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Hepatitis A virus (HAV) is a worldwide, acute self-limiting disease
transmitted via the fecal–oral route. Hepatocyte injury is caused by a
cytopathic and immunologic response, which can result in jaundice and
increased liver function tests. Treatment measures are usually
supportive and aimed toward prevention (pre-exposure and postexposure) through vaccination.
Hepatitis B virus (HBV) is a bloodborne pathogen that is transmitted
through percutaneous or perinatal exposure, blood products, or sexual
contact. HBV has an acute phase with resolution and a chronic phase.
Over the course of decades, the chronic phase can lead to hepatic
cirrhosis and death. Patients with chronic infection require treatment
with peginterferon, nucleoside and nucleotide reverse transcriptase (RT)
inhibitors. Several effective prophylactic strategies (immunizations and
nucleoside or nucleotide RT inhibitors) are used to prevent HBV
Hepatitis C virus (HCV) is a bloodborne pathogen that is transmitted
primarily through percutaneous exposure, blood products, or sexual
contact. HCV has an acute and a chronic phase. The chronic phase can
lead to cirrhosis, decompensated liver disease, hepatocellular carcinoma,
and death. Acute clinical manifestations are similar to those for HAV
and HBV. Treatment of chronic HCV infection (genotypes 1 to 6) is
with direct-acting antivirals (DAAs).
Hepatitis Dvirus (HDV) is a small RNA virus that requires coinfection
with HBV for replication. HDV transmission is most likely associated
with percutaneous exposure. HDV, in combination with HBV, leads to
a much higher risk of acute liver failure. Prevention strategies rely on
successful immunization of HBV.
Hepatitis E virus is similar to HAV and is transmitted via the fecal–oral
route, especially through contaminated water, which is found more
common in developing countries. Recovery from acute illness usually
There are five distinctly separate hepatitis viruses that cause liver disease. A sixth
virus also has been identified, but has yet to be implicated in liver disease. Four of
these viruses are RNA viruses, and one is a DNA virus.
can be distinguished by serologic assays and, in some instances, by genotyping.
Although progress in the area of disease prevention has improved, advances in
treatment of certain viral infections have been limited because of the large amount of
viruses produced and their rapid mutation. For instance, the hepatitis C virus (HCV)
replicates approximately 1 trillion virus particles (virions) daily, compared with 100
billion HBV virions daily and 10 billion HIV virions daily.
the virology, epidemiology, pathogenesis, natural history, diagnosis, clinical
manifestations, prevention, and treatment strategies for viral hepatitis A through E.
CAUSATIVE AGENTS AND CHARACTERISTICS
Viral hepatitis is a major cause of morbidity and mortality in the United States.
least five distinct pathogens are responsible for viral hepatitis. These hepatotrophic
viruses are identified by the letters A through E as follows: (a) type A hepatitis
caused by hepatitis A virus (HAV), (b) type B hepatitis caused by hepatitis B virus
(HBV), (c) type C hepatitis caused by HCV, (d) type D or delta hepatitis caused by
the HBV-associated hepatitis D virus (HDV), and (e) type E hepatitis caused by the
hepatitis E virus (HEV). Hepatitis A through E viruses differ in their immunologic
characteristics and epidemiologic patterns (Table 80-1).
is the primary mode of infection for HAV and HEV, whereas parenteral and sexual
transmission is characteristic of HBV, HCV, and HDV infections.
viruses primarily affect nonhepatic organ systems and may secondarily induce a
hepatitis-like syndrome. These include the Epstein–Barr virus (infectious
mononucleosis), cytomegalovirus, herpes simplex viruses, varicella-zoster virus, and
rubella, rubeola, and mumps viruses.
Characteristics of Hepatitis Viruses
HAV Nonenveloped SS RNA Fecal–oral None Low
HBV Enveloped DS DNA Parenteral
HCV Enveloped SS RNA Parenteral
HDV Enveloped SS RNA Parenteral
HEV Nonenveloped SS RNA Fecal–oral None Low–Moderate
virus; SS, single-stranded; RNA, ribonucleic acid; DNA, deoxyribonucleic acid.
Definitions of Acute and Chronic Hepatitis
Viral hepatitis can present as either an acute or chronic illness. Acute hepatitis is
defined as an illness with a discrete date of onset with jaundice or increased serum
aminotransferase concentrations greater than 10 times the upper limit of normal
and does not exceed 6 months. Chronic hepatitis is a prolonged inflammatory
condition of the liver that involves ongoing hepatocellular necrosis for ≥6 months
beyond the onset of acute illness.
4,5 The most common causes of chronic viral
3 Drug-induced and autoimmune chronic hepatitis occur
less frequently; metabolic disorders and HDV chronic hepatitis are relatively rare.
