2
Climate, Ecology, and Infectious Disease

OVERVIEW

As depicted in the convergence model of infectious disease emergence, illustrated in Figure SA-4, climate interacts with, and can alter, the complex ecological relationships underlying infectious disease transmission patterns. This chapter examines such interactions from several perspectives:

  • Their consequences throughout the aquatic-marine food web, which defines ecological relationships for water-dwelling animals

  • In patterns of distribution and transmission dynamics of individual infectious diseases (cholera, Rift Valley fever, chikungunya, and plague)

  • Their effects on the dynamics of plant diseases, and their effects on agriculture and natural ecosystems

  • As manifested in the public health challenges posed by climate change to human populations in the Arctic

Research on the effects of climate variation on infectious disease incidence and geographic range in these diverse contexts is providing the basis for developing climate-based early warning systems for disease risk. Such studies also represent a necessary first step toward anticipating how climate change may alter infectious disease dynamics in various ecological frameworks.

In her workshop presentation, Leslie Dierauf, director of the U.S. Geological Survey’s National Wildlife Health Center in Madison, Wisconsin, described the apparent and predicted effects of climate on a broad cross-section of animal species that inhabit fresh- and saltwater ecosystems, as well as the intertidal



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement



Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.

OCR for page 104
2 Climate, Ecology, and Infectious Disease OVERVIEW As depicted in the convergence model of infectious disease emergence, illustrated in Figure SA-4, climate interacts with, and can alter, the complex ecological relationships underlying infectious disease transmission patterns. This chapter examines such interactions from several perspectives: • Their consequences throughout the aquatic-marine food web, which defines ecological relationships for water-dwelling animals • In patterns of distribution and transmission dynamics of individual infec- tious diseases (cholera, Rift Valley fever, chikungunya, and plague) • Their effects on the dynamics of plant diseases, and their effects on agri- culture and natural ecosystems • As manifested in the public health challenges posed by climate change to human populations in the Arctic Research on the effects of climate variation on infectious disease incidence and geographic range in these diverse contexts is providing the basis for devel- oping climate-based early warning systems for disease risk. Such studies also represent a necessary first step toward anticipating how climate change may alter infectious disease dynamics in various ecological frameworks. In her workshop presentation, Leslie Dierauf, director of the U.S. Geologi- cal Survey’s National Wildlife Health Center in Madison, Wisconsin, described the apparent and predicted effects of climate on a broad cross-section of animal species that inhabit fresh- and saltwater ecosystems, as well as the intertidal 0

OCR for page 104
0 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE zones that unite aquatic and marine environments. Ecological connections among these environments are illustrated in Figure SA-8, which depicts the marine food web. Dierauf also emphasized the physical connectedness of aquatic and marine environments, which makes it possible for infectious diseases of fish and wild- life to move from freshwater sources to intertidal zones to marine environments, affecting species that may not have encountered these disease agents before. Salmon, for example, hatch in small freshwater streams, travel hundreds of kilo- meters downstream to the ocean where they live for several years, only to return to the same streams where they hatched to spawn and die shortly thereafter. Thus, she observed, “if the temperature of the streams changes or the fish themselves pick up novel disease agents, because a vector, or an intermediate host, or a disease agent thrives in the new warmer environment, infectious disease may result.” Evidence-based studies of the effects of climate change on the health of aquatic and marine wildlife are few, Dierauf reported; therefore, current under- standing of this topic derives from such sources as historical comparisons (of climatic conditions and of animal health and behaviors), long-term ecological research, correlation studies, and recognition of the physical, chemical, and biological processes governing climate change. Following the flow of water from inland streams to estuaries and into the open ocean, Dierauf considered the possible impacts of climate change in each of the three main elements of the aquatic continuum and how these changes may affect the health of their animal inhabitants. In freshwater ecosystems, extreme weather events that produce flooding can trigger overwhelming influxes of nutrients into ecosystems. Storms can cause a range of environmental disturbances; Dierauf described the release of Nile tila- pia into Mississippi streams from aquaculture facilities damaged by Hurricane Katrina. Several emerging diseases of inland aquatic animals, described and depicted in Box SA-2 in the Summary and Assessment, may also be influenced by climate change. Intertidal areas, such as salt marshes and estuaries, are essential for main- taining a delicate balance among many complex and interactive variables (such as temperature, light, salinity, wave action, sea level rise, erosion, and sediment deposition) that characterize the transition from freshwater to saltwater environ- ments, Dierauf explained. Storms, such as hurricanes, greatly affect intertidal zones. Heavy inland rainfall increases the speed and volume of the run-off that reaches estuaries, while marine storms drive saltwater and its contents past the intertidal buffer, affecting inland ecosystem health. Climate change is expected to produce a range of important effects on oceans (as well as on large, deep-water lakes such as the Great Lakes), according to Dierauf. These include increased wave intensity, increased nutrient turnover, changes in nutrients, and changes in the food web. In addition, she noted, higher

OCR for page 104
0 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS concentrations of atmospheric carbon dioxide are dramatically increasing the acidity of ocean waters, which in turn is weakening the carbonate shells and skeletons of many marine species that comprise coral reef systems. She also noted the effects of harmful algal blooms (HABs), which are thought to result from nutrient influxes to the ocean (see Summary and Assessment). HABs appear to be increasing in both frequency and size as the climate warms, she said; this could result from increased upwelling of nutrients within the ocean or changes in ocean currents, as well as from the effects of extreme weather events inland. “What we do know is that HABs are affecting and often killing living things in the food web, like zooplankton, shellfish, fish, birds, and marine mammals, like manatees,” she said. Ocean warming, which is reducing the availability of food and sea ice for marine mammals, may also be compromising their resistance to infectious dis- ease, Dierauf said. “Already, climate change and thinning of sea ice has reduced the time mother polar bears have to build the fat stores they need to sustain themselves over winter and to feed their young come spring when they emerge from their dens,” she noted. Faced with shortages of food in their native waters, some marine mammals move to new territories where they both encounter and introduce novel disease agents (see Summary and Assessment). “Climate change and climate variability will affect aquatic and marine spe- cies worldwide,” Dierauf concluded. “We must act now at personal, professional, local, and global levels to protect vulnerable ecosystems and the aquatic and marine species that depend on these habitats for survival.” In contrast to the broad perspective on the effect of climate change on aquatic ecosystems offered by Dierauf, this chapter’s first paper, by Rita Colwell of the University of Maryland, focuses on the specific and well-characterized effects of climate on cholera, a water-borne disease that affects an estimated 100,000 people per year, resulting in 10,000 deaths. The incidence and distribution of cholera are controlled by water temperature, precipitation patterns, and water salinity—all of which are influenced by global climate—and conducted through a complex web of ecological relationships. Sanitation and infrastructure also play a role in the incidence and distribution of cholera. Colwell noted, however, that “by simply educating women to filter drinking water through several layers of ‘sari cloth,’ we were able to reduce cholera incidence by 50 percent.” Colwell described how, over the course of decades, she and coworkers deduced the circumstances under which the causal agent of cholera, the bacterium Vibrio cholerae, is transmitted to humans by the plankton species with which the bacterium associates. This knowledge led to the development of remote sensing systems capable of predict- ing the onset of cholera epidemics in the Ganges delta, known as the “home of cholera,” because of its long history of epidemic disease. This chapter’s second paper also describes the use of remote sensing to monitor the effects of climate variation on specific infectious diseases. Speaker Jean-Paul Chretien, of the Department of Defense Global Emerging Infections

OCR for page 104
07 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE Surveillance and Response System (DOD-GEIS), and coauthors describe the use of satellite and epidemiological data to examine connections between the El Niño/Southern Oscillation (ENSO) and recent epidemics of two mosquito-borne viral diseases: Rift Valley fever (RVF) and chikungunya fever. In the first case, the association of RVF outbreaks in East Africa with periods of heavy rainfall, which occur during the El Niño phase of ENSO, led researchers to develop a model to forecast RVF risk in that region based on vegetation density (a marker for rain- fall), as measured by satellite (Linthicum et al., 1999). The authors describe the operation of this model in the El Niño season of 2006-2007, when its prediction of elevated risk of disease prompted intensified surveillance for RVF in Kenya and, ultimately, to an international effort to stem a pending epidemic. Chikungunya fever caused a series of outbreaks along the Kenyan coast in 2004, from which it apparently spread to several western Indian Ocean islands and India, resulting in the largest chikungunya fever epidemic on record (Chretien et al., 2007). At the time of the initial outbreaks in Kenya, a regional drought— corresponding to the La Niña phase of ENSO—had gripped the region. Chretien and coauthors discuss several possible, nonexclusive mechanisms connecting the epidemic with the drought, some of which may have also have influenced the first appearance of chikungunya fever in Europe in 2007. In the chapter’s third paper, speaker Nils Stenseth of the University of Oslo provides a much longer view of climate variation and its effects on infectious dis- ease dynamics. Throughout recorded history, the various forms of plague, caused by the bacterium Yersinia pestis and transmitted by fleas among a wide range of hosts, are known to have caused both endemic and epidemic disease. Stenseth examines the dynamic ecology and epidemiology of plague in its ancient reser- voir in Central Asia, and compares these patterns with local climate variation over the course of decades (as recorded in regular measurements of temperature and rainfall) and centuries (as reflected in tree-ring data for the past 1,000 years). Using data collected twice annually between 1949 and 1995 in Kazakhstan, a focal region for plague where human cases are regularly reported, Stenseth and colleagues determined that Y. pestis prevalence increases dramatically in its primary host, the great gerbil (Rhombomys opimus), during warmer springs and wetter summers (Stenseth et al., 2006). Rodent populations also tend to increase under these conditions and, along with them, the possibility that plague will be transmitted to humans. Analyses of historical climate variation, as reflected in tree-ring patterns, suggest that similar warm, wet conditions existed in Central Asia during the onset of the Black Death in the fourteenth century, as well as in the years preceding a mid-nineteenth-century plague pandemic. As Earth’s climate warms, warmer springs and wetter summers are expected to become more common in Central Asia (as well as in North America) therefore raising the possibility that plague activity—and therefore the potential for epidemic disease—will increase. “Although the number of human cases of plague is relatively low, it would

