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Microbes and Human-Caused Environmental Change BIOL/ENVS 313, Spring 2015, Wednesdays 1:10-4:00 Readings Jan. 28 1a. The Anthropocene , as seen by pathogens 1b. Human ecology and the origin of infectious disease in our history. 1a. Cohan Ch. 1. (Lewis and Maslin, 2015)† Lewis and Maslin try to define the beginning point of the Anthropocene in terms that all the other geological epochs have been defined—in terms of noticeable changes in rocks and so on. They claim that 1610 and 1964 fit these criteria. However, I argue that their criteria might be too stringent. Are biologists constrained to demarcate today’s species only in terms that a paleontologist would recognize? When we have more information, why not use it? 1b. Cohan Ch. 2. Hunting and disease (Wolfe, 2011), Ch. 2 Wolfe’s Chapter 2 presents the fateful evolutionary transition in the chimp-human lineage (after it separated from the lines leading to gorillas and other great apes, but before humans and chimps diverged as separate lineages) toward hunting. His emphasis, of course, is on how hunting yields a superhighway of infection opportunities. What is really interesting about this chapter is that the entire story of hunting and disease transmission is couched in the context of the history of HIV, first in monkeys, then in their predators (chimps), and then in the chimps’ predators (humans).

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Microbes and Human-Caused Environmental ChangeBIOL/ENVS 313, Spring 2015, Wednesdays 1:10-4:00

Readings

Jan. 28 1a. The Anthropocene, as seen by pathogens

1b. Human ecology and the origin of infectious disease in our history.

1a. Cohan Ch. 1.(Lewis and Maslin, 2015)†Lewis and Maslin try to define the beginning point of the Anthropocene in terms that all the other geological epochs have been defined—in terms of noticeable changes in rocks and so on. They claim that 1610 and 1964 fit these criteria. However, I argue that their criteria might be too stringent. Are biologists constrained to demarcate today’s species only in terms that a paleontologist would recognize? When we have more information, why not use it?

1b. Cohan Ch. 2.

Hunting and disease(Wolfe, 2011), Ch. 2Wolfe’s Chapter 2 presents the fateful evolutionary transition in the chimp-human lineage (after it separated from the lines leading to gorillas and other great apes, but before humans and chimps diverged as separate lineages) toward hunting. His emphasis, of course, is on how hunting yields a superhighway of infection opportunities. What is really interesting about this chapter is that the entire story of hunting and disease transmission is couched in the context of the history of HIV, first in monkeys, then in their predators (chimps), and then in the chimps’ predators (humans).

Hunting and HIV(Gao et al., 1999); (Hahn et al., 2000); (Bailes et al., 2003); (Keele et al., 2009); (Worobey et al., 2008); (Quammen, 2012), Section VIIIGao et al. give the phylogenetic evidence for the origins of HIV in humans from multiple infections from chimpanzees; more recent and extensive data are given by Hahn et al. Bailes et al. demonstrate that the SIV of chimpanzees originated as a hybrid between the SIV’s of two monkey species that are common prey of chimpanzees. Note that SIV is not ancient in chimpanzees. Very recent data by Keele et al. shows that SIV produces AIDS in chimps. Worobey discusses phylogenetic evidence that the modern plague of HIV began through infection from

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chimpanzees around 1900, with rapid spread within humans from Kinshasa around 1960. Section VIII of Quammen’s Spillover (“The Chimp and the River”) gives a gripping reenactment of the origins and early spread of HIV, along with the scientific underpinning.

Agriculture and acute diseases(Diamond, 1997), Chapter 11; (Moodley et al., 2009); (Mindell, 2006), Ch. 3; (Pearce-Duvet, 2006)Diamond’s Ch. 11 explains why hunter-gatherers have only diseases that are chronic or intermittent and why the acute diseases are diseases of crowds; thus, their maintenance in humanity required the invention of agriculture (with higher population densities). Moodley gives an example of a chronic disease pathogen that is so anciently established in humans that its phylogeny mirrors that of the human hosts. The chapter also describes the kinds of diseases that can be maintained in small populations (chronic and zoonotic diseases). Diamond presents the reasons why early farmers (and worse, city dwellers) were so prone to diseases: their filthy lifestyle (and not leaving camp frequently as do nomads) and the diseases they acquired from their domestic animals. Mindell’s chapter discusses the importance of phylogenetic thinking in public health (identifying unknown disease organisms and finding their closest relatives) and in unraveling the history of our diseases.

