Hepatitis E (ICD-10-GM B17.2: Acute viral hepatitis E) is an inflammation of the liver caused by the hepatitis E virus (HEV). Hepatitis E virus belongs to the group of RNA viruses. It used to be considered part of the family Caliciviridae, but is now considered to belong to the monotypic family Hepeviridae (genus Orthohepevirus). HEV genotypes 1-5 can be distinguished. Genotypes 1-4 are human pathogenic (“causing disease to humans”): HEV 1 and HEV 2 are mostly responsible for rice infection. HEV 3 and HEV 4 occur in humans and animals (especially pigs). Genotypes 5 and 6 occur only in wild boar in Japan.Recently, genotypes 5 and 6 have been detected in wild boar and genotypes 7 and 8 in camels. In Europe, North America, and Australia, most cases of hepatitis E are caused by HEV genotype 3, which is autochthonous (“indigenous”). In Asia and Africa, the main HEV genotypes encountered are 1 and 2, where humans are the only known reservoir. Natural reservoirs of the pathogen in animals are pigs (raw pork from domestic pigs), sheep, monkeys, rats, and mice. Recent studies have shown that the hepatitis E pathogen with genotype 3 is also widespread in German wild boar and deer (= zoonosis (animal disease)). The infestation rate is about 15%. The risk groups include above all hunters, forestry workers, pig breeders or slaughterhouse employees. Transmission here occurs through the consumption of contaminated pork and game meat. Occurrence: Hepatitis E occurs worldwide. Major epidemics have occurred primarily in Africa (North and West Africa), Asia, the Middle East, and Mexico – particularly in connection with flood disasters or in refugee camps. Recently, isolated cases of hepatitis E acquired in Germany have also been reported, especially with a chronic course. The incidence of hepatitis E is not subject to seasonal fluctuations. Transmission of the pathogen (route of infection) occurs by contact or smear infection (fecal-oral: infections in which pathogens excreted with feces (fecal) are ingested via the mouth (oral), e.g., through contaminated drinking water and/or contaminated food with HEV genotypes 1 and 2): In this case, zoonotic transmission mainly occurs via consumption of inadequately cooked pork or game meat and products made from them. Filter-feeding organisms (e.g., mussels) can accumulate HEV found in water and thus also serve as a source of infection. The virus can also be transmitted parenterally (e.g., through contaminated blood products). Human-to-human transmission (e.g., among household members) is possible in travel-associated HEV-1 and -2 infections through contact transmission (smear infection). However, HEV-3 infections acquired in Germany appear to be only extremely rarely (if ever) directly transmissible from person to personRisk groups include primarily travelers to India, Central/South America, Africa, or the Commonwealth of Independent States (CIS). The incubation period (time from infection to onset of disease) is usually 15 to 64 days. Sex ratio: males are more commonly affected than females. The reason for the male predominance is unclear. Frequency peak: the disease rarely occurs in those under 20 years of age. The prevalence (disease incidence) for anti-HEV (antibodies to HEV) is 16.8% in Germany. It is the second most common cause of acute viral hepatitis. The incidence (frequency of new cases) is about 0.3 cases per 100,000 inhabitants per year. The duration of infectivity (contagiousness) has not been conclusively clarified. The virus can be detected in the stool about one week before to 4 weeks after the onset of jaundice. In the case of chronic infections, it must be assumed that the virus is excreted as long as the infection persists. Meanwhile, HEV RNA as well as HEV antigens have been detected in the urine of patients with acute or chronic viral infection. Course and prognosis: Acute hepatitis E infection follows a similar course to hepatitis A. Both diseases are hardly distinguishable by clinical symptoms. Both diseases can hardly be distinguished from each other on the basis of clinical symptoms. In immunocompetent patients, the disease is clinically inapparent in more than 99% of cases and usually cures without sequelae.If the infection is symptomatic, spontaneous improvement and healing usually occurs after about two to three weeks. In elderly persons, patients with chronic liver disease (pre-existing steatosis hepatis/fatty liver or fibrosis) and pregnant women, fulminant courses with acute or acute-on-chronic liver failure (ACLF) can be observed.Chronic courses with HEV occur in immunodeficiency (e.g. HIV infection) or under immunosuppression. In these cases, only mildly elevated transaminases are detectable.The lethality (mortality relative to the total number of people with the disease) for hepatitis E (HEV genotype 1) is reported to be 0.5-4% for clinical cases in Asia; lethality considering seroprevalence (percentage of patients testing serologically positive) in hepatitis E outbreaks yields a lower lethality rate of 0.07-0.6%. In pregnancy and in patients with chronic liver disease, fulminant hepatitis can occur with a lethality rate of up to 20%. Chronic courses have also been described in immunosuppressed patients (e.g., after organ transplantation). Hepatitis E leads to a cure in 98 % of cases (exception: pregnant women). Vaccination: A vaccine against hepatitis E (genotype 1) has been approved in China since the beginning of 2012. So far, it has not been clearly proven whether this vaccine also protects against the European HEV genotype 3. In Germany, the disease is notifiable according to the Infection Protection Act (IfSG). Notification has to be made in cases of suspected disease, illness, as well as death Since Jan. 1, 2020, blood products in Germany must be tested for HEV contamination.