OCR for page 104
0 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS be a mistake to overlook its threat to humanity, because of the disease’s inherent communicability, rapid spread, rapid clinical course, and high mortality if left untreated,” Stenseth notes. Moreover, he adds, even a minor plague outbreak can result in panic, with severe economic repercussions; a 1994 plague outbreak in India that caused 50 deaths also led to a nationwide collapse in tourism and trade, costing the nation an estimated $600 million (Fritz et al., 1996). “Plague remains a fairly poorly understood threat that we cannot afford to ignore,” Stenseth concludes. “Only by knowing more about how the eco-epidemiological plague systems in the different parts of the world will respond to given climate scenarios can we take the necessary precautionary measures to reduce the risks of human infections.” While climate-based early warning systems for human disease are in an early stage of development, plant disease forecasting systems based on variables such as temperature and precipitation have been used for many years, according to speaker Karen Garrett of Kansas State University. However, she adds, these well- established models will need to be adapted (based on sound science) to account for climate change, as will plant disease management policies that flow from climate-based forecasts. In her contribution to this chapter, Garrett establishes a framework for this critical effort. She describes standard methods for managing plant disease, reviews observed effects of climate variation on plant diseases and their implications given projected future climatic conditions, and discusses research and policy needs for plant disease management in response to climate change. In considering the consequences of climate change for plant health, Garrett emphasizes threshold effects: environmental perturbations that produce disproportionate ecological upheaval. Examples of such thresholds include longer growing seasons; pathogen introductions and range shifts; pathogen overwinter- ing; and the removal of constraints on pathogen reproduction at a critical popula- tion size. Much as it has been argued that the most effective available protective mea- sures against the adverse human health effects of climate change are basic public health interventions (see Campbell-Lendrum in Chapter 4), Garrett observes that “the good news for formulation of strategies for plant disease management under changing climate conditions is that much of what needs to be done is the same with or without climate change.” Thus, she advocates research to advance our understanding of plants’ adaptive capacities and mechanisms, and policies to encourage the development of “diverse, flexible, and resilient agricultural systems that can adapt more readily to new climatic conditions.” The chapter’s final paper, by Alan Parkinson of the Centers for Disease Control and Prevention’s (CDC’s) Arctic Investigations Program in Anchor- age, Alaska, presents a panoramic view of the public health challenges faced by people living in the Arctic, where the physical effects of climate change are dramatically apparent. Temperatures in this region have increased at nearly twice the global average over the past century, causing widespread melting of land and

OCR for page 104
0 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE sea ice (see Figure SA-13; Borgerson, 2008; IPCC, 2007). These conditions are exposing the Arctic’s human inhabitants, many of whom have limited access to public health and/or sanitation services, to an increasingly broad range of infectious disease threats (among other health challenges). Parkinson describes the observed and projected effects of climate change in the Arctic environment, discusses the direct effects of higher ambient temperatures on the health of Arctic inhabitants, and catalogs the many ways in which climate change may increase the risk of infectious disease for Arctic residents. Indeed, Parkinson observes, infectious disease risks are already increasing in the Arctic through the indirect influence of climate change on the populations and ranges of disease vector species (e.g., mosquitoes, ticks) and the population den- sity and range of reservoir hosts that can transmit disease (e.g., rodents, foxes). Flooding and the loss of permafrost are also damaging the sanitation infrastruc- ture of Arctic communities, thereby increasing the risk of water-borne infectious diseases, respiratory diseases, and skin infections. Meanwhile, increasing mean ambient temperatures raise the risk of food-borne diseases, particularly for Arctic residents who rely on traditional methods of subsistence and food preservation (e.g., fermentation, air-drying, burying). In the face of these public health challenges, Parkinson recommends a range of public health responses, including monitoring of high-risk, climate-sensitive infectious diseases with potentially large public health impacts (e.g., water-borne diseases such as giardiasis), prompt investigation of infectious disease outbreaks that may be related to climate change, and research on the relationship between climate and infectious disease emergence to guide early detection and public health interventions. He also encourages the creation of infectious disease moni- toring networks to connect typically small, isolated Arctic communities and link them to regional, national, and international health organizations. Such networks would encourage the standardization of monitoring methods, the sharing of data, and the detection of infectious disease trends over a larger geographic area. THE MARINE ENVIRONMENT AND HUMAN HEALTH: THE CHOLERA MODEL Rita Colwell, Ph.D. University of Maryland Cholera, a disease I have studied for more than 30 years, is a model of the complex interactions between climate, ecology, environment, and weather related to epidemics of infectious diseases. Revealing cholera’s secrets has required inter- 1 Chairman, Canon U.S. Life Sciences, Inc., and Distinguished University Professor at both the University of Maryland at College Park and at the Johns Hopkins University Bloomberg School of Public Health.

OCR for page 104
0 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS disciplinary research examining all of these influences, as well as a point of view that I call biocomplexity: recognizing that infectious diseases operate on a wide range of time and space scales. Thus, we employ gene probes, environmental measurements (ground truth), and other precise techniques for pathogen detec- tion, but at the same time, we take a holistic approach that integrates informa- tion from the atomic to the atmospheric—and perhaps, in some cases, even the cosmic—in order to build a predictive model for cholera outbreaks. Cholera is a significant, global public health problem, as shown in Table 2-1. Annually, it results in approximately 100,000 hospitalizations and approximately 10,000 deaths, varying from year to year. A few cases of cholera appear each year in the United States, usually associated with seafood harvested from closed beds near sewage outfalls in the Gulf of Mexico. Most of my group’s research on cholera has focused on the Ganges delta, which feeds into the Bay of Bengal. This area is known as the home of cholera due to spring and fall epidemics, of varying but predictable intensity, that have recurred there for hundreds of years (see Figure 2-1). During the monsoon sea- son, flooding rains wash nutrients down from the Himalayas, while winds drive water from the Bay of Bengal up into the Ganges and its tributaries, creating ideal conditions (discussed later) for cholera outbreaks. The fall 2007 epidemic, which followed massive flooding, was catastrophic. The Center for Diarrheal Disease TABLE 2-1 Cholera Cases Officially Reported to WHO, 2004—Selected Countries Number Mortality Country of Cases Imported Deaths Rate (%) Benin 642 9 1.40 Burundi 819 14 1.71 Cameroon 8,005 137 1.71 Comoros 1 0 0.00 Côte d’Ivoire 105 9 8.57 DROC (Congo) 7,665 228 2.97 Niger 2,178 57 2.62 Nigeria 3,186 185 5.81 Somalia 4,490 26 0.58 Uganda 3,380 91 2.69 Tanzania 10,319 272 2.64 Zambia 12,149 373 3.07 Zimbabwe 119 9 7.56 India 4,695 7 0.15 Japan 66 55 0 0.00 Singapore 11 1 1 9.09 Total 57,830 56 1,418 2.45 SOURCE: WHO (2005).

OCR for page 104
 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE FIGURE 2-1 Bangladesh border, barrier islands, and location of Dacca, Matlab, Math- baria, and Bakerganj. SOURCE: Printed with permission from Google. 2-1 Bitmapped Research in Dacca admitted about a thousand new cases per day for almost 30 days and had to use temporary space to house cholera victims. We are working to create predictive models to provide advance warning of conditions that produce severe epidemics in this region of the world. However, V. cholerae, the bacterium, is a natural inhabitant of rivers, estu- aries, and coastal waters throughout the world. Currently, we are sequencing approximately 50 different strains of Vibrio cholerae, the causative agent of cholera collected from many geographic locations to examine their genetic rela- tionships. Preliminary sequencing studies of V. cholerae collected at a depth of 2,000 m at a site located off the coast of Oregon indicate that those isolates may represent ancestral strains; interestingly, one strain studied in detail has genes in common with other Vibrio pathogens, as well, including Vibrio vulnificus and Vibrio parahaemolyticus, the latter being the most common food-borne pathogen in Asian countries, where raw seafood is consumed.

