Yellow fever (yellow fever) is an acute infectious disease caused by yellow fever virus, transmitted by mosquitoes. The main clinical manifestations are fever, yellow stain, hemorrhage and so on. The disease is mainly in the tropical regions of Central and South America and Africa, through the mosquito and non-human primates between the periodic occurrence of natural infection cycle. First, the pathogenesis of yellow fever virus (yellow fever virus) belongs to the Flaviviridae (Flavivirus) of the genus Flavivirus, virus particles are spherical, 37-50 nm in diameter, outside the lipid envelope, the surface has spines. The viral genome is a single-stranded positive-stranded RNA with a molecular weight of approximately 3.8 × 106. A typical yellow fever virus contains 10,862 nucleotides, consisting of a single read frame of 10,233 nucleotides and a shorter non-coding region at the 5′ end and a non-coding region at the 3′ end. Three structural and eight non-structural proteins are encoded. The viral E protein is the major envelope glycoprotein and contains viral hemagglutinins and neutralizing antigenic determinants. the M protein causes increased infectivity of the virus and forms the surface structure of the viral particle. The virus is weakly resistant and is easily and rapidly inactivated by heat, ether, sodium deoxycholate and commonly used disinfectants. Yellow fever virus can produce cross-serological reactions with other members of the flavivirus family such as dengue virus, West Nile virus, and St. Louis encephalitis virus. Second, the epidemiology (a) the source of infection. People and monkeys infected with yellow fever are the main source of infection of this disease. The main source of infection for the urban type is the patient and the latent infection, especially the patient within 4 days of onset. The main source of infection for the jungle type is monkeys and other non-human primates. Mosquitoes sucking the blood of patients or sick monkeys after 9-12 days is infectious. Infected mosquitoes can carry the virus for life, and can be transmitted by the egg. Yellow fever recessive infection and light cases are far more serious patients, these cases play an extremely important role in the spread of the disease. (B) the transmission route. The disease is transmitted by mosquito bite. Aedes aegypti mosquito is the only vector of urban-type yellow fever to people – Aedes aegypti – people cycle. Jungle-type vector mosquito species are more complex, including Aedes africanus, Aedes simpson, blood mosquito genus (Hemagogus), Sabethes mosquito genus (Sabethes), etc., to monkey – Aedes africanus or blood mosquito genus, etc. – monkey cycle, people are infected by mosquito bites because they enter the jungle. (C) crowd susceptibility. People are generally susceptible to yellow fever virus. In the urban type because most of the adults due to infection and immunity, so the patients are mostly children. In the jungle type, most of the patients are adult males. After infection, lasting immunity can be obtained, and no reinfection has been found. (D) epidemic characteristics. 1, regional distribution: yellow fever is mainly prevalent in Africa and Central and South America 44 tropical countries, of which 33 countries in Africa (Benin, Chad, Congo, Guinea, Equatorial Guinea, Ethiopia, Ghana, Ivory Coast, Nigeria, Sierra Leone, Sudan, Uganda, Zaire, Cape Verde, Burundi, Eritrea, Gambia, Guinea (Bissau), Rwanda, Sao Tome and Principe, Somalia, Tanzania, Cameroon, Kenya, Liberia, Mali, Angola, Burkina Faso, Gabon, Mauritania, Senegal, Togo, Central African Republic), and 11 countries in South America (Brazil, Bolivia, British Guiana, Colombia, Ecuador, French Guiana, Panama, Peru, Suriname, Paraguay and Venezuela). 2, seasonal distribution: the disease develops throughout the year, with more cases in March-April. Asian regions, including China, although in geography, climate, mosquitoes, monkeys and other conditions similar to the above-mentioned areas, most areas also have Aedes aegypti mosquitoes, before March 12, 2016, no epidemic or confirmed cases of the disease were reported in China. Third, the pathogenesis and pathological changes (a) pathogenesis. The pathogenesis of yellow fever is not fully understood. Target cell damage may be caused by the direct action of the virus. The liver is the main target organ, due to damage to hepatocytes and yellow staining and prolonged prothrombin time, etc., while the kidney, heart, etc. are seen to be involved. Cytokines such as TNF produced by macrophages in the liver and spleen, oxygen radical accumulation, endothelial cell injury, microthrombosis and DIC are possible causes of multi-organ damage and shock. (ii) Pathological changes. The disease can cause a wide range of histopathological changes, of which the liver pathological changes are the most diagnostically specific. The liver may be mildly enlarged, with necrosis of the central parenchymal cells of the hepatic lobules, or in severe cases, necrosis of the entire hepatic lobules may occur, with the necrotic cells showing glassy and eosinophilic changes, but without obvious inflammatory reaction and fibrous tissue hyperplasia; if there is an inflammatory reaction, it is mostly due to complications. The kidney was enlarged, with acute tubular necrosis and steatosis, and the glomerulus was also destroyed. Special staining revealed positive Schiff staining of the basement membrane, and protein-like material was deposited in the glomerular capsule lumen and proximal tubular lumen. The myocardium showed fatty degeneration, cloudy swelling and degeneration. The spleen was congested and there was a marked decrease in lymphocytes in the spleen and lymph nodes, which were replaced by large monocytes and histiocytes. There are small foci of hemorrhage and edema in the brain tissue. In addition, hemorrhage in the skin and gastrointestinal mucosa and a small amount of fluid in the thoracic and abdominal cavities are also seen. Clinical manifestations The incubation period is 3-6 days. The clinical manifestations of the disease vary greatly, and the condition can range from mild self-limiting to lethal infection. The typical clinical course can be divided into the following four phases. (i) Viremia phase. Acute onset with chills, fever, up to 39-40°C, and relatively slow pulse. Severe headache, back pain, generalized muscle pain, nausea, vomiting. Conjunctival and facial congestion, epistaxis, epigastric discomfort, and significant pressure pain. Dark urine and proteinuria may be present. The symptoms last for 3-5 days. (ii) Remission period. A remission period of 12-24 hours occurs 3-5 days after the onset of infection, which is characterized by a decrease in body temperature, disappearance of headache, and improvement in the general basic condition. The virus is cleared from the body during this period, and non-infectious immune complexes can be detected in the blood. Mild patients can be cured in this period. (iii) Period of liver and kidney damage. This period lasts for 3-8 days, and about 15-25% of patients enter this period after the remission period. Body temperature rises again, systemic symptoms reappear, frequent vomiting, epigastric pain, etc. Jaundice appears and gradually deepens, with bleeding manifestations such as petechiae, petechiae, epistaxis, extensive bleeding from mucous membranes, and even hemorrhage from the cavity. Abnormal renal function with decreased urine output and proteinuria. Cardiac damage is seen on the electrocardiogram with ST-T segment abnormalities, and a few may develop acute myocardial dilatation. Cerebral edema, elevated cerebrospinal fluid protein but not high white blood cells may be present. Hypertension, tachycardia, shock, and intractable eruptions suggest a poor prognosis. Approximately 20-50% of patients in this phase die 7-10 days after onset. (iv) Recovery period. Patients in this phase are extremely fatigued and weak and can last for 2-4 weeks. Patients have also been reported to die during the recovery period, partly due to cardiac arrhythmias. Elevated transaminases may persist until several months after recovery.