How Viral Hepatitis Spreads

Hepatitis A
Hepatitis A virus is found in the feces of infected persons. It is usually spread from
person to person by ingesting food or water contaminated with fecal matter.
Hepatitis A virus can be transmitted through:

Drinking contaminated water.

Being in close contact with an infected person.

Eating food that was handled by a person with the virus, who did not carefully
wash their hands after using the bathroom.

Hepatitis B
Unfortunately, hepatitis B often has a stigma attached to it because it can be
contracted through socially unaccepted behavior, such as injecting illegal drugs or
engaging in unprotected sex.
However, many people do not realize that, most of the time, a person infected with
hepatitis B is an innocent victim who has encountered the virus through:

Birth, when his or her mother who was infected with hepatitis B passed the
virus on. (Most common)

A transfusion with blood that has not been screened for the hepatitis B virus
(HBV).

Direct contact with blood from an open wound.

Sharing contaminated toothbrushes or razors.

Improperly cleaned tattooing needles.

Improperly cleaned medical or dental tools.

It is important to note that most people who are infected with hepatitis B have no
symptoms, yet they can still transmit the disease and are at risk of developing liver
cancer.

Hepatitis C
The mode of transmission for hepatitis C is similar to hepatitis B, however, there are
a few differences. Hepatitis C virus is spread through:

Blood transfusions and organ transplants that have not been screened for
hepatitis C.

Sharing of needles during injected drug use.

Birth: a small number infected mother can pass the virus to her baby.

Sexual contact: very rarely, hepatitis C can be spread through sex.

Misconceptions
Many misconceptions exist about hepatitis B and C, especially regarding the way in
which it spreads. Hepatitis B and C cannot be transmitted by:

Food or water (however, hepatitis A can be transmitted in this manner).

Casual contact, such as hugging, shaking hands or kissing.

Sneezing or coughing.

Breastfeeding.

What Is Hepatitis?
The Liver
Your liver is the largest organ in your body and plays an essential role in regulating
life processes. It performs many vital functions such as:

Converting food into chemicals for life and growth

Detoxifying and removing substances poisonous to the body

Manufacturing important substances needed by the rest of the body

You simply cannot live without your liver.

Hepatitis
Hepatitis is inflammation of the liver. It may occur with limited or no
symptoms but sometimes leads to fever and jaundicea yellowish tint to the skin,

eyeballs and urine that is caused by a build-up of bile in the body. The three main
forms of hepatitiscalled A, B and Care all caused by a virus.
According to the Center for Disease Control, viral hepatitis is the leading cause of
liver cancer and the most common reason for liver transplantation. In the United
States, an estimated 1.2 million Americans are living with chronic hepatitis B and 3.2
are living with chronic hepatitis C. Many do not know they are infected. Each year an
estimated 25,000 persons become infected with Hepatitis A; 43,000 with hepatitis B,
and 17,000 with hepatitis C.
Acute Viral Hepatitis
Acute viral hepatitis is the inflammation of the liver caused by a hepatitis virus. In
most cases, the disease onsets suddenly and lasts only a few weeks. It can cause
anything from symptoms of the flu to fatal liver failure. The symptoms, if any,
usually develop quickly and may include: loss of appetite, nausea, fever, vomiting,
and abdominal pain. In most people, special treatment is not needed, however, people
with severe acute hepatitis may require hospitalization. People with acute viral
hepatitis usually recover in 4 to 8 weeks and should avoid alcohol until they have
fully recovered.
Chronic Viral Hepatitis
Chronic viral hepatitis is the inflammation of the liver caused by a virus that lasts at
least 6 months. For most people, there are usually no symptoms until serious liver
damage has developed. If symptoms manifest, they often include fatigue, poor
appetite, and abdominal discomfort. Chronic viral hepatitis is most commonly caused
by hepatitis B and hepatitis C virus and can lead to complications such as cirrhosis,
liver failure, and liver cancer if left unmonitored and/or treated.
Different Types of Hepatitis
Viral Hepatitis
Hepatitis A is caused by the hepatitis A virus and is usually transmitted through
contaminated food or water. Typically, hepatitis A has milder symptoms than hepatitis

