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5 Infectious Disease Emergence: Past, Present, and Future OVERVIEW Emerging infections, as defined by Stephen Morse of Columbia University in his contribution to this chapter, are infections that are rapidly increasing in incidence or geographic range, including such previously unrecognized diseases as HIV/AIDS, severe acute respiratory syndrome (SARS), Ebola hemorrhagic fever, and Nipah virus encephalitis. Among his many contributions to efforts to recognize and address the threat of emerging infections, Lederberg co-chaired the committees that produced two landmark Institute of Medicine (IOM) reports, Emerging Infections: Microbial Threats to Health in the United States (IOM, 1992) and Microbial Threats to Health (IOM, 2003), which provided a cru- cial framework for understanding the drivers of infectious disease emergence (Box WO-3 and Figure WO-13). As the papers in this chapter demonstrate, this framework continues to guide research to elucidate the origins of emerging infectious threats, to inform the analysis of recent patterns of disease emergence, and to identify risks for future disease emergence events so as to enable early detection and response in the event of an outbreak, and perhaps even predict its occurrence. In the chapter’s first paper, Morse describes two distinct stages in the emer- gence of infectious diseases: the introduction of a new infection to a host popu- lation, and the establishment within and dissemination from this population. He considers the vast and largely uncharacterized “zoonotic pool” of possible human pathogens and the increasing opportunities for infection presented by ecological upheaval and globalization. Using hantavirus pulmonary syndrome and H5N1 influenza as examples, Morse demonstrates how zoonotic pathogens 

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 MICROBIAL EVOLUTION AND CO-ADAPTATION gain access to human populations. While many zoonotic pathogens periodically infect humans, few become adept at transmitting or propagating themselves, Morse observes. Human activity, however, is making this transition increasingly easy by creating efficient pathways for pathogen transmission around the globe. “We know what is responsible for emerging infections, and should be able to prevent them,” he concludes, through global surveillance, diagnostics, research, and above all, the political will to make them happen. The authors of the chapter’s second paper, workshop presenter Mark Woolhouse and Eleanor Gaunt of the University of Edinburgh, draw several gen- eral conclusions about the ecological origins of novel human pathogens based on their analysis of human pathogen species discovered since 1980. Using a rigor- ous, formal methodology, Woolhouse and Gaunt produced and refined a catalog of the nearly 1,400 recognized human pathogen species. A subset of 87 species have been recognized since 1980—and are currently thought to be “novel” patho- gens. The authors note four attributes of these novel pathogens that they expect will describe most future emergent microbes: a preponderance of RNA viruses; pathogens with nonhuman animal reservoirs; pathogens with a broad host range; and pathogens with some (perhaps initially limited) potential for human-human transmission. Like Morse, Woolhouse and Gaunt consider the challenges faced by novel pathogens to become established in a new host population and achieve efficient transmission, conceptualizing Morse’s observation that “many are called but few are chosen” in graphic form, as a pyramid. It depicts the approximately 1,400 pathogens capable of infecting humans, of which 500 are capable of human-to- human transmission, and among which fewer than 150 have the potential to cause epidemic or endemic disease; evolution—over a range of time scales—drives pathogens up the pyramid. The paper concludes with a discussion of the public health implications of the pyramid model, which suggests that ongoing global ecological change will continue to produce novel infectious diseases at or near the current rate of three per year. In contrast to other contributors to this chapter, who focus on what, why, and where infectious diseases emerge, Jonathan Eisen, of the University of California, Davis, considers how new functions and processes evolve to generate novel pathogens. Eisen investigates the origin of microbial novelty by integrating evolutionary analyses with studies of genome sequences, a field he terms “phy- logenomics.” In his essay, he illustrates the results of such analyses in a series of “phylogenomic tales” that describe the use of phylogenomics to predict the function of uncharacterized genes in a variety of organisms, and in elucidating the genetic basis of a complex symbiotic relationship involving three species. Knowledge of microbial genomes, and the functions they encode, is severely limited, Eisen observes. Among 40 phyla of bacteria, for example, most of the available genomic sequences were from only three phyla; sequencing of Archaea and Eukaryote genomes has proceeded in a similarly sporadic manner. To fill

