The jaundice has prompted the appellation "yellow fever" and other designations such as mal de Siam, fièvre jaune, gelbfieber, and virus amaril, whereas the hemorrhaging of black blood underlies the name vomito negro ("black vomit"). Known early in the New World as "Barbados distemper," "bleeding fever," maladie de Siam, el peste, and "yellow jack" (from ships' quarantine flags), the disease has had some 150 names.
Characteristics
Yellow fever is normally a disease of nonhuman primates,
particularly monkeys. Mosquitoes transmit the disease among them – but
not mosquitoes that ordinarily bite humans. This form of the disease is
jungle yellow fever or sylvan yellow fever; it is enzootic, meaning that transmission is from monkey to mosquito to monkey.
When the disease leaves the treetops, and mosquitoes (such as Aedes africanus and Aedes simpsoni in Africa, and species of Haemogogus in the Americas) begin transmission from nonhuman primate to mosquito to human, the disease is called endemic yellow fever. When the virus is carried by an infected human to populated areas, where transmission is from human to A. aegypti mosquito to human, the disease is termed epidemic yellow fever or urban yellow fever.
The habits of the female A. aegypti have much to do with
shaping the characteristics of an epidemic. She is a domestic mosquito,
living close to humans, depending on them for blood meals, and breeding
in nearby loci of water. Her range is short, at most a few hundred
yards, meaning that she requires a fairly dense human population.
Because A. aegypti can survive only days without water
(although her eggs can survive for years in dehydrated form) and
requires water in which to breed, adequate rainfall is a prerequisite
for epidemic yellow fever. Warm weather is another prerequisite: A. aegypti will not bite in temperatures under 62°F and hibernates in extended chilly weather.
The virus also has some distinctive requirements, especially for
transmission – a process in which humans are best thought of as the
site where the virus changes mosquitoes. This exchange can take place
only during the first 3–6 days of infection of the yellow fever victim
while the virus still remains in the blood (viremia); after the
virus has entered the mosquito, it must incubate for another 9–18 days
before the mosquito can infect another human. After this period of
extrinsic incubation, however, the mosquito remains infective for the
remainder of its life, which could be upward of 180 days, although
generally the lifespan of the female A. aegypti is closer to a month or two.
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In the Americas, epidemic yellow fever declined during the twentieth century, essentially because of efforts to eradicate A. aegypti
in population centers. The last outbreak occurred in Trinidad in 1954.
Nonetheless, the virus remains alive in the monkeys of Central and
South America; consequently, some human cases are still reported among
people who work or live close to the forests. Most cases occur in
regions of Brazil, Ecuador, Venezuela, Colombia, and Peru that are
drained by river networks contributing to the Orinoco, Magdalena, and
Amazon systems. Earlier in the twentieth century, human cases were also
reported fairly regularly in Central America, Bolivia, Argentina, and
Paraguay.
In Africa, severe yellow fever epidemics still occur; a notable
example, in Ethiopia in 1961, cost thousands of lives. Still more
recently, a major outbreak in Nigeria claimed thousands more, and yet
another was ongoing at the turn of the twenty-first century. A vast
belt of endemic yellow fever stretches across Africa, but isolated
cases are only irregulary reported.
One mystery surrounding yellow fever is its lack of incidence in Asia, despite the presence of Aedes
mosquitoes. Some think that the mosquitoes themselves are resistant to
infection. Others suspect that a population may support only so many
arboviruses and that entrenched ones such as dengue and Japanese encephalitis may have forestalled the advance of yellow fever.
A yellow fever attack confers lifetime immunity on the host. Because
the disease generally reserves severe symptoms for young adults and
treats children more gently, whole populations in endemic or frequently
visited areas can become more or less immune, with yellow fever just
another childhood ailment. Under such circumstances, epidemics never
occur unless groups of newcomers arrive, as was the case with
immigrants, soldiers, and sailors reaching the Americas. It was this
phenomenon that gave rise to yellow fever nicknames such as "strangers'
fever," the "disease of acclimation," and "patriotic fever."
Many in the New World came to believe that blacks possessed a
special ability to resist yellow fever. Most slaves reaching the
Americas originated within the African endemic zone and would have
acquired immunity before ever stepping aboard ship. Thus it is possible
to explain blacks' refractoriness to yellow fever as acquired immunity.
On the other hand, genetic selection for yellow fever resistance as
a result of prolonged exposure cannot be discounted, for many of the
West African descendants of those first arrivals to the Americas lived
for generations in areas untouched by yellow fever, yet, without any
opportunity to acquire immunity in advance, suffered much less than
whites when the disease finally did make an appearance. It has been
suggested that related arboviruses or flaviviruses (dengue or Japanese
encephalitis, for example) may confer some cross-protection against
yellow fever, whereas others believe that certain strains of the
illness may vary in mildness or severity, depending on the groups of
individuals under attack. In this latter connection, it may be
significant that Chinese in the New World were reputed to be almost as
resistant to the illness as blacks, because although yellow fever has
never invaded Asia, dengue and Japanese encephalitis are endemic to
much of the region.