Symptoms of Hepatitis A Infection
Hepatitis A may cause no symptoms at all when it is contracted, especially in children. Such individuals will only know they were infected (and have become immune – you can only get hepatitis A once) by getting a blood test later in life. Approximately 10 to 12 days after exposure, HAV is present in blood and is excreted via the biliary system into the feces (CDC, 2009c). Peak titers occur during the 2 weeks before onset of illness. Although virus is present in the blood, its concentration is much higher in feces. Virus excretion begins to decline at the onset of clinical illness, and decreases significantly by 7 to 10 days after onset of symptoms. Most infected persons no longer excrete virus in the feces by the third week of illness. Children may excrete virus longer than adults.
Seventy percent of hepatitis A infections in children younger than six years of age are asymptomatic; in older children and adults, infection tends to be symptomatic with more than 70% of those infected developing jaundice (CDC, 2009c). Symptoms typically begin about 28 days after contracting HAV, but can begin as early as 15 days or as late as 50 days after exposure and include muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever, and malaise. After a few days of the aforementioned symptoms, jaundice (also termed “icterus”) sets in. Jaundice is a yellowing of the skin, eyes and mucous membranes that occurs because bile flows poorly through the liver and backs up into the blood. The urine will also turn dark with bile and the stool light or clay-colored from lack of bile. When jaundice sets in, the initial systemic manifestations (such as fever and headache) begin to subside.
In general, symptoms usually last less than 2 months, although 10% to 15% of symptomatic persons have prolonged or relapsing disease for up to 6 months. It is not unusual, however, for blood tests to remain abnormal for six months or more. The jaundice so commonly associated with hepatitis A can linger for a prolonged period in some infected persons – sometimes as long as eight months. Additionally, pruritus, or severe “itchiness” of the skin, can also persist for several months after the onset of symptoms. These conditions are frequently accompanied by diarrhea, anorexia, and fatigue. Relapse is possible with hepatitis A, typically within three months of the initial onset of symptoms. Although relapse is more common in children, it does occur with some regularity in adults. The vast majority of persons who contract hepatitis A fully recover, and do not develop chronic hepatitis. Persons do not carry hepatitis A long-term as with hepatitis B and C.
Fulminant Hepatitis A
Fulminant hepatitis A is a rare but devastating complication of an HAV infection; as many as 50% of individuals with acute liver failure may die or require emergency liver transplantation (Taylor et al., 2006). Elderly patients and patients with chronic liver disease are at a higher risk of fulminant hepatitis A. In parallel with a declining incidence of acute HAV infection in the general population, however, the incidence of fulminant HAV appears to be decreasing (Taylor et al., 2006).
HAV infects the liver’s parenchymal cells (internal liver cells). Once a cell has been penetrated by the viral particles, the hepatitis A virus releases its own toxins that cause, in essence, a hostile takeover of the host cell’s system. The cell then produces new viral components that are released into the bile capillaries or tubes that run between the liver’s parenchymal cells. This process results in the death of liver cells, called hepatic necrosis. The fulminant form of hepatitis occurs when this necrotic process kills so many liver cells - upwards of three-quarters of the liver’s total cell count - that the liver can no longer perform its job. Aside from the loss of liver function, fulminant hepatic failure can lead to encephalopathy and cerebral edema. Encephalopathy is a brain disorder that causes central nervous system depression and abnormal neuromuscular function. Cerebral edema is a swelling of the brain that can result in dangerous intracranial pressure. Intracranial hypertension leading to brain stem death and sepsis with multiple organ failure are the leading causes of death in individuals with fulminant hepatic failure (Detry, 2006).
Treatment of those suffering from fulminant hepatic failure turns largely on the victim’s status. Those who have not become encephalopathic generally undergo an intense course of supportive treatment. But for those whose liver failure is so complete that it has lead to encephalopathy or cerebral edema, timely liver transplantation is often the only option. For these unlucky few, the process of necrosis has left their liver scarred and useless. Unfortunately, many patients with irreversible liver failure do not receive a transplant because of contraindications or the unavailability of donor livers (Feldman, 2002).
Persons most at risk of suffering fulminant hepatitis A include those with:
- Pre-existing chronic liver disease (Gilkson, et al., 1992)
- Chronic hepatitis B
- Chronic hepatitis C (there are 3.9 million such persons in the U.S. [MMWR, Oct. 9, 1999])
- Alcohol-induced chronic hepatitis or cirrhosis
- Older individuals, over the age of 50