HAV and HEV are self-limiting infections that rarely progress to chronic hepatitis.
Serologic Evaluation in Presumed Chronic Hepatitis
Serologies are useful in diagnosing viral hepatitis. Antibodies against hepatitis A
presence of immunoglobulin M (IgM) anti-HAV. If HBsAg is present, further testing
for hepatitis B envelope antigen (HBeAg) and HBV DNA confirms the presence of
active viral replication and viral load, respectively. Testing for hepatitis D antibody
(anti-HDV) should also be performed in patients with HBV infection to evaluate the
possibility of coinfection. If serology is negative, rare but treatable causes of chronic
active hepatitis should be further ruled out. These include alcoholic liver disease,
disease, alpha-1-antitrypsin deficiency, and drug-induced chronic active hepatitis.
Drugs associated with reversible chronic active hepatitis syndrome include
Hepatitis A virus is an icosahedral, nonenveloped virus measuring 28 nm diameter. It
is a single-stranded, positive-sense, linear RNA enterovirus of the Picornaviridae
HAV has a worldwide distribution.
13,14 The prevalence of infection is related to
the quality of the water supply, level of sanitation, and age.
unreliable because the disease is frequently mild and often unrecognized, resulting in
under-reporting. The primary mode of transmission is from person to person via the
15,16 The virus is sturdy and resists degradation by drying,
environmental conditions (temperatures as high as 56°C and as low as −20°C),
gastric acid (pH 3.0), and digestive enzymes in the upper gastrointestinal (GI) tract.
Therefore, HAV is easily spread within a population. Fecally contaminated water or
food is a significant mode of transmission.
16,17 Children are considered a relatively
common reservoir, but rarely exhibit clinical symptoms.
In 2014, the overall incidence rate of HAV infection was 0.4 cases per 100,000
population in the United States.
19 HAV infection could occur from common-source
water supplies, waterborne outbreaks of HAV are uncommon.
vaccination was recommended for persons at high risk of infection and children
living in communities at high risk. However, due to the significant number of cases of
HAV disease still occurring in the United States, HAV vaccination recommendations
have expanded. In 2006, the Advisory Committee on Immunization Practices (ACIP)
recommended routine vaccination for all children aged 12 to 23 months in the United
Exceedingly rare causes of HAV include transfusion of blood or blood products
collected from donors during the viremic phase of their infection and from contact
with experimentally infected nonhuman primates.
16,21 Percutaneous transmission is
rare because no asymptomatic carrier state for HAV exists and the incubation period
16 Occupations at risk for HAV infection include sewage workers, hospital
cleaning personnel, day-care staff, and pediatric nurses.
preventable (e.g., vaccination) infection in travelers visiting locations with poor
Although the exact mechanism of injury is unknown,
17,23,24 viral replication occurs
within the liver, or hepatocytes. Subsequent hepatocyte death results in viral
elimination and eventual resolution of the clinical illness.
After exposure to HAV, usually via ingestion of HAV from material contaminated
with feces, the virus resides and replicates in the hepatocytes within hours or days
after infection. Following the translational and replication processes, HAV is
released into the bile canaliculi and is transported to the intestine, where it is
excreted in the feces at concentrations ranging up to 10
17 This occurs during the subclinical stage (incubation period) or anicteric
prodromal period (14–21 days) of the infection before alanine aminotransferase
(ALT) levels become elevated and clinical symptoms or jaundice occurs.
contagiousness of the infection is highest during this period and is significantly
reduced following the onset of symptoms or jaundice. HAV infection could occur in
two clinical courses varying from subclinical hepatitis (asymptomatic), usually
observed in children, to anicteric hepatitis (symptoms without jaundice) or icteric
hepatitis that occurs in adults and could result in fulminant hepatitis and death,
especially among adults older than 50 years.
18 Chronic HAV infection usually does
not manifest because of the robust humoral and cellular immune responses,
particularly natural killer cells, CD4
humoral immunity plays a pivotal role in viral clearance leading to viremia declines
after the presence of neutralizing antibodies.
25 Typically, the course of HAV includes
an incubation phase, an acute hepatitis phase, and a convalescent phase. Complete
clinical recovery is usually seen in all patients within 6 months after HAV infection.
jaundice of his eyes and skin and sought medical attention.
diazepam 5 mg at bedtime (HS) as needed (PRN) for “muscle spasms,” but he has not taken diazepam for
admission, for which he takes phenytoin 400 mg PO every HS.
tender, enlarged liver and right upper quadrant pain. Laboratory tests reveal the following values:
White blood cell (WBC) count: 5,500 cells/μL
Aspartate transaminase (AST): 120 units/L
Alanine aminotransferase (ALT): 240 units/L
Alkaline phosphatase: 86 units/L
Phenytoin concentration: 12 mg/L (normal: 10–20 mg/L)
The incubation period for HAV is 15 to 50 days (average 28 days) after
inoculation. The host is usually asymptomatic during this stage of the infection; thus,
E.T. is beyond the inoculation phase of the disease. Because HAV titers are highest
in the acute-phase fecal samples, the period of infectivity is 14 and 21 days, before
the onset of jaundice, to 7 or 8 days after jaundice. Therefore, E.T. should be
considered infectious at this time. In HAV infections, acute-phase serum and saliva
are less infectious than fecal samples, whereas urine and semen samples are not
infectious. Family members and persons recently in immediate contact with E.T.
