Vector-Borne Diseases

5.1 Introduction

  • Charles B. Beard
    Centers for Disease Control and Prevention
  • Rebecca J. Eisen
    Centers for Disease Control and Prevention
  • Christopher M. Barker
    University of California, Davis
  • Jada F. Garofalo
    Centers for Disease Control and Prevention
  • Micah Hahn
    Centers for Disease Control and Prevention
  • Mary Hayden
    National Center for Atmospheric Research
  • Andrew J. Monaghan
    National Center for Atmospheric Research
  • Nicholas H. Ogden
    Public Health Agency of Canada
  • Paul J. Schramm
    Centers for Disease Control and Prevention

Vector-borne diseases are illnesses that are transmitted by vectors, which include mosquitoes, ticks, and fleas. These vectors can carry infective pathogens such as viruses, bacteria, and protozoa, which can be transferred from one host (carrier) to another. In the United States, there are currently 14 vector-borne diseases that are of national public health concern. These diseases account for a significant number of human illnesses and deaths each year and are required to be reported to the National Notifiable Diseases Surveillance System at the Centers for Disease Control and Prevention (CDC). In 2013, state and local health departments reported 51,258 vector-borne disease cases to the CDC (Table 5.1).

Table 5.1: Summary of Reported Case Counts of Notifiable Vector-Borne Diseases in the United States.

Diseases 2013 Reported Cases Median (range) 2004–2013b
   Lyme disease 36,307 30,495 (19,804–38,468)
   Spotted Fever Rickettsia 3,359 2,255 (1,713–4,470)
   Anaplasmosis/Ehrlichiosis 4,551 2,187 (875–4,551)
   Babesiosisb 1,792 1,128 (940–1,792)
   Tularemia 203 136 (93–203)
   Powassan 15 7 (1–16)
   West Nile virus 2,469 1,913 (712–5,673)
   Malariac 1,594 1,484 (1,255–1,773)
   Dengueb,c 843 624 (254–843)
   California serogroup viruses 112 78 (55–137)
   Eastern equine encephalitis 8 7 (4–21)
   St. Louis encephalitis 1 10 (1–13)
   Plague 4 4 (2–17)

a State Health Departments are required by law to report regular, frequent, and timely information about individual cases to the CDC in order to assist in the prevention and control of diseases. Case counts are summarized based on annual reports of nationally notifiable infectious diseases.9,10,11,12,13,14,15,16,17,18

b Babesiosis and dengue were added to the list of nationally notifiable diseases in 2011 and 2009, respectively. Median and range values encompass cases reported from 2011 to 2013 for babesiosis and from 2010 to 2013 for dengue.

c Primarily acquired outside of the United States and based on travel-related exposures.

Vectors and hosts involved in the transmission of these infective pathogens are sensitive to climate change and other environmental factors which, together, affect vector-borne diseases by influencing one or more of the following: vector and host survival, reproduction, development, activity, distribution, and abundance; pathogen development, replication, maintenance, and transmission; geographic range of pathogens, vectors, and hosts; human behavior; and disease outbreak frequency, onset, and distribution.1

The seasonality, distribution, and prevalence of vector-borne diseases are influenced significantly by climate factors, primarily high and low temperature extremes and precipitation patterns.1 Climate change can result in modified weather patterns and an increase in extreme events (see Ch. 1: Introduction) that can affect disease outbreaks by altering biological variables such as vector population size and density, vector survival rates, the relative abundance of disease-carrying animal (zoonotic) reservoir hosts, and pathogen reproduction rates. Collectively, these changes may contribute to an increase in the risk of the pathogen being carried to humans.

Climate change is likely to have both short- and long-term effects on vector-borne disease transmission and infection patterns, affecting both seasonal risk and broad geographic changes in disease occurrence over decades. However, models for predicting the effects of climate change on vector-borne diseases are subject to a high degree of uncertainty, largely due to two factors: 1) vector-borne diseases are maintained in nature in complex transmission cycles that involve vectors, other intermediate zoonotic hosts, and humans; and 2) there are a number of other significant social and environmental drivers of vector-borne disease transmission in addition to climate change. For example, while climate variability and climate change both alter the transmission of vector-borne diseases, they will likely interact with many other factors, including how pathogens adapt and change, the availability of hosts, changing ecosystems and land use, demographics, human behavior, and adaptive capacity.2,3 These complex interactions make it difficult to predict the effects of climate change on vector-borne diseases.

The risk of introducing exotic pathogens and vectors not currently present in the United States, while likely to occur, is similarly difficult to project quantitatively.4,5,6 In recent years, several important vector-borne pathogens have been introduced or reintroduced into the United States. These include West Nile virus, dengue virus, and chikungunya virus. In the case of the 2009 dengue outbreak in southern Florida, climate change was not responsible for the reintroduction of the virus in this area, which arrived via infected travelers from disease-endemic regions of the Caribbean.7 In fact, vector populations capable of transmitting dengue have been present for many years throughout much of the southern United States, including Florida.8 Climate change has the potential to increase human exposure risk or disease transmission following shifts in extended spring and summer seasons as dengue becomes more established in the United States. Climate change effects, however, are difficult to quantify due to the adaptive capacity of a population that may reduce exposure to vector-borne pathogens through such means as air conditioning, screens on windows, vector control, and public health practices.

This chapter presents case studies of Lyme disease and West Nile virus infection in relation to weather and climate. Although ticks and mosquitoes transmit multiple infectious pathogens to humans in the United States, Lyme disease and West Nile virus infection are the most commonly reported tick-borne and mosquito-borne diseases in this country (Table 5.1). In addition, a substantial number of studies have been conducted to elucidate the role of climate in the transmission of these infectious pathogens. These broad findings, together with the areas of uncertainty from these case studies, are generalizable to other vector-borne diseases.1


Figure 5.1: Climate Change and Health—Lyme Disease

Figure 5.1: Climate Change and Health—Lyme Disease
This conceptual diagram illustrates the key pathways by which climate change influences human exposure to Lyme disease and the potential resulting health outcomes (center boxes). These exposure pathways exist within the context of other factors that positively or negatively influence health outcomes (gray side boxes). Key factors that influence vulnerability for individuals are shown in the right box, and include social determinants of health and behavioral choices. Key factors that influence vulnerability at larger scales, such as natural and built environments, governance and management, and institutions, are shown in the left box. All of these influencing factors can affect an individual’s or a community’s vulnerability through changes in exposure, sensitivity, and adaptive capacity and may also be affected by climate change. See Ch. 1: Introduction for more information.

5.2 Lyme Disease

State of the Science

Blacklegged tick

In the eastern United States, Lyme disease is transmitted to humans primarily by blacklegged (deer) ticks.

Lyme disease is a tick-borne bacterial disease that is endemic (commonly found) in parts of North America, Europe, and Asia. In the United States, Lyme disease is caused by the bacterium Borrelia burgdorferi sensu stricto (B. burgdorferi; one of the spiral-shaped bacteria known as spirochetes) and is the most commonly reported vector-borne illness. It is primarily transmitted to humans in the eastern United States by the tick species Ixodes scapularis (formerly I. dammini), known as blacklegged ticks or deer ticks, and in the far western United States by I. pacificus, commonly known as western blacklegged ticks.19 Illness in humans typically presents with fever, headache, fatigue, and a characteristic skin rash called erythema migrans. If left untreated, infection can spread to joints, the heart, and the nervous system.20 Since 1991, when standardized surveillance and reporting of Lyme disease began in the United States, case counts have increased steadily.21 Since 2007, more than 25,000 Lyme disease cases have been reported annually.22 The geographic distribution of the disease is limited to specific regions in the United States (Figure 5.2), transmission occurs seasonally, and year-to-year variation in case counts and in seasonal onset is considerable.20,21,23 Each of these observations suggest that geographic location and seasonal climate variability may play a significant role in determining when and where Lyme disease cases are most likely to occur.

Although the reported incidence of Lyme disease is greater in the eastern United States compared with the westernmost United States,20,21 in both geographical regions, nymphs (small immature ticks) are believed to be the life stage that is most significant in pathogen transmission from infected hosts (primarily rodents) to humans (Figure 5.2, Figure 5.3).24,25 Throughout the United States, the majority of human cases report onset of clinical signs of infection during the months of June, July, and August. The summer is a period of parallel increased activity for both blacklegged and western blacklegged ticks in the nymphal life stage (the more infectious stage) and for human recreational activity outdoors.21,25

Infection rates in humans vary significantly from year to year. From 1992 to 2006, variation in case counts of Lyme disease was as high as 57% from one year to the next.21 Likewise, the precise week of onset of Lyme disease cases across states in the eastern United States, where Lyme disease is endemic, differed by as much as 10 weeks from 1992 to 2007. Much of this variation in timing of disease onset can be explained by geographic region (cases occurred earlier in warmer states in the mid-Atlantic region compared with cooler states in the North); however, the annual variation of disease onset within regions was notable and linked to winter and spring climate variability (see “Annual and Seasonal Variation in Lyme Disease” below).23


Figure 5.2: Changes in Lyme Disease Case Report Distribution

Figure 5.2: Changes in Lyme Disease Case Report Distribution
Maps show the reported cases of Lyme disease in 2001 and 2014 for the areas of the country where Lyme disease is most common (the Northeast and Upper Midwest). Both the distribution and the numbers of cases have increased. (Figure source: adapted from CDC 2015)65

The geographic and seasonal distributions of Lyme disease case occurrence are driven, in part, by the life cycle of vector ticks (Figure 5.3). Humans are only exposed to Lyme disease spirochetes (B. burgdorferi) in locations where both the vector tick populations and the infection-causing spirochetes are present.26 Within these locations, the potential for contracting Lyme disease depends on three key factors: 1) tick vector abundance (the density of host-seeking nymphs being particularly important), 2) prevalence of B. burgdorferi infection in ticks (the prevalence in nymphs being particularly important), and 3) contact frequency between infected ticks and humans.27 To varying degrees, climate change can affect all three of these factors.

