Hepatitis A is a common cause of acute hepatic inflammation and jaundice worldwide, and until 2004 it was the most commonly reported type of hepatitis in the United States.¹ A combination of widespread vaccination, food safety practices, and improved sanitation decreased the incidence of hepatitis A in the United States from the 1970s until 2015. However, infection rates have recently increased because of large community outbreaks in susceptible individuals.²

Epidemiology

Worldwide, an estimated 1.4 million cases of hepatitis A are reported each year, and it remains a major infectious disease for most of the world's population.³ Before the development and implementation of the hepatitis A vaccine, annual cases of acute infection in the United States were reported in the tens of thousands, peaking at 59,606 cases in 1971.⁴ Following the licensing of the first vaccine, the annual number of U.S. cases fell by 92% between 1995 and 2010.¹ This decline in cases occurred after only moderate vaccination coverage was achieved, indicating a substantial herd immunity effect.⁵ However, the United States has seen a steep increase in cases, driven by several person-to-person and food-related outbreaks beginning in 2016.^4,6,7 These episodes, along with several outbreaks in Europe over the past five years, have led to resurgences of hepatitis A in areas considered low-endemic regions.^3,8 The lack of widespread adult immunity in the affected nations, whether due to poor immunization rates or few previous infections, provides fuel for outbreaks.⁹ Advances in virus genotyping have allowed researchers to track outbreak origin and trajectory.¹⁰

Transmission and Risk Factors

Hepatitis A virus is a nonenveloped positive-strand RNA virus classified as a picornavirus, whose only natural host is humans.¹ Remarkably stable in many environments and able to survive on surfaces for weeks, hepatitis A virus is transmitted through ingestion of infected stool particles.^11–13 The virus is absorbed in the stomach and intestines, travels to the liver via the portal circulation, and replicates in hepatocytes.^11,12 Detectable virus appears in blood and feces approximately 10 to 12 days after infection and may be excreted in stool for up to three weeks after the onset of symptoms.^1,12 Viral shedding may begin weeks before symptom onset, contributing to the scope of outbreaks.^4,12 Close interpersonal or sexual contact with an infected person and consumption of contaminated food or water are the most common routes of infection.^4,14 Less commonly, infection has resulted from injection drug use or blood transfusion.^4,12,14 Risk factors for contracting hepatitis A and characteristics that increase the risk of complications from infection are listed in Table 1.²

Presentation and Complications

An incubation phase of approximately 30 days (range = 15 to 50) is followed by the development of infectious symptoms in most adults and children six years and older.^4,12 Approximately 70% of children younger than six years remain asymptomatic.⁴ Patients often initially experience nonspecific flulike symptoms of fever, malaise, nausea with vomiting, and abdominal pain that may progress to the classic findings of dark urine and jaundice in 70% of adults and older children.^4,12 Although less common, diarrhea, joint pain, pruritus, and skin eruptions may also occur.¹² Hepatomegaly and jaundice are the most common examination findings, occurring in 78% and 40% to 80% of patients, respectively.¹²