B or C. Illness from hepatitis A is usually brief, and infection with the virus does not
lead to chronic liver disease or liver cancer.
Hepatitis B is caused by the hepatitis B virus and is usually transmitted through the
blood of another person with hepatitis B or from mother to child during birth. There
are usually no symptoms until there are serious liver complications. When symptoms
do appear, they may include high fever, jaundice and abdominal pain. Untreated
chronic hepatitis B can lead to cirrhosis and/or liver cancer.
Hepatitis C is also passed on through contaminated blood and is caused by the
hepatitis C virus. Infection with the hepatitis C virus is the number-one reason for
liver transplant in the U.S. Unlike hepatitis A and B, there is no vaccine to prevent
hepatitis C.
Alcoholic Hepatitis
Alcoholic hepatitis is the inflammation of the liver caused by the long-term heavy
intake of alcohol. Symptoms include enlargement of the liver, development of fluids
in the abdomen, and elevation of liver enzymes. Alcoholic hepatitis can progress to
cirrhosis if heavy alcohol use continues.
Autoimmune Hepatitis
Autoimmune hepatitis is the inflammation of the liver resulting from the body's own
immune system attacking the liver. This disease is chronic and usually has very minor
symptoms. When symptoms do occur, it usually includes fatigue, abdominal
discomfort, itching, jaundice, enlarged liver, and nausea. If left untreated,
automimmune hepatitis can lead to cirrhosis and liver failure.
Non-alcoholic Fatty Liver Disease
Non-alcoholic fatty liver disease occurs in people with fatty liver who have no history
of alcohol use. Symptoms may include fatigue, pain in the upper right abdomen, and
weight loss. In the most severe cases, non-alocholic fatty liver disease can progress to
liver failure.
http://www.asianpacificlivercenter.org/hepatitis/Pages/Is_There_a_Vaccine.aspx

Discussion
Epidemiology of Hepatitis A Infection
Hepatitis A virus (HAV) is the leading cause of acute viral hepatitis worldwide.
Indeed, in some developing areas of the world, HAV seropositivity is close
to 100%[1] . Overall, hepatitis A infection in the United States is much lower in
industrialized countries[2] . Data from 1988 to 1994 in the NHANES III (National
Health and Nutrition Examination Survey) revealed particularly high seroprevalence
rates in the United States among poor, immigrant, and Latino populations[3] . In more
recent surveillance data, the most frequent risk for HAV infection was travel outside
the United States or Canada[4] . In the United States, HAV causes approximately
45% of all cases of acute viral hepatitis and 12% of all cases of acute liver failure[5] .
The incidence of HAV in the United States has declined more than 90% since the
availability of the hepatitis A vaccine in 1995. In 2010, the Centers for Disease
Control and Prevention (CDC) received 1,670 reported cases of acute symptomatic
hepatitis A infection and this represented the lowest number of cases per year
ever reported[6] . The CDC estimates that the actual numbers of symptomatic acute
HAV infections and total new infections in 2010 were 7,000 and 17,000, respectively.
Transmission, and Risk Factors
Hepatitis A virus is primarily transmitted via the fecal-oral route and is most
commonly acquired via ingestion of contaminated food or during sexual activity[1] .
Food can be contaminated at the time of harvesting, packaging, or meal preparation,
and multi-state outbreaks have been associated with ingestion of fresh and frozen
produce. Undercooked bivalves have also been implicated in hepatitis A outbreaks.
Although transmission of HAV can occur through serum, blood products in the
United States do not routinely undergo screening for HAV because transfusion-related
hepatitis A infection rarely occurs. This low transmission rate is attributed to the

virus' short incubation period and exclusion of patients with jaundice from blood
donation. Vertical transmission is exceedingly rare. In the United States, the leading
three risk factors for hepatitis A infection are (1) sexual or household contact, (2)
international travel and (3) male-male sexual activity (Figure 1)[2] . In a more recent
population-based surveillance study conducted during 2005 to 2007, the reported risk
factors for HAV acquisition were international travel (48.5%), contact with a case
(14.8%), employee or child in a day care center (7.6%), exposure to food or
waterborne common-source outbreak (7.3%), illicit drug use (4.3%), and men who
have sex with men (3.9%)[4] . Although needle sharing is likely responsible for
transmission in some instances among injection drug users, poor hygiene, with
resultant fecal-oral transmission, may play a role in the passage of hepatitis A among
injection-drug users[7] . Children and employees at daycare facilities (and their
contacts) are at higher risk for hepatitis A. No risk factor is identified in more than
30% of cases.
Clinical Course
The incubation phase lasts from 2 to 7 weeks (mean 28-30 days). Prodromal
symptoms are non-specific and often include anorexia, fever, nausea, and malaise
(Figure 2). Jaundice typically appears within 1 week after symptom onset and occurs
in 70 to 80% of the adult population, but in less than 10% of children younger than 6
years of age. Bilirubinuria may precede jaundice by a few days and dark urine is a
common presenting complaint. Jaundice and hepatomegaly are the most commonly
observed

physical

examination

abnormalities(Figure

3)[8] .

Extra-hepatic

manifestations may occur, but with less frequency than that observed in hepatitis B or
C (Figure 4). The acute illness can be disabling; patients missed an average of 9 days
of work in one food-borne outbreak[9] and 12 days in another outbreak that involved
homosexual men[10] . After the onset of jaundice, most constitutional symptoms
abate quickly, although some patients complain of residual fatigue for several weeks.