Aside from short periods of time when they are feeding on hosts (less than three weeks of their two- to three-year life cycle), ticks spend most of their lives off of hosts in various natural landscapes (such as woodlands or grasslands) where weather factors including temperature, precipitation, and humidity affect their survival and host-seeking behavior. In general, both low and high temperatures increase tick mortality rates, although increasing humidity can increase their ability to tolerate higher temperatures.28,29,30,31,32,33,34,35,36,37 Within areas where tick vector populations are present, some studies have demonstrated an association among temperature, humidity, and tick abundance.38,39,40 Factors that are less immediately dependent on climate (for example, landscape and the relative proportions within a community of zoonotic hosts that carry or do not carry Lyme disease-causing bacteria) may be more important in smaller geographic areas.41,42 Temperature and humidity also influence the timing of host-seeking activity,31,34,35,43 and can influence which seasons are of highest risk to the public.

In summary, weather-related variables can determine geographic distributions of ticks and seasonal activity patterns. However, the importance of these weather variables in Lyme disease transmission to humans compared with other important predictors is likely scale-dependent. In general, across the entire country, climate-related variables often play a significant role in determining the occurrence of tick vectors and Lyme disease incidence in the United States (for example, Lyme disease vectors are absent in the arid Intermountain West where climate conditions are not suitable for tick survival). However, within areas where conditions are suitable for tick survival, other variables (for example, landscape and the relative proportions within a community of zoonotic hosts that carry or do not carry Lyme disease-causing bacteria) are more important for determining tick abundance, infection rates in ticks, and ultimately human infection rates.38,44,45

Observed Trends and Measures of Human Risk

Geographic Distribution of Ticks

Because the presence of tick vectors is required for B. burgdorferi transmission to humans, information on where vector tick species live provides basic information on where Lyme disease risk occurs. Minimum temperature appears to be a key variable in defining the geographic distribution of blacklegged ticks.38,44,46 Low minimum temperatures in winter may lead to environmental conditions that are unsuitable for tick population survival. The probability of a given geographic area being suitable for tick populations increases as minimum temperature rises.44 In the case of the observed northward range expansion of blacklegged ticks into Canada, higher temperatures appear to be a key factor affecting where, and how fast, ticks are colonizing new localities.47,48,49,50,51

Maximum temperatures also significantly affect where blacklegged ticks live.38,44 Higher temperatures increase tick development and hatching rates, but reduce tick survival and egg-laying (reproduction) success.29

Declines in rainfall amount and humidity are also important in limiting the geographic distribution of blacklegged ticks. Ticks are more likely to reside in moister areas because increased humidity can increase tick survival.34,37,38,44,46,48 

Geographic Distribution of Infected Ticks

Climate variables have been shown to be strong predictors of geographic locations in which blacklegged ticks reside, but less important for determining how many nymphs live in a given area or what proportion of those ticks is infected.38,39 The presence of uninfected nymphs and infected nymphs can vary widely over small geographic areas experiencing similar temperature and humidity conditions, which supports the hypothesis that factors other than weather play a significant role in determining nymph survival and infection rates.36,38,39,40,43 Additional studies that modeled nymphal density within small portions of the blacklegged tick range (north-central states and Hudson River Valley, NY), and modeling studies that include climate and other non-biological variables indicate only a weak relationship to nymphal density.52,53 Nonetheless, climate variables can be used to model nymphal density in some instances. For example, in a single county in northern coastal California with strong climate gradients, warmer areas with less variation between maximum and minimum monthly water vapor in the air were characteristic of areas with elevated concentrations of infected nymphs.40 However, it is likely that differences in animal host community structure, which vary with climatic conditions (for example, relative abundances of hosts that carry or do not carry Lyme disease-causing bacteria), influenced the concentration of infected nymphs.36,54

Geographic Distribution of Lyme Disease

Though there are links between climate and tick distribution, studies that look for links between weather and geographical differences in human infection rates do not show a clear or consistent link between temperature and Lyme disease incidence.45,55,56


Annual and Seasonal Variation in Lyme Disease

Temperature and precipitation both influence the host-seeking activity of ticks, which may result in year-to-year variation in the number of new Lyme disease cases and the timing of the season in which Lyme disease infections occur. However, identified associations between precipitation and Lyme disease incidence, or temperature and Lyme disease incidence, are limited or weak.57,58 Overall, the association between summer moisture and Lyme disease infection rates in humans remains inconsistent across studies.

House finch

Birds such as the house finch are the natural host of West Nile virus.

The peak period when ticks are seeking hosts starts earlier in the warmer, more southern, states than in northern states.43 Correspondingly, the onset of human Lyme disease cases occurs earlier as the growing degree days (a measurement of temperature thresholds that must be met for biological processes to occur) increases, yet, the timing of the end of the Lyme disease season does not appear to be determined by weather-related variables.23 Rather, the number of potential carriers (for example, deer, birds, and humans) likely influences the timing of the end of the Lyme disease season.

The effects of temperature and humidity or precipitation on the seasonal activity patterns of nymphal western blacklegged ticks is more certain than the impacts of these factors on the timing of Lyme disease case occurrence.35,36 Peak nymphal activity is generally reached earlier in hotter and drier areas, but lasts for shorter durations. Host-seeking activity ceases earlier in the season in cooler and more humid conditions. The density of nymphal western blacklegged ticks in north-coastal California consistently begins to decline when average daily maximum temperatures are between 70°F (21°C) and 73.5°F (23°C), and when average maximum daily relative humidity decreases below 83%–85%.35,36

Projected Impacts

Warmer winter and spring temperatures are projected to lead to earlier annual onset of Lyme disease cases in the eastern United States (see “Research Highlight” below) and in an earlier onset of nymphal host-seeking behavior.59 Limited research shows that the geographic distribution of blacklegged ticks is expected to expand to higher latitudes and elevations in the future and retract in the southern United States.60 Declines in subfreezing temperatures at higher latitudes may be responsible for improved survival of ticks. In many woodlands, ticks can find refuge from far-subzero winter air temperatures in the surface layers of the soil.61,62 However, a possibly important impact of climate change will be acceleration of the tick life cycles due to higher temperatures during the spring, summer, and autumn, which would increase the likelihood that ticks survive to reproduce.51,63 This prediction is consistent with recent observations of the spread of I. scapularis in Canada.48,64

To project accurately the changes in Lyme disease risk in humans based on climate variability, long-term data collection on tick vector abundance and human infection case counts are needed to better understand the relationships between changing climate conditions, tick vector abundance, and Lyme disease case occurrence.


5.3 West Nile Virus

State of the Science

West Nile virus (WNV) is the leading cause of mosquito-borne disease in the United States. From 1999 to 2013, a total of 39,557 cases of WNV disease were reported in the United States.73 Annual variation is substantial, both in terms of case counts and the geographic distribution of cases of human infection (Figure 5.5).73 Since the late summer of 1999, when an outbreak of WNV first occurred in New York City,74 human WNV cases have occurred in the United States every year. After the introduction of the virus to the United States, WNV spread westward, and by 2004 WNV activity was reported throughout the contiguous United States.75,76 Annual human WNV incidence remained stable through 2007, decreased substantially through 2011, and increased again in 2012, raising questions about the factors driving year-to-year variation in disease transmission.75 The locations of annual WNV outbreaks vary, but several states have reported consistently high rates of disease over the years, including Arizona, California, Colorado, Idaho, Illinois, Louisiana, New York, North Dakota, South Dakota, and Texas.73,75


Figure 5.5: Incidence of West Nile Neuroinvasive Disease by County in the United States

Figure 5.5: Incidence of West Nile Neuroinvasive Disease by County in the United States
Maps show the incidence of West Nile neuroinvasive disease in the United States for 2010 through 2013. Shown as cases per 100,000 people. (Data source: CDC 2014)73

The majority (70% to 80%) of people infected with WNV do not show symptoms of the disease. Of those infected, 20% to 30% develop acute systemic febrile illness, which may include headache, myalgias (muscle pains), rash, or gastrointestinal symptoms; fewer than 1% experience neuroinvasive disease, which may include meningitis (inflammation around the brain and spinal cord), encephalitis (inflammation of the brain), or myelitis (inflammation of the spinal cord) (see Section 5.4 “Populations of Concern” below).77 Because most infected persons are asymptomatic (showing no symptoms), there is significant under-reporting of cases.78,79,80 More than three million people were estimated to be infected with WNV in the United States from 1999 to 2010, resulting in about 780,000 illnesses.77 However, only about 30,700 cases were reported during the same time span.73


Humans can be infected from a bite of a mosquito that has previously bitten an infected bird.

