Fevers and Colds|
Dec
05
Filed Under (Health) by drfever
peterhutch asked:
Yellow fever can be recognized from historic texts stretching back 400 years. Infection causes a wide spectrum of disease, from mild symptoms to severe illness and death. The “yellow” in the name is explained by the jaundice that affects some patients, causing yellow eyes and yellow skin.
Yellow fever is difficult to recognize, especially during the early stages. It can easily be confused with malaria, typhoid, rickettsial diseases, haemorrhagic viral fevers (e.g. Lassa), arboviral infections (e.g. dengue), leptospirosis, viral hepatitis and poisoning (e.g. carbon tetrachloride). A laboratory analysis is required to confirm a suspect case. Blood tests (serology assays) can detect yellow fever antibodies that are produced in response to the infection. Several other techniques are used to identify the virus itself in blood specimens or liver tissue collected after death. These tests require highly trained laboratory staff using specialized equipment and materials.
Yellow fever causes epidemics that can affect 20% of the population. When epidemics occur in unvaccinated populations, case-fatality rates may exceed 50%. No treatment beyond supportive care exists. Yellow fever is common in West and Central Africa and in parts of South America. Periodic epidemics in Africa lead to hundreds of thousands of cases. Yellow fever is a very rare cause of illness in U.S. travelers.
Yellow fever transmission predominately occurs in areas of sub-Saharan Africa and South America 15° north and 10° south of the equator. It has never been documented in Asia. Yellow fever epidemics were dominant in Africa from 1986-1991, with close to 20,000 cases and 6000 deaths. This is considered to be grossly underestimated because of underreporting. These epidemics commonly include 30-1000 cases and have fatality ratios of 20-50%. In areas of West Africa, 200,000 endemic cases may occur annually.
The disease occurs only in sub-Saharan Africa and tropical South America (see Maps 4-15 and 4-16), where it is endemic and intermittently epidemic (see Table 4-23 for a list of countries in the endemic zone). Areas considered endemic for yellow fever have evidence of yellow fever transmission to humans and/or its potential, due to the presence of both a competent vector and YFV in nonhuman primates. In Africa, where most cases are reported, a variety of mosquitoes transmit the virus. The case-fatality rate of yellow fever in Africa is highly variable but approximates 20%. Infants and children are at greatest risk of severe disease.
Two live, attenuated yellow fever vaccines, strains 17D-204 and 17DD, were derived in parallel in the 1930s. Historical data suggest that these “17D vaccines”have identical safety and immunogenicity profiles. Despite a marked reduction in the world-wide incidence of yellow fever in the last five decades due to the extensive use of 17D vaccines and mosquito eradication programs, at least seven tropical South American countries (Bolivia, Brazil, Colombia, Ecuador, French Guiana, Peru, and Venezuela) and much of sub-Saharan Africa currently experience yellow fever epidemics. However, the actual areas of yellow fever virus activity far exceed the infected zones officially reported for epidemics.
Yellow fever decimated American troop populations in the Spanish-American War, prompting the appointment of a Yellow Fever Commission. Dr. Walter Reed (for whom the famous army hospital is named) was named to head it. In September 1900, his commission concluded the virus vector was the mosquito and that yellow fever could be experimentally transmitted from one human via infected blood. Without an animal model, the studies relied on human volunteers. Although the commission was actively attempting to infect humans with potentially lethal doses of virus, they were pioneers in the first forms of informed consent.
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Yellow fever can be recognized from historic texts stretching back 400 years. Infection causes a wide spectrum of disease, from mild symptoms to severe illness and death. The “yellow” in the name is explained by the jaundice that affects some patients, causing yellow eyes and yellow skin.
Yellow fever is difficult to recognize, especially during the early stages. It can easily be confused with malaria, typhoid, rickettsial diseases, haemorrhagic viral fevers (e.g. Lassa), arboviral infections (e.g. dengue), leptospirosis, viral hepatitis and poisoning (e.g. carbon tetrachloride). A laboratory analysis is required to confirm a suspect case. Blood tests (serology assays) can detect yellow fever antibodies that are produced in response to the infection. Several other techniques are used to identify the virus itself in blood specimens or liver tissue collected after death. These tests require highly trained laboratory staff using specialized equipment and materials.
Yellow fever causes epidemics that can affect 20% of the population. When epidemics occur in unvaccinated populations, case-fatality rates may exceed 50%. No treatment beyond supportive care exists. Yellow fever is common in West and Central Africa and in parts of South America. Periodic epidemics in Africa lead to hundreds of thousands of cases. Yellow fever is a very rare cause of illness in U.S. travelers.
Yellow fever transmission predominately occurs in areas of sub-Saharan Africa and South America 15° north and 10° south of the equator. It has never been documented in Asia. Yellow fever epidemics were dominant in Africa from 1986-1991, with close to 20,000 cases and 6000 deaths. This is considered to be grossly underestimated because of underreporting. These epidemics commonly include 30-1000 cases and have fatality ratios of 20-50%. In areas of West Africa, 200,000 endemic cases may occur annually.
The disease occurs only in sub-Saharan Africa and tropical South America (see Maps 4-15 and 4-16), where it is endemic and intermittently epidemic (see Table 4-23 for a list of countries in the endemic zone). Areas considered endemic for yellow fever have evidence of yellow fever transmission to humans and/or its potential, due to the presence of both a competent vector and YFV in nonhuman primates. In Africa, where most cases are reported, a variety of mosquitoes transmit the virus. The case-fatality rate of yellow fever in Africa is highly variable but approximates 20%. Infants and children are at greatest risk of severe disease.
Two live, attenuated yellow fever vaccines, strains 17D-204 and 17DD, were derived in parallel in the 1930s. Historical data suggest that these “17D vaccines”have identical safety and immunogenicity profiles. Despite a marked reduction in the world-wide incidence of yellow fever in the last five decades due to the extensive use of 17D vaccines and mosquito eradication programs, at least seven tropical South American countries (Bolivia, Brazil, Colombia, Ecuador, French Guiana, Peru, and Venezuela) and much of sub-Saharan Africa currently experience yellow fever epidemics. However, the actual areas of yellow fever virus activity far exceed the infected zones officially reported for epidemics.
Yellow fever decimated American troop populations in the Spanish-American War, prompting the appointment of a Yellow Fever Commission. Dr. Walter Reed (for whom the famous army hospital is named) was named to head it. In September 1900, his commission concluded the virus vector was the mosquito and that yellow fever could be experimentally transmitted from one human via infected blood. Without an animal model, the studies relied on human volunteers. Although the commission was actively attempting to infect humans with potentially lethal doses of virus, they were pioneers in the first forms of informed consent.
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