OCR for page 104
2 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS The Ecology of Cholera My laboratory accomplished the first isolation of Vibrio cholerae from the Chesapeake Bay more than two decades ago, and we now know that this bacte- rium is found in estuaries of similar salinity, (ca. 15 parts per thousand), where the water temperature rises seasonally to 15ºC or higher and where an influx of nutrients encourages plankton blooms (Colwell, 1996). Other species of Vibrio, including V. parahaemolyticus and V. vulnificus, also thrive under these condi- tions. One of my current graduate students, Brad Haley, has just returned from Iceland, where he was able to isolate V. cholerae at locations where geothermal effluent flows into bays. Clearly, water temperature is critical to the growth of this pathogen. Vibrio cholerae also has a dormant state, which it assumes between epi- demics and during which it cannot be cultured but can be detected with probes (fluorescent antibodies and gene signature sequences). Only during the peak of the zooplankton bloom, in the spring and the fall, is V. cholerae easily culturable. We were able to show that by adding nalidixic acid and nutrient (yeast extract) to water containing the quiescent bacterium, we can stimulate cell elongation and metabolism. Another important discovery was that cholera is transmitted by plankton. Thus, it is not enough to say that its growth correlates with sea surface tempera- ture and salinity; it is important to recognize the ecological interactions that pro- duce these correlations. There is a commensal relationship—which may prove to be symbiosis—between Vibrio bacteria and zooplankton. Vibrios are chitinolytic (i.e., capable of breaking down chitin, the material that forms the carapaces of zooplankton and crustaceans (e.g., crabs, shrimp). V. cholerae also produces a powerful proteolytic enzyme that the bacterium apparently uses to perform an additional function for zooplankton: breaking down its egg sac, enabling the eggs to disperse into the water column. We are discovering that interactions between V. cholerae and various zooplankton species are quite intricate; for example, certain strains of the bacterium attach preferentially to certain species of zooplankton (Rawlings et al., 2007). All of this leads to the conclusion that V. cholerae is integral to marine ecosystems, and therefore cannot be eradicated. The Epidemiology of Cholera We have determined in earlier studies that between 10,000 and 50,000 Vib- rio cholerae bacteria may be attached to an individual copepod (the zooplankton favored by V. cholerae). A liter of water drawn by a villager from a pond in Bangladesh between epidemics may contain 10 copepods. However, during a zooplankton bloom, that concentration can increase a hundredfold or more per liter, carrying a dose of cholera bacteria sufficient to cause cholera. The severity of the disease is dose dependent: a low concentration of bacterial cells will pro-

OCR for page 104
 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE duce mild diarrhea; hospitalized cases—which represent about 25 percent of all infections—require more since one million bacteria per milliliter has been shown to be required to produce the disease. Thus, it has been estimated that only 25 percent of those with cholera end up in hospitals and many more may have been infected (Colwell and Huq, 2004). Cholera is a disease with rapid onset. Within 24 to 48 hours, the typical patient can lose up to 18 liters of fluid. If that fluid can be replenished quickly, either intravenously or through oral rehydration (using a simple mixture of bicar- bonate of soda, table salt, and sugar), recovery is fairly rapid. From years of study in Bangladesh, we have determined several factors that interact and are associated with the massive annual biennial (spring and fall) cholera epidemics, so that we can predict the onset and severity of epidemics. Our recent research focuses on the communities of Mathbaria and Bakerganj, which are located in the barrier islands region of the Ganges delta (see Figure 2-1). Mangrove-based ecosystems are abundant in copepods. Thus, the Vibrio population is also abundant, and during the zooplankton/Vibrio bloom, cholera results from drinking untreated water. In Bakerganj and Mathbaria, copepods comprise the majority of zooplankton species. We now have evidence that the severity of a given local cholera epidemic can be determined by copepod population dynamics, with intense epidemics occurring during times of abundance of those copepod species to which epidemic strains of V. cholera preferentially attach. We are currently conducting a seasonal study of zooplankton species in an attempt to determine which species carry V. cholera and to identify factors that influence population size; we will use this information, with other environmental data, to build a predictive capacity for cholera epidemics. We are also using our knowledge of cholera epidemiology to help the people of Bangladesh to avoid contracting cholera. In one study, for example, we found that by simply educating women to filter drinking water through several layers of sari cloth, we were able to reduce cholera incidence by 50 percent. This result supported our hypothesis that plankton and particulates—to which the bacteria are attracted—transmit cholera and when removed by simple filtration, the inci- dence of the disease is significantly reduced. Predictive Models of Cholera Currently, the spring bloom of phytoplankton in the Bay of Bengal can be measured by satellite sensors that measure chlorophyll intensity and, therefore, the phytoplankton population. Phytoplankton blooms are followed by zooplank- ton blooms, but the latter cannot yet be measured directly by satellite sensors. However, the zooplankton peak can be inferred using a series of calculations from measurements of the phytoplankton populations that precede the zooplankton

OCR for page 104
 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS population peak. This information taken together with salinity, temperature, and other environmental factors, provides a more complete picture. We have also gathered ground truth data over the past 10 years in the Bak- erganj area, including conductivity of the water, presence of inorganic nutrients, temperature, and salinity. With these data, we are able to improve our prediction of the timing and, possibly, the severity of cholera epidemics. In our original work, we were able to use satellite imagery to measure sea surface temperature and sea surface height in the Bay of Bengal. As shown in Figure 2-2, the correlation of chlorophyll and temperature data, measured by sat- ellite sensors, provides a predictive capacity for conditions conducive to cholera outbreaks. We are currently working on a predictive model that takes into account ocean currents to monitor the movement of plankton into the Bay of Bengal estu- aries from the southern tip of India. This could provide as much as a 3-month warning prior to an impending cholera outbreak. In Latin America, the 1991-1992 El Niño event corresponded with a cholera epidemic that was initially attributed to the dumping of ballast water by a ship in the harbor of Lima, Peru (Gil et al., 2004). We were able to disprove this hypoth- esis by demonstrating that cholera outbreaks had occurred in three different cities along the coast of Peru, starting before the peak of the 1991-1992 El Niño event. The epidemic more likely resulted from the effect of increased sea surface tem- peratures on existing plankton and V. cholerae populations. Our most sophisticated predictive model for cholera incorporates chloro- phyll, sea surface height, temperature, and extensive ground truth data. Within a few years, the National Oceanic and Atmospheric Administration (NOAA) will launch a satellite that may provide salinity data. We are also refining our model, based on the 40 years of data accumulated on cholera in Bangladesh and in India, which we are presently analyzing. Nevertheless, with the analyses we have performed to date—sea surface temperature and sea surface height from satellite sensors; measurements of chlorophyll intensity (corrected for the time lag from chlorophyll-phytoplankton bloom to the zooplankton bloom that feeds on the phytoplankton); and measurements of vibrio dispersion in the water—we are able to determine significant correlations and, thus, a foundation from which to predict cholera epidemics. Conclusion Climate change is likely to increase the burden of cholera in Bangladesh, but even greater suffering will occur if sea levels rise to predicted levels, displacing millions of people. However, our interdisciplinary, international (as demonstrated by our large number of collaborators from many countries), and biocomplex- ity approach to studying cholera extends well beyond Bangladesh and even beyond the disease itself. By gaining an understanding of the complex interac- tions between infectious disease, ecology, and the physical environment, we can

OCR for page 104
 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS standardization, data-sharing, and the detection of infectious disease trends over a larger geographic area. This capacity is essential for the development of strate- gies to minimize the negative effects of climate change on the health of Arctic residents in the future. REFERENCES Overview References Borgerson, S. G. 2008. Arctic meltdown: the economic and security implications of global warming. Foreign Affairs 87(2):63-77. Chretien, J. P., A. Anyamba, S. A. Bedno, R. F. Breiman, R. Sang, K. Sergon, A. M. Powers, C. O. Onyango, J. Small, C. J. Tucker, and K. J. Linthicum. 2007. Drought-associated chi- kungunya emergence along coastal East Africa. American Journal of Tropical Medicine and Hygiene 76(3):405-407. Fritz, C. L., D. T. Dennis, M. A. Tipple, G. L. Campbell, C. R. McCance, and D. J. Gubler. 1996. Surveillance for pneumonic plague in the United States during an international emergency: a model for control of imported emerging diseases. Emerging Infectious Diseases 2(1):30-36. IPCC (Intergovernmental Panel on Climate Change). 2007. Climate change 2007: the physical science basis. Contribution of Working Group I to the fourth assessment report of the IPCC. Cambridge, UK: Cambridge University Press. Linthicum, K. J., A. Anyamba, C. J. Tucker, P. W. Kelley, M. F. Myers, and C. J. Peters. 1999. Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya. Science 285(5426):397-400. Stenseth, N. C., N. I. Samia, H. Viljugrein, K. L. Kausrud, M. Begon, S. Davis, H. Leirs, V. M. Dubyanskiy, J. Esper, V. S. Ageyev, N. L. Klassovskiy, S. B. Pole, and C. Kung-Sik. 2006. Plague dynamics are driven by climate variation. Proceedings of the National Academy of Sci- ences 103(35):13110-13115. Colwell References Colwell, R. R. 1996. Global climate and infectious disease: the cholera paradigm. Science 274(5295):2025-2031. Colwell, R. R., and A. Huq. 1994. Vibrios in the environment: viable but nonculturable Vibrio cholerae. In: Vibrio cholerae and cholera: molecular to global perspectives, edited by I. K. Wachsmuth, O. Olsvik, and P. A. Blake. Washington, DC: American Society for Micro- biology. Pp. 117-133. Gil, A. I., V. R. Louis, I. N. Rivera, E. Lipp, A. Huq, C. F. Lanata, D. N. Taylor, E. Russek-Cohen, N. Choopun, R. B. Sack, R. R. Colwell. 2004. Occurrence and distribution of Vibrio cholerae in the coastal environment of Peru. Environmental Microbiology 6(7):699-706. Rawlings, T., G. M. Ruiz, and R. R. Colwell. 2007. Association of Vibrio cholerae O1 El Tor and O139 Bengal with the copepods Acartia tonsa and Eurytemora affinis. Applied Environmental Microbiology 73(24):7926-7933. WHO (World Health Organization). 2005. Weekly epidemiological record 80(31):261-268, http:// www.who.int/wer/2005/wer8031.pdf (accessed May 1, 2008).