West Nile virus is maintained in transmission cycles between birds (the natural hosts of the virus) and mosquitoes (Figure 5.6). The number of birds and mosquitoes infected with WNV increases as mosquitoes pass the virus from bird to bird starting in late winter or spring. Human infections can occur from a bite of a mosquito that has previously bitten an infected bird.81 Humans do not pass on the virus to biting mosquitoes because they do not have sufficient concentrations of the virus in their bloodstreams.82,83 In rare instances, WNV can be transmitted through blood transfusions or organ transplants.82,84 Peak transmission of WNV to humans in the United States typically occurs between June and September, coinciding with the summer season when mosquitoes are most active and temperatures are highest.85


Figure 5.6: Climate Impacts on West Nile Virus Transmission

Figure 5.6: Climate Impacts on West Nile Virus Transmission

Observed Impacts and Indicators

Mosquito vectors and bird hosts are required for WNV to persist, and the dynamics of both are strongly affected by climate in a number of ways. Geographical variation in average climate constrains the ranges of both vectors and hosts, while shorter-term climate variability affects many aspects of vector and host population dynamics. Unlike ticks, mosquitoes have short life cycles and respond more quickly to climate drivers over relatively short timescales of days to weeks. Impacts on bird abundance are often realized over longer timescales of months to years due to impacts on annual reproduction and migration cycles.

WNV has been detected in 65 mosquito species and more than 300 bird species in the United States,85 although only a relatively small number of these species contribute substantively to human infections. Three Culex (Cx.) mosquito species are the primary vectors of the virus in different regions of the continental United States, and differences in their preferred breeding habitats mean that climate change will likely impact human WNV disease risk differently across these regions (Figure 5.5). Bird species that contribute to WNV transmission include those that develop sufficient viral concentrations in their blood to transmit the virus to feeding mosquitoes.86,87 As with mosquitoes, the bird species involved in the transmission cycle are likely to respond differently to climate change, increasing the complexity of projecting future WNV risk.

Impacts of Climate and Weather

Climate, or the long-term average weather, is important for defining WNV’s transmission range limits because extreme conditions—too cold, hot, wet, or dry—can alter mosquito and bird habitat availability, increase mortality in mosquitoes or birds, and/or disrupt viral transmission. WNV is an invasive pathogen that was first detected in the United States just over 15 years ago, which is long enough to observe responses of WNV to key weather variables, but not long enough to observe responses to climate change trends.

Climate change may influence mosquito survival rates through changes in season length, although mosquitoes are also able to adapt to changing conditions. For example, mosquitoes that transmit WNV are limited to latitudes and altitudes where winters are short enough for them to survive.88 However, newly emerged adult female mosquitoes have some ability to survive cold temperatures by entering a reproductive arrest called diapause as temperatures begin to cool and days grow shorter in late summer.89,90 These females will not seek a blood meal until temperatures begin to warm the following year. Even during diapause, very harsh winters may reduce mosquito populations, as temperatures near freezing have been shown to kill diapausing Cx. tarsalis.91

During the warmer parts of the year, Culex mosquitoes must have aquatic habitat available on a nearly continuous basis because their eggs hatch within a few days after they are laid and need moisture to remain viable. The breeding habitats of WNV vectors vary by species, ranging from fresh, sunlit water found in irrigated crops and wetlands preferred by Cx. tarsalis to stagnant, organically enriched water sources such as urban storm drains, unmaintained swimming pools, or backyard containers used by Cx. pipiens and Cx. quinquefasciatus92,93,94

WNV has become endemic within a wide range of climates in the United States, but there is substantial geographic variation in the intensity of virus transmission. Part of this geographic variation can be attributed to the abundance and distributions of suitable bird hosts.95 Important hosts, such as robins, migrate annually between summer breeding grounds and winter foraging areas.86,96 Migrating birds have shown potential as a vehicle for long-range virus movement.97,98 Although the timing of migration is driven by climate, the impact of climate change-driven migration changes on WNV transmission have not yet been documented by scientists. Climate change has already begun to cause shifts in bird breeding and migration patterns,99 but it is unknown how these changes may affect WNV transmission.

Temperature is the most studied climate driver of the dynamics of WNV transmission. It is clear that warm temperatures accelerate virtually all of the biological processes that affect transmission: accelerating the mosquito life cycle,100,101,102,103,104 increasing the mosquito biting rates that determine the frequency of contact between mosquitoes and hosts,105,106 and increasing viral replication rates inside the mosquito that decrease the time needed for a blood-fed mosquito to be able to pass on the virus.107,108,109 These relationships between increasing temperatures and the biological processes that affect WNV transmission suggest a subsequent increase in risk of human disease.110,111,112,113 However, results from models have suggested that extreme high temperatures combined with decreased precipitation may decrease mosquito populations.114

Precipitation can create aquatic breeding sites for WNV vectors,115,116 and in some areas snowpack increases the amount of stored water available for urban or agricultural systems, which provide important habitat for WNV vectors,117,118 although effects depend on human water management decisions and vary spatially.101 Droughts have been associated with increased WNV activity, but the association between decreased precipitation and WNV depends on location and the particular sequence of drought and wetting that precedes the WNV transmission season.119,120,121,122

The impact of year-to-year changes in precipitation on mosquito populations varies among the regions of the United States and is affected by the typical climate of the area as well as other non-climate factors, such as land use or water infrastructure and management practices. In the northern Great Plains—a hotspot for WNV activity—increased precipitation has been shown to lead to higher Cx. tarsalis abundance a few weeks later.116 In contrast, in the typically wet Pacific Northwest, weekly precipitation was found to be unrelated to subsequent mosquito abundance.123 In urban areas, larvae (aquatic immature mosquitoes) may be washed out of their underground breeding habitats by heavy rainfall events, making drier conditions more favorable for WNV transmission.110,124,125 In rural areas or drier regions, increased precipitation or agricultural irrigation may provide the moisture necessary for the development of breeding habitats.121

Impacts of Long-Term Climate Trends

The relatively short period of WNV’s transmission in the United States prevents direct observation of the impacts of long-term climate trends on WNV incidence. However, despite the short history of WNV in the United States, there are some lessons to be learned from other mosquito-borne diseases with longer histories in the United States.

Western equine encephalomyelitis virus (WEEV) and St. Louis encephalitis virus (SLEV) were first identified in the 1930s and have been circulating in the United States since that time. Like WNV, both viruses are transmitted primarily by Culex mosquitoes and are climate-sensitive. WEEV outbreaks were associated with wet springs followed by warm summers.118,126 Outbreaks of SLEV were associated with hot, dry periods when urban mosquito production increased due to stagnation of water in underground systems or when cycles of drought and wetting set up more complex transmission dynamics.127,128

Despite climatic warming that would be expected to favor increased WEEV and SLEV transmission, both viruses have had sharply diminished incidence during the past 30 to 40 years.129,130 Although the exact reason for this decline is unknown, it is likely a result of non-climate factors, such as changes in human behavior or undetected aspects of viral evolution. Several other mosquito-borne pathogens, such as chikungunya and dengue, have grown in importance as global health threats during recent decades; however, a link to climate change induced disease expansion in the United States has not yet been confirmed. These examples demonstrate the variable impact that climate change can have on different mosquito-borne diseases and help to explain why the direction of future trends in risk for WNV remain unclear.

Projected Impacts

Given WNV’s relatively short history in the United States, the described geographic variation in climate responses, and the complexity of transmission cycles, projecting the future distribution of WNV under climate change remains a challenge. Despite the growing body of work examining the connections between WNV and weather, climate-based seasonal forecasts of WNV outbreak risk are not yet available at a national scale. Forecasting the annual presence of WNV disease on the basis of climate and other ecological factors has been attempted for U.S. counties, with general agreement between modeled expectations and observed data, but more quantitative predictions of disease incidence or the risk for human exposure are needed.131

Longer-term projections of WNV under climate change scenarios are also rare. WNV is projected to increase in much of the northern and southeastern United States due to rising temperatures and declining precipitation, respectively, with the potential for decreased occurrence across the central United States.132 Future projections show that the season when mosquitoes are most abundant will begin earlier and end later, possibly resulting in fewer mosquitoes in mid-summer in southern locations where extreme heat is predicted to coincide with decreased summer precipitation.114

5.4 Populations of Concern

Climate change will influence human vulnerability to vector-borne disease by influencing the seasonality and the location of exposures to pathogens and vectors. These impacts may influence future disease patterns; certain vector-borne diseases may emerge in areas where they had previously not been observed and other diseases may become less common in areas where they had previously been very common. As such, some segments of the U.S. population may be disproportionately affected by, or exposed to, vector-borne diseases in response to climate change (see also Ch. 9: Populations of Concern).

