of hepatitis to have. To confirm the diagnosis, the patient’s blood is tested for the presence of the antibody against Hep C, Anti-HCV. Presence of Anti-HCV is a marker of infection. This antibody is not a protective antibody. The incubation period for this virus is 15-150 days.

This is a fulminant (aggressive) type of hepatitis. More than 70-85% of these patients go on to develop chronic hepatitis. Of those, 30% will get cirrhosis of the liver. Once a diagnosis of Hep C is confirmed, the patient is tested every 3-6 months and Anti-HCV titers are monitored. Rising titers is a marker of a progressing illness. Dropping titers is a marker of resolution of the infection. Recovery occurs when the patient completely sheds Anti-HCV. Rising titers will be associated with an elevation of liver enzymes SGPT (ALT) and SGOT (AST).

  • ALT comes from the cytosol of the hepatocytes and AST comes from the mitochondria of the hepatocytes. Swelling of the liver cells due to inflammation as in hepatitis, results in ALT levels being markedly elevated. ALT is always higher than AST levels with hepatitis.
  • Cirrhosis of the liver is associated with necrosis or death of the liver cells. So AST levels will be markedly elevated.
  • In cirrhosis, AST levels are always greater than ALT levels.

1.5. Hepatitis D

Hepatitis D occurs with Hep B as a co-infection or superinfection. Due to the presence of two viruses, it is a more fulminant type of hepatitis.

  • The incubation period of Hep. D is thus limited to two to six months.