OCR for page 104
 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE Chretien et al. References Anyamba, A., K. J. Linthicum, R. Mahoney, C. J. Tucker, and P. W. Kelley. 2002. Mapping potential risk of Rift Valley fever outbreaks in African savannas using vegetation index time series data. Photogrammetric Engineering and Remote Sensing 68(2):137-145. Anyamba, A., J. P. Chretien, J. Small, C. J. Tucker, and K. J. Linthicum. 2006. Developing global climate anomalies suggest potential disease risks for 2006-2007. International Journal of Health Geographics 5:60. Bedno, S. A., C. O. Onyango, C. Njugana, R. Sang, S. Gaydos, K. Sergon, and R. F. Breiman. 2006. Outbreak of chikungunya in Lamu, Kenya, 2004. Paper presented at the International Confer- ence on Emerging Infectious Diseases, Atlanta, GA. CDC (Centers for Disease Control and Prevention). 1998. Rift Valley fever—East Africa, 1997-1998. Morbidity and Mortality Weekly Report 47(13):261-264. Chretien, J, P., and K. J. Linthicum. 2007. Chikungunya in Europe—what’s next? Lancet 370(9602):1805-1806. Chretien, J. P., A. Anyamba, S. A. Bedno, R. F. Breiman, R. Sang, K. Sergon, A. M. Powers, C. O. Onyango, J. Small, C. J. Tucker, and K. J. Linthicum. 2007. Drought-associated chi- kungunya emergence along coastal East Africa. American Journal of Tropical Medicine and Hygiene 76(3):405-407. FAO (Food and Agriculture Organization). 2006. Possible RVF activity in the Horn of Africa. EMPRES Watch. IOM (Institute of Medicine). 2003. Microbial threats to health: emergence, detection, and response. Washington, DC: The National Academies Press. IPCC (Intergovernmental Panel on Climate Change). 2007a. Climate change 2007: the physical science basis. Contribution of Working Group I to the fourth assessment report of the IPCC. Cambridge, UK: Cambridge University Press. Chapter 3. ———. 2007b. Climate change 2007: the physical science basis. Contribution of Working Group I to the fourth assessment report of the IPCC. Cambridge, UK: Cambridge University Press. Chapter 10. Kovats, R. S., M. J. Bouma, S. Hajat, E. Worrall, and A. Haines. 2003. El Niño and health. Lancet 362(9394):1481-1489. Linthicum, K. J., F. G. Davies, C. L. Bailey, and A. Kairo. 1984. Mosquito species encountered in a flooded grassland dambo in Kenya. Mosquito News 44:228-232. Linthicum, K. J., A. Anyamba, C. J. Tucker, P. W. Kelley, M. F. Myers, and C. J. Peters. 1999. Climate and satellite indicators to forecast Rift Valley fever epidemics in Kenya. Science 285(5426):397-400. Mavalankar, D., P. Shastri, and P. Raman. 2007. Chikungunya epidemic in India: a major public-health disaster. Lancet Infectious Disease 7(5):306-307. Peters, C. J., and K. J. Linthicum. 1994. Rift Valley fever. In Handbook of zoonoses, Second edition, edited by G. B. Beran. Boca Raton, FL: CRC Press, Inc. Rezza, G., L. Nicoletti, R. Angelini, R. Romi, A. C. Finarelli, M. Panning, P. Cordioli, C. Fortuna, S. Boros, F. Magurano, G. Silvi, P. Angelini, M. Dottori, M. G. Ciufolini, G. C. Majori, and A. Cassone. 2007. Infection with chikungunya virus in Italy: an outbreak in a temperate region. Lancet 370(9602):1840-1846. Save the Children Alliance. 2007 (January 11). Horn of Africa emergency statement, http://www. savethechildren.net/alliance/media/newsdesk/2007-01-01.html (accessed March 4, 2008). Sergon, K., C. Njuguna, R. Kalani, V. Ofula, C. Onyango, L. S. Konongoi, S. Bedno, H. Burke, A. M. Dumilla, J. Konde, M. K. Njenga, R. Sang, and R. F. Breiman. 2008. Seroprevalence of chikungunya virus (CHIKV) infection on Lamu Island, Kenya, October 2004. American Journal of Tropical Medicine and Hygiene 78(2):333-337.

OCR for page 104
70 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS Tsetsarkin, K. A., D. L. Vanlandingham, C. E. McGee, and S. Higgs. 2007. A single mutation in Chi- kungunya virus affects vector specificity and epidemic potential. PLoS Pathogens 3(12):e201. UN (United Nations). 2004. Kenya flash appeal, http://www.un.org/depts/ocha/cap/kenya.html (ac- cessed March 4, 2008). ———. 2006. Global survey of early warning systems: an assessment of capacities, gaps, and oppor- tunities towards building a comprehensive global early warning system for all natural hazards, http://www.unisdr.org/ppew/info-resources/ewc3/Global-Survey-of-Early-Warning-Systems.pdf (accessed March 4, 2008). Watts, D. M., D. S. Burke, B. A. Harrison, R. E. Whitmire, and A. Nisalak. 1987. Effect of tempera- ture on the vector efficiency of Aedes aegypti for dengue 2 virus. American Journal of Tropical Medicine and Hygiene 36(1):143-152. WHO (World Health Organization). 2004. Using climate to predict infectious disease outbreaks: a review, http://www.who.int/globalchange/publications/oeh0401/en/ (accessed March 4, 2008). ———. 2006. Chikungunya and dengue in the south west Indian Ocean, http://www.who.int/csr/ don/2006_03_17/en/ (accessed March 4, 2008). ———. 2007a. Outbreaks of Rift Valley fever in Kenya, Somalia and United Republic of Tanzania, December 2006-April 2007. Weekly Epidemiological Record 82(20):169-178. ———. 2007b. Health action in crises. Highlights No 0— to  January 2007, http://www.who. int/hac/donorinfo/highlights/highlights_140_08_14jan2007.pdf (accessed March 4, 2008). Stenseth References Achtman, M., K. Zurth, G. Morelli, G. Torrea, A. Guiyoule, and E. Carniel. 1999. Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis. Proceedings of the National Academy of Sciences 96(24):14043-14048. Anyamba, A., J. P. Chretien, J. Small, C. J. Tucker, and K. J. Linthicum. 2006. Developing global climate anomalies suggest potential disease risks for 2006-2007. International Journal of Health Geographics 5:60. Baltazard, M., Y. Karimi, M. Eftekhari, M. Chamsa, and H. H. Mollaret. 1963. La conservation interépizootique de la peste en foyer invétéré hypothèses de travail. Bulletin de la Société de Pathologie Exotique 56:1230-1241. Ben Ari, T., A. Gershunov, K. L. Gage, T. Snäll, P. Ettestad, K. L. Kausrud, and N. C. Stenseth. 2008. Human plague in U.S.: the importance of regional and local climate. Biology Letters (in review). Blanc, G. 1956. Une opinion non conformiste sur le mode de transmission de la peste. Revue d’Hygiéne et de Médecine Sociale 4(6):532-562. Chamberlain, N. 2004. Plague, http://www.kcom.edu/faculty/chamberlain/Website/lectures/lecture/ plague.htm (accessed July 1, 2008). Cohn, S. K., Jr. 2002. The Black Death transformed: disease and culture in early Renaissance Europe. London, UK: Edward Arnold Publishers. Davis, S., M. Begon, L. De Bruyn, V. S. Ageyev, N. L. Klassovskiy, S. B. Pole, H. Viljugrein, N. C. Stenseth, and H. Leirs. 2004. Predictive thresholds for plague in Kazakhstan. Science 304(5671):736-738. Davis, S., H. Leirs, H. Viljugrein, N. C. Stenseth, L. De Bruyn, N. Klassovskiy, V. Ageyev, and M. Begon. 2007. Empirical assessment of a threshold model for sylvatic plague. Journal of the Royal Society Interface 4(15):649-657. Drancourt, M., L. Houhamdi, and D. Raoult. 2006. Yersinia pestis as a telluric, human ectoparasite- borne organism. Lancet Infectious Diseases 6(4):234-241.