In addition to climate factors, multiple non-climate factors also influence human exposure to vector-borne pathogens.7,133,134,135,136,137 Some of these include factors from an environmental or institutional context (Figure 5.1), such as pathogen adaptation and change, changes in vector and host population and composition, changes in pathogen infection rates, and vector control or other public health practices (pesticide applications, integrated vector management, vaccines, and other disease interventions). Other non-climate factors that influence vulnerability to vector-borne disease include those from a social and behavioral context, such as outdoor activity, occupation, landscape design, proximity to vector habitat, and personal protective behaviors (applying repellents before spending time in tick habitat, performing tick checks, and bathing after being outdoors).138 For Lyme disease, behavioral factors, especially the number of hours spent working or playing outdoors in tick habitat as well as proximity to dense shrubbery, can increase exposure to the ticks that transmit the bacteria that causes Lyme disease.139 For example, outdoor workers in the northeastern United States are at higher risk for contact with blacklegged ticks and, therefore, are at a greater risk for contracting Lyme disease.140,141,142 If outdoor workers are working in areas where there are infected mosquitoes, occupational exposures can also occur for WNV.143

Individual characteristics, such as age, gender, and immune function, may also affect vulnerability by influencing susceptibility to infection.21,80,140,143,144,145 Lyme disease is more frequently reported in children between 5 and 9 years of age and in adults between the ages of 55 and 59,21 and advanced age and being male contribute to a higher risk for severe WNV infections.79,144,145

The impacts of climate change on human vulnerability to vector-borne disease may be minimized by individual- or community-level adaptive capacity, or the ability to reduce the potential exposures that may be caused by climate change. For example, socioeconomic status and domestic protective barriers, such as screens on windows and doors, can limit exposures to vector-borne pathogens.7,134,135,136,137 From 1980 to 1999, the infected mosquito counts in Laredo, Texas, were significantly higher than in three adjoining Mexican states—yet, while there were only 64 cases of dengue fever reported in Texas, more than 62,000 dengue fever cases were reported in the Mexican states.137 In Texas, socioeconomic factors and adaptive measures, including houses with air conditioning and intact screens, contributed to the significantly lower dengue incidence by reducing human–mosquito contact.137 The adaptive capacity of a population may augment or limit the impacts of climate change to human vulnerability for vector-borne disease.137

Climate factors are useful benchmarks to indicate seasonal risk and broad geographic changes in disease occurrence over decades. However, human vulnerability to vector-borne disease is more holistically evaluated by examining climate factors with non-climate factors (environmental or institutional context, social and behavioral context, and individual characteristics). Ultimately, a community’s capacity to adapt to both the climate and non-climate factors will affect population vulnerability to vector-borne disease.

5.5 Emerging Issues

Some vector-borne diseases may be introduced or become re-established in the United States by a variety of mechanisms. In conjunction with trade and travel, climate change may contribute by creating habitats suitable for the establishment of disease-carrying vectors or for locally sustained transmission of vector-borne pathogens. Examples of emerging vector-borne diseases in the United States include the West Nile virus introduction described above, recent outbreaks of locally acquired dengue in Florida7,146 and southern Texas,147 and chikungunya cases in the Caribbean and southern Florida,148 all of which have raised public health concern about emergence and re-emergence of these mosquito-borne diseases in the United States. Collecting data on the spread of disease-causing insect vectors and the viruses that cause dengue and chikungunya is critical to understanding and predicting the threat of emergence or reemergence of these diseases. Understanding the role of climate change in disease emergence and reemergence would also require additional research.

5.6 Research Needs

In addition to the emerging issues identified above, and based on their review of the literature, the authors highlight the following areas for potential scientific research activity on vector-borne disease. Climate and non-climate factors interact to determine the burden of vector-borne diseases on humans, but the mechanisms of these processes are still poorly understood.149 Evidence-based models that include vector–host interaction, host immunity, pathogen evolution, and land use, as well as socioeconomic drivers of transmission, human behavior, and adaptive capacity are needed to facilitate a better understanding of the mechanisms by which climate and non-climate factors drive vector-borne disease emergence. Socioeconomic and human behavioral factors, in particular, appear to limit vector-borne diseases, even in neighboring cities.136,137 This is a fertile area for future research, and one that is particularly relevant for increasing our adaptive capacity to address future vector-borne disease threats.

Numerous studies have identified associations between vector-borne diseases and weather or climate, but most have focused on risk mapping or estimating associations of broad aggregates of temperature and precipitation with disease-related outcomes. A move beyond correlative associations to a more mechanistic understanding of climate’s impacts on the discrete events that give rise to transmission is needed. Models must also be accompanied by empirical research to inform their parameters. Climate effects are complex, and models frequently borrow information across vector species and pathogens or make simplifying assumptions that can lead to incorrect conclusions.150 

The risk for vector-borne diseases is highly variable geographically and over time. Monitoring responses of pathogens to climate change at a continental scale requires coordinated, systematically collected long-term surveillance datasets to document changes in vector occurrence, abundance, and infection rates. Collecting these data will provide a clearer understanding of how external drivers work in conjunction with climate change to determine the risk for human exposure to vector-borne disease. 

Future assessments can benefit from research activities that:

  • evaluate how climatic variables, socioeconomic factors, and human behavior influence vector-borne disease occurrence and are expected to affect human adaptive capacity and the ability to respond to future disease threats;
  • enhance long-term, systematic data collection on vector and pathogen distributions to detect changes over time. Such datasets must span a range of land-use types, including urban areas, and should be coupled with data on human disease;
  • utilize mechanistic models that provide an evidence-based view of climate’s impacts on vector-borne diseases by explicitly accounting for the series of discrete but intertwined events that give rise to transmission. Models should be supported and validated by data specific to the disease system and include a realistic assessment of parameter uncertainty and variability;
  • study the natural maintenance cycles of vector-borne pathogen evolution, emergence, and transmission as well as how climatic variables influence these cycles.