The symptoms of acute viral hepatitis caused by HAV, HBV, HCV, HDV, and
HEV are similar. The onset of symptoms in HAV infection, however, is less
insidious than those seen with HBV and HCV infection.
HAV infection present a week or more before the onset of jaundice. The likelihood
of having symptoms is related to age. In children younger than 6 years of age, 70% of
infections are asymptomatic, whereas older children and adults have symptomatic
disease with jaundice occurring in more than 70% of cases.
symptoms of acute HAV infection, including the nonspecific prodromal symptoms of
fatigue, weakness, anorexia, nausea, and vomiting. Abdominal pain and
hepatomegaly are common. Less common symptoms include fever, headache,
arthralgias, myalgias, and diarrhea. Within 1 to 2 weeks of the onset of prodromal
symptoms, patients may enter an icteric phase with symptoms, including clay-colored
stools, dark urine, scleral icterus, and jaundice. The dark urine is caused by
bilirubin, generally occurring shortly before the onset of jaundice. E.T. should be
questioned about the presence of pale stools (light gray or yellow), which usually is
observed during the icteric phase. His scleral icterus is strongly suggestive of viral
hepatitis. Icteric infections usually occur in adults and are 3.5 times more common
than the nonicteric presentation that is seen in children.
The results of E.T.’s liver function tests (e.g., elevations in AST, ALT, and total
bilirubin) also are consistent with viral hepatitis. Serum transaminase concentrations
increase during the prodromal phase (usually ALT > AST) of HAV infection, peaking
before the onset of jaundice. These concentrations are often greater than 500 units/L
and decline at an initial rate of 75%/week, followed by a slower rate of decline
thereafter. Serum bilirubin peaks after aminotransferase activity and rarely exceeds
10 mg/dL. Total bilirubin levels decline more slowly than aminotransferases and
generally normalize within 3 months. Right upper quadrant tenderness, mild liver
enlargement, and splenomegaly may also be present in patients with acute HAV
With the appearance of jaundice, prodromal pruritus and extrahepatic
manifestations can occur, usually in patients with a more protracted illness. E.T.
should be monitored for additional manifestations of HAV infection, including
immune complex-associated rash, leukocytoclastic vasculitis, glomerulonephritis,
cryoglobulinemia (less likely than with HCV), and arthritis.
Diagnostic methods for detecting HAV antigen and anti-HAV are listed in Figure 80-
1. Detection of IgM antibodies to HAV in a patient who presents with clinical
characteristics of hepatitis, or in an asymptomatic patient with elevated
transaminases, is consistent with acute HAV infection. HAV IgG appears after IgM
and is indicative of previous exposure and immunity to HAV, whereas a rising IgG is
consistent with recent exposure.
5,26 Anti-HAV IgM is commonly present throughout
the disease course (16–40 weeks), usually peaking early and declining to
undetectable levels 3 to 4 months after the initial infection.
infected with HAV have IgM present for up to 6 months and occasionally longer.
HAV IgG appears early in the convalescent phase and is detectable for decades after
the acute infection resolves, with a slowly declining titer.
immunosorbent assay (ELISA) and radioimmunoassay methods of antibody detection
are sensitive, specific, and reliable to diagnose acute HAV infection. E.T. has a
positive IgM anti-HAV, consistent with acute HAV infection. He has a negative IgM
anti-HBc test, ruling out acute HBV infection.
HAV infection is usually a self-limiting disease and rarely leads to serious
complications including fulminant liver failure and death.
