Hepatitis A

Following improved sanitation and hygiene, and the introduction of HAV vaccination in 1995, the number of infections has declined by nearly 95%.

However, between 2016 in 2018 an estimated 15,000 reported cases have occurred, largely associated with outbreaks related to drug use,homelessness, and men having sex with men.

Formally outbreaks were related to small events associated with consumption of contaminated food, child care centers, or unvaccinated travelers returning from endemic settings.

Approximately 26,000 cases reported annually in the US prior to HAV vaccine.

Currently most commonly identified factor among reported cases of acute infection is contact with an infected household member or sexual partner.

Additional risk factors include: international travel, men who have sex with men, daycare workers, injection drug abuse, eating raw shellfish from contaminated water, sporadic food outbreaks and blood transfusion with acute hepatitis.

Peak infectivity occurs during the two-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus is highest in the stool.

Illness usually associated with an abrupt onset with fever, malaise, nausea, anorexia, abdominal discomfort, dark urine, and jaundice.

Nearly 50% of reported cases a definitive source cannot be identified.

HAV is primarily transmitted I directy via the fecal-oral route and is acquired by ingestion of contaminated food or water or directly through sexual or a direct contact with an infected individual.

Replicates only within the liver after being ingested and absorbed in the stomach and small intestine and then reaching the liver

The replicating virus is released from the liver cells into bile and then secreted into the stool.

In 2005 estimated 42,000 cases of acute infection in the U.S.

Since the advent of hepatitis a vaccine in 1995 the frequency of acute hepatitis A has been steadily declining if all age groups.

Presently, annual incidence is 1.5 cases per 100,000 persons an 85% decline in new cases since 1995

symptoms of HIV infection are indistinguishable from other causes of acute viral hepatitis.

Diagnosis is established by serological testing, typically during the acute or early convalescent phase.

70% of infected children younger than 6 years are asymptomatic.

Young children are the main source of transmission in the community.

Severity of symptoms increases with age.

Among children aged 0 to 4 years fewer than 10% have jaundice, and this percentage increased to 30-40 percent among children aged 5 to 9 years, 60 to 80% among those 10-17 years, in 1890% among adults aged 18 years or older.

Typically, signs and symptoms last less than two months, although 10 to 15% of patients may have prolonged the relapsing disease lasting up to six months.

Patients with chronic diseases are at higher risk for a complicated process.

Patients with chronic liver diseases such as chronic hepatitis C or alcoholic liver disease are at risk for a more severe infection than are healthy people.

Patients with immunosuppression may have a prolonged recovery and a more variable course of disease.

Most patients experience symptoms approximately one month after contact with virus.

Symptoms are nonspecific and include: nausea, fatigue, diarrhea, anorexia, fever, right upper quadrant pain, and jaundice, the latter seen in less than 10% of young children and the majority of older children and adults.

Symptoms usually last 1-2 weeks, but some may experience a prolonged period of jaundice up to several months duration.

Up to 10% of patients experience a recurrence of acute symptoms after seemingly have recovered from the initial process.

Rarely immune responses to the virus can result in arthritis and glomerulonephritis.

Risk of dying by acute infection is 1%, but varies with age in that 2.2% of those over the age of 50 years will die of acute infection.

Recovery provides life long antibody protection.

More than 75% of adults have symptoms.

Average incubation period of 28 days (range 15-50 days).

Most patients have complete and uneventful recovery.

Permanent damage unlikely.

100 deaths annually related to fulminant infection in the U.S.

Case fatality rate for HAV infection increases with age with 1.8% rate for adults greater than 50 years of age compared with 0.6% for patients less than 15 years of age.

Patients with chronic liver disease are at increased risk for liver failure.

One-third of population has serologic evidence of previous hepatitis A infection, with a 9% prevalence among children 6-11 years and up to 75% in adults over the age of 70 years.

Peak infectivity, as determined by viral shedding in the stool, occurs approximately two weeks prior to the development of clinical symptoms, although prolonged shedding can occur especially in children.

HAV nucleic acid amplification tests are also available but rarely required to establish a diagnosis.

Laboratory findings include: marked increases in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) reflecting the severity of the lover inflammation and injury.

Anti-HAV IgM establishes the diagnosis of acute hepatitis A and appears in symptomatic patients 5-10 days before symptom onset.

Anti-HAV IgM can remain elevated 3-12 months following infection.

Anti-HAVOIGG generally process for the duration of a patient’s life following infection with vaccination and presents right before or at the time of symptom onset in case of acute infection.

The serum bilirubin maybe elevated, the prothrombin time may elevated and the serum albumin levels will fall.

Incidence has decreased as a result of childhood vaccination.

Immune globulin recommended for postexposure prophylaxis in the U.S.

Hepatitis A vaccine is effective for postexposure prophylaxis