The SIR model of acute diseasesWikipedia on Epidemic Modeling (http://en.wikipedia.org/wiki/Epidemic_model)The Wikipedia reference gives an introduction to the SIR model of acute diseases (susceptible, infected, recovered).

Geographic origins of diseases(Wolfe et al., 2007); (Diamond, 2002)Wolfe et al. show that the temperate-origin diseases tend to be the crowd epidemic diseases, while none of the tropical-origin diseases are in this category. Wolfe et al. chart the origins of our epidemic pathogens, finding the most coming from domestic animals, then some from apes and rodents, and some origins yet to be identified. Diamond’s 2002 paper is a wide-ranging short review of why agriculture developed in certain localities and why agriculture led to the acquisition of new acute-disease pathogens.

Feb. 4 2a. The ecology of 2a.

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spillovers—how humans become exposed to novel diseases. 2b. The evolution of spillovers—how a wild-animal pathogen becomes humanized

What is it with bats?(Quammen, 2012), Ch. VII, “Celestial Hosts”; (Plowright et al., 2011); (McNeil, 2013); (Olival et al., 2013); (Zhang et al., 2013)Bats are the reservoirs for Hendra, SARS, and Nipah, and it turns out that it just gets worse. David Quammen’s book Spillover has a wonderful chapter on the role of bats in emerging viruses of humans. First, we see that added to the list of chiropteranoses (my invention for a bat zoonosis; you heard it here first) is Marburg for sure, and likely its close relative Ebola. Next, we see some extremely intriguing theory for why bats are responsible for so many human diseases and why only now. One aspect of this is the huge size of many bat populations, and their extremely high densities. This means that SIR diseases can do just fine within bat species. Then the chapter gets into the question of why now there have been so many diseases emerging into humans from bats. An interesting hypothesis is being developed and tested by Raina Plowright. The idea is that in previous times bats lived in contiguous forest, with much dispersal of bats across a huge set of highly connected populations. This would have led to a low level of endemic disease everywhere. Then as forests became fragmented, and human habitations and farms offered a great source of food, bat populations became highly fragmented as well, and habituated to living in high densities around humans, with little migration between bat populations associated with different cities. In this model, a large number of susceptible bats would accumulate in any given locality until a migrating infected bat re-ignites the infection. Then there would be a huge number of bats at one time that could potentially infect humans. Making the situation worse is that the bats are largely living in close proximity to humans. The McNeil Times article and the Olival article present data that the Ebola Virus is in bats in Bangladesh. This indicates what has been suspected, that bats can transport a virus for which they are a reservoir immense distances. Zhang et al. present genomic data that may explain bats’ propensity to harbor some nasty viruses: they are missing some immunity genes, while other immunity genes have been under strong positive selection.

Other recent diseases from bats and camels(Azhar et al., 2014); (Kupferschmidt, 2015)†; (Zaki et al., 2012); (Hazelton et al., 2013); (Quammen, 2012), Ch. 4Azhar et al. provide evidence that the recent MERS epidemic spread into humans from camels. (They gave us smallpox; what is it with camels?)

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Here is an ethics issue for you (from Kupferschmidt). It seems that the most effective way to limit MERS spillovers would be to vaccinate camels, and a promising vaccine is on the way. However, MERS does little or no harm to camels, and so camel owners say they’re not interested in having their camels vaccinated.Zaki et al. present yet another case of a novel infectious disease brought to humans (most likely) through bats. Also, Hazelton et al. discuss another pathogen reaching humans from bats, Hendra virus. Quammen’s Ch. 4 discusses SARS virus.