OCR for page 104
7 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE Duplantier, J. M., J. B. Duchemin, S. Chanteau, and E. Carniel. 2005. From the recent lessons of the Malagasy foci towards a global understanding of the factors involved in plague reemergence. Veterinary Research 36(3):437-453. Esper, J., S. G. Shiyatov, V. S. Mazepa, R. J. S. Wilson, D. A. Graybill, and G. Funkhouser. 2003. Temperature-sensitive Tien Shan tree ring chronologies show multi-centennial growth trends. Climate Dynamics 21(7/8):8p. Frigessi, A., M. Holden, C. Marshall, H. Viljugrein, N. C. Stenseth, L. Holden, V. Ageyev, and N. L. Klassovskiy. 2005. Bayesian population dynamics of interacting species: great gerbils and fleas in Kazakhstan. Biometrics 61(1):230-238. Fritz, C. L., D. T. Dennis, M. A. Tipple, G. L. Campbell, C. R. McCance, and D. J. Gubler. 1996. Surveillance for pneumonic plague in the United States during an international emergency: a model for control of imported emerging diseases. Emerging Infectious Diseases 2(1):30-36. Gage, K. L., and M. Y. Kosoy. 2005. Natural history of plague: perspectives from more than a century of research. Annual Review of Entomology 50(1):505-528. Galimand, M., A. Guiyoule, G. Gerbaud, B. Rasoamanana, S. Chanteau, E. Carniel, and P. Courvalin. 1997. Multidrug resistance in Yersinia pestis mediated by a transferable plasmid. New England Journal of Medicine 337(10):677-680. Guiyoule, A., F. Grimont, I. Iteman, P. A. Grimont, M. Lefevre, and E. Carniel. 1994. Plague pan- demics investigated by ribotyping of Yersinia pestis strains. Journal of Clinical Microbiology 32(3):634-641. Guiyoule, A., G. Gerbaud, C. Buchrieser, M. Galimand, L. Rahalison, S. Chanteau, P. Courvalin, and E. Carniel. 2001. Transferable plasmid-mediated resistance to streptomycin in a clinical isolate of Yersinia pestis. Emerging Infectious Diseases 7(1):43-48. Hall, F. G., G. Collatz, S. Los, E. Brown de Colstoun, and D. Landis, eds. 2005. ISLSCP Initiative II. DVD/CD-ROM. Hinnebusch, B. J., M.-L. Rosso, T. G. Schwan, and E. Carniel. 2002. High-frequency conjugative transfer of antibiotic resistance genes to Yersinia pestis in the flea midgut. Molecular Microbiol- ogy 46(2):349-354. Hotez, P. J., D. H. Molyneux, A. Fenwick, E. Ottesen, S. Ehrlich Sachs, and J. D. Sachs. 2006. Incor- porating a rapid-impact package for neglected tropical diseases with programs for HIV/AIDS, tuberculosis, and malaria. PLoS Medicine 3(5):e102. Huntington, T. G. 2006. Evidence for intensification of the global water cycle: review and synthesis. Journal of Hydrology 319(1-4):83-95. Inglesby, T. V., D. T. Dennis, D. A. Henderson, J. G. Barlett, M. S. Ascher, E. Eitzen, A. D. Fine, A. M. Friedlander, J. Hauer, J. F. Koerner, M. Layton, J. McDade, M. T. Osterholm, T. O’Toole, G. Parker, T. M. Perl, P. K. Russell, M. Schoch-Spana, and K. Tonat. 2000. Plague as a biologi- cal weapon. Journal of the American Medical Association 283(17):2281-2290. IPCC (Intergovernmental Panel on Climate Change). 2007. Climate change 2007: impacts, adapta- tion, and vulnerability. Contribution of Working Group II to the fourth assessment report of the Intergovernmental Panel on Climate Change. Cambridge, UK: Cambridge University Press. Chapter 8. Kausrud, K., H. Viljugrein, A. Frigessi, M. Begon, S. Davis, H. Leirs, V. Dubyanskiy, and N. C. Stenseth. 2007. Climatically driven synchrony of gerbil populations allows large-scale plague outbreaks. Proceedings: Biological Sciences 274(1621):1963-1969. Kausrud, K. L., H. Viljugrein, A. Frigessi, M. Begon, S. Davis, H. Leirs, T. Ben Ari, and N. C. Stenseth. 2008. The epidemiological history of plague in Central Asia: a paleoclimatic modelling study Proceedings of the National Academy of Sciences (in review). Koirala, J. 2006. Plague: disease, management, and recognition of act of terrorism. Infectious Disease Clinics of North America 20(2): viii, 273-287.

OCR for page 104
72 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS Laudisoit, A., H. Leirs, R. H. Makundi, S. Van Dongen, S. Davis, S. Neerinckx, J. Deckers, and R. Libois. 2007. Plague and the human flea, Tanzania. Emerging Infectious Diseases 13(5):687-693. Los, S., G. Collatz, P. Sellers, C. Malmström, N. Pollack, R. Defries, L. Bounoua, M. Parris, C. Tucker, and D. Dazlich. 2000. A global 9-year biophysical land surface data set from NOAA AVHRR data. Journal of Hydrometeorology 1:183-199. Mudur, G. 1995. India’s pneumonic plague outbreak continues to baffle. British Medical Journal 311(7007):706. Park, S., K. S. Chan, H. Viljugrein, L. Nekrassova, B. Suleimenov, V. S. Ageyev, N. L. Klassovskiy, S. B. Pole, and N. C. Stenseth. 2007. Statistical analysis of the dynamics of antibody loss to a disease-causing agent: plague in natural populations of great gerbils as an example. Journal of the Royal Society Interface 4(12):57-64. Parkhill, J., B. W. Wren, N. R. Thomson, R. W. Titball, M. T. G. Holden, M. B. Prentice, M. Sebai- hia, K. D. James, C. Churcher, K. L. Mungall, S. Baker, D. Basham, S. D. Bentley, K. Brooks, A. M. Cerdeno-Tarraga, T. Chillingworth, A. Cronin, R. M. Davies, and P. Davis. 2001. Genome sequence of Yersinia pestis, the causative agent of plague. Nature 413(6855):523-527. Parmenter, R. R., E. P. Yadav, C. A. Parmenter, P. Ettestad, and K. L. Gage. 1999. Incidence of plague associated with increased winter-spring precipitation in New Mexico. American Journal of Tropical Medicine and Hygiene 61(5):814-821. Pettorelli, N., J. O. Vik, A. Mysterud, J.-M. Gaillard, C. J. Tucker, and N. C. Stenseth. 2005. Using the satellite-derived NDVI to assess ecological responses to environmental change. Trends in Ecology and Evolution 20(9):503-510. Raoult, D., and G. Aboudharam. 2000. Molecular identification by “suicide PCR” of Yersinia pes- tis as the agent of medieval Black Death. Proceedings of the National Academy of Sciences 97(23):12800-12803. Samia, N. I., K.-S. Chan, and N. C. Stenseth. 2007. A generalized threshold mixed model for ana- lyzing nonnormal nonlinear time series, with application to plague in Kazakhstan. Biometrika 94(1):101-118. Schrag, S. J., and P. Wiener. 1995. Emerging infectious diseases: what are the relative roles of ecology and evolution? Trends in Ecology and Evolution 10(8):319-324. Scott, S., and C. J. Duncan. 2001. Biology of plagues: evidence from historical populations. Cam- bridge, UK: Cambridge University Press. Stenseth, N. C. 1999. Population cycles in voles and lemmings: density dependence and phase de- pendence in a stochastic world. Oikos 87(3):427-460. Stenseth, N. C., A. Mysterud, G. Ottersen, J. W. Hurrell, C. Kung-Sik, and M. Lima. 2002. Ecological effects of climate fluctuations. Science 297(5585):1292-1296. Stenseth, N. C., N. I. Samia, H. Viljugrein, K. L. Kausrud, M. Begon, S. Davis, H. Leirs, V. M. Dubyanskiy, J. Esper, V. S. Ageyev, N. L. Klassovskiy, S. B. Pole, and C. Kung-Sik. 2006. Plague dynamics are driven by climate variation. Proceedings of the National Academy of Sciences 103(35):13110-13115. Stenseth, N. C., B. B. Atshabar, M. Begon, S. R. Belmain, E. Bertherat, E. Carniel, K. L. Gage, H. Leirs, and L. Rahalison. 2008. Plague: past, present, and future. PLoS Medicine 5(1):e3. Treydte, K. S., G. H. Schleser, G. Helle, D. C. Frank, M. Winiger, G. H. Haug, and J. Esper. 2006. The twentieth century was the wettest period in northern Pakistan over the past millennium. Nature 440(7088):1179-1182. Twigg, G. 1984. The Black Death: a biological reappraisal. London, UK: Batsform Academic and Educational. WHO (World Health Organization). 2003. Plague, Algeria. Weekly Epidemiological Record 78(29):253. ———. 2005. Plague. Weekly Epidemiological Record 80(15):138-140. Yersin, A. 1894. La peste bubonique à Hong-Kong. Annales de l’Institut Pasteur 8:662-667.

