Hepatitis A Flashcards
(42 cards)
To what family and genus does HAV belong?
HAV is a member of the genus Heparnavirus in the family Picornaviridae family.
What is the geographical distribution of HAV?
Worldwide.
What is the incidence of HAV infection?
Globally, an estimated 1.4 million cases occur each year.
How is HAV transmitted?
HAV is usually transmitted by the fecal-oral route (either via person-to-person contact or consumption of contaminated food or water). Risk factors for HAV transmission include residence in or travel to areas to poor sanitation, household or sexual contact with another person with hepatitis A, homosexual activity in men, exposure to daycare centers, exposure to residential institutions, and illicit drug use. Bloodborne transmission can occur but is uncommon.
How is HAV not transmitted?
Maternal-fetal transmission has not been described.
Can HAV cause outbreaks?
Hepatitis A can occur sporadically or in an epidemic form.
Write short notes on the pathogenesis of HAV infection.
Hepatic injury occurs as a result of the host immune response to hepatitis A virus (HAV). Viral replication occurs in the hepatocyte cytoplasm; hepatocellular damage and destruction of infected hepatocytes is mediated by human leukocyte antigen–restricted, HAV-specific CD8+ T lymphocytes and natural killer cells. Interferon-gamma appears to have a central role in promoting clearance of infected hepatocytes. An excessive host response (denoted by a marked reduction of circulation HAV RNA during acute infection) is associated with severe hepatitis.
What’s the incubation period of HAV?
The incubation period of hepatitis A infection averages 28 days (range 15 to 50 days).
How does HAV infection usually present?
Acute hepatitis A virus (HAV) infection in adults is usually a self-limited illness.
What are the typical findings on history and examination in patients with HAV infection?
More than 70 percent of adults with HAV have symptomatic illness, which begins with abrupt onset of nausea, vomiting, anorexia, fever, malaise, and abdominal pain. Within a few days to a week, dark urine (bilirubinuria) appears; pale stools (lacking bilirubin pigment) may also be observed. These are followed by jaundice and pruritus (40 to 70 percent of cases). The early signs and symptoms usually diminish when jaundice appears, and jaundice typically peaks within two weeks.
Physical findings include fever, jaundice, scleral icterus, hepatomegaly (80 percent of cases), and abdominal pain. Less common findings include splenomegaly and extrahepatic manifestations such as skin rash and arthralgias.
Discuss the lab findings typically found in patients with HAV infection.
Laboratory abnormalities include elevations of serum aminotransferases (often >1000 international units/dL), serum bilirubin (typically ≤10 mg/dL), and alkaline phosphatase (up to 400 U/L). The serum aminotransferase elevations precede the bilirubin elevation. Serum aminotransferases peak approximately one month after exposure to the virus and then decline by approximately 75 percent per week. The serum bilirubin concentration usually declines within two weeks of peak levels. Other laboratory abnormalities include elevations of acute-phase reactants and inflammatory markers.
When are patients with HAV infectious?
Infected individuals are contagious during the incubation period and remain so for about a week after jaundice appears. HAV replicates in the liver and is shed in the stool in high concentrations from two to three weeks before to one week after onset of clinical illness.
How do patients generally fare in typical HAV infection?
Full clinical and biochemical recovery is observed within two to three months in 85 percent of patients, and complete recovery is observed by six months in nearly all patients. HAV infection does not become chronic, and individuals cannot become reinfected after recovering from infection.
Can HAV cause acute liver failure?
Yes.
Write a short note on acute liver failure in HAV infection.
Fulminant hepatic failure develops in less than 1 percent of patients with hepatitis A; it occurs most commonly among patients with underlying liver disease, particularly chronic hepatitis C virus infection.
(and those >50 and those with other liver diseases, e.g. HBV)
HAV infection can cause extra-hepatic manifestations. Say which patients are at greatest risk for these and which manifestations are the most common.
Extrahepatic manifestations occur most commonly in patients who have protracted illness such as relapsing or cholestatic hepatitis. The most common extrahepatic manifestations include evanescent rash and arthralgias (occurring in 10 to 15 percent of patients).
What other conditions can be caused by HAV infection and what is the likely underlying mechanism?
