Hepatitis, viral: A and E
D E FI N I T ION
Hepatitis caused by infection with the RNA viruses, hepatitis A (HAV) or
hepatitis E virus (HEV), that follow an acute course without progression to chronic carriage.
AE T IOLOGY HAV
is a picornavirus and HEV is a calicivirus. Both are small non-enveloped
single-stranded linear RNA viruses of 7500 nucleotides, with transmission by the
faecal–oral route.
Both viruses replicate in hepatocytes and are secreted into bile. Liver inflammation and
hepatocyte necrosis is caused by the immune response, with targeting of infected cells by
CD8þ T cells and natural killer cells. Histology shows inflammatory cell infiltration
(neutrophils, macrophages, eosinophils and lymphocytes) of the portal tracts, zone 3
necrosis and bile duct proliferation.
E P IDEMIOLOGY HAV
is endemic in the developing world, infection often occurs subclinically.
In the developed world, better sanitation means that seroprevalence is lower,
age of exposure " and hence is more likely to be symptomatic. Annual UK incidence is
5000 cases (seroprevalence 5%).
HEV is endemic in Asia, Africa and Central America.
H ISTORY
Incubation period for HAV or HEV is 3–6 weeks.
Prodromal period:
Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and
vomiting.
Hepatitis:
Prodrome followed by dark urine, pale stools and jaundice lasting 3 weeks.
Occasionally, itching and jaundice last several weeks in HAV infection (owing to
cholestatic hepatitis).
EXAMINA T I ON
Pyrexia, jaundice, tender hepatomegaly, spleen may be palpable (20%).
Absence of stigmata of chronic liver disease, although a few spider naevi may appear,
transiently.
INVE S T I G A T IONS
Blood:
LFT ("" AST and ALT, " bilirubin, " AlkPhos), " ESR. In severe cases, # albumin and
" platelets.
Viral serology:
Hepatitis A: Anti-HAV IgM (during acute illness, disappearing after 3–5 months), anti-HAV
IgG (recovery phase and lifelong persistence).
Hepatitis E:
Anti-HEV IgM (" 1–4 weeks after onset of illness), anti-HEV IgG. Hepatitis B and C
viral serology is also necessary to rule out these infections.
Urinalysis:
Positive for bilirubin, " urobilinogen.
MANAGEMENT
No specific management. Bed rest and symptomatic treatment (e.g.
antipyretics, antiemetics). Colestyramine for severe pruritus.
Prevention and control:
Public health: Safe water, sanitation, food hygiene standards. Both are notifiable diseases.
Personal hygiene and sensible dietary precautions when travelling.
Immunization (HAV only): Passive immunization with IM human immunoglobulin is only
effective for a short period. Active immunization with attenuated HAV vaccine offers safe
and effective immunity for those travelling to endemic areas, high-risk individuals (e.g.
residents of institutions).
COM P L IC A T I ONS
Fulminant hepatic failure develops in 0.1% cases of HAV, 1–2%of HEV
but up to 20% in pregnant women. Cholestatic hepatitis with prolonged jaundice and
pruritus may develop after HAV infection.
Hepatitis, viral: A and E (continued)
Post-hepatitis syndrome: Continued malaise for weeks to months.
PROGNOSIS
Recovery is usual within 3–6 weeks. Occasionally, a relapse during recovery.
There are no chronic sequelae. Fulminant hepatic failure carries an 80% mortality.
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