OCR for page 104
7 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE Zhang, Z., Z. Li, Y. Tao, M. Chen, X. Wen, L. Xu, H. Tian, and N. C. Stenseth. 2007. Relationship between increase rate of human plague in China and global climate index as revealed by cross- spectral analysis and cross-wavelet analysis. Integrative Zoology 2(3):144-153. Ziegler, P. 1969. The Black Death. Wolfeboro Falls, NH: Alan Sutton Publishing Inc. Garrett References Anagnostakis, S. L. 2000. Revitalization of the majestic chestnut: chestnut blight disease. APSnet, http://www.apsnet.org/online/feature/chestnut/ (accessed March 28, 2008). Anderson, P. K., A. A. Cunningham, N. G. Patel, F. J. Morales, P. R. Epstein, and P. Daszak. 2004. Emerging infectious diseases of plants: pathogen pollution, climate change and agrotechnology drivers. Trends in Ecology and Evolution 19(10):535-544. Bai, G., and G. Shaner. 2004. Management and resistance in wheat and barley to Fusarium head blight. Annual Review of Phytopathology 42:135-161. Bergot, M., E. Cloppet, V. Pérarnaud, M. Déqué, B. Marçais, and M.-L. Desprez-Loustau. 2004. Simulations of potential range expansion of oak disease caused by Phytophthora cinnamomi under climate change. Global Change Biology 10:1539-1552. Brasier, C. M. 2001. Rapid evolution of introduced plant pathogens via interspecific hybridization. BioScience 51(2):123-133. Burdon, J. J., P. H. Thrall, and L. Ericson. 2006. The current and future dynamics of disease in plant communities. Annual Review of Phytopathology 44:19-39. Chakraborty, S., A. V. Tiedemann, and P. S. Teng. 2000. Climate change: potential impact on plant diseases. Environmental Pollution 108(3):317-326. Cheatham, M. R., M. N. Rouse, P. D. Esker, S. Ignacio, W. Pradel, R. Raymundo, A. H. Sparks, G. A. Forbes, T. R. Gordon, and K. A. Garrett. Beyond yield: plant disease in the context of ecosystem services. Phytopathology (in revision). Cline, W. R. 2007. Global warming and agriculture: impact estimates by country. Washington, DC: Center for Global Development and Peterson Institute for International Economics. Coakley, S. M., H. Scherm, and S. Chakraborty. 1999. Climate change and plant disease management. Annual Review of Phytopathology 37:399-426. Daily, G. C., ed. 1997. Nature’s services: societal dependence on natural ecosystems. Washington, DC: Island Press. De Wolf, E. D., and S. A. Isard. 2007. Disease cycle approach to plant disease prediction. Annual Review of Phytopathology 45:203-220. Desprez-Loustau, M.-L., C. Robin, G. Reynaud, M. Déqué, V. Badeau, D. Piou, C. Husson, and B. Marçais. 2007. Simulating the effects of a climate-change scenario on the geographical range and activity of forest-pathogenic fungi. Canadian Journal of Plant Pathology 29:101-120. Eviner, V. T., and G. E. Likens. 2008. Effects of pathogens on terrestrial ecosystem function. In Infec- tious disease ecology: effects of ecosystems on disease and of disease on ecosystems, edited by R. Ostfeld, F. Keesing, and V. Eviner. Princeton, NJ: Princeton University Press. Pp. 260-283. Fletcher, J., and J. P. Stack. 2007. Agricultural biosecurity: threats and impacts for plant pathogens. In Global infectious disease surveillance and detection. Washington, DC: The National Academies Press. Pp. 86-94. Frank, E. E. 2007. Rust and drought effects on gene expression and phytohormone concentration in big bluestem. M.S. Thesis, Kansas State University, Manhattan, Kansas. Garrett, K. A., and R. L. Bowden. 2002. An Allee effect reduces the invasive potential of Tilletia indica. Phytopathology 92:1152-1159. Garrett, K. A., S. P. Dendy, E. E. Frank, M. N. Rouse, and S. E. Travers. 2006. Climate change effects on plant disease: genomes to ecosystems. Annual Review of Phytopathology 44:489-509.

OCR for page 104
7 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS Garrett, K. A., L. N. Zúñiga, E. Roncal, G. A. Forbes, C. C. Mundt, Z. Su, and R. J. Nelson. Intra- specific functional diversity in hosts and its effect on disease risk across a climatic gradient. Ecological Applications (in revision). He, Z. L., T. J. Gentry, C. W. Schadt, L. Y. Wu, J. Liebich, S. C. Chong, Z. J. Huang, W. M. Wu, B. H. Gu, P. Jardine, C. Criddle, and J. Zhou. 2007. GeoChip: a comprehensive microarray for investigating biogeochemical, ecological and environmental processes. ISME Journal 1:67-77. Hijmans, R. J., G. A. Forbes, and T. S. Walker. 2000. Estimating the global severity of potato late blight with GIS-linked disease forecast models. Plant Pathology 49(6):697-705. Isard, S. A., S. H. Gage, P. Comtois, and J. M. Russo. 2005. Principles of the atmospheric pathway for invasive species applied to soybean rust. BioScience 55(10):851-861. Jeger, M. J., and M. Pautasso. 2008. Plant disease and global change—the importance of long-term data sets. New Phytologist 177(1):8-11. Johnson, R. C. 2008. Gene banks pay big dividends to agriculture, the environment, and human welfare. PLoS Biology 6(6):e148. Lobell, D. B., M. B. Burke, C. Tebaldi, M. D. Mastrandrea, W. P. Falcon, and R. L. Naylor. 2008. Priori- tizing climate change adaptation needs for food security in 2030. Science 319(5863):607-610. Madden, L., and M. Wheelis. 2003. The threat of plant pathogens as weapons against U.S. crops. Annual Review of Phytopathology 41:155-176. Magarey, R. D., G. A. Fowler, D. M. Borchert, T. B. Sutton, and M. Colunga-Garcia. 2007. NAPPFAST: an Internet system for the weather-based mapping of plant pathogens. Plant Disease 91(4):336-345. Margosian, M. L., K. A. Garrett, J. M. S. Hutchinson, and K. A. With. Connectivity of the American agricultural landscape: assessing the national risk of crop pest and disease spread. BioScience (in revision). McDonald, B. A., and C. Linde. 2002. Pathogen population genetics, evolutionary potential, and durable resistance. Annual Review of Phytopathology 40:349-379. Mitchell, C. E., P. B. Reich, D. Tilman, and J. V. Groth. 2003. Effects of elevated CO 2, nitrogen deposition, and decreased species diversity on foliar fungal plant disease. Global Change Biol- ogy 9(3):438-451. Nelson, R. J., R. L. Naylor, and M. M. Jahn. 2004. The role of genomics research in improvement of “orphan” crops. Crop Science 44:1901-1904. Oerke, E. C., H. W. Dehne, F. Schönbeck, and A. Weber. 1994. Crop production and crop protection. Amsterdam, The Netherlands: Elsevier Science, B.V. Parker, I. M., and G. S. Gilbert. 2004. The evolutionary ecology of novel plant-pathogen interactions. Annual Review of Ecology, Evolution and Systematics 35:675-700. Patt, A., P. Suarez, and C. Gwata. 2005. Effects of seasonal climate forecasts and participatory workshops among subsistence farmers in Zimbabwe. Proceedings of the National Academy of Sciences 102(35):12623-12628. Peng, S., J. Huang. J. E. Sheehy, R. C. Laza, R. M. Visperas, X. H. Zhong, G. S. Centeno, G. S. Khush, and K. G. Cassman. 2004. Rice yields decline with higher night temperature from global warm- ing. Proceedings of the National Academy of Sciences 101(27):9971-9975. Pimentel, D., L. Lach, R. Zuniga, and D. Morrison. 2000. Environmental and economic costs of nonindigenous species in the United States. BioScience 50(1):53-65. Pivonia, S., and X. B. Yang. 2004. Assessment of the potential year-round establishment of soybean rust throughout the world. Plant Disease 88(5):523-529. Redak, R. A., A. H. Purcell, J. R. S. Lopes, M. J. Blua, R. F. Mizell, and P. C. Andersen. 2004. The biology of xylem fluid-feeding insect vectors of Xylella fastidiosa and their relation to disease epidemiology. Annual Review of Entomology 49:243-270. Riesenfeld, C. S., P. D. Schloss, and J. Handelsman. 2004. Metagenomics: genomic analysis of mi- crobial communities. Annual Review of Genetics 38:525-552.

