The latitudinal temperature gradient in the tropics is relatively shallow. Not only does this make latitudinal studies more difficult, but it portends relatively higher extinction rates for midtropical species of restricted geographic range and limited dispersal capabilities. Elevational shifts provide the only published data for range shifts in the tropics, where upslope range shifts have been demonstrated for plants and vertebrate animals (Colwell et al. 2008; Pounds et al. 2005). Unlike most temperate areas, in the lowland tropics there is no community of species adapted to even hotter areas available to replace those species that shift their ranges upslope or poleward. Thus, the species diversity of lowland tropical areas is expected to decrease as global tem- peratures rise (Colwell et al. 2008). However, extinctions are likely to be selective. Specialist species with relatively narrow niche breadth (especially in terms of physiological tolerances, habitat, and diet requirements) are most likely to suffer, whereas more adaptable generalist species may thrive, with potentially impor- tant consequences for pathogen transmission (Mills 2006). Range shifts may not be restricted to lati- tudinal and elevational dimensions. Several host and vector species are restricted to specific habitat types. The frequency of occurrence of hosts, vectors, or pathogens in these habitat types helps to define relative risk of disease to humans associated with these habitats (Mills and Childs 1998). Effects of climate change on the species composition of plant and ani- mal communities are poorly understood. Range shifts in response to climate change are unlikely to affect entire communities or assem- blages in unison (Root and Schneider 2002). Species will migrate at different rates and according to their own motility, tolerances, and physiological constraints. Thus, species assemblages are likely to change: Some species in new areas will experience increased popula- tion densities and competitive release, allow- ing colonization of habitats from which they were formerly excluded, whereas others may experience increased pressures and decreased population densities as new competitors or predators move into their ranges or they are unable to migrate as climate change leaves them stranded on shrinking islands of suitable habitat. This concept was illustrated by several high-altitude rodent and insectivore species in Yosemite National Park that are now restricted to only a portion of their former range (Moritz et al. 2008) (Figure 1). Changes in population density. Climate change has been associated with conditions that alter the carrying capacity of ecosystems for some plant or animal populations (Gage et al. 2008; Sutherst 2004). Such changes can result in dramatic increases, or some- times decreases, in host or vector population Climate change and zoonotic and vector-borne disease densities. Examples from vector-borne diseases are numerous. Populations of Aedes mosqui- toes (vector for the agent of Rift Valley fever in East Africa) (Table 1) increase dramatically after periods of high rainfall associated with El Niño Southern Oscillation (ENSO) events (Anyamba et al. 2001; Linthicum et al. 1999). Increases in mosquitoes and mosquito-borne malaria were associated with ENSO events in South America (Barrera et al. 1999; Bouma and Dye 1997; Bouma et al. 1997) and south- ern Africa (Mabaso et al. 2007). Increasing temperatures also can decrease the develop- ment time of mosquitoes allowing greater population densities to be reached (Gage et al. 2008). Increased incidence of malaria was linked to precipitation and higher tempera- tures in Kenya (Githeko and Ndegwa 2001) and Madagascar (Bouma 2003). Conversely, reduced rainfall in Senegal and Niger was asso- ciated with decreases in malaria (Julvez et al. 1997; Mouchet et al. 1996), presumably result- ing from decreased mosquito reproduction. The effects of environmental extremes on vertebrate host populations can be pronounced. High summer temperatures have resulted in increased mortality of hosts, such as bats in tropical or subtropical areas (Welbergen et al. 2008) or increased overwinter survivorship of species in temperate areas (Straile and Stenseth 2007). After an ENSO event in 1997, inves- tigators recorded increased rainfall, improved quality of vegetation, and increased popula- tion density of North American deer mice (Peromyscus maniculatus) in the southwestern United States. These events preceded increased numbers of HPS cases in the area over 3 years (Yates et al. 2002). Increased rainfall was also associated with outbreaks of HPS in Paraguay (Williams et al. 1997) and Panama (Ruedas et al. 2004). Similarly, human plague (a flea- borne zoonotic disease caused by the bacte- rium Yersinia pestis; Table 1) in the western United States was influenced by the effects of above-normal temperatures and status of the Pacific Decadal Oscillation (PDO). The PDO resulted in precipitation increases (Ari et al. 2008) that were believed to enhance small-mammal food resources and flea sur- vival (Enscore et al. 2002; Parmenter et al. 1999). Although less attention has been paid to decreases in host populations, lower rain- fall is accompanied by decreasing populations of North American deer mice in the south- western United States (Yates et al. 2002), whereas increasing rainfall during cold periods was associated with abrupt population declines in some ecosystems (Calisher et al. 2005). Changes in prevalence of infection in host or vector populations. The increases in host or vector populations discussed above can lead to increased frequency of contact between hosts or between hosts and vectors (density-dependent transmission) (Begon et al. 2002) and increased prevalence of infection in host or vector populations. The increased North American deer mouse popu- lation density in the southwestern United States that followed the 1997 ENSO was fol- lowed, a year later, by increased prevalence of hantavirus infection in North American deer mouse populations [Centers for Disease Control and Prevention (CDC) 1999; Yates et al. 2002]. This delayed density-dependent increase in infection in host populations may be a general phenomenon affecting horizon- tally transmitted pathogens in wildlife hosts in strongly seasonal climates (Madhav et al. 2007; Mills et al. 1999). Similarly, as rodent populations increase above certain thresh- olds, the likelihood of plague epizootics also may increase (Davis et al. 2004). Precipitation and temperature influence the appearance of plague epizootics among Asian gerbils (Stenseth et al. 2006) and epizootics among prairie dogs in Colorado were linked to ENSO events (Stapp et al. 2004). Prevalence of infection for other VBZDs might be increased by other mechanisms besides density-dependent transmission. Environmental changes that lead to increased stress in hosts can decrease host immune response, resulting in increased probability of infection as well as higher pathogen loads and increased pathogen shedding by a variety of host species (Nelson et al. 1995), including hosts for hantaviruses (Demas and Nelson 1998; Klein et al. 2004; Lehmer et al. 2007) and arenaviruses (Barnard et al. 1996). Changes in pathogen load. Temperatures can have profound effects on the development of pathogens and pathogen loads in arthro- pod vectors (Gage et al. 2008; Sutherst 2004). Malaria parasites develop in mosquito vec- tors only within certain temperature ranges (Patz and Olson 2006). Similarly, Y. pestis, the etiological agent of plague, develops and expresses biofilm efficiently only at tempera- tures < 28°C. Biofilm facilitates Y. pestis trans- mission by causing infected fleas to increase feeding attempts and regurgitate Y. pestis back 3,500 3,000 ) 2,500 m ( ion 2,000 t v a 1,500 e l E 1,000 500 0 1920 2006 Peromyscus truei Chaetodipus californicus Tamias alpinus Figure 1. Elevational distribution of the piñon deer mouse (Peromyscus truei), the California pocket mouse (Chaetodipus californicus), and the alpine chipmunk (Tamias alpinus) in Yosemite National Park, California, 1920 and 2006 (Moritz et al. 2008). Environmental Health Perspectives • volume 118 | number 11 | November 2010 1509