Other conditions related to immune complex disease and vasculitis also occur, including: ●Leukocytoclastic vasculitis (most often apparent on the legs and buttocks; biopsy demonstrates anti-HAV immunoglobulin (Ig)M and complement in the blood vessel walls) ●Arthritis ●Glomerulonephritis ●Cryoglobulinemia ●Optic neuritis ●Transverse myelitis ●Toxic epidermal necrolysis ●Myocarditis ●Thrombocytopenia ●Aplastic anemia ●Red cell aplasia
What are the complications of HAV infection?
Complications of acute hepatitis A infection include cholestatic hepatitis, relapsing hepatitis, and autoimmune hepatitis.
Write short notes on cholestatic hepatitis secondary to HAV infection. Cover:
- Incidence
- Clinical course
- Imaging
- Treatment/Recovery
Prolonged cholestasis is characterized by a protracted period of jaundice (lasting >3 months); it occurs among fewer than 5 percent of patients with acute hepatitis A infection
.
The course of cholestatic hepatitis is usually characterized by marked jaundice, pruritus, fever, weight loss, diarrhea, and malaise. Laboratory findings include markedly elevated serum bilirubin (often >10 mg/dL) and alkaline phosphatase, modest elevation of serum aminotransferases, and elevated serum cholesterol. Peak bilirubin levels may be reached in the eighth week or later.
In general, cholestatic hepatitis resolves spontaneously with no sequelae; recognition is important to avoid unnecessary testing. Ultrasonography is appropriate to exclude biliary obstruction; cholangiography or liver biopsy are usually not necessary.
Treatment is usually supportive; there is no role for corticosteroids. Cholestyramine may be administered if pruritus is bothersome.
Write short notes on relapsing hepatitis secondary to HAV infection. Cover;
- Incidence and duration
- Clinical course and extra-hepatic manifestations
- Multiple relapses
- Imaging
- Recovery
Up to 10 percent of patients experience a relapse of symptoms during the six months after acute illness. The duration of clinical relapse is generally less than 3 weeks, although biochemical relapse may last as long as 12 months
The clinical course usually consists of apparent clinical recovery after acute infection with near normalization of the serum aminotransferases, followed by biochemical (and, in some cases, clinical) relapse; clinical manifestations of relapse are often milder than the initial episode. HAV can be recovered from stool during relapse episodes, so such patients should be considered infectious.
Multiple relapses can occur. In one series including 297 adults with acute hepatitis A infection, relapse was observed in 13 percent of patients (of whom 22 percent had more than one relapse); approximately half of patients were asymptomatic during the relapses. Development of extrahepatic manifestations (such as arthritis, vasculitis, nephritis, and cryoglobulinemia) during relapse has been described.
In general, patients with relapsing hepatitis have complete recovery; recognition is important to avoid unnecessary testing. Ultrasonography is appropriate to exclude biliary obstruction in patients with significant jaundice; cholangiography or liver biopsy are usually not necessary.
Comment on the relationship between HAV and autoimmune hepatitis.
Rarely, HAV infection may serve as a trigger for development of autoimmune hepatitis in susceptible individuals.
How is the diagnosis of HAV infection established?
The diagnosis is established by detection of serum immunoglobulin (Ig)M anti-HAV antibodies.
Describe the use of IgM anti-HAV antibodies in the diagnosis of HAV infection.
Serum IgM antibodies are detectable at the time of symptom onset, peak during the acute or early convalescent phase of the disease, and remain detectable for approximately three to six months. Among patients with relapsing hepatitis, serum IgM antibodies persist for the duration of this pattern of disease.
Detection of serum IgM antibodies in the absence of clinical symptoms may reflect prior hepatitis A infection with prolonged persistence of IgM, a false-positive result, or asymptomatic infection (which is more common in children <6 years of age than older children or adults).
Comment on the presence of IgG anti-HAV antibodies in the serum.
Serum IgG antibodies appear early in the convalescent phase of the disease, remain detectable for decades, and are associated with lifelong protective immunity. Detection of anti-HAV IgG in the absence of anti-HAV IgM reflects past infection or vaccination rather than acute infection.
