form of liver disease characterized by inflammation of the liver
due to infection with the hepatitis E virus (HEV). Usually a
mild disease, hepatitis E but can in rare cases prove fatal,
particularly in pregnant women.
HEV is transmitted via food or
drink that has been handled by an infected person, or through
infected water supplies in areas where fecal matter may get into
the water. Consumption of uncooked deer meat is important risk
factor for infection with HEV in Japan. Hepatitis E is rare in
the US and Canada. It is more common in tropical and subtropical
regions of the world.
The finding of anti-HEV antibodies in blood is evidence for
prior infection with HEV. There is currently no vaccine or
treatment for hepatitis E, although anti-viral drugs may be
Hepatitis E disease occur in both
sporadic and epidemic forms and is primarily associated with the
ingestion of faecally contaminated drinking water. Little
secondary household transmission has been documented to occur
unlike HAV. Hepatitis E was first documented in New Delhi in
1955 when 29000 cases of icteric hepatitis occurred following
the contamination of the city's drinking water. Several other
large epidemics have occurred since in the Indian subcontinent
and the USSR;
The Delhi Epidemic 1955-56
Ahmedaban, India 1975-76
Pune, India 1978
Tashkent, USSR 1983
were originally thought to be due to HAV but retrospective
analysis of stored serum identified HEV as the causative agent.
Epidemics have also been reported from parts of China, Africa
and Mexico. Sporadic cases predominantly occur in the Indian
subcontinent. One notable feature of hepatitis E is the
relatively low incidence of clinical disease in case contacts.
For example, only 2.4% of household contacts of HE cases
developed clinical illness during the 1981-82 epidemic in
Kathmandu Valley, whereas the secondary attack rate for HAV was
10 to 20% among household contacts in the same region.
HEV has a slightly longer
incubation period than HAV (2-9 weeks, mean = 6 weeks) Like HAV,
the disease is usually self-limiting. The clinical attack rate
is from 0.7 to 10%. Virus particles are present in the faeces
just before the onset of jaundice and the appearance of
antibodies. The particles are 27- 30 nm. There is a good animal
model available. Various strains of HEV had been isolated in
different primates. A particular strain may produce disease in
one type of animal but not another. Therefore, different strains
appears to have different host susceptibilities. However,
cross-protection can be demonstrated between different strains.
Therefore, the antigen responsible for producing neutralizing
antibodies appears to be the similar.
Clinically, the disease is similar
to hepatitis A, but carried a higher mortality, especially
amongst pregnant women. HAV has a mortality of 0.1 - 0.2%, in
contrast with HEV which carries a mortality of 1-2%. In pregnant
women, the case-fatality rate can be as high as 10-20%. The case
fatality of HAV for pregnant women is the same as in the general
population. The highest attack rate occurred among the 15 - 40
age group. Hepatitis E Accounts for 12-50% of clinical hepatitis
in the Indian subcontinent.
Certain questions about the virus
remains unanswered, Firstly, why should those aged between 15-40
should be predominantly affected. This implies that infection
either occurs sub clinically or not at all in younger
individuals. This is supported by a study carried out in Kenya
during an investigation of an HEV outbreak among refugees. Also
why should the disease carry a higher mortality amongst pregnant
women which is not the case with HAV and HBV. The unexpected
high mortality rate in HE-infected pregnant women may reflect a
unique feature of viral replication and pathogenesis of disease
in these women. Indigenous immunoglobulin had been reported to
be of use in the prophylaxis against hepatitis E.
Commercial assays are becoming available for the detection of
IgG using recombinant antigens and synthetic polypeptides. The
sensitivity and specificity of these assays are highly
questionable as they tend to give a high seropositive rate eg.
there is a seropositive rate of 2% in the US eventhough there
had not been any reported cases of hepatitis E in the US. The
IgM response is unreliable and is thought to only occur in 50%
Causes and Symptoms
There are at least two strains of
HEV, one found in Asia and another in Mexico. The virus may
start dividing in the gastrointestinal tract, but it grows
mostly in the liver. After an incubation period (the time from
when a person is first infected by a virus until the appearance
of the earliest symptoms) of two to eight weeks, infected
persons develop fever, may feel nauseous, lose their appetite,
and often have discomfort or actual pain in the right upper part
of the abdomen where the liver is located. Some develop
yellowing of the skin and the whites of the eyes (jaundice).
Most often the illness is mild and disappears within a few weeks
with no lasting effects. Children younger than 14 years and
persons over age 50 seldom have jaundice or show other clinical
signs of hepatitis.
Hepatitis E never becomes a
chronic (long-lasting) illness, but on rare occasions the acute
illness damages and destroys so many liver cells that the liver
can no longer function. This is called fulminant liver failure,
and may cause death. Pregnant women are at much higher risk of
dying from fulminant liver failure; this increased risk is not
true of any other type of viral hepatitis. The great majority of
patients who recover from acute infection do not continue to
carry HEV and cannot pass on the infection to others.
Symptoms of Hepatitis E
Symptoms of hepatitis E do not
occur in everyone who has the disease. If they do occur,
hepatitis E symptoms usually appear abruptly and go away within
a couple of weeks. Symptoms may include:
In a number of people, these
symptoms may be confused with stomach flu symptoms, especially
in the early stages.
Pregnant women (especially those
in their third trimester) appear to be exceptionally susceptible
to severe disease.
HEV can be found by
microscopically examining a stool sample, but this is not a
reliable test, as the virus often dies when stored for a short
time. Like other hepatitis viruses, HEV stimulates the body's
immune system to produce a substance called an antibody, which
can swallow up and destroy the virus. Blood tests can determine
elevated antibody levels, which indicate the presence of HEV
virus in the body. Unfortunately, such antibody blood tests are
not widely available.
Most attempts to use blood serum
containing HEV antibody to prevent hepatitis in those exposed to
HEV have failed. Hopefully, this approach can be made to work so
that pregnant women living in endemic areas can be protected. No
vaccine is available, though several are being tested. It also
is possible that effective anti-viral drugs will be found. The
best ways to prevent hepatitis E are to provide safe drinking
water and take precautions to use sterilized water and beverages
How Is Hepatitis E Spread?
Hepatitis E transmission typically
occurs through what is known as "fecal-oral transmission. “If an
puts something in the mouth that
has been contaminated with the stool of an infected person (even
if it looks clean), infection can occur.
Most infections result from contamination of water supplies,
such as after monsoon flooding. Unlike hepatitis A (which is
also spread through the fecal-oral route), transmission of the
hepatitis E virus rarely occurs through contact with a household
member or sex partner who has been infected. Casual contact --
as in the usual office, factory, or school setting -- does not
spread the virus.
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