  1. Allan, B. F., F. Keesing, and R. S. Ostfeld, 2003: Effect of forest fragmentation on Lyme disease risk. Conservation Biology, 17, 267-272. doi:10.1046/j.1523-1739.2003.01260.x | Detail
  2. Ashley, S. T., and V. Meentemeyer, 2004: Climatic analysis of Lyme disease in the United States. Climate Research, 27, 177-187. doi:10.3354/cr027177 | Detail
  3. Bacon, R. M., K. J. Kugeler, and P. S. Mead, 2008: Surveillance for Lyme disease--United States, 1992-2006. Morbidity and Mortality Weekly Report - Surveillance Summaries, 57, 1-9. PMID: 18830214 | Detail
  4. Barker, C. M., B. G. Bolling, W. C. Black, C. G. Moore, and L. Eisen, 2009: Mosquitoes and West Nile virus along a river corridor from prairie to montane habitats in eastern Colorado. Journal of Vector Ecology, 34, 276-293. doi:10.1111/j.1948-7134.2009.00036.x | Detail
  5. Beasley, D. W., A. D. Barrett, and R. B. Tesh, 2013: Resurgence of West Nile neurologic disease in the United States in 2012: What happened? What needs to be done? Antiviral Research, 99, 1-5. doi:10.1016/j.antiviral.2013.04.015 | Detail
  6. Bennett, C. M., and A. J. McMichael, 2010: Non-heat related impacts of climate change on working populations. Global Health Action, 3, 5640. doi:10.3402/gha.v3i0.5640 | Detail
  7. Bertrand, M. R., and M. L. Wilson, 1996: Microclimate-dependent survival of unfed adult Ixodes scapularis (Acari: Ixodidae) in nature: Life cycle and study design implications. Journal of Medical Entomology, 33, 619-627. doi:10.1093/jmedent/33.4.619 | Detail
  8. Bouchard, C., G. Beauchamp, P. A. Leighton, R. Lindsay, D. Belanger, and N. H. Ogden, 2013: Does high biodiversity reduce the risk of Lyme disease invasion? Parasites & Vectors, 6, 195. doi:10.1186/1756-3305-6-195 | Detail
  9. Bowen, G. S., T. L. Schulze, C. Hayne, and W. E. Parkin, 1984: A focus of Lyme disease in Monmouth County, New Jersey. American Journal of Epidemiology, 120, 387-394. PMID: 6475916 | Detail
  10. Brien, J. D., J. L. Uhrlaub, A. Hirsch, C. A. Wiley, and J. Nikolich-Žugich, 2009: Key role of T cell defects in age-related vulnerability to West Nile virus. The Journal of Experimental Medicine, 206, 2735-2745. doi:10.1084/jem.20090222 | Detail
  11. Brownstein, J. S., T. R. Holford, and D. Fish, 2003: A climate-based model predicts the spatial distribution of the Lyme disease vector Ixodes scapularis in the United States. Environmental Health Perspectives, 111, 1152-1157. doi:10.1289/ehp.6052 | Detail
  12. Brownstein, J. S., T. R. Holford, and D. Fish, 2005: Effect of climate change on Lyme disease risk in North America. EcoHealth, 2, 38-46. doi:10.1007/s10393-004-0139-x | Detail
  13. Brunkard, J. M., E. Cifuentes, and S. J. Rothenberg, 2008: Assessing the roles of temperature, precipitation, and ENSO in dengue re-emergence on the Texas-Mexico border region. Salud Publica Mex, 50, 227-234. doi:10.1590/S0036-36342008000300006 | Detail
  14. Brunner, J. L., M. Killilea, and R. S. Ostfeld, 2012: Overwintering survival of nymphal Ixodes scapularis (Acari: Ixodidae) under natural conditions. Journal of Medical Entomology, 49, 981-987. doi:10.1603/me12060 | Detail
  15. Busch, M. P., and others, 2006: West Nile virus infections projected from blood donor screening data, United States, 2003. Emerging Infectious Diseases, 12, 395-402. doi:10.3201/eid1203.051287 | Detail
  16. Calhoun, L. M., M. Avery, L. A. Jones, K. Gunarto, R. King, J. Roberts, and T. R. Burkot, 2007: Combined sewage overflows (CSO) are major urban breeding sites for Culex quinquefasciatus in Atlanta, Georgia. The American Journal of Tropical Medicine and Hygiene, 77, 478-484. URL | Detail
  17. Carson, P. J., and others, 2012: Neuroinvasive disease and West Nile virus infection, North Dakota, USA, 1999–2008. Emerging Infectious Diseases, 18, 684-686. doi:10.3201/eid1804.111313 | Detail
  18. CDC, 2005: Notice to readers: Final 2004 reports of Notifiable Diseases. MMWR. Morbidity and Mortality Weekly Report, 54, 770-780. URL | Detail
  19. CDC, 2006: Notice to readers: Final 2005 Reports of Notifiable Diseases. MMWR. Morbidity and Mortality Weekly Report, 55, 880-881. URL | Detail
  20. CDC, 2007: Notice to readers: Final 2006 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 56, 853-863. URL | Detail
  21. CDC, 2008: Notice to readers: Final 2007 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 57, 901,903-913. URL | Detail
  22. CDC, 2009: Notice to readers: Final 2008 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 58, 856-869. URL | Detail
  23. CDC, 2010: Notice to readers: Final 2009 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 59, 1027-1039. URL | Detail
  24. CDC, 2011: Notice to readers: Final 2010 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 60, 1088-1101. URL | Detail
  25. CDC, 2012: Notice to readers: Final 2011 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 61, 624-637. URL | Detail
  26. CDC, 2014: Notice to readers: Final 2013 Reports of Nationally Notifiable Infectious Diseases. MMWR. Morbidity and Mortality Weekly Report, 63, 702-715. URL | Detail
  27. CDC, cited 2014: Surveillance Resources: ArboNET. Centers for Disease Control and Prevention, Arboviral Diseases Branch. URL | Detail
  28. CDC, cited 2015: Lyme Disease: Data and Statistics: Maps- Reported Cases of Lyme Disease – United States, 2001-2014. Centers for Disease Control and Prevention. URL | Detail
  29. CDC, cited 2015: Ticks: Life Cycle of Hard Ticks that Spread Disease. Centers for Disease Control and Prevention. URL | Detail
  30. CDC, cited 2015: Reported Cases of Lyme Disease by Year, United States, 1995-2013. Centers for Disease Control and Prevention. URL | Detail
  31. CDC, cited 2015: Lyme Disease: Preventing Tick Bites on People. Centers for Disease Control and Prevention. URL | Detail
  32. Centers for Disease Control and Prevention (CDC), 2013: Notice to readers: Final 2012 Reports of Nationally Notifiable Infectious Diseases. Morbidity and Mortality Weekly Report, 62, 669-682. PMID: 24133698 | Detail
  33. Chuang, T. W., M. B. Hildreth, D. L. Vanroekel, and M. C. Wimberly, 2011: Weather and land cover influences on mosquito populations in Sioux Falls, South Dakota. Journal of Medical Entomology, 48, 669-679. doi:10.1603/me10246 | Detail
  34. Clover, J. R., and R. S. Lane, 1995: Evidence implicating nymphal Ixodes pacificus (Acari, ixodidae) in the epidemiology of Lyme disease in California. The American Journal of Tropical Medicine and Hygiene, 53, 237-240. | Detail
  35. Darsie, R. F., and R. A. Ward, 2005: Identification and Geographical Distribution of the Mosquitos of North America, North of Mexico. University Press of Florida, 383 pp. | Detail
  36. DeGroote, J. P., R. Sugumaran, S. M. Brend, B. J. Tucker, and L. C. Bartholomay, 2008: Landscape, demographic, entomological, and climatic associations with human disease incidence of West Nile virus in the state of Iowa, USA. International Journal of Health Geographics, 7, 19. doi:10.1186/1476-072x-7-19 | Detail
  37. Dennis, D. T., T. S. Nekomoto, J. C. Victor, W. S. Paul, and J. Piesman, 1998: Forum: Reported Distribution of Ixodes scapularis and Ixodes pacificus (Acari: Ixodidae) in the United States. Journal of Medical Entomology, 35, 629-638. doi:10.1093/jmedent/35.5.629 | Detail
  38. Dick, O. B., J. L. San Martín, R. H. Montoya, J. del Diego, B. Zambrano, and G. H. Dayan, 2012: The history of dengue outbreaks in the Americas. American Journal of Tropical Medicine and Hygiene, 87, 584-593. doi:10.4269/ajtmh.2012.11-0770 | Detail
  39. Diuk-Wasser, M. A., and others, 2006: Spatiotemporal Patterns of Host-Seeking Ixodes scapularis Nymphs (Acari: Ixodidae) in the United States. Journal of Medical Entomology, 43, 166-176. doi:10.1093/jmedent/43.2.166 | Detail
  40. Diuk-Wasser, M. A., and others, 2010: Field and climate-based model for predicting the density of host-seeking nymphal Ixodes scapularis, an important vector of tick-borne disease agents in the eastern United States. Global Ecology and Biogeography, 19, 504-514. doi:10.1111/j.1466-8238.2010.00526.x | Detail
  41. Diuk-Wasser, M. A., and others, 2012: Human Risk of Infection with Borrelia burgdorferi, the Lyme Disease Agent, in Eastern United States. The American Journal of Tropical Medicine and Hygiene, 86, 320-327. doi:10.4269/ajtmh.2012.11-0395 | Detail
  42. Dodson, B. L., L. D. Kramer, and J. L. Rasgon, 2012: Effects of larval rearing temperature on immature development and West Nile virus vector competence of Culex tarsalis. Parasites & Vectors, 5, 199. doi:10.1186/1756-3305-5-199 | Detail
  43. Dohm, D. J., M. L. O'Guinn, and M. J. Turell, 2002: Effect of environmental temperature on the ability of Culex pipiens (Diptera: Culicidae) to transmit West Nile virus. Journal of Medical Entomology, 39, 221-225. doi:10.1603/0022-2585-39.1.221 | Detail
  44. Dusek, R. J., R. G. McLean, L. D. Kramer, S. R. Ubico, A. P. Dupuis, G. D. Ebel, and S. C. Guptill, 2009: Prevalence of West Nile virus in migratory birds during spring and fall migration. The American Journal of Tropical Medicine and Hygiene, 81, 1151-1158. doi:10.4269/ajtmh.2009.09-0106 | Detail
  45. Eisen, L., C. M. Barker, C. G. Moore, W. J. Pape, A. M. Winters, and N. Cheronis, 2010: Irrigated agriculture is an important risk factor for West Nile virus disease in the hyperendemic Larimer-Boulder-Weld area of north central Colorado. Journal of Medical Entomology, 47, 939-951. doi:10.1093/jmedent/47.5.939 | Detail
  46. Eisen, L., R. J. Eisen, and R. S. Lane, 2002: Seasonal activity patterns of Ixodes pacificus nymphs in relation to climatic conditions. Medical and Veterinary Entomology, 16, 235-244. doi:10.1046/j.1365-2915.2002.00372.x | Detail
  47. Eisen, R. J., and others, 2010: A spatially-explicit model of acarological risk of exposure to Borrelia burgdorferi-infected Ixodes pacificus nymphs in northwestern California based on woodland type, temperature, and water vapor. Ticks and Tick-Borne Diseases, 1, 35-43. doi:10.1016/j.ttbdis.2009.12.002 | Detail
  48. Eisen, R. J., L. Eisen, and R. S. Lane, 2004: Habitat-related variation in infestation of lizards and rodents with Ixodes ticks in dense woodlands in Mendocino County, California. Experimental and Applied Acarology, 33, 215-233. doi:10.1023/B:Appa.0000032954.71165.9e | Detail
  49. Eisen, R. J., L. Eisen, M. B. Castro, and R. S. Lane, 2003: Environmentally related variability in risk of exposure to Lyme disease spirochetes in northern California: Effect of climatic conditions and habitat type. Environmental Entomology, 32, 1010-1018. doi:10.1603/0046-225X-32.5.1010 | Detail
  50. Eldridge, B. F., 1987: Diapause and related phenomena in Culex mosquitoes: Their relation to arbovirus disease ecology. Current Topics in Vector Research, 4, 1-28. doi:10.1007/978-1-4612-4712-8_1 | Detail
  51. Estrada-Peña, A., 2002: Increasing habitat suitability in the United States for the tick that transmits Lyme disease: A remote sensing approach. Environmental Health Perspectives, 110, 635-640. URL | Detail
  52. Falco, R. C., D. F. McKenna, T. J. Daniels, R. B. Nadelman, J. Nowakowski, D. Fish, and G. P. Wormser, 1999: Temporal relation between Ixodes scapularis abundance and risk for Lyme disease associated with erythema migrans. American Journal of Epidemiology, 149, 771-776. URL | Detail
  53. Finch, C., M. S. Al-Damluji, P. J. Krause, L. Niccolai, T. Steeves, C. F. O’Keefe, and M. A. Diuk-Wasser, 2014: Integrated assessment of behavioral and environmental risk factors for Lyme disease infection on Block Island, Rhode Island. PLoS ONE, 9, e84758. doi:10.1371/journal.pone.0084758 | Detail
