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140 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS

found that climate influences plague dynamics through the rodent-host and flea-vector relationship. Simulating backwards, Kausrud et al. (2008) successfully predicted human plague patterns in Kazakhstan from 1904 to 1950. Using tree-ring data extending back in time to 1000 A.D., this model allows us to compare model predictions with historical plague epidemiology. Analysis suggests an eco-epidemiological basis for considering the Black Death epidemic as having originated in central Asia during climatically favorable conditions (for the plague system). The same model, used for prediction forward, suggests that expected climate change will sustain and possibly increase plague activity in central Asia.

Effect of Climate on Plague Dynamics in Other Regions of the World

Based upon our work on the Kazakh data, we are now extending our interest to other parts of the world. Together with Zhang et al. (2007), I have been involved in some preliminary analysis of data on human plague cases from China. These show a clear effect of large-scale climate influence. Unpublished work that I have done in cooperation with a student of mine (Ben Ari et al., 2008) similarly shows that the number of human plague cases in the western United States is strongly influenced by the Pacific Decadal Oscillation (PDO) and the number of days with above-normal temperatures. In short, a warmer and wetter climate is associated with increased prevalence level of the plague bacterium in the rodent reservoir, which subsequently might lead to an increased number of human cases. These results match up nicely with the previously published cascade model by Parmenter et al. (1999) emphasizing that the climate connection works partly through the rodent-host dynamics and the flea-vector dynamics (see Figure 2-17) in the same region.

Additional Reasons for Being Concerned: Bioterror

As indicated in the introduction, we should not overlook the fact that plague has been weaponized throughout history—from catapulting diseased corpses over city walls, to dropping infected fleas from airplanes, to refined modern aerosol formulations (Inglesby et al., 2000; Koirala, 2006). The weaponization research carried out on plague from the 1930s through the 1990s fueled biological warfare fears that may actually have stimulated research on infectious disease surveillance and response strategies. More recently, however, the fears of small-scale bioter-rorism and a desire by government authorities to more fully control all access to plague materials increase the danger of stifling basic research on plague ecology, epidemiology, and pathophysiology that is required to improve its clinical management in endemic areas. Terrorist use of an aerosol released in a confined space could result in significant mortality and widespread panic (Inglesby et al., 2000; Koirala, 2006), and no one would want the knowledge and materials for weaponizing plague to fall into the hands of non-state actors. However, the

Increased rodent food sources

Increased rodent food sources

Effects of Increased Precipitation

February - March (Major effect) t

July - August

February - March

(Minor effect)

Effects of Increased Precipitation

February - March (Major effect) t

July - August

February - March

(Minor effect)

Increased soil moisture and available hosts

Cool summer (15-18 months after first wet winter) (Major effect)

High rodent densities favor epizootic spread

Cool summer (15-18 months after first wet winter) (Major effect)

Cool temperatures favor survival of infected fleas

Increased human plague risks

FIGURE 2-17 The modified trophic cascade model of Parmenter et al. (1999).

SOURCE: Adapted from Parmenter et al. (1999) with permission from the American Journal of Tropical Medicine and Hygiene.

142 GLOBAL CLIMATE CHANGE AND EXTREME WEATHER EVENTS

need for scientifically sound studies of the dynamics of infection, transmission, outbreak management, and improved surveillance and monitoring systems has never been greater.

Conclusion: It Is Unwise to Neglect Plague

In conclusion, it should be noted that although plague may not match the so-called big three diseases (malaria, HIV/AIDS, and tuberculosis; see Hotez et al., 2006) in numbers of human cases, it by far exceeds these diseases in pathogenicity and rapid spread under the right environmental conditions. Plague should be seen not only as a historical curiosity but as a reemerging disease of the twenty-first century. Plague should not continue to be neglected and relegated to the sidelines; it is a disease which should concern us today.

Plague remains a fairly poorly understood threat that we cannot afford to ignore. Nevertheless, much progress has recently been made toward understanding the dynamics of the full plague eco-epidemiological system, and not the least how it responds to climate variation and change. We know that climate does affect the dynamics (and indeed the level) of plague. However, it is difficult at present to say what that effect will be. For example, in central Asia there might be higher levels of plague in the rodent reservoir populations, if current climate prognoses for the region materialize. Also, higher levels in the wildlife reservoir will automatically lead to a greater chance of people being infected by the plague bacillus. In other places of the world there might be lower plague levels in the reservoirs—we simply do not know, but we ought to know if we are to be maximally prepared for what happens should climate change. It is certain, though, that the picture regarding plague might be much more serious than conveyed by Anyamba et al. (2006). Only by knowing more about how the eco-epidemiological plague systems in different parts of the world will respond to given climate scenarios can we take the necessary precautionary measures to reduce the risks associated with human infections. Indeed, knowing how climate is affecting the components of the eco-epidemiological system depicted in Figure 2-13, and subsequently how these climate drivers might change the dynamics of the system, will put us in a greatly improved position for predicting where and under what environmental conditions the risk of human plague infections might increase and where and under what conditions it might decrease (or remain unchanged). Much of the insight derived from studying particular plague systems will be general and applicable to other plague systems—and indeed to other vector-borne infectious disease systems. However, since the involved host and vector species are different from one part of the world to another (indeed, the plague eco-epidemiological system is characterized by a whole suite of rodent host species and their associated fleas, differing from one place to another), studies similar to those that I have summarized for central Asia are greatly needed. Such additional studies may help us to understand which insights derived from the central-Asian studies may or may not be generalized to other places where

CLIMATE, ECOLOGY, AND INFECTIOUS DISEASE 143

plague occurs. Such additional studies will further help us develop more region-specific prediction regarding what might happen should climate change in some specific way.

Acknowledgments

I thank Tamara Ben Ari for having read and commented on an earlier version of this paper; furthermore, I thank her and Kyrre Linné Kausrud for allowing me to summarize yet unpublished work. Over the years working on plague dynamics, I have benefited enormously from collaboration with several colleagues, most importantly Herwig Leirs, Hildegunn Viljugrein, Mike Begon, Kung-Sik Chan, Noelle I. Samia, Stephen Davis, Kyrre Linné Kausrud, Tamara Ben Ari, Lise Heier, Elisabeth Carniel, Mark Achtman, Kenneth L. Gage, Vladimir S. Ageyev, Nikolay L. Klassovskiy, and Sergey B. Pole. I have learned a lot from them—any misunderstandings of what they have tried to teach me is due solely to my own shortcomings. On a more administrative side, I would like to thank Dr. M. Pletschette for his stimulating encouragement, which made me start working on plague in the first case. My work on plague has been generously funded over the years through the European Union Projects (ISTC K-159, STEPICA [INCO-COPERNICUS, ICA 2-CT2000-10046], as well as Marie Curie Early Stage Training grant to CEES), the Norwegian Research Council, and my own university and center. Last, but not least, I extend my thanks to the many hundreds of Kazakh plague zoologists who collected so many data over all these years.

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