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Acute Viral Hepatitis (Hepatitis A, D, E)
Acute hepatitis with a predominant hepatocellular pattern of liver injury may occur as a consequence of a diverse spectrum of etiologies, including both nonhepatotrophic and hepatotrophic viruses. Among the latter group, hepatitis A, hepatitis B, and hepatitis E infections are the most common source for acute viral hepatitis. Acute hepatitis D infection may also occur rarely in context of coexisting acute hepatitis B infection or as a superinfection in patients with chronic hepatitis B infection. Other viruses associated with acute viral hepatitis include cytomegalovirus (CMV), herpes simplex virus (HSV), and Epstein-Barr virus (EBV), which are less often associated with icteric hepatitis.
Hepatitis A
Hepatitis A virus (HAV) is phylogenetically distinct from the other hepatitis viruses and belongs to a new genus described as Hepatovirus. HAV is a nonenveloped virus capable of surviving in a variety of external environments, such as dried feces and live oysters, for a prolonged time, and it can withstand relatively warm temperatures. Major modes of transmission are fecal-oral and person to person and through contaminated food and water. The incubation period is generally 1 to 2 weeks. Viral shedding in the stool often occurs before symptoms develop. Recent outbreaks of acute hepatitis A in major US cities, including San Diego and Salt Lake City in 2017 to 2018, have raised attention of public health agencies to this source of acute viral hepatitis.
The typical course of acute HAV and other viral hepatitis infections is shown in Figs. 165.1 to 165.3 .
Clinical Picture
Acute HAV infection may present clinically in a manner similar to any other form of acute hepatitis. Moderate to marked elevation of serum transaminases (aminotransferases) may be present. The likelihood of jaundice increases with increasing length of exposure. Neonates and children are often asymptomatic. In fact, in many areas of the developing world, a large proportion of the population appears to have been previously exposed to HAV, based on the presence of positive anti-HAV antibody.
Several clinical patterns of HAV infection may be recognized. Acute infection may be completely asymptomatic, especially in very young patients. Many patients have symptomatic acute icteric hepatitis and may have all the characteristic symptoms, such as fatigue, lethargy, nausea, abdominal pain, and anorexia. Occasionally, a cholestatic variant may be observed, with prolonged jaundice and a highly cholestatic pattern of liver test abnormalities. Relapsing hepatitis has been reported in some patients, with apparent remissions and relapses that may last several months. Cholestasis and relapsing hepatitis do not increase mortality risk. In a small subset of patients, fulminant hepatitis may occur, necessitating urgent liver transplantation. Aplastic anemia is another rare but serious complication of acute HAV.
The incidence of these serious complications is less than 5%. Mortality risk in patients older than 50 is significantly greater than among younger patients. Chronic hepatitis is not observed among patients with acute HAV infection.
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