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Key facts
Hepaii s E is a viral liver disease that can cause mild to severe illness.
It is spread by faecal-oral (or stool to mouth) transmission when a person ingests food
or drink contaminated by an infected person’s stool.
The disease is closely associated with poor sanitai on and a lack of personal hygiene
habits, such as hand-washing.
There are an esi mated 14 million symptomai c cases of hepaii s E worldwide; 300 000
deaths and 5200 si llbirths occur annually.
Epidemics can grow rapidly and with high mortality among pregnant women.
There is evidence of foodborne transmission of hepaii s E.
Improved sanitai on is the most eff eci ve way to combat the disease.
There is no commercially available vaccine for this infeci on.
Hepaii s E (HEV) was not recognized as a disi nct human disease uni l 1980. Hepaii s E is caused by infeci on with the hepaii s E virus, a non-enveloped, posii ve-sense, single-stranded RNA virus. Four genotype, 1, 2, 3 and 4 been recognized for HEV. Each HEV genotype appears to have a specifi c geographic distribui on. Genotype 1 HEV has been isolated from human cases of epidemic and sporadic hepaii s E in parts of Asia and Africa, where the disease is highly endemic. Genotype 2 sequences, fi rst reported from an outbreak of hepaii s E in Mexico, have subsequently been reported from cases in western Africa. Genotype 3 HEV, fi rst idenifi ed in a few rare cases of locally-acquired hepaii s E in the United States has subsequently been reported from human cases in several industrialized countries in Europe as well as in Asia and Pacifi c, Genotype 4 HEV has been found in sporadic cases with acute hepaii s from China, Taiwan, Japan and Vietnam. All genotypes share at least one major serologically cross-reaci ve epitope and belong to a single serotype. Genotype 3 and 4 isolates of HEV appear to be somewhat less pathogenic in humans than those from genotypes 1 and 2.
Although man is considered the natural host for HEV, ani bodies to HEV or closely-related viruses have been detected in primates and several other animal species.
How is HEV transmitted?
HEV is transmit ed via the faecal-oral route. Hepaii s E is a waterborne disease, and contaminated water or food supplies have been implicated in major outbreaks. Consumpi on of faecal-contaminated drinking water has given rise to epidemics, and the ingesi on of raw or uncooked shellfi sh has been the source of sporadic cases in endemic areas. There is a possibility of zoonoi c spread of the virus, since several non-human primates, pigs, cows, sheep, goats and rodents are suscepi ble to infeci on. The risk factors for HEV infeci on are related poor sanitai on in large areas of the world, and HEV shedding in feces.
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Person-to-person transmission is uncommon. There is no evidence for sexual transmission or for transmission by transfusion.
Where is HEV a problem?
The highest rates of infeci on occur in regions where low standards of sanitai on promote the transmission of the virus. Epidemics of hepaii s E have been reported in Central and South-East Asia, North and West Africa, and in Mexico, especially where faecal contaminai on of drinking water is common. However, sporadic cases of hepaii s E have also been reported elsewhere and serological surveys suggest a global distribui on of strains of hepaii s E.
When is a HEV infection life-threatening?
In general, hepaii s E is a self-limii ng viral infeci on followed by recovery. Prolonged viraemia or faecal shedding are unusual and chronic infeci on does not occur.
Occasionally, a fulminant form of hepaii s develops, with overall pai ent populai on mortality rates ranging between 0.5% - 4.0%. Fulminate hepaii s occurs more frequently in pregnancy and regularly induces a mortality rate of 20% among pregnant women in the third trimester. There is evidence that acute HEV in persons with chronic HBV or HCV infeci ons could have severe hepaii s and liver funci on failure.
The disease
The incubai on period following exposure to HEV ranges from 3 to 8 weeks, with a mean of 40 days. The period of communicability is unknown. There are no chronic infeci ons reported.
Hepaii s E virus causes acute sporadic and epidemic viral hepaii s. Symptomai c HEV infeci on is most common in young adults aged 15 – 40 years. Although HEV infeci on is frequent in children, it is mostly asymptomai c or causes a very mild illness without jaundice (anicteric) that goes undiagnosed.
Typical signs and symptoms of hepaii s include jaundice (yellow discolourai on of the skin and sclera of the eyes, dark urine and pale stools), anorexia (loss of appei te), an enlarged, tender liver (hepatomegaly), abdominal pain and tenderness, nausea and vomii ng, and fever, although the disease may range in severity from subclinical to fulminant.
Diagnosis
Since cases of hepaii s E are not clinically disi nguishable from other types of acute viral hepaii s, diagnosis is made by blood tests which detect elevated ani body levels of specifi c ani bodies to hepaii s E in the body or by reverse transcriptase polymerase chain reaci on (RT-PCR). Unfortunately, such tests are not widely available.
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provision of safe drinking water and proper disposal of sanitary waste;
monitoring of disease incidence;
determination of source of infection and mode of transmission by epidemiologic
At present, no commercially available vaccine exists for the preveni on of hepaii s E. However, several studies for the development of an eff eci ve vaccine against hepaii s E are in progress.
Prevention
As almost all HEV infeci ons are spread by the faecal-oral route, good personal hygiene, high quality standards for public water supplies and proper disposal of sanitary waste have resulted in a low prevalence of HEV infeci ons in many well developed sociei es.
For travelers to highly endemic areas, the usual elementary food hygiene precaui ons are recommended. These include avoiding drinking water and/or ice of unknown purity and eai ng uncooked shellfi sh, uncooked fruits or vegetables that are not peeled or prepared by the traveler.
Treatment
Hepaii s E is a viral disease, and as such, ani bioi cs are of no value in the treatment of the infeci on. There is no hyper immune E globulin available for pre- or post-exposure prophylaxis. HEV infeci ons are usually self-limited, and hospitalizai on is generally not required. No available therapy is capable of altering the course of acute infeci on.
As no specifi c therapy is capable of altering the course of acute hepaii s E infeci on, preveni on is the most eff eci ve approach against the disease. Hospitalizai on is required for fulminant hepaii s and should be considered for infected pregnant women.
Guidelines for epidemic measures
Determinai on of the mode of transmission. Idenifi cai on of the populai on exposed to increased risk of infeci on.
Eliminai on of a common source of infeci on.
Improvement of sanitary and hygienic praci ces to eliminate faecal contaminai on of food and