OCR for page 104
7 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE Rizzo, D. M., M. Garbelotto, and E. A. Hansen. 2005. Phytophthora ramorum: integrative research and management of an emerging pathogen in California and Oregon forests. Annual Review of Phytopathology 43:309-335. Roesch, L. F., R. R. Fulthorpe, A. Riva, G. Casella, A. K. M. Hadwin, A. D. Kent, S. H. Daroub, F. A. O. Camargo, W. G. Farmerie, and E. W. Triplett. 2007. Pyrosequencing enumerates and contrasts soil microbial diversity. ISME Journal 1:283-290. Rouse, M. N. 2007. Diversity of a disease resistance gene homolog in Andropogon gerardii (Poaceae) is correlated with precipitation. M.S. Thesis, Kansas State University, Manhattan, Kansas. Roy, B. A., S. Gusewell, and J. Harte. 2004. Response of plant pathogens and herbivores to a warming experiment. Ecology 85:2570-2571. Rush, C. M., R. Riemenschneider, J. M. Stein, T. Boratynski, R. L. Bowden, and M. H. Royer. 2005. Status of karnal bunt of wheat in the United States 1996-2004. Plant Disease 89(3):212-223. Stack, J. P., and J. Fletcher. 2007. Plant biosecurity infrastructure for disease surveillance and diag- nostics. In Global infectious disease surveillance and detection. Washington, DC: The National Academies Press. Pp. 95-102. Stokstad, E. 2007. Plant pathology: deadly wheat fungus threatens world’s bread baskets. Science 315(5820):1786-1787. Travers, S. E., M. D. Smith, J. Bai, S. H. Hulbert, J. E. Leach, P. S. Schnable, A. K. Knapp, G. A. Milliken, P. A. Fay, A. Saleh, and K. A. Garrett. 2007. Ecological genomics: making the leap from model systems in the lab to native populations in the field. Frontiers in Ecology and the Environment 5:19-24. UNEP (United Nations Environment Programme). 2004. Childhood pesticide poisoning: information for advocacy and action. Châtelaine, Switzerland: United Nations Environment Programme. Villanueva, H., R. Raymundo, H. Juarez, W. Perez, and G. Forbes. In preparation. The article and journal titles were not available at the time of publication. Waldrop, M. P., and M. K. Firestone. 2006. Response of microbial community composition and func- tion to soil climate change. Microbial Ecology 52:716-724. Webb, K. M., J. Bai, I. Oña, K. A. Garrett, T. W. Mew, C. M. Vera Cruz, and J. E. Leach. In prepara- tion. The article and journal titles were not available at the time of publication. Widmark, A.-K., B. Andersson, A. Cassel-Lundhagen, M. Sandström, and J. E. Yuen. 2007. Phy- tophthora infestans in a single field in southwest Sweden early in spring: symptoms, spatial distribution and genotypic variation. Plant Pathology 56:573-579. Woods, A., K. D. Coates, and A. Hamann. 2005. Is an unprecedented Dothistroma needle blight epidemic related to climate change? BioScience 55(9):761-769. Zhu, Y., H. Chen, J. Fan, Y. Wang, Y. Li, J. Chen, J. Fan, S. Yang, L. Hu, H. Leung, T. W. Mew, P. S. Teng, Z. Wang, and C. C. Mundt. 2000. Genetic diversity and disease control in rice. Nature 406(6797):718-722. Zhu, Y., H. Fang, Y. Wang, J. X. Fan, S. Yang, T. W. Mew, and C. Mundt. 2005. Panicle blast and canopy moisture in rice cultivar mixtures. Phytopathology 95(4):433-438. Parkinson References AMAP (Arctic Monitoring and Assessment Programme). 2003. AMAP Assessment 2002: human health in the Arctic. Oslo, Norway: Arctic Monitoring and Assessment Program. Arctic Council. 2005. Arctic climate impact assessment scientific report. New York: Cambridge University Press. Pp. 863-960. Baggett, H. C., T. W. Hennessy, R. Leman, C. Hamlin, D. Bruden, and A. Reasonover. 2003. An outbreak of community-onset methicillin resistant Staphylococcus aureus skin infections in southwestern Alaska. Infection Control and Hospital Epidemiology 24(6):397-402.

OCR for page 104
7 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS Baggett, H. C., T. W. Hennessy, K. Rudolph, D. Bruden, A. Reasonover, and A. J. Parkinson. 2004. Community-onset methicillin-resistant Staphylococcus aureus, associated with antibiotic use and cytotoxin Panton-Valentine leukocidin during a furnunculosis outbreak in rural Alaska. Journal of Infectious Diseases 189(9):1565-1573. Bjerregaard, P., K. T. Young, E. Dewailly, and S. O. E. Ebbesson. 2004. Indigenous health in the Arctic: an overview of the circumpolar Inuit population. Scandinavian Journal of Public Health 32(5):390-395. Borgerson, S. G. 2008. Arctic meltdown: the economic and security implications of global warming. Foreign Affairs 87(2):63-77. Bruce, M. G., S. L. Deeks, T. Zulz, D. Bruden, C. Navarro, M. Lovegren, L. Jette, K. Kristinsson, G. Sigmundsdottir, K. Brinklov Jensen, O. Lovoll, J. P. Nuorti, E. Herva, A. Nystedt, A. Sjostedt, A. Koch, T. W. Hennessy, and A. J. Parkinson. 2008a. International Circumpolar Surveillance for invasive pneumococcal disease, 1999-2005. Emerging Infectious Diseases 14(1):25-33. Bruce, M. G., S. L. Deeks, T. Zulz, C. Navarro, C. Palacios, C. Case, C. Hemsley, T. W. Hennessy, A. Corriveau, B. Larke, I. Sobel, M. Lovegren, C. DeByle, R. Tsang, and A. J. Parkinson. 2008b. Epidemiology of Haemophilus influenzae serotype A, North American Arctic 2000-2005. Emerging Infectious Diseases 14(1):48-55. Bulkow, L. R., R. J. Singleton, R. A. Karron, L. H. Harrisson, and Alaska RSV Study Group. 2002. Risk factors for severe respiratory syncytial virus infection among Alaska Native children. Pediatrics 109(2):210-216. Castrodale, L. J., M. Beller, J. F. Wilson, P. M. Schantz, D. P. McManus, L. H. Zhang, F. G. Fallico, and F. D. Sacco. 2002. Two atypical cases of cystic echinococcosis (Echinococcus granulosis) in Alaska 1999. American Journal of Tropical Medicine and Hygiene 66(3):325-327. CDC (Centers for Disease Control and Prevention). 2001. Botulism outbreak associated with eating fermented food—Alaska. Morbidity and Mortality Weekly Report 50(32):680-682. Christensen, J., P. Poulsen, and K. Ladefoged. 2004. Invasive pneumococcal disease in Greenland. Scandinavian Journal of Infectious Diseases 36(5):325-329. Curtis, T., S. Kvernmo, and P. Bjerregaad. 2005. Changing living conditions, life style and health. International Journal of Circumpolar Health 64(5):442-450. Dawar, M., L. Moody, J. D. Martin, C. Fung, J. Isaac-Renton, and D. M. Patrick. 2002. Two outbreaks of botulism associated with fermented salmon roe—British Columbia, August 2001. Canadian Communicable Disease Reports 28(6):45-49. Degani, N., C. Navarro, S. Deeks, and M. Lovegren. 2008. Invasive bacterial diseases in northern Canada. Emerging Infectious Diseases 14(1):34-40. Frumkin, H., J. Hess, G. Luber, J. Maliay, and M. McGeehin. 2008. Climate change: the public health response. American Journal of Public Health 98(3):435-445. Furgal, C. 2005. Monitoring as a community response for climate change and health. International Journal of Circumpolar Health 64(5):440-441. Gessner, B. D., N. S. Weiss, and C. M. Nolan. 1998. Risk factors for pediatric tuberculosis infec- tion and disease after household exposure to adult index cases in Alaska. Jornal de Pediatria 132(3):509-513. Haines, A., R. S. Kovars, D. Campbell-Lendrun, and C. Corvalan. 2006. Climate change and human health: impacts, vulnerability, and mitigation. Lancet 360(9528):2101-2109. Hennessy, T., T. Ritter, R. C. Holman, D. L. Bruden, K. L. Yorita, L. Bulkow, J. E. Cheek, R. J. Singleton, and J. Smith. 2008. Relationship between in-home water service and the risk of respitatory tract, skin, and gastrointestinal tract infections among Alaska Natives. American Journal of Public Health 98(5):1-8. Hess, J., J. Malilay, and A. J. Parkinson. In press. Climate change: the importance of place and places of special risk. American Journal of Preventive Medicine.