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 INFECTIOUS DISEASE EMERGENCE these gaps in our knowledge of the “tree of life,” his group has begun an initiative called the Genomic Encyclopedia of Bacteria and Archaea. Eisen describes this effort and advocates the further integration of information on microbial phylog- eny, genetic sequence, and gene function with biogeographical data, in order to produce a “field guide to microbes.” The chapter’s final paper, by Peter Daszak of the Consortium for Conser- vation Medicine, Wildlife Trust, makes the leap from knowing how infectious diseases emerge to predicting where, and under what circumstances, an emergent disease event is likely to occur. Daszak presents several examples of his group’s efforts to build predictive approaches to infectious disease emergence based on a thorough understanding of the underlying ecology. These include construct- ing a model to predict relative risks for Nipah virus reemergence in Malaysia, where a 1999 outbreak devastated a thriving pig farming industry; identifying likely sources by which West Nile virus could spread to Hawaii, the Galapagos, and Barbados; and determining likely reservoirs of H5N1 influenza for specific geographic locations worldwide. Daszak’s group constructed a database of emerging infectious disease “events” first reported in human populations between 1940 and 2004, which they have used to examine correspondences between events and ecological variables, such as human population density and wildlife diversity, in a geographical con- text. These analyses have revealed “hotspots” for infectious disease emergence. Daszak discusses the implications of hotspot location for global infectious disease surveillance, and describes how he and coworkers have used their knowledge of hotspots to target surveillance for Nipah virus in India, and also to discover a virus with zoonotic potential in Bangladesh. EMERGING INFECTIONS: CONDEMNED TO REPEAT? Stephen S. Morse, Ph.D.1 Columbia University We have all learned about the importance of infectious diseases throughout history, including the Plague of Justinian (541-542), the first known pandemic on record (McNeill, 1976), and the Black Death in the fourteenth century. Stanley Falkow, who is included in this volume, has extensively studied Yersinia pestis, the responsible organism, and given us important insights into its pathogenesis. Another devastating disease that was once much feared is smallpox, which is said to have killed more people than all the wars in history. The eradication of small- pox was therefore a triumph of public health. Ironically, smallpox has the unique property of being the only species to date that human beings have intentionally 1 Professor of epidemiology and founding director of the Center for Public Health Preparedness at the Mailman School of Public Health.

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 MICROBIAL EVOLUTION AND CO-ADAPTATION driven to extinction. While we have unintentionally driven so many species to extinction, it is nice to know we can actually intentionally do some good. Chol- era was, of course, a very big concern in the nineteenth century and remains a concern today, especially in places like Bangladesh, as Gerald Keusch of Boston University and a member of the Forum can affirm. The 1918 influenza pandemic is one of our paradigms of a nightmare emerg- ing infectious disease event. It may very well have been the greatest natural disaster in the early days of the twentieth century. The “official” mortality esti- mates keep rising as investigators keep finding data from further away, in devel- oping countries and more remote places. But that pandemic is thought to have accounted for about 50 million or more deaths, depending on how you want to count it, and is obviously a matter of great concern. Despite that, we have had years of complacency about infectious diseases, partly for reasons already discussed—the antibiotic era, immunizations, improved public health measures—all of which have led to the fact that we now live longer and tend to die later of chronic diseases. Unfortunately, this has not been true everywhere. It has not been true in many developing countries. Infectious dis- eases remain the major causes of morbidity and mortality in much of the world. But in this paper, I would like to concentrate on emerging infections, the ones that are not previously recognized and that seem to appear suddenly and almost mysteriously—if you will, The Andromeda Strain (Crichton, 1969). Figure WO-7 graphically shows a number of examples. Of course, there are also forgot- ten infections that reappear. We sometimes call those “reemerging infections.” I tend to think of most of the “reemerging” infections as reminding us that many infectious diseases in our highly mechanized modern societies, with the standard of living we enjoy, have been pushed to the margins, but have never been entirely eliminated. So when public health measures are relaxed or are abandoned because of lack of money or complacency—complacency being a very big problem—you then see forgotten infections reappearing. An example is diphtheria in the former Soviet Union and Eastern Europe in the early 1990s when those countries no longer had the money to maintain their immunization programs. It reminds us that many of these diseases may be forgotten, but they are not gone. HIV/AIDS is, of course, the infection that got our attention initially and made it possible at least to think about shaking ourselves out of the growing complacency about infectious diseases. HIV infection and AIDS, starting from obscurity, rose to become a leading cause of death in the United States by 1993 (Figure 5-1). There are recent reports dating HIV to the early twentieth cen- tury, but it didn’t appear to take off until mid-century. You can find a molecular example of HIV in Zaire in 1969, but that is almost a one-off, and then there were reports of a few cases in the 1970s in Africa, if anyone had been paying attention. Then suddenly, in the early 1980s, it appeared in the United States and took off like the proverbial rocket to overtake all other causes of death in healthy young people. Of course, this is the same age group killed in the 1918 flu, but also the

