Hepatitis E is caused by the hepatitis E virus (HEV), a naked single-stranded RNA virus which is usually divided into four genotypes with different characteristics (1). Genotypes 1 and 2 are predominant in developing countries with poor sanitary conditions, where the contagion is passed on via the faecal-oral transmission route between humans. Outbreaks of these genotypes can occur both sporadically and in large epidemics, and are characterised by a staggering mortality rate of up to 25 % among pregnant patients (2).
In Europe however, genotype 3 is dominant, and infects a wide range of mammals, although the main reservoir seems to be porcine (1). The primary cause of hepatitis E infections in the human population is probably ingestion of contaminated food or direct contact with porcine faeces, although there are also well-documented cases of infection through blood products (3, 4). The incubation period varies from 2 to 8 weeks with an average of 40 days (5).
In otherwise healthy humans the HEV infection is usually asymptomatic. In patients who show symptoms, these are usually mild and non-specific. Symptoms disappear after a few days but can persist for a few weeks (6, 7), although serious infections also occur (8). The most common symptoms are jaundice, fatigue and fever (9). No increase in mortality has been described among pregnant patients infected with genotype 3 (1); however the infection can become chronic in immunosuppressed individuals as well as cause an exacerbation of pre-existing chronic hepatitis with potentially serious consequences (5).
There are no official statistics regarding the prevalence or incidence of hepatitis E in Norway as it is rarely tested for. Hepatitis E is considered to be an infectious disease which is harmful to public health, and reporting of this disease to the Norwegian Surveillance System for Communicable Diseases (MSIS) was mandatory in the period from 1991– 2002. As few as 24 cases were reported in the entire period (10), and in all these cases transmission of the disease had occurred outside of Norway. However, the Norwegian Institute of Public Health, reported in a personal communication that some cases have since been registered where transmission might have occurred in Norway.
In Europe the seroprevalence of anti-HEV IgG in the general population varies between 4.6 % and 16 % (1). In one study, HEV IgG was found in 9.3 % of the general population in Sweden (11). The prevalence is dependent on age, region, occupation and choice of diagnostic test. An approximation of the incidence of the disease can be obtained by studying the number of HEV RNA-positive blood donations. This was done in England in 2012 – 2013, where 0.04 % of 225 000 blood donations tested were found to be positive. The infections were of genotype 3 (4).
No registered drugs exist to treat hepatitis E, although treatments with ribavarin and pegylated interferon have both been attempted in cases of chronic HEV infection in immunosuppressed patients with promising results (12). No internationally approved vaccines against the disease exist. In China a vaccine with the trade name Hecolin has been shown to provide protection against genotype 4 which is predominant in China, although its efficacy against the remaining genotypes has yet to be determined (13).
In the case described in this paper, only IgG and IgM HEV antibodies were discovered, and no viraemia could be ascertained in the ensuing PCR analysis. This is scarcely surprising since the virus is typically removed from the bloodstream in about 5 weeks after infection (10) – and in this case the diagnostic blood test was performed about 2 months after admission.
This constitutes the first documented case of transmission of hepatitis E in Norway. The published literature can, however, be interpreted as pointing to a considerable number of unrecorded infections, and thus to an underestimated incidence rate of hepatitis E in Europe (1).