  54. Forrester, N. L., J. L. Kenney, E. Deardorff, E. Wang, and S. C. Weaver, 2008: Western equine encephalitis submergence: Lack of evidence for a decline in virus virulence. Virology, 380, 170-172. doi:10.1016/j.virol.2008.08.012 | Detail
  55. Gage, K. L., T. R. Burkot, R. J. Eisen, and E. B. Hayes, 2008: Climate and vectorborne diseases. American Journal of Preventive Medicine, 35, 436-450. doi:10.1016/j.amepre.2008.08.030 | Detail
  56. García-Rejón, J. E., and others, 2008: Gonotrophic cycle estimate for Culex quinquefasciatus in Mérida, Yucatán, México. Journal of the American Mosquito Control Association, 24, 344-348. doi:10.2987/5667.1 | Detail
  57. Gardner, A. M., G. L. Hamer, A. M. Hines, C. M. Newman, E. D. Walker, and M. O. Ruiz, 2012: Weather variability affects abundance of larval Culex (Diptera: Culicidae) in storm water catch basins in suburban Chicago. Journal of Medical Entomology, 49, 270-276. doi:10.1603/ME11073 | Detail
  58. Gibney, K. B., and others, 2012: Modifiable Risk Factors for West Nile Virus Infection during an Outbreak--Arizona, 2010. The American Journal of Tropical Medicine and Hygiene, 86, 895-901. doi:10.4269/ajtmh.2012.11-0502 | Detail
  59. Gubler, D. J., P. Reiter, K. L. Ebi, W. Yap, R. Nasci, and J. A. Patz, 2001: Climate variability and change in the United States: Potential impacts on vector- and rodent-borne diseases. Environmental Health Perspectives, 109, 223-233. doi:10.2307/3435012 | Detail
  60. Guerra, M., and others, 2002: Predicting the risk of Lyme disease: Habitat suitability for Ixodes scapularis in the north central United States. Emerging Infectious Diseases, 8, 289-297. doi:10.3201/eid0803.010166 | Detail
  61. Harrigan, R. J., H. A. Thomassen, W. Buermann, and T. B. Smith, 2014: A continental risk assessment of West Nile virus under climate change. Global Change Biology, 20, 2417-2425. doi:10.1111/gcb.12534 | Detail
  62. Hartley, D. M., C. M. Barker, A. Le Menach, T. Niu, H. D. Gaff, and W. K. Reisen, 2012: Effects of temperature on emergence and seasonality of West Nile virus in California. The American Journal of Tropical Medicine and Hygiene, 86, 884-894. doi:10.4269/ajtmh.2012.11-0342 | Detail
  63. Hayes, E. B., N. Komar, R. S. Nasci, S. Montgomery, D. R. O'Leary, and G. L. Campbell, 2005: Epidemiology and transmission dynamics of West Nile virus disease. Emerging Infectious Diseases, 11, 1167-1173. doi:10.3201/eid1108.050289a | Detail
  64. IOM, 2003: Microbial Threats to Health: Emergence, Detection, and Response. M.S. Smolinski, Hamburg, M.A., and Lederberg, J., Eds., Institute of Medicine. The National Academies Press, 398 pp. doi:10.17226/10636 | Detail
  65. Johnson, B. J., and M. V. K. Sukhdeo, 2013: Drought-induced amplification of local and regional West Nile virus infection rates in New Jersey. Journal of Medical Entomology, 50, 195-204. doi:10.1603/me12035 | Detail
  66. Jones, K. E., N. G. Patel, M. A. Levy, A. Storeygard, D. Balk, J. L. Gittleman, and P. Daszak, 2008: Global trends in emerging infectious diseases. Nature, 451, 990-993. doi:10.1038/nature06536 | Detail
  67. Khatchikian, C. E., M. Prusinski, M. Stone, P. B. Backenson, I. N. Wang, M. Z. Levy, and D. Brisson, 2012: Geographical and environmental factors driving the increase in the Lyme disease vector Ixodes scapularis. Ecosphere, 3, art85. doi:10.1890/ES12-00134.1 | Detail
  68. Kilpatrick, A. M., 2011: Globalization, land use, and the invasion of West Nile virus. Science, 334, 323-327. doi:10.1126/science.1201010 | Detail
  69. Kilpatrick, A. M., and S. E. Randolph, 2012: Drivers, dynamics, and control of emerging vector-borne zoonotic diseases. The Lancet, 380, 1946-1955. doi:10.1016/s0140-6736(12)61151-9 | Detail
  70. Kilpatrick, A. M., M. A. Meola, R. M. Moudy, and L. D. Kramer, 2008: Temperature, viral genetics, and the transmission of West Nile virus by Culex pipiens mosquitoes. PLoS Pathogens, 4, e1000092. doi:10.1371/journal.ppat.1000092 | Detail
  71. Kilpatrick, A. M., P. Daszak, M. J. Jones, P. P. Marra, and L. D. Kramer, 2006: Host heterogeneity dominates West Nile virus transmission. Proceedings of the Royal Society B: Biological Sciences, 273, 2327-2333. doi:10.1098/rspb.2006.3575 | Detail
  72. Komar, N., 2003: West Nile virus: Epidemiology and ecology in North America. The Flaviviruses: Detection, Diagnosis and Vaccine Development, T. Chambers and Monath, T., Eds., Elsevier Academic Press, 185-234. doi:10.1016/s0065-3527(03)61005-5 | Detail
  73. Lanciotti, R. S., and others, 1999: Origin of the West Nile Virus responsible for an outbreak of encephalitis in the northeastern United States. Science, 286, 2333-2337. doi:10.1126/science.286.5448.2333 | Detail
  74. Landesman, W. J., B. F. Allan, R. B. Langerhans, T. M. Knight, and J. M. Chase, 2007: Inter-annual associations between precipitation and human incidence of West Nile Virus in the United States. Vector-Borne and Zoonotic Diseases, 7, 337-343. doi:10.1089/vbz.2006.0590 | Detail
  75. Lane, R. S., J. E. Kleinjan, and G. B. Schoeler, 1995: Diel activity of nymphal Dermacentor occidentalis and Ixodes pacificus (Acari: Ixodidae) in relation to meteorological factors and host activity periods. Journal of Medical Entomology, 32, 290-299. doi:10.1093/jmedent/32.3.290 | Detail
  76. Lane, R. S., J. Piesman, and W. Burgdorfer, 1991: Lyme borreliosis: Relation of its causative agent to its vectors and hosts in North America and Europe. Annual Review of Entomology, 36, 587-609. doi:10.1146/annurev.en.36.010191.003103 | Detail
  77. Leighton, P. A., J. K. Koffi, Y. Pelcat, L. R. Lindsay, and N. H. Ogden, 2012: Predicting the speed of tick invasion: An empirical model of range expansion for the Lyme disease vector Ixodes scapularis in Canada. Journal of Applied Ecology, 49, 457-464. doi:10.1111/j.1365-2664.2012.02112.x | Detail
  78. Levi, T., F. Keesing, K. Oggenfuss, and R. S. Ostfeld, 2015: Accelerated phenology of blacklegged ticks under climate warming. Philosophical Transactions of the Royal Society B: Biological Sciences, 370. doi:10.1098/rstb.2013.0556 | Detail
  79. Lindsay, L. R., I. K. Barker, G. A. Surgeoner, S. A. McEwen, T. J. Gillespie, and J. T. Robinson, 1995: Survival and development of Ixodes scapularis (Acari: Ixodidae) under various climatic conditions in Ontario, Canada. Journal of Medical Entomology, 32, 143-152. doi:10.1093/jmedent/32.2.143 | Detail
  80. LoGiudice, K., S. T. Duerr, M. J. Newhouse, K. A. Schmidt, M. E. Killilea, and R. S. Ostfeld, 2008: Impact of host community composition on Lyme disease risk. Ecology, 89, 2841-2849. doi:10.1890/07-1047.1 | Detail
  81. Mail, G. A., and R. A. McHugh, 1961: Relation of temperature and humidity to winter survival of Culex pipiens and Culex tarsalis. Mosquito News, 21, 252-254. | Detail
  82. Manore, C. A., J. K. Davis, R. C. Christofferson, D. M. Wesson, J. M. Hyman, and C. N. Mores, 2014: Towards an early warning system for forecasting human west nile virus incidence. PLOS Currents: Disasters, 6. doi:10.1371/currents.outbreaks.f0b3978230599a56830ce30cb9ce0500 | Detail
  83. Mather, T. N., M. L. Wilson, S. I. Moore, J. M. Ribeiro, and A. Spielman, 1989: Comparing the relative potential of rodents as reservoirs of the Lyme disease spirochete (Borrelia burgdorferi). American Journal of Epidemiology, 130, 143-150. PMID: 2787105 | Detail
  84. McCabe, G. J., and J. E. Bunnell, 2004: Precipitation and the occurrence of Lyme disease in the northeastern United States. Vector-Borne and Zoonotic Diseases, 4, 143-148. doi:10.1089/1530366041210765 | Detail
  85. Mead, P. S., 2015: Epidemiology of Lyme disease. Infectious Disease Clinics of North America, 29, 187-210. doi:10.1016/j.idc.2015.02.010 | Detail
  86. Monaghan, A. J., S. M. Moore, K. M. Sampson, C. B. Beard, and R. J. Eisen, 2015: Climate change influences on the annual onset of Lyme disease in the United States. Ticks and Tick-Borne Diseases, 6, 615-622. doi:10.1016/j.ttbdis.2015.05.005 | Detail
  87. Moore, S. M., R. J. Eisen, A. Monaghan, and P. Mead, 2014: Meteorological influences on the seasonality of Lyme disease in the United States. The American Journal of Tropical Medicine and Hygiene, 90, 486-496. doi:10.4269/ajtmh.13-0180 | Detail
  88. Morin, C. W., and A. C. Comrie, 2013: Regional and seasonal response of a West Nile virus vector to climate change. Proceedings of the National Academy of Sciences of the United States of America, 110, 15620-15625. doi:10.1073/pnas.1307135110 | Detail
  89. Mostashari, F., and others, 2001: Epidemic West Nile encephalitis, New York, 1999: Results of a household-based seroepidemiological survey. The Lancet, 358, 261-264. doi:10.1016/S0140-6736(01)05480-0 | Detail
  90. Mount, G. A., D. G. Haile, and E. Daniels, 1997: Simulation of Management Strategies for the Blacklegged Tick (Acari: Ixodidae) and the Lyme Disease Spirochete, Borrelia burgdorferi. Journal of Medical Entomology, 34, 672-683. doi:10.1093/jmedent/34.6.672 | Detail
  91. Needham, G. R., and P. D. Teel, 1991: Off-host physiological ecology of ixodid ticks. Annual Review of Entomology, 36, 659-681. doi:10.1146/annurev.en.36.010191.003303 | Detail
  92. Nelms, B. M., P. A. Macedo, L. Kothera, H. M. Savage, and W. K. Reisen, 2013: Overwintering biology of Culex (Diptera: Culicidae) mosquitoes in the Sacramento Valley of California. Journal of Medical Entomology, 50, 773-790. doi:10.1603/me12280 | Detail
  93. Nett, R. J., M. J. Kuehnert, M. G. Ison, J. P. Orlowski, M. Fischer, and J. E. Staples, 2012: Current practices and evaluation of screening solid organ donors for West Nile virus. Transplant Infectious Disease, 14, 268-277. doi:10.1111/j.1399-3062.2012.00743.x | Detail
  94. NIOSH, 2005: Recommendations for Protecting Outdoor Workers from West Nile Virus Exposure. 16 pp., Department of Health and Human Services, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. URL | Detail
  95. Ogden, N. H., and others, 2006: Climate change and the potential for range expansion of the Lyme disease vector Ixodes scapularis in Canada. International Journal for Parasitology, 36, 63-70. doi:10.1016/j.ijpara.2005.08.016 | Detail
  96. Ogden, N. H., and others, 2008: Risk maps for range expansion of the Lyme disease vector, Ixodes scapularis, in Canada now and with climate change. International Journal of Health Geographics, 7, 24. doi:10.1186/1476-072X-7-24 | Detail
  97. Ogden, N. H., C. Bouchard, K. Kurtenbach, G. Margos, L. R. Lindsay, L. Trudel, S. Nguon, and F. Milord, 2010: Active and passive surveillance and phylogenetic analysis of Borrelia burgdorferi elucidate the process of Lyme disease risk emergence in Canada. Environmental Health Perspectives, 118, 909-914. doi:10.1289/ehp.0901766 | Detail
  98. Ogden, N. H., J. K. Koffi, Y. Pelcat, and L. R. Lindsay, 2014: Environmental risk from Lyme disease in central and eastern Canada: A summary of recent surveillance information. Canada Communicable Disease Report, 40, 74-82. URL | Detail
  99. Ogden, N. H., M. Radojević, X. Wu, V. R. Duvvuri, P. A. Leighton, and J. Wu, 2014: Estimated effects of projected climate change on the basic reproductive number of the Lyme disease vector Ixodes scapularis. Environmental Health Perspectives, 122, 631-638. doi:10.1289/ehp.1307799 | Detail
  100. Ostfeld, R. S., C. D. Canham, K. Oggenfuss, R. J. Winchcombe, and F. Keesing, 2006: Climate, deer, rodents, and acorns as determinants of variation in Lyme-disease risk. Plos Biology, 4, e145. doi:10.1371/Journal.Pbio.0040145 | Detail
  101. Owen, J., F. Moore, N. Panella, E. Edwards, R. Bru, M. Hughes, and N. Komar, 2006: Migrating birds as dispersal vehicles for West Nile virus. EcoHealth, 3, 79-85. doi:10.1007/s10393-006-0025-9 | Detail