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 INFECTIOUS DISEASE EMERGENCE FIGURE 5-1 Leading causes of death in young adults, United States, 1987-2005. Red line: Rise of HIV infection to become leading cause of death. SOURCE: CDC (2008). Figure 5-1 COLOR Original file colors very people we generally expect to have the best survival rate. They have survived childhood and we expect that they ought to be fine. As shown in Figure 5-1, all the other causes of death were unchanged during that period. HIV was therefore quite a surprise. When you think about it, this does seem rather like The Andromeda Strain. We had thousands of years of experience with infections, some of them historically recorded in some detail. Some of these are still unidentified, and we still argue about what they were. But a disease that actu- ally kills by undermining the immune system directly was a novel mechanism of pathogenesis. How often does one find a new mechanism of pathogenesis in an infectious disease, considering the thousands of years of experience that we have had? I think it was quite remarkable. Since its peak (around 1995), the HIV/AIDS death rate in the young adult population in the United States has dropped (Figure 5-1), thanks largely to the fact that a few effective drugs were finally developed, including in particular the protease inhibitors. As a result, the trend reached a plateau and has recently been going down. HIV/AIDS is now a treatable disease, with many lives saved among those who can afford the medication. But it also worries me that this fortunate situation may not last very long. Inevitably, antiviral resistance has already been identified in some patients. Another concern is that some of the younger people have now become quite complacent about this disease, not knowing the devasta- tion that many of us witnessed in the 1980s, before it could be effectively treated. We are seeing young people now regarding this with less seriousness than they should. So there we are, facing complacency again. If there is a bottom line to the