supportive care and medical treatment of serious complications. Intravenous (IV)
fluid and electrolyte replacement, nutritional support, and the use of antiemetics may
be necessary for some patients. Antipyretics (acetaminophen) should not be used
because the risk of fulminant hepatic failure (FHF) could increase. Considering that
hemolysis or acute kidney injury is possible, a regular assessment of renal function
with a complete blood count (CBC) should be performed. Patients should abstain
from alcohol during the acute phase of the disease. After resolution of symptoms and
serum biochemical abnormalities, moderate alcohol intake is no longer
contraindicated. In general, prognosis after HAV infection is very good. Long-term
immunity accompanies HAV infection, and recurrence or chronic hepatitis usually
Adjustment of Medication Doses
Dosage adjustments for hepatically eliminated drugs in the setting of liver disease
are difficult to predict. This is because hepatic metabolism is complex, involving
numerous oxidative and conjugative pathways that are variably affected in hepatic
disease. In renal disease, creatinine serves as an endogenous marker to predict the
clearance of renally eliminated drugs. In hepatic disease, however, no reliable
endogenous markers exist to predict drug hepatic clearance. Laboratory tests that
approximate the synthetic function of the liver (e.g., albumin, PT) and biliary
clearance (bilirubin) are used to estimate the degree of hepatic impairment, but these
tests are not dependable in predicting alterations in pharmacokinetic parameters for
hepatically metabolized drugs. Unnecessary and potentially hepatotoxic medications
should be avoided during the acute phase of the illness. When drug therapy is
indicated with agents that undergo hepatic elimination, it is prudent to use the lowest
doses possible to achieve the desired therapeutic effect.
E.T. should be advised to discontinue diazepam because this medication
undergoes extensive hepatic biotransformation and limited data suggest this agent
accumulates in the setting of acute viral hepatitis.
therapy for muscle spasms, he should either decrease the diazepam dose or consider
using an alternative agent (e.g., lorazepam) that does not accumulate in acute viral
29 Patients with acute viral hepatitis do not require phenytoin dosage
30 Because E.T.’s plasma phenytoin concentration is within the desired
therapeutic range, no dosage adjustment is needed.
Prevention of hepatitis A infection can be achieved through immunoprophylactic
measures. Immunoprophylaxis may be passive, active, or a combination of both. I
passive immunization, temporary protective antibody in the form of immunoglobulin
is administered. In active immunization, a vaccine is administered to induce the
formation of protective antibody.
3 months from now and wonders whether he should receive prophylaxis for HAV.
Before hepatitis A vaccine was available, the only therapy for pre-exposure
prophylaxis of hepatitis A infection was immunoglobulin. Although passive
immunization with immunoglobulin alone is highly effective in preventing HAV
the duration of protection is short. When used for pre-exposure
prophylaxis (e.g., in travelers who are allergic to a vaccine component or decide
against vaccination), a dose of 0.02 mL/kg of immunoglobulin administered
intramuscularly (IM) confers protection for less than 3 months, and an IM dose of
0.06 mL/kg confers protection for 5 months or longer.
Recommended Doses of Hepatitis A Vaccines
Age at Vaccination Dose (Volume)
Children 12 months–18 years 720 ELISA units (0.5 mL) 0, 6–12
Adults >19 years 1,440 ELISA units (1.0 mL) 0, 6–12
Children 12 months–18 years 25 units (0.5 mL) 0, 6–18
Adults >19 years 50 units (1.0 mL) 0, 6
aEnzyme-linked immunosorbent assay (ELISA) units.
Active immunization with hepatitis A vaccine has largely supplanted the use of
immunoglobulin for pre-exposure prophylaxis of infection caused by HAV. Two
types of the inactivated, monovalent hepatitis A vaccines are available in the United
States and globally: Havrix and Vaqta. Both vaccines are formalin-inactivated
preparations of attenuated HAV strains.
32 The manufacturers use differing units to
express antigen content of their respective vaccines. Havrix dosages are expressed in
ELISA units, and Vaqta dosages are expressed as units of hepatitis A antigen. These
vaccines are developed to provide long-term immunity. They are free of thimerosal
and mercury as preservatives and are safe and effective for children and adults.
Havrix is available in two formulations that differ according to age: for persons 12
months to 18 years of age, 720 ELISA units (0.5 mL)/dose in a two-dose schedule;
and for persons 19 years and older, 1,440 ELISA units (1.0 mL)/dose in a two-dose
27,31,32 Havrix is injected IM into the deltoid muscle with a
booster dose administered 6 to 12 months later. The pediatric Havrix formulation
(three-dose schedule) is no longer available. Vaqta is available in two formulations
that differ according to the person’s age: for persons 12 months to 18 years of age, 25
units (0.5 mL) in a two-dose schedule; and for persons 19 years and older, 50 units
(1.0 mL) per dose in a two-dose schedule (Table 80-2).
27,31,32 Likewise, this vaccine
is injected IM into the deltoid muscle with a booster dose administered 6 to 18
The US Food and Drug Administration (FDA) has also licensed a combined HAV
and HBV vaccine (Twinrix) for use in persons aged 18 years and older. Twinrix is
composed of the same antigenic components used in Havrix and Engerix-B. Each
dose of Twinrix contains at least 720 ELISA units of inactivated HAV and 20 mcg of
34,35 Twinrix does not contain thimerosal and mercury as
preservatives and is safe and effective for children and adults.
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