Other reports in this collection
Mosquitoes transmit many viruses, more than 100 of which are known to infect humans—causing illness ranging from acute viral syndrome to severe and sometimes fatal encephalitis and hemorrhagic fever. The natural transmission cycles of these viruses are complex and usually involve birds or rodents as well as several mosquito species; each region of the world has its own unique viruses (Gubler and Roehrig, 1998). These viruses have become important global emergent/resurgent public health problems in recent years, causing widespread epidemics (Gubler 1996, 1998a).
Yellow fever—a virus that occurs naturally in the rain forests of Africa and South America in an enzootic cycle involving lower primates and mosquitoes—also can cause major urban epidemics in a cycle involving Aedes aegypti that is identical to dengue (Monath, 1988). As such, it has similar weather and climate sensitivity to dengue. Yellow fever was effectively controlled in the 1950s and 1960s through vaccination (Africa) and mosquito control (the Americas). With reinvasion of most large American tropical urban centers by Aedes aegypti in the past 30 years (Gubler, 1989), the region is at its highest risk for urban epidemics in 50 years (Gubler, 1998c). Once urban epidemics of yellow fever begin to occur in tropical America, it is expected that this virus will move very quickly via modern transportation to Asia and the Pacific, where it has never occurred (Gubler, 1998c).
Several mosquito-borne viruses cause encephalitis, including eastern equine
encephalitis (EEE), western equine encephalitis (WEE), St. Louis encephalitis
(SLE), La Crosse encephalitis (LAC), and Venezuelan equine encephalitis (VEE)
in the Americas; Japanese encephalitis (JE) in Asia; Murray Valley encephalitis
(MVE) and Kuniin (KUN) in Australia; and West Nile (WN) and Rift Valley fever
(RVF) viruses in Africa (Gubler and Roehrig 1998). WN virus also occurs in west
and central Asia, the Middle East, and Europe and recently was introduced into
the United States, where it caused a major epidemic in New York City (Asnis
et al., 2000; Komar, 2000). All of these viruses have birds (EEE, WEE, SLE,
JE, MVE, KUN, WN) or rodents (LAC, VEE) as natural reservoir hosts. The natural
host for RVF is not known, but large ungulates act as amplifying hosts.
Epidemics of these diseases occur when their natural ecology is disturbed in
some way (Gubler and Roehrig, 1998). This could include environmental changes
such as meteorological changes or forest clearing, changes in population densities
and structure of the mosquito or vertebrate host, or genetic changes in the
viruses. All of these diseases are very climate-sensitive, but it is difficult
to know how climate change will influence their distribution and incidence because
of the complexities of their transmission cycles in nature. For example, in
the United States, WEE and SLE could expand their geographic distribution northward,
and WEE could disappear from most of the country (Reeves et al., 1994). Climate
change also may have an effect on endemic/enzootic arboviruses in Australia
(Russell, 1998; Tong et al., 1998; Bi et al., 2000). Thus, there probably would
be positive and negative impacts, depending on the disease.
Floods may cause an immediate decrease in mosquito populations because of loss of breeding sites. However, disease risk may rise as floodwaters recede and vector populations increase, but only if the virus is present (Nasci and Moore, 1998). This underscores the need to have effective surveillance systems and prevention strategies in place to monitor disease and control vector activity, as well as the need for more research on the transmission dynamics of vector-borne diseases.
There are two principal clinical types of leishmaniasis—visceral and cutaneous—which is caused by a range of species of Leishmania parasites. The parasites are transmitted by sandflies, of which the two most important genera are Phlebotomus in Europe and Asia and Lutzomyia in the Americas. In central Asia and Europe, leishmaniasis has become an important co-infection with human imunodeficiency virus (HIV) (Alvar et al., 1997; WHO/UNAIDS, 1998). Sandflies are very sensitive to temperature, and increases in temperature also may increase daily mortality rates. Phlebotominae are sensitive to sudden temperature changes and prefer regions with small differences between maximum and minimum temperatures. Thomson et al. (1999) mapped P. orientalis in Sudan and found that the geographic distribution was best explained by mean annual maximum daily temperature and soil type. One study on leishmaniasis in Italy indicates that climate change may expand the range of one vector (P. perniciosus) but decrease the range of another (P. perfiliewi) (Kuhn, 1997). A 3°C increase in temperature could increase the geographic and seasonal distribution of P. papatasi in southwest Asia, provided other ecological requirements are met (Cross and Hyams, 1996; Cross et al., 1996).
The southern limit of leishmaniasis and vectors in South America is the extreme north of Argentina (Curto de Cassas and Carcavallo, 1995; Marcondes et al., 1997). There have been no systematic studies of the relationship between climate parameters and vectors or human cases in the Americas. Climate change could affect the geographical distribution of these vector species in Brazil, Paraguay, Bolivia, and Argentina (Carcavallo and Curto de Casas, 1996).
|
Other reports in this collection |
|