Like malaria epidemics, dengue fever epidemics depend

on temperature (Fig. 120-5). Higher temperatures increase the rate of

larval development and accelerate the emergence of adult Aedes mosquitoes.
The daily temperature range may also influence dengue virus
transmission, with a smaller range corresponding to a higher transmission
potential. Temperatures <15°C or >36°C substantially reduce

pg 343
Dengue is the most important of the human arboviral infections, with
almost half of the world’s population at risk. Occurring in the range of
Aedes mosquitoes, dengue virus infection imposes a heavy burden of
morbidity and mortality worldwide, with as many as 50–200 million
infections, 500,000 severe cases, and 20,000 deaths annually. Dengue
virus is a flavivirus and exists in four serotypes (DENV1–4) that 3403
circulate independently of one another; immunity to one serotype does not confer
immunity to the others.
Dengue is transmitted primarily by Aedes aegypti and secondarily by Aedes albopictus.
The original life cycle of dengue virus was most likely similar to that of yellow fever,
consisting of sylvatic transmission from mosquitoes to nonhuman primates and back to
mosquitoes; over the past few centuries, the virus has adapted to an urban and periurban
mosquito–human–mosquito cycle as well. Dengue and its more severe manifestations,
dengue hemorrhagic fever and dengue shock syndrome, were first described in outbreaks
in Japan in 1943 and Hawaii in 1945. However, clinically similar diseases had been
reported during the previous two centuries in a geographic band extending from India
south to Queensland, Australia, and east through Polynesia; in addition, there had been
occasional outbreaks in areas as disparate as Greece, Panama, and southern Texas.
The ecology of dengue changed dramatically in the second half of the twentieth
century, led by the successful invasion by A. aegypti of the global tropics after World
War II, with the postwar dispersion of troops and materiel. From its ancestral roots in
Southeast Asia, all four dengue serotypes spread globally in the tropics. DENV2 had
been introduced into West Africa by the 1960s and established both sylvatic enzootic
nonhuman primate and urban endemic human cycles. Travel and commerce facilitated
importations, probably through both viremic human hosts and infected mosquitoes. In the
Americas in particular, a campaign to eradicate A. aegypti, which is also the principal
vector of yellow fever, failed in the mid-1970s, and both A. aegypti and dengue virus,
especially DENV2, rapidly reinvaded their prior habitat; thus dengue reemerged as a
major arboviral disease extending from the southern United States in the north, through
northern Argentina in the south. Recent outbreaks have occurred along the U.S.–Mexico
border and in the state of São Paulo in Brazil, where DENV1, DENV2, and DENV4 are
co-circulating.
Dengue’s emergence and spread have been intimately linked to human activity. In
particular, globalization, with the movement of viremic people and mosquitoes through
modern transportation of both passengers and goods, has been critical to dengue’s
success. One particular adaptation has also facilitated its urban spread: Aedes is able to
breed in standing water associated with human habitation, such as cisterns, ornamental
ponds, puddles, and water trapped in abandoned tires. This ability of Aedes has allowed
dengue to be one of the only two known arboviruses (the other being Zika) that are
adapted to an urban environment and can replicate entirely in a mosquito-to-human cycle.
Together, these factors have led to widespread dengue transmission in a band extending
across the tropics worldwide.