  102. PAHO, cited 2014: Chikungunya. Pan American Health Organization. URL | Detail
  103. Parham, P. E., and others, 2015: Climate, environmental and socio-economic change: Weighing up the balance in vector-borne disease transmission. Philosophical Transactions of the Royal Society B: Biological Sciences, 370. doi:10.1098/rstb.2013.0551 | Detail
  104. Parmesan, C., 2006: Ecological and evolutionary responses to recent climate change. Annual Review of Ecology, Evolution, and Systematics, 37, 637-669. doi:10.1146/annurev.ecolsys.37.091305.110100 | Detail
  105. Pealer, L. N., and others, 2003: Transmission of West Nile virus through blood transfusion in the United States in 2002. New England Journal of Medicine, 349, 1236-1245. doi:10.1056/NEJMoa030969 | Detail
  106. Pecoraro, H. L., H. L. Day, R. Reineke, N. Stevens, J. C. Withey, J. M. Marzluff, and J. S. Meschke, 2007: Climatic and landscape correlates for potential West Nile virus mosquito vectors in the Seattle region. Journal of Vector Ecology, 32, 22-28. doi:10.3376/1081-1710(2007)32[22:CALCFP]2.0.CO;2 | Detail
  107. Pepin, K. M., and others, 2012: Geographic variation in the relationship between human Lyme disease incidence and density of infected host-seeking Ixodes scapularis nymphs in the eastern United States. The American Journal of Tropical Medicine and Hygiene, 86, 1062-1071. doi:10.4269/ajtmh.2012.11-0630 | Detail
  108. Petersen, L. R., A. C. Brault, and R. S. Nasci, 2013: West Nile virus: Review of the literature. JAMA: The Journal of the American Medical Association, 310, 308-315. doi:10.1001/jama.2013.8042 | Detail
  109. Petersen, L. R., and E. B. Hayes, 2004: Westward ho?--The spread of West Nile virus. New England Journal of Medicine, 351, 2257-2259. doi:10.1056/NEJMp048261 | Detail
  110. Petersen, L. R., P. J. Carson, B. J. Biggerstaff, B. Custer, S. M. Borchardt, and M. P. Busch, 2013: Estimated cumulative incidence of West Nile virus infection in US adults, 1999-2010. Epidemiology & Infection, 141, 591-595. doi:10.1017/S0950268812001070 | Detail
  111. Piesman, J., 1989: Transmission of Lyme disease spirochetes (Borrelia-Burgdorferi). Experimental and Applied Acarology, 7, 71-80. doi:10.1007/Bf01200454 | Detail
  112. Radke, E. G., and others, 2012: Dengue outbreak in Key West, Florida, USA, 2009. Emerging Infectious Diseases, 18, 135-137. doi:10.3201/eid1801.110130 | Detail
  113. Ramos, M. M., and others, 2008: Epidemic dengue and dengue hemorrhagic fever at the Texas–Mexico border: Results of a household-based seroepidemiologic survey, December 2005. The American Journal of Tropical Medicine and Hygiene, 78, 364-369. URL | Detail
  114. Reeves, W. C., S. M. Asman, J. L. Hardy, M. M. Milby, and W. K. Reisen, 1990: Epidemiology and Control of Mosquito-Borne Arboviruses in California, 1943-1987. California Mosquito and Vector Control Association, 508 pp. | Detail
  115. Reiner, R. C., and others, 2013: A systematic review of mathematical models of mosquito-borne pathogen transmission: 1970-2010. Journal of the Royal Society Interface, 10. doi:10.1098/rsif.2012.0921 | Detail
  116. Reisen, W. K., 1995: Effect of temperature on Culex tarsalis (Diptera: Culicidae) from the Coachella and San Joaquin Valleys of California. Journal of Medical Entomology, 32, 636-645. doi:10.1093/jmedent/32.5.636 | Detail
  117. Reisen, W. K., D. Cayan, M. Tyree, C. M. Barker, B. Eldridge, and M. Dettinger, 2008: Impact of climate variation on mosquito abundance in California. Journal of Vector Ecology, 33, 89-98. doi:10.3376/1081-1710(2008)33[89:iocvom]2.0.co;2 | Detail
  118. Reisen, W. K., R. P. Meyer, M. M. Milby, S. B. Presser, R. W. Emmons, J. L. Hardy, and W. C. Reeves, 1992: Ecological observations on the 1989 outbreak of St. Louis encephalitis virus in the southern San Joaquin Valley of California. Journal of Medical Entomology, 29, 472-482. doi:10.1093/jmedent/29.3.472 | Detail
  119. Reisen, W. K., Y. Fang, and A. C. Brault, 2008: Limited interdecadal variation in mosquito (Diptera: Culicidae) and avian host competence for Western equine encephalomyelitis virus (Togaviridae: Alphavirus). The American Journal of Tropical Medicine and Hygiene, 78, 681-686. URL | Detail
  120. Reisen, W. K., Y. Fang, and V. M. Martinez, 2005: Avian host and mosquito (Diptera: Culicidae) vector competence determine the efficiency of West Nile and St. Louis encephalitis virus transmission. Journal of Medical Entomology, 42, 367-375. doi:10.1603/0022-2585(2005)042[0367:ahamdc]2.0.co;2 | Detail
  121. Reisen, W. K., Y. Fang, and V. M. Martinez, 2006: Effects of temperature on the transmission of West Nile virus by Culex tarsalis (Diptera: Culicidae). Journal of Medical Entomology, 43, 309-317. doi:10.1093/jmedent/43.2.309 | Detail
  122. Reiter, P., and others, 2003: Texas lifestyle limits transmission of dengue virus. Emerging Infectious Diseases, 9, 86-89. doi:10.3201/eid0901.020220 | Detail
  123. Rollend, L., D. Fish, and J. E. Childs, 2013: Transovarial transmission of Borrelia spirochetes by Ixodes scapularis: A summary of the literature and recent observations. Ticks and Tick-Borne Diseases, 4, 46-51. doi:10.1016/j.ttbdis.2012.06.008 | Detail
  124. Rosenberg, R., M. A. Johansson, A. M. Powers, and B. R. Miller, 2013: Search strategy has influenced the discovery rate of human viruses. Proceedings of the National Academy of Sciences of the United States of America, 110, 13961-13964. doi:10.1073/pnas.1307243110 | Detail
  125. Rueda, L. M., K. J. Patel, R. C. Axtell, and R. E. Stinner, 1990: Temperature-dependent development and survival rates of Culex quinquefasciatus and Aedes aegypti (Diptera: Culicidae). Journal of Medical Entomology, 27, 892-898. doi:10.1093/jmedent/27.5.892 | Detail
  126. Ruiz, M. O., and others, 2010: Local impact of temperature and precipitation on West Nile virus infection in Culex species mosquitoes in northeast Illinois, USA. Parasites & Vectors, 3, Article 19. doi:10.1186/1756-3305-3-19 | Detail
  127. Schulze, T. L., and R. A. Jordan, 2003: Meteorologically Mediated Diurnal Questing of Ixodes scapularis and Amblyomma americanum (Acari: Ixodidae) Nymphs. Journal of Medical Entomology, 40, 395-402. doi:10.1603/0022-2585-40.4.395 | Detail
  128. Schulze, T. L., R. A. Jordan, C. J. Schulze, and R. W. Hung, 2009: Precipitation and Temperature as Predictors of the Local Abundance of Ixodes scapularis (Acari: Ixodidae) Nymphs. Journal of Medical Entomology, 46, 1025-1029. doi:10.1603/033.046.0508 | Detail
  129. Schwartz, B. S., and M. D. Goldstein, 1990: Lyme disease in outdoor workers: Risk factors, preventive measures, and tick removal methods. American Journal of Epidemiology, 131, 877-885. | Detail
  130. Schwartz, B. S., M. D. Goldstein, and J. E. Childs, 1994: Longitudinal study of Borrelia burgdorferi infection in New Jersey outdoor workers, 1988-1991. American Journal of Epidemiology, 139, 504-512. | Detail
  131. Shaman, J., J. F. Day, and M. Stieglitz, 2004: The spatial-temporal distribution of drought, wetting, and human cases of St. Louis encephalitis in southcentral Florida. The American Journal of Tropical Medicine and Hygiene, 71, 251-261. URL | Detail
  132. Shaman, J., J. F. Day, and M. Stieglitz, 2005: Drought-induced amplification and epidemic transmission of West Nile virus in southern Florida. Journal of Medical Entomology, 42, 134-141. doi:10.1093/jmedent/42.2.134 | Detail
  133. Shaman, J., J. F. Day, and N. Komar, 2010: Hydrologic conditions describe West Nile virus risk in Colorado. International Journal of Environmental Research and Public Health, 7, 494-508. doi:10.3390/ijerph7020494 | Detail
  134. Shaman, J., K. Harding, and S. R. Campbell, 2011: Meteorological and hydrological influences on the spatial and temporal prevalence of West Nile virus in Culex mosquitos, Suffolk County, New York. Journal of Medical Entomology, 48, 867-875. doi:10.1603/ME10269 | Detail
  135. Soverow, J. E., G. A. Wellenius, D. N. Fisman, and M. A. Mittleman, 2009: Infectious disease in a warming world: How weather influenced West Nile virus in the United States (2001–2005). Environmental Health Perspectives, 117, 1049-1052. doi:10.1289/ehp.0800487 | Detail
  136. Stafford III, K. C., 1994: Survival of immature Ixodes scapularis (Acari: Ixodidae) at different relative humidities. Journal of Medical Entomology, 31, 310-314. doi:10.1093/jmedent/31.2.310 | Detail
  137. Stromdahl, E. Y., and G. J. Hickling, 2012: Beyond Lyme: Aetiology of tick-borne human diseases with emphasis on the south-eastern United States. Zoonoses and Public Health, 59, 48-64. doi:10.1111/j.1863-2378.2012.01475.x | Detail
  138. Subak, S., 2003: Effects of climate on variability in Lyme disease incidence in the northeastern United States. American Journal of Epidemiology, 157, 531-538. doi:10.1093/aje/kwg014 | Detail
  139. Tran, P. M., and L. Waller, 2013: Effects of landscape fragmentation and climate on Lyme disease incidence in the northeastern United States. Ecohealth, 10, 394-404. doi:10.1007/s10393-013-0890-y | Detail
  140. Tuite, A. R., A. L. Greer, and D. N. Fisman, 2013: Effect of latitude on the rate of change in incidence of Lyme disease in the United States. CMAJ Open, 1, E43-E47. doi:10.9778/cmajo.20120002 | Detail
  141. USGS, cited 2014: Dengue Fever (Locally Acquired) Human 2013. Cumulative data as of May 7, 2014. United States Geological Survey. URL | Detail
  142. Vail, S. G., and G. Smith, 1998: Air temperature and relative humidity effects on behavioral activity of blacklegged tick (Acari: Ixodidae) nymphs in New Jersey. Journal of Medical Entomology, 35, 1025-1028. doi:10.1093/jmedent/35.6.1025 | Detail
  143. Walter, N. M., and C. S. Hacker, 1974: Variation in life table characteristics among three geographic strains of Culex pipiens quinquefasciatus. Journal of Medical Entomology, 11, 541-550. | Detail
  144. Wegbreit, J., and W. K. Reisen, 2000: Relationships among weather, mosquito abundance, and encephalitis virus activity in California: Kern County 1990-98. Journal of the American Mosquito Control Association, 16, 22-27. | Detail
  145. Weiss, D., D. Carr, J. Kellachan, C. Tan, M. Phillips, E. Bresnitz, M. Layton, and West Nile Virus Outbreak Response Working Group, 2001: Clinical findings of West Nile virus infection in hospitalized patients, New York and New Jersey, 2000. Emerging Infectious Diseases, 7, 654-658. | Detail
  146. WHO, cited 2015: Dengue and Severe Dengue. Fact Sheet No. 117. World Health Organization. URL | Detail
  147. Wimberly, M. C., A. Lamsal, P. Giacomo, and T. -W. Chuang, 2014: Regional variation of climatic influences on West Nile virus outbreaks in the United States. The American Journal of Tropical Medicine and Hygiene, 91, 677-684. doi:10.4269/ajtmh.14-0239 | Detail
  148. Winters, A. M., R. J. Eisen, S. Lozano-Fuentes, C. G. Moore, W. J. Pape, and L. Eisen, 2008: Predictive spatial models for risk of West Nile virus exposure in eastern and western Colorado. The American Journal of Tropical Medicine and Hygiene, 79, 581-590. URL | Detail
  149. Yuval, B., and A. Spielman, 1990: Duration and regulation of the developmental cycle of Ixodes dammini (Acari: Ixodidae). Journal of Medical Entomology, 27, 196-201. doi:10.1093/jmedent/27.2.196 | Detail
  150. Zou, S., G. A. Foster, R. Y. Dodd, L. R. Petersen, and S. L. Stramer, 2010: West Nile fever characteristics among viremic persons identified through blood donor screening. The Journal of Infectious Diseases, 202, 1354-1361. doi:10.1086/656602 | Detail