Jaundice typically resolves within two weeks[11] . Most cases of hepatitis A are selflimited, and 85% of people show complete resolution of symptoms by 3 months[8] .
Hepatitis A carries no risk for chronic hepatitis. Less common presentations of
hepatitis A include cholestatic hepatitis, relapsing hepatitis, and acute hepatic failure.
In recent years, fewer than 100 HAV-related deaths per year have been reported[6] .
In rare instances, hepatitis A infection may trigger autoimmunehepatitis[12] .
Relapsing Hepatitis A
Hepatitis A infection relapses in approximately 5 to 10% of cases (range 1.5 to 20%),
typically within several weeks after apparent resolution of the original illness[1,13] .
The severity of the relapse is variable and often resembles the initial presentation with
manifestations that can include jaundice, elevated hepatic aminotransferase levels,
and fecal shedding of the virus. Patients with relapse may have a greater risk of
developing either short-term cholestasis[1] or immune-related manifestations, such
as purpura, arthralgias, and nephritis[13] . Nevertheless, patients with relapsing
hepatitis A infection should generally expect a full recovery. A review of several cases
of relapsing hepatitis A suggested steroids may expedite recovery[13] . The existing
published case series have involved too few patients to accurately identify risk factors
for relapse. Available data suggest that multiple relapses appear to be highly unusual,
but may be more common in children[14] .
Cholestatic Hepatitis A
Cholestatic hepatitis A occurs in fewer than 10% of cases and is characterized by
serum bilirubin greater than 10 mg/dL and a prolonged period of jaundice (usually
greater than 12 weeks)[8] . Surprisingly, serum alkaline phosphatase is usually
normal or only slightly elevated in patients with cholestatic hepatitis A infection[14] .
In many cases, patients may experience a protracted clinical illness with pruritis,
nausea, diarrhea, or malabsorption[1] . Most experts recommended treating

cholestatic hepatitis A infection with oral prednisone at 40 mg/day, followed by a

slow 4 week taper[15] . A marked decline in serum bilirubin typically occurs within
several days of initiating corticosteroid treatment. In general, patients with a
prolonged period of jaundice and serologic evidence of acute hepatitis A do not
require an invasive work-up for jaundice; an abdominal ultrasound to exclude biliary
obstruction should suffice.
Acute Liver Failure and Mortality
Acute liver failure associated with hepatitis A infection infrequently develops, but has
profound clinical importance when it does occur. The most widely accepted criteria
for the diagnosis of acute liver failure consists of (1) evidence of a coagulation
abnormality (prolongation in prothrombin time by 4 to 6 seconds or an INR greater
than or equal to 1.5); (2) any degree of altered sensorium; (3) no history of
preexisting cirrhosis; and (4) a duration of illness less than 26 weeks[16] . The term
acute liver failure is often used interchangeably with the terms fulminant hepatitis or
fulminant hepatic failure, but the term acute liver failure is preferred. Patients with
acute liver failure should be hospitalized and managed in an intensive care unit;
moreover, the medical facility should have the capacity to perform liver
transplantation. Among cases of HAV infection reported to the CDC in 2002, 25%
were hospitalized[2] . In 2010, among the 1670 reported cases of acute HSV,
approximately 1% died[6] . These CDC statistics (involving reported cases) probably
vastly overestimate the true hospitalization and death rates when considering all
patients with hepatitis A, since many patients with mild disease either remain
undiagnosed or do not get reported. A recent review of hepatitis A-related deaths in
California revealed an age-adjusted mortality of 1.2 deaths per 1 million
person years[17] . Fatality is unusual in children, and the risk increases significantly
in persons older than40[1,17] . Mortality rates appear to be greater among patients
with underlying liver disease, regardless of the cause[1] . Acute hepatic failure carries

a high mortality rate, as only 35 to 40% of patients with acute hepatic failure caused
by HAV infection will recoverspontaneously[18,19] . Since more than 65% of
patients

with

acute

liver

failure

from

hepatitis

A will

survive

after

livertransplantation[14] , these patients with acute hepatic failure should receive an