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 MICROBIAL EVOLUTION AND CO-ADAPTATION theme of the Forum on Microbial Threats, it is that we cannot afford to be com- placent anymore. What are emerging infections? I always like informally to define emerging infections as those that would knock a really important story off the front page of the newspaper, whether the runaway bride or the Texas polygamy case, at least for a day or two. However, I do have a more formal definition: those infections that are rapidly increasing in incidence or geographic range. In some cases, these are novel, previously unrecognized diseases. But, as I am going to show you, many of them are not The Andromeda Strain. They do not come from space. Actually, in many cases, they have already existed in nature. Very often, anthropogenic causes—often as unintended consequences of things we do—are important in the emergence of these infections. There are many examples. You can pick your favorite: Ebola in 1976; han- tavirus pulmonary syndrome, which I will discuss briefly in a moment; Nipah, which Peter Daszak addressed at the workshop (and his group has done some excellent work on this); SARS; and, of course, influenza, which still continues to surprise us. You could think of the many events shown in Figure 5-2 as “a thousand points of light” (or at least those of you who are old enough to remember the first President Bush). But these are really a lot of little fires all over the world, most of which we did not spot in time before they became big brush fires or even wild- fires. That includes many examples, such as West Nile virus entering the United States in 1999, the enteropathogenic Escherichia coli (made famous by the “Jack in the Box” case2), and a number of others, including SARS, of course. I have divided the process of disease emergence into two steps, for analysis: (1) what I call introduction, where these “Andromeda-like” infections are coming from; and (2) establishment and dissemination, which (fortunately for us) is much harder for most of these agents to achieve. The basic lesson there is that many may be called, but few are chosen. In this two-step process, as you all know, the opportunities are increasing thanks to ecological changes and globalization, which gives the microbes great opportunities to travel along with us, and to travel very quickly. Even medical technologies have played an inadvertent role in helping to disseminate emerging infections. I will spend most of my time talking about what seems to be the most myste- rious step—and I hope we can demystify it a bit here—and that is the introduction of a “new” infection. What we now know is that many of these infections, exotic as they may seem, are often zoonotic. Some of them do not do very much, and 2 In 1993, four children died and hundreds became ill after eating undercooked hamburger pat- ties contaminated by E. coli bacteria at Jack in the Box restaurants (see http://www.about-ecoli. com/ecoli_outbreaks/view/jack-in-the-box-e-coli-outbreak).

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FIGURE 5-2 Global examples of emerging and reemerging infectious diseases, some of which are discussed in the main text. Red represents Figure 5-2 COLOR.eps newly emerging diseases; blue, reemerging or resurging diseases; black, a “deliberately emerging” disease. bitmap image SOURCE: Reprinted from Morens et al. (2004) with permission from Macmillan Publishers Ltd. Copyright 2004.  landscape

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00 MICROBIAL EVOLUTION AND CO-ADAPTATION may cause no infection at all; while others may cause a truly dramatic infection, like Ebola. So that zoonotic pool, if I may use that term, is not fully chlorinated, and it is a rich source of potential emerging pathogens. There is so much biodiversity out there, including a tremendous biodiversity of microbes. Some of that biodi- versity—we do not know how much, even now—is still untapped. Changes in the environment may increase the frequency of contact with a natural host carrying an infection, and therefore increase our chances of encoun- tering microorganisms previously unknown to humans. Of course, the role of food animals, as well as wildlife (one of the subjects of Peter Daszak’s contribu- tion to this volume), has come very much to fore in recent years. There are a number of examples associated with activities like agriculture, food-handling practices, and, for the vector biologists, of course, changes in water ecosystems. Table 5-1 lists just some of these cases. The basic point is that there are a number of ecological changes, many of them anthropogenic, which provide new opportunities for pathogens to emerge and gain access to human populations. Think of these as a sort of microbial explorers, discovering new niches—us—and exploring new territory. It is important not to overlook the very important role of evolution as well. One role is obviously what evolution has already been doing for a long time, lead- ing to the biodiversity of pathogens that we see existing in nature. It is remark- able, when you think about how great that biodiversity is. We don’t even know how many viruses human beings are subject to, even how many inhabit us at this very moment. But when I think about just the herpesviruses, which are pretty well studied, that number could be very large indeed. There are eight known human herpesviruses, and at least six of them—you might argue, even seven of them, except for Human herpesvirus 8, the one that causes Kaposi’s sarcoma—are ubiq- TABLE 5-1 New Opportunities for Pathogens: Ecological Changes Agriculture Hantaan, Argentine hemorrhagic fever, Nipah, West Nile (Israel), possibly pandemic influenza Food-handling practices SARS, H5N1 influenza, HIV?, enteropathogenic E. coli Dams, changes in water ecosystems Rift Valley fever, other vectorborne diseases, Schistosomiasis Deforestation, reforestation Kyasanur Forest, Lyme disease Climate changes Hantavirus pulmonary syndrome (HPS), vectorborne diseases