OCR for page 104
77 CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE Hoberg, E. P., L. Polley, E. J. Jenins, S. J. Kutz, A. M. Vetch, and B. T. Elkin. 2008. Integrated ap- proaches and empiric models for investigation of parasitic diseases in northern wildlife. Emerg- ing Infectious Diseases 14(1):10-17. Holts, D. W., C. Hanns, T. O. O’Hara, J. Burek, and R. Franz. 2005. New distribution records of Echinococcus multilocularis in the brown lemming from Barrow, Alaska. Journal of Wildlife Diseases 41(1):257-259. IOM (Institute of Medicine). 1992. Emerging infections: microbial threats to health in the United States. Washington, DC: National Academy Press. ———. 2003. Microbial threats to health: emergence, detection, and response. Washington, DC: The National Academies Press. Karron, R. A., R. J. Singleton, L. Bulkow, A. J. Parkinson, D. Kruse, I. DeSmet, C. Indorf, K. M. Petersen, D. Leombruno, D. Hurlburt, M. Santosham, and L. H. Harrison. 1999. Severe respiratory syncytial virus disease in Alaska Native children. Journal of Infectious Diseases 180(1):41-49. Kurkela, S., O. Rätti, E. Huhtamo, N. Y. Uzcátegui, P. J. Nuorti, J. Laakkonen, T. Manni, P. Helle, A. Vaheri, and O. Vapalahti. 2008. Sindbis virus infection in resident birds, migratory birds, and humans, Finland. Emerging Infectious Diseases 14(1):41-47. Leclair, D., J. W. Austin, J. Faber, B. Cadieux, and B. Blanchfield. 2004. Toxicity of aged seal meat challenged with Clostridium botulinum type E. Federal Food Safety and Nutrition Research Meeting, Ottawa, Ontario, October 4-5. Lindgren, E., and R. Gustafson. 2001. Tick-borne encephalitis in Sweden and climate change. Lancet 358(9275):16-18. McLaughlin, J. B., A. Depoala, C. A. Bopp, K. A. Martinek, N. Napolilli, C. Allison, S. Murry, E. C. Thompson, M. M. Bird, and T. P. Middaugh. 2005. Emergence of Vibrio parahaemolyticus gastroenteritis associated with consumption of Alaskan oysters and its global implications. New England Journal of Medicine 353(14):1463-1470. McMahon, B. J., M. G. Bruce, T. W. Hennessy, D. L. Bruden, F. Sacco, H. Peters, D. A. Hurlburt, J. M. Morris, A. L. Reasonover, G. Dailde, D. E. Berg, and A. J. Parkinson. 2007. Reinfection after successful eradication of Helicobacter pylori—a 2 year prospective study in Alaska Natives. Alimentary Pharmacology and Therapeutics 23(8):1215-1223. Meyer, A., K. Ladefoged, P. Poulsen, and A. Kock. 2008. Population-based survey of invasive bacte- rial diseases, Greenland, 1995-2004. Emerging Infectious Diseases 14(1):76-79. Nayha, S. 2005. Environmental temperature and mortality. International Journal of Circumpolar Health 64(5):451-458. Netesov, S. V., and L. J. Conrad. 2001. Emerging infectious diseases in Russia 1990-1999. Emerging Infectious Diseases 7(1):1-5. Nguyen, D., J. F. Proulx, J. Westley, L. Thibert, S. Dery, and M. A. Behr. 2003. Tuberculosis in the Inuit community of Quebec, Canada. American Journal of Respiratory and Critical Care Medicine 168(11):1353-1357. Ogden, N. H., A. Maarouf, I. K. Barker, M. Bigras-Poulin, L. R. Lindsay, M. G. Morshed, C. J. O’Callaghan, F. Ramay, D. Waltner-Twews, and D. F. Charron. 2005. Climate change and the potential for range expansion of the Lyme disease vector Ixodes scapularis in Canada. International Journal of Parasitology 36(1):63-70. Orr, P., B. Lorencz, R. Brown, R. Kielly, B. Tan, D. Holton, H. Clugstone, L. Lugtig, C. Pim, S. McDonald, G. Hammond, M. Moffatt, J. Spika, D. Manuel, W. Winther, D. Milley, H. Lior, and N. Sinuff. 1994. An outbreak of diarrhea due to verotoxin-producing Esherichia coli in the Canadian Northwest Territories. Scandinavian Journal of Infectious Diseases 26(6):675-684. Parkinson, A. J., and J. C. Butler. 2005. Potential impact of climate change on infectious disease emergence in the Arctic. International Journal of Circumpolar Health 64(5):478-486. Parkinson, A. J., M. Bruce, and T. Zultz. 2008. International circumpolar surveillance, and arctic network for surveillance of infectious diseases. Emerging Infectious Diseases 14(1):18-24.

OCR for page 104
7 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS Pettersson, L., J. Boman, P. Juto, M. Evander, and C. Ahlm. 2008. Outbreak of Puumala virus infec- tion, Sweden. Emerging Infectious Diseases 14(5):808-810. Proulx, J. F., V. Milor-Roy, and J. Austin. 1997. Four outbreaks of botulism in Ungava Bay Nunavik, Quebec. Canadian Communicable Disease Report 23(4):30-32. Rausch, R. 2003. Cystic echinococcosis in the Arctic and sub-Arctic. Parasitology 127(suppl): S73-S85. Revich, B. A. 2008. Climate change alters human health in Russia. Studies on Russian Economic Development 19(3):311-317. Richter-Menge, J., S. Nghiem, D. Perovich, and I. Rigor. 2008. Sea ice cover. In Arctic report card, 2007, www.arctic.noaa.gov//reportcard/seaice.html (accessed April 4, 2008). Rudolph, K. M., M. J. Crain, A. J. Parkinson, and M. C. Roberts. 1999. Characterization of a multidrug- resistant clone of invasive Streptococcus pneumoniae serotype 6B in Alaska by using pulsed- field gel electrophoresis and PspA typing. Journal of Infectious Diseases 180(5):1577-1583. Rudolph, K. M., A. J. Parkinson, A. L. Reasonover, L. R. Bulkow, D. J. Parks, and J. C. Butler. 2000. Serotype distribution and antimicrobial resistance patterns of invasive isolates of Streptococcus pneumoniae: Alaska 1991-1998. Journal of Infectious Diseases 182(2):490-496. Schweiger, A., R. W. Ammann, D. Candinas, P. A. Clavien, J. Eckert, B. Gottstein, N. Halkic, B. Muellhaupt, J. Reichen, P. E. Tarr, P. R. Torgerson, and P. Deplazes. 2007. Human al- veolar echinococcus after fox population increase Switzerland. Emerging Infectious Diseases 13(6):878-882. Singleton, R., L. Hammitt, T. Hennessy, L. Bulkow, D. DeByle, A. Parkinson, T. E. Cottle, H. Peters, and J. C. Butler. 2006. The Alaska Haemophilus influenzae type b experience: lessons in control- ling a vaccine-preventable disease. Pediatrics 118(2):421-429. Skarphédinsson, S., M. Jensen, and K. Kristiansen. 2005. Survey of tickborne infections in Denmark. Emerging Infectious Diseases 11(7):1055-1061. Sobel, J., N. Tucker, A. Sulka, J. McMaughlin, and S. Maslanka. 2004. Foodborne botulism in the United States, 1990-2000. Emerging Infectious Diseases 10(9):1606-1611. Søborg, C., B. Søborg, S. Pouelsen, G. Pallisgaard, S. Thybo, and J. Bauer. 2001. Doubling of tu- berculosis incidence in Greenland over an 8 year period (1990-1997). International Journal of Tuberculosis and Lung Disease 5(3):257-265. Sørensen, H. C., K. Albøge, and J. C. Misfeldt. 1993. Botulism in Ammassalik. Ugeskrift for Laeger 115(2):108-109. Stefansson Arctic Institute. 2004. Arctic human development report. Akureyri, Iceland: Stefansson Arctic Institute. Van Caeseele, P., A. Macaulay, P. Orr, F. Aoki, and B. Martin. 2001. Rapid pharmacotherapeutic inter- vention for an influenza A outbreak in the Canadian Arctic: lessons from Sanikiluaq experience. International Journal of Circumpolar Health 60(4):640-648. Wainwright, R. B., W. L. Heyward, J. P. Middaugh, C. L. Hatheway, A. P. Harpster, and T. R. Bender. 1988. Foodborne botulism in Alaska 1947-1985: epidemiology and clinical findings. Journal of Infectious Diseases 157(6):1158-1162. Walters, L. L., S. J. Tyrrell, and R. E. Shope. 1999. Seroepidemiology of California and Bunyamwera (Bunyaviridae) serogroup virus infections in native populations of Alaska. American Journal of Tropical Medicine and Hygiene 60(5):806-821. Warren, J. A., J. E. Berner, and T. Curtis. 2005. Climate change and human health: infrastructure impacts to small remote communities in the North. International Journal of Circumpolar Health 64(5):487-497. Young, T. K. 2008. Circumpolar health indicators: sources, data, and maps. Circumpolar Health Supplements 3:55-78.