expedited evaluation for potential liver transplantation as soon as possible after
presentation.
Laboratory Findings and Diagnosis of Acute HAV
Soon after inoculation, HAV is carried via the bloodstream to the liver where it
replicates within hepatocytes. The virus is shed into the bile ducts and excreted in the
stool. Viremia and fecal shedding of the virus peak in the two weeks prior to the onset
of clinical symptoms (Figure 5). Fecal shedding of the virus likely continues for at
least a week after symptoms begin, and the period of shedding can be longer in
children (in some cases up to several months)[14] . Low-level viremia may persist for
18-30 days after the onset ofsymptoms[14] . Although PCR can detect HAV in blood
and stool, the technique is time-consuming, costly, and rarely used outside of the
research setting. Hepatocellular injury becomes evident by the marked elevation in
hepatic aminotransferase levels (often greater than 500 units/L) which peak shortly
after the prodromal period. After peaking, serum hepatic aminotransferase levels
decline by approximately 75% per week[11] . Serum bilirubin levels are also
elevated, but they do not usually exceed 10 g/dL. The decrease in serum bilirubin
levels typically lags behind the fall in serum hepatic aminotransferase levels[11] .
Serum IgM anti-HAV is almost always detectable at the onset of symptoms, and IgG
anti-HAV levels rise soon thereafter (Figure 5). Measurement of serum IgM antiHAV remains the diagnostic test of choice. In the setting of acute HAV infection, the
IgM anti-HAV has a sensitivity of nearly 100%, specificity of 99%, and a positive
predictive value of 88%[20] . Rarely, a patient with symptomatic early acute hepatitis
A will have a negative result, but a repeat test should become positive in 1-2 weeks.

The IgM levels characteristically peak before 3 months and gradually decline until
they become undetectable. The IgG levels, however, remain elevated and confer
lifelong immunity.
Monitoring and Treatment
Most experts would recommend that any patient with moderate to severe acute
hepatitis should have immediate measurement of prothrombin time (PT) with
international normalized ratio (INR) and should be evaluated for subtle signs of
encephalopathy, including lethargy or irritability[14,16] . If liver function is normal
or minimally abnormal, and there is no evidence for encephalopathy, patients and
their family members or caregiver should be counseled to monitor for changes in
sensorium, and close clinical follow-up should be arranged. There is no specific
antiviral therapy for acute hepatitis A infection. Most patients can be treated
symptomatically as an outpatient with laboratory and clinical follow-up. In general,
patients with acute HAV infection who do not develop acute liver failure will have
complete recovery without any permanent sequelae. For patients who present withor
develop more severe disease, including PT INR of 1.5 or greater, or significant
symptoms such as nausea and vomiting, hospitalization is usually required.
Hospitalization is mandatory for patients with acute liver failure (PT INR of 1.5 or
greater and encephalopathy); in this situation, the patient should be admitted to an
intensive care unit (ICU) and contact inititated with a liver transplantation center,
since patients with acute liver failure can rapidly deteriorate.
Tes Fungsi Hati pada Kelainan Hepatobilier
Jenis Kelainan Bilirubin
Aminotransf Alkaline
Albumin
erase

phosphatas
e

Prothrombin
Time

Hemolisis

N 5 U/L
85%

Normal

Normal

Normal

Normal

Normal

Normal

Biasanya

berhubungan

dengan

bilirubin

indirek.
Tidak
Hepatoselular

bilirubinuria.
Bilirubin direk dan Meningkat,

nekrosis akut indirek

(viral,

ada

mungkin biasanya

drug, meningkat

>500 IU

sampai

normal, jika >5x

penignkata

dibawah control
dan

hepatotoxin.

Peningkatan diikuti ALT>AST

AHF)

dengan peningkatan

normal.

>3x

tidak

dikoreksi dengan

aminotransferase

vitamin

Bilirubinuria

parenteral,
prognosis

Bilirubin direk dan Meningkat,

Normal

Hepatocellula

indirek

sampai >3x kan

prolonged

r Disorders

meningkat

peningkata

menurun

ketika dikoreksi

n normal.

dengan

Kebanya

K parenteral.
Kebanyakan

mungkin biasanya
<300 IU

Bilirubinuria
Alcoholic

Bilirubin direk dan AST:ALT >2 Normal

hepatitis

indirek

Cirrosis

meningkat

alcoholic

Bilirubinuria

hepatis

Kebanya

menjadi buruk.
Kebanyakan

Chronic

mungkin kemungkinan sampai >3x kan

sirosis.

peningkata
atau n normal.

fails

vitamin

prolonged

fails

menurun

ketika dikoreksi

dengan

vitamin

K parenteral.

Intra dan extra Bilirubin direk dan Normal

Meningkat,

Normal,

Normal,

hepatic

indirek

kebanyakan

kecuali

terjadi

kolestasis

meningkat

peningkatan

>4x

kronik

prolonged,

(obstructive

Bilirubinuria

sedang

peningkata

mungkin sampai

jaundice)

IU
Normal

Meningkat,

infiltratif

sampai

kebanyakan

(tumor,

sedikit

>4x

granulomata,

meningkat.

peningkata

partial

dikoreksi dengan

Jarang >500 n normal.

Penyakit

Biasanya normal.

bile

duct
obstruction)

n normal.

jika

vitamin
Normal

parenteral.
Normal.