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0 INFECTIOUS DISEASE EMERGENCE uitous in the human population. They can be found all over the world. Several of them are present at very high prevalence in the human population. That just gives you an idea of some of that great biodiversity. As it happens, these herpesviruses are all specialized for humans. There are, of course, herpes- viruses of other species. So a lot of coevolution between host and pathogen goes on as well. Of course, there is adaptation to new hosts and environments through natu- ral selection. We see this with influenza most notably, but with many other examples—the coronaviruses, like SARS—as well. Of course, antimicrobial resis- tance has been mentioned so many times. If anyone needs to be convinced about the role of evolution in the world, I think this is a pretty good demonstration—one of the rare examples in which you can do in vitro exactly the same thing as what happens in the real world, just on a different scale. There are many case studies. I’ll briefly discuss a few, just to illustrate some key points. Hantavirus pulmonary syndrome was ironically one of the first things to happen suddenly in the United States after the original Institute of Medicine Emerging Infections report came out in October 1992. Hantavirus pulmonary syndrome suddenly appeared in the southwestern United States in the following spring and summer. My friend Richard Preston wrote a book called The Hot Zone. He has a very philosophical chapter at the end where he talks about the “revenge of the rainfor- est.” I think it is a good thought, in that we should be kinder to our environment, for many good reasons. The rainforests are great sources of biodiversity and, to a great extent, that biodiversity was largely unexplored. But an emerging infection can occur anywhere. Even the southwestern United States, which looks so dry, arid, and inhospitable to life, has its share, different from the rainforest, but just as significant. Jim Hughes, who is a Forum member and was the director of the National Center for Infectious Diseases (NCID) at the Centers for Disease Control and Prevention (CDC) at the time of the outbreak, knows this story firsthand. Start- ing in the late spring and then going through the summer of 1993, people started appearing at emergency departments and clinics with respiratory distress. Many of them were hospitalized. I believe the case fatality rate at that time was about 60 percent, even with treatment. It is a little lower now, but it is still hovering near 40 to 50 percent. The health departments did the usual investigations: There is a pocket of plague in that area, so the local health departments tested for that. Another possi- bility could be influenza out of season. These, and other likely possibilities, were ruled out. The state health departments then called in CDC, which did a number of tests and identified, perhaps surprisingly, a hantavirus as the most likely cul- prit. This was tested both by serology and, later, shedding of virus was tested by polymerase chain reaction (PCR). Of course, when you think of hantavirus, you

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0 MICROBIAL EVOLUTION AND CO-ADAPTATION usually think of rodents, with a few minor exceptions. So a number of rodent species trapped near patients’ homes were tested. The most frequent rodent was apparently also the most frequently infected: Peromyscus maniculatus, the deer mouse. This is a very successful and prolific rodent that is essentially the major wild rodent in this entire area. Ruth Berkelman likes to refer to this as your typi- cal hardworking single mom, as shown in the illustration (Figure 5-3). Of course, once a test was developed and people started looking for the virus, they were able to find it in a great number of other places, including serum and tissue samples that had been saved earlier because the etiology was unknown, but FIGURE 5-3 A deer mouse (Peromyscus maniculatus), natural host for the Sin Nombre (hantavirus pulmonary syndrome) Figure 5-3.eps virus, with her young. SOURCE: Image courtesy of Bet Zimmerman, www.sialis.org. bitmap image

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0 INFECTIOUS DISEASE EMERGENCE FIGURE 5-4 Hantaviruses of the Americas. Viruses associated with human disease are Figure 5-4 COLOR.eps shown in bold. bitmap image SOURCE: Adapted from Peters (1998) with permission from ASM Press and Jim Mills. inverted colors odd—cases of acute respiratory distress. There were even some cases outside the geographic range of Peromyscus maniculatus, which turned out to be hantaviruses that were natural infections of other rodent species. This point is illustrated in Figure 5-4 (I thank C. J. Peters, then at CDC, for the illustration). Before 1993, the United States had one known hantavirus, not associated with human disease (Prospect Hill virus) and another hantavirus of rats, Seoul virus, and related variants that could be found in port cities; neither was associated with serious acute disease in the United States. After 1993, we had to add another: the virus that causes hantavirus pulmonary syndrome. Then, when people started looking for hantaviruses, there was no shortage of previously unrecognized cases. In Figure 5-4, the virus names in bold have been associated with human disease, while many others have not. So throughout North and South America, suddenly there was a whole rash of hantaviruses that nobody knew existed.

