Yellow fever is an acute arboviral (arthropod-borne) infection caused by the yellow fever virus, a
flavivirus. The illness is characterized by high fever, jaundice and
encephalopathy in its severe form. The disease occurs in focal outbreaks in Africa, the Caribbean and Central
and South America. This condition is prevented by the 17 Dattenuated live vaccine strain, which should be given
to travellers to endemic areas and to indigenous populations in outbreaks. There are infrequent occurrences of
importation of yellow fever to Europe, which can present as PUO or viral haemorrhagic fever.
Distribution and incidence
Sub-Saharan tropical Africa (especially West Africa), the Caribbean islands (most recently Trinidad) and
South America (Brazil, Peru, Bolivia, Ecuador, Venezuela and Colombia) are the areas affected by yellow fever.
Relatively small numbers of cases occur every year in these areas, although cases in isolated areas may go unreported.
Transmission and epidemiology
In South America, and Central and East Africa, a jungle cycle involves monkey-mosquito-monkey and maintains the virus in
the mosquito reservoir. Haemagogus mosquitoes are the vector. The epidemiology in savannah and
forest-savannah areas involves other Aedes species with humans and monkeys. The insect vector passes infection to the
next generation of mosquitoes by transovarial transmission. Non-immune persons of all races, all ages and
both sexes are susceptible to infection. Prior exposure to other flaviviruses produces some degree of
cross-protection. Men are at particular risk of infection because of occupations
that take them into forests.
Pathology and pathogenesis
The liver is the main organ involved and shows mid-zonalnecrosis of hepatocytes. Councilman bodies result from
the degeneration of hepatocytes. The kidneys show acute tubular necrosis which may relate to shock and
hypovolaemia. There may be haemorrhage into mucous membranes and the skin, associated with the bleeding
tendency that is common in yellow fever. The underlying pathogenic mechanisms are poorly understood.
There is a range of severity of disease, from mild to severe
life-threatening illness. The latter constitutes a minority of all those infected. The incubation period is about 6
days before the onset of headache and fever. More severe illness is associated with marked limb pains. Proteinuria is
usual High fever, headache, severe limb and back pain, chillsassociated with fetor, haemorrhages in the gums,
and nosebleeds are early features in severe cases. There may then be a short period of remission of symptoms for up to24 hours before the recurrence of fever with
vomiting and jaundice. Bleeding into the gut, skin and other sites is usual in severe cases. Occasional cases are seen with
organ damage limited to the heart or kidneys, causing cardiac orrenal failure. Bleeding and renal failure are the main
causes of the high mortality (up to 50%) in severe cases. Resolution in severe cases can take from 3 days to 6 weeks.
The clinical features in severe cases suggest the diagnosis, but in milder cases without evidence of organ
dysfunction the diagnosis may not be made. Virus can be isolated most often from blood taken in the first 4 days of clinical
illness. Rising antibody titres in paired sera may also give the diagnosis, but serological tests may not be easy to interpret
in people exposed to related viruses.
In mild cases the range of febrile illnesses to be considered is extensive and includes malaria, typhoid, the prodromalphase of viral hepatitis, leptospirosis and
rickettsial diseases. The presence of jaundice with fever prompts consideration of leptospirosis, malaria, East African
trypanosomiasis, typhoid, biliary tract sepsis and Marburgvirus diseases. Ebola virus fever and Lassa fever are
other causes of haemorrhagic fever, although marked jaundice is not usual.
Laboratory features Anaemia, leukopenia and thrombocytopenia are usual features in more severe cases. Conjugated bilirubin
levels and transaminases are high in jaundiced cases. Coagulation abnormalities comprise prolonged prothrombin
time, reduced fibrinogen levels and detectable fibrin degradation products. Renal failure with proteinuria, oliguria
and raised creatinine and urea may occur.
Prevention and control
All travellers to endemic areas - apart from pregnant women, infants under 1 year and
immuno suppressed patients - should receive the attenuated 17D yellow fever vaccine. Patients with yellow fever should be nursed
under mosquito nets to prevent mosquitoes becoming infected. Vaccination is used to help control epidemics.