Conditions · Infectious and tropical diseases
Yellow fever !
Yellow fever is a mosquito-borne viral disease of the tropics. Most cases are mild, but a minority develop jaundice, bleeding and liver and kidney failure.
Updated 2026-11-01
Structures involved
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Microorganisms that cause it
Why it happens
- Apoptosis: the intrinsic and extrinsic pathways
- Functions of the liver
- Heme breakdown and bilirubin
- Liver: lobule, acinus, hepatocytes, sinusoids, Kupffer cells
What it is
An acute viral haemorrhagic fever caused by the yellow fever virus (a flavivirus) and spread by mosquitoes. Most infections are mild or silent, but some people progress to a toxic phase with hepatitis, jaundice, bleeding and kidney failure.
Who gets it
Endemic in tropical Africa and South America; Colombia is one of the Latin American countries considered at risk, with sylvatic transmission in forested areas such as the Amazon, Orinoquia and Andean foothills. It is a notifiable disease in Colombia, and vaccination is free in the national programme. Africa carries most of the world burden.
Causes
- Yellow fever virus, an RNA flavivirus (same family as dengue and Zika)
- Sylvatic cycle: Haemagogus and Sabethes mosquitoes transmit the virus between monkeys and to people who enter the forest
- Urban cycle: Aedes aegypti can spread it from person to person in towns
Risk factors
- Living in or travelling to endemic areas without vaccination
- Forest work: farming, logging, mining, hunting
- Unknown or unverifiable vaccination history
- Low vaccination coverage in the community
Pathophysiology
After an infected bite the virus replicates in lymph nodes and spreads through the blood. It targets the liver, causing midzonal hepatocyte necrosis with apoptotic hepatocytes (Councilman bodies), which produces jaundice and coagulopathy. Kidney injury, myocardial damage and a cytokine storm with capillary leak lead to bleeding and shock in severe cases.
Classification
- Asymptomatic or mild infection
- Acute (infection) phase: fever, myalgia, headache
- Period of remission lasting hours to a day or two
- Toxic (intoxication) phase: jaundice, haemorrhage, liver and kidney failure
Symptoms and signs
- Sudden fever, chills, headache and back and muscle pain
- Nausea, vomiting and marked weakness
- Relative bradycardia despite high fever (Faget sign)
- In the toxic phase: jaundice, abdominal pain and recurrent fever
- Bleeding from gums, nose or gut (black vomit), and reduced urine output
Diagnosis
- Clinical
- Fever with jaundice or bleeding in someone with exposure in an endemic area and no verified vaccination. Every suspected case must be notified to the public health surveillance system.
- Tests
- RT-PCR on blood in the first days; later, IgM ELISA confirmed by neutralisation tests (PRNT) because of cross-reaction with other flaviviruses. Very high transaminases (AST often higher than ALT), raised bilirubin, prolonged clotting times, thrombocytopenia, rising creatinine and proteinuria. Histology (post mortem) shows midzonal necrosis and Councilman bodies.
- Imaging
- Not diagnostic. Abdominal ultrasound may be used to exclude biliary obstruction.
Differential diagnosis
- Dengue (severe dengue)
- Severe malaria
- Leptospirosis (Weil disease)
- Acute viral hepatitis
- Other viral haemorrhagic fevers and toxic hepatitis
Goal of treatment
There is no specific antiviral. Care aims to support the patient through the acute illness: keep hydration and perfusion, correct bleeding and coagulopathy, protect liver and kidney function, and treat secondary infections.
Treatment
- Acute
- Hospital supportive care: fluids, control of fever with paracetamol (avoiding aspirin and NSAIDs because of bleeding risk), blood products for haemorrhage and coagulopathy.
- Acute
- Intensive care for the toxic phase: vasopressor support, dialysis for acute kidney injury, management of liver failure and encephalopathy.
- Medical
- Antibiotics for secondary bacterial infections; experimental antivirals only within research protocols.
- Follow-up
- Close monitoring of vital signs, urine output, bleeding, glucose, liver tests and clotting; mosquito net for the patient during the viraemic phase to avoid further transmission.
Complications
- Fulminant hepatitis and liver failure
- Acute kidney injury
- Haemorrhage and disseminated intravascular coagulation
- Myocarditis, arrhythmias and shock
- Secondary bacterial infection and death
Prognosis
Most people with the mild form recover fully and gain lifelong immunity. Up to about half of those who enter the toxic phase die, usually within 7 to 10 days.
Prevention
- Vaccination with the live attenuated vaccine; one dose gives lifelong protection for most people
- Vaccination at least 10 days before travel to risk areas, with the international certificate
- Mosquito control and protection from bites (long sleeves, repellent, nets)
- Prompt notification of suspected cases to trigger outbreak control
Test yourself
Think of the answer, then tap the question to see it.
Which liver finding is classic in yellow fever?
Midzonal (zone 2) hepatocyte necrosis with apoptotic eosinophilic hepatocytes called Councilman bodies.
What is the Faget sign?
Relative bradycardia: a pulse slower than expected for the height of the fever.
Which mosquitoes transmit sylvatic yellow fever in South America?
Haemagogus and Sabethes species; Aedes aegypti drives the urban cycle.
What is the main measure to prevent yellow fever?
Vaccination with the live attenuated vaccine, which gives long-lasting immunity after a single dose in most people.
Related conditions
- Dengue
- Malaria
- Leptospirosis
- Viral hepatitis
- Acute liver failure
- Acute kidney injury
- Viral haemorrhagic fevers (Ebola and others)
- Zika virus infection
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Yellow fever (World Health Organization (WHO), 2025); Fiebre Amarilla (Ministerio de Salud y Protección Social de Colombia, 2025).
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