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 Figure 5-21 COLOR.eps FIGURE 5-21 Global richness map of the geographic origins of EID events from 1940 to 2004. The map is derived for EID events caused by all pathogen types. Circles represent one degree grid cells, and the area of the circle is proportional to the number of events in the cell. bitmap image SOURCE: Jones et al. (2008). landscape

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 INFECTIOUS DISEASE EMERGENCE the greatest numbers of EID events. We corrected for that by geographically plotting the coordinates of every author—about 17,000 of them—of every paper published in the Journal of Infectious Diseases (JID) for the last 20 years, and used this information in our analyses. We were able to use this database to address some key questions in emerg- ing disease biology. First, whether EIDs are really on the rise (Jones et al., 2008). Decade by decade, from the 1940s to the 1990s, the number of EID events has increased significantly, even after accounting for the increasing num- bers of scientists over this period. This has another implication: It is reasonable to expect that this trend will continue in the future. We also found that a major- ity of EID events were associated with drug-resistant microbes. Second, we were able to examine whether zoonoses such a HIV/AIDS, which are the most high-profile EIDs, are truly the most significant threat. We found that zoonoses emerging from wildlife (i.e., HIV, SARS, Ebola and Nipah viruses) are indeed significantly rising over time and during the 1990s, represented the dominant type of emerging disease. Testing Hypotheses We used our database approach to examine two simple questions: (1) Is dis- ease emergence an “anthropogenic” process (i.e., are human changes to demog- raphy, the environment, and other factors the key drivers of EIDs)? (2) Can we obtain a more accurate map of the emerging disease “hotspots”—the regions most likely to cause the next new emerging disease? To test these theories, we first found a way around the dilemma of not know- ing where the diversity of pathogens resides by assuming that each mammalian species harbors a similar number of host-specific pathogens. If this is true, then the global distribution of wildlife diversity approximates the potential zoonotic pathogen diversity. In our analysis, we used a global dataset on mammalian host richness. We then used a simple multiple logistic regression to assess the correlation between the risk of an EID historically and some key factors thought respon- sible for disease emergence, correcting for reporter bias with the dataset on JID authors. We addressed the first hypothesis by testing global human population density against EID risk and showed that this is a significant predictor of risk for each group of pathogen. This specifically shows that the risk of a disease emerg- ing (not spreading) is dependent on human population density (i.e., those regions with dense human populations and presumably lots of human-driven changes are most likely to lead to a new EID). By plotting out our risk measures globally, we were able to produce the first ever global distribution maps of emerging disease risk, corrected for reporter bias, and based on correlated trends in EIDs. These predictive maps of EID “hotspots” show different global distribution patterns when we sorted EID events