Very Likely
≥9 in 10
≥2 in 3
As Likely as Not
≈ 1 in 2
≤ 1 in 3
Very Unikely
≤1 in 10

Confidence Level

Very High Strong evidence (established theory, multiple sources, consistent results, well documented and accepted methods, etc.), high consensus
High Moderate evidence (several sources, some consistency, methods vary and/or documentation limited, etc.), medium consensus
Medium Suggestive evidence (a few sources, limited consistency, models incomplete, methods emerging, etc.), competing schools of thought
Low Inconclusive evidence (limited sources, extrapolations, inconsistent findings, poor documentation and/or methods not tested, etc.), disagreement or lack of opinions among experts

Documenting Uncertainty: This assessment relies on two metrics to communicate the degree of certainty in Key Findings. See Appendix 4: Documenting Uncertainty for more on assessments of likelihood and confidence.

Key Finding 1: Changing Distributions of Vectors and Vector-Borne Diseases

Climate change is expected to alter the geographic and seasonal distributions of existing vectors and vector-borne diseases [Likely, High Confidence].

Key Finding 2: Earlier Tick Activity and Northward Range Expansion

Ticks capable of carrying the bacteria that cause Lyme disease and other pathogens will show earlier seasonal activity and a generally northward expansion in response to increasing temperatures associated with climate change [Likely, High Confidence]. Longer seasonal activity and expanding geographic range of these ticks will increase the risk of human exposure to ticks [Likely, Medium Confidence].

Key Finding 3: Changing Mosquito-Borne Disease Dynamics

Rising temperatures, changing precipitation patterns, and a higher frequency of some extreme weather events associated with climate change will influence the distribution, abundance, and prevalence of infection in the mosquitoes that transmit West Nile virus and other pathogens by altering habitat availability and mosquito and viral reproduction rates [Very Likely, High Confidence]. Alterations in the distribution, abundance, and infection rate of mosquitoes will influence human exposure to bites from infected mosquitoes, which is expected to alter risk for human disease [Very Likely, Medium Confidence].

Key Finding 4: Emergence of New Vector-Borne Pathogens

Vector-borne pathogens are expected to emerge or reemerge due to the interactions of climate factors with many other drivers, such as changing land-use patterns [Likely, High Confidence]. The impacts to human disease, however, will be limited by the adaptive capacity of human populations, such as vector control practices or personal protective measures [Likely, High Confidence].