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 MICROBIAL EVOLUTION AND CO-ADAPTATION according to their origins (e.g., zoonotic diseases from wildlife; vector-borne pathogens; drug-resistant pathogens; Jones et al., 2008). For EIDs of wildlife origin (the high-profile zoonoses), these hotspots are primarily tropical areas where wildlife diversity is highest, and particularly where human density is also high, as occurs in southern Brazil, northern India and Bangladesh, and Southeast Asia (Figure 5-22). However, Europe and the United States also have significant potential for zoonotic disease emergence, due to continued, high-level environ- mental changes. However, perhaps one of the key findings of our analysis is that if we plot out the geographic distribution of all 17,000 JID authors, we find that the global effort for infectious disease research has largely focused on regions from where the next EID is least likely to emerge. Indeed, few EID hotspots—located pri- marily in developing countries—are under thorough surveillance for infectious pathogens (Jones et al., 2008). We therefore concluded that global efforts to detect emerging infections should be slightly refocused to the Tropics if we are to rapidly intervene with this process of emergence. Using Predictive Approaches: “Smart Surveillance” Can we use this hotspot approach to increase our capacity for preventing the next EID? If we return to Nipah virus, we see that this emerging pathogen fits into the high-profile group of zoonoses that are lethal to humans and have emerged from wildlife in tropical regions. During the last decade, antibodies to this patho- gen have been reported in bats across Southeast Asia, South Asia, Madagascar, China, and even continental Africa. But this knowledge has been gleaned through different groups working independently and often serendipitously. There has been no focused, global surveillance for viruses related to NiV in bats. If we examine the wildlife zoonotic disease hotspot map (Figure 5-22) in one of the highest risk regions, Bangladesh, the human population has been subject to a series of repeated outbreaks of NiV with higher case-fatality rates than in Malaysia (average around 70 percent), evidence of foodborne infection, and evidence of up to five chains of human-to-human transmission. Bangladesh has the densest population of any country on Earth that is not an urban city-state: 2,595 people per square mile, as compared with a global average of 128 persons per square mile (the United States has 80 people per square mile; http://www. worldatlas.com, 2006). The country also has surprisingly high wildlife diversity, given its population. Thus, it appears that in Bangladesh, Nipah virus is closer to stage three, or pandemic emergence. This raises important questions: Why were there no programs to identify NiV in Bangladesh once the virus was discovered in Malaysia? What other regions globally might harbor spillover of NiV or related viruses? What other zoonotic pathogens might be lurking in the South Asia hot- spot within bats or other wildlife hosts? I propose that a more efficient strategy to address future emerging diseases

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FIGURE 5-22 Global distribution of the relative risk of an EID event. Maps are derived for EID events caused by (a) zoonotic pathogens Figure 5-22 COLOR.eps from wildlife; (b) zoonotic pathogens from nonwildlife; (c) drug-resistant pathogens; and (d) vector-borne pathogens. Green corresponds to bitmap image lower values; red to higher values. landscape SOURCE: Jones et al. (2008). 

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 MICROBIAL EVOLUTION AND CO-ADAPTATION is to combine rigorous analyses of the fine-scale ecological and demographic changes within hotspot regions (the risk factors) with state-of-the-art molecular approaches to viral discovery. This will give us a more accurate predictive model for future disease emergence, and better definition of the size and diversity of the zoonotic pool. Techniques such as pyrosequencing and mass tag polymerase chain reaction (PCR) will rapidly decrease the expense and logistical challenges involved in identifying new viral groups, and if applied to key groups of wildlife species (those most often responsible for disease emergence in the past) within hotspot regions, will provide the most cost-effective way to proactively address the EID challenge. This model for virus-hunting in the future is, of course, still somewhat crude. It is impossible, for example, to determine the future ability of a novel virus to jump hosts successfully to humans, and its likely pathogenicity. However, by focusing first on viral groups known to be pathogenic, and by target- ing viral discovery within these clades, significant progress can be made toward dealing with the EID threat. Acknowledgments The work described in this chapter was carried out by a large number of collaborators, including members of the Henipavirus Ecology Research Group (HERG),14 especially Jon Epstein (Consortium for Conservation Medicine) and Juliet Pulliam (Fogarty International Center). The work on West Nile virus and avian influenza was led by A. Marm Kilpatrick (Consortium for Conservation Medicine, University of California Santa Cruz) and the hotspots analyses were conducted in collaboration with Kate Jones (Institute of Zoology) and Marc A. Levy (Center for International Earth Science Information Network, Columbia). This work was supported in part by a National Institutes of Health/National Science Foundation “Ecology of Infectious Diseases” award from the John E. Fogarty International Center R01-TW00824, by core funding to the Consortium for Conservation Medicine from the V. Kann Rasmussen Foundation and is published in collaboration with the Australian Biosecurity Cooperative Research Center for Emerging Infectious Diseases (AB-CRC). REFERENCES Overview References 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. 14 See http://www.henipavirus.org.

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