Bushmeat(Wolfe, 2011), Ch. 8; (LeBreton et al., 2007); (Peeters et al., 2002); (Wolfe et al., 2005)†Wolfe discusses several changes in agricultural industry that increase the likelihood of a dangerous new pandemic sweeping through humanity: bushmeat hunting in areas never before accessed by human hunters; immunosuppression of many who handle bushmeat; the huge densities of agricultural animals and their access to pathogens from outside the stockyards; feeding diseased animals to other animals; and the exotic pet industry. LeBreton et al. present data on how frequently immunosuppressed people are potentially exposed to viruses through bushmeat butchering. Peeters et al. demonstrate the dangers of future human infections from SIV’s from the bushmeat markets of Cameroon. Wolfe et al. provide evidence of infection of bushmeat hunters by simian T-lymphotropic viruses, and they argue that infectious by new zoonotic diseases is an ongoing process for bushmeat hunters.

Hanta viruses(Dearing and Dizney, 2010)Dearing and Dizney discuss the effects of increasing El Niño events (predicted with global climate change) on Hanta virus outbreaks, such as seen with the emergence of the Sin Nombre virus in the Four Corners region of the US. (We’ll discuss this next week.)

2b.Evolution and ecology of host jumps(Wolfe et al., 2007); (Woolhouse and Gaunt, 2007); (Woolhouse et al., 2005); (Veyrier et al., 2009); (Allison et al., 2012); (Wolfe, 2011), Ch. 5; (Anonymous, 2009), URL: http://www.who.int/mediacentre/factsheets/fs262/en/ ;

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(Jackson and Charleston, 2004); (Streicker, 2013); (Streicker et al., 2010); (Streicker et al., 2012)Wolfe et al. (2007) has a section on the stages from being an occasional zoonosis to being a fully human pathogen—Figure 1 is widely cited. Woolhouse and Gaunt provide a somewhat simpler version of the steps toward becoming a human pathogen, and they discuss sources of new human viruses. Woolhouse et al. discuss some interesting examples of host jumps. (We don’t need to focus on their modeling.) Veyrier et al. use a genomic analysis to show the role of horizontal genetic transfer in providing new proteins for infecting new host species. Allison et al. show the potential importance of “bridge hosts,” which can facilitate adaptation from one host to another; in this case, the bridge host was raccoons, on the way from cats to dogs for canine parvovirus. This also illustrates the importance of changes in existing genes in yielding adaptation to a new host (in contrast to acquisition of new genes). Jackson and Charleston use a phylogenetic approach to show how we can identify viruses that easily jump hosts versus those that don’t. The WHO fact sheet details transmission of Nipah virus, which apparently was able to sustain itself within humans for some time before the R0 became too low. Streicker explains his phylogenetic analyses of repeated cross-species jumps of rabies across bat species, and found that phylogenetic similarity is a better predictor of ease of jump than ecological overlap.

Evolution of Plague(Sun et al., 2014)Sun et al. present how Yersinia pestis, transmitted by fleas, evolved recently from an ancestor that was transmitted by the fecal-oral route.

Feb. 11

3a. Evolutionary fine-tuning of a pathogen’s virulence.

3b. Global warming and infectious disease

3a. Evolutionary fine-tuning of a pathogen’s virulence(Ewald, 1993)*; (Walther and Ewald, 2004); (Ariën et al., 2007)*; (Ariën et al., 2005)*; (Kouri et al., 2015)†; (Pantazis et al., 2014)†; (Payne et al., 2014)†; (Cairns, 2014)†; (Knell, 2004)*; (Pepperell et al., 2013).The Ewald paper is a very brief synopsis of Ewald’s 1994 blockbuster book Evolution of Infectious Disease. The Scientific American article explains Ewald’s hypotheses about how the mode of transmission of a pathogen, as well as the pathogen’s survival in the environment (outside of hosts), should be expected to determine the level of virulence. The more recent Walther and Ewald paper gives some data supporting the Ewald hypotheses regarding the effect of persistence in the

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environment on virulence evolution. The Ariën 2007 paper explains two ways that natural selection may have favored lower virulence in HIV-1: that lower rates of opportunity for sexual transmission may select for less virulent viruses (the Ewald hypothesis) and that higher levels of immune diversity in a human population may result in lower virulence. Ariën in 2005 gives evidence that historical HIV viruses were less virulent than more recent ones, in head-to-head competition experiments. On the other hand, Pantazis et al. find evidence for a higher virulence in Europe. Kouri et al. offer evidence for an extremely virulent new form of HIV that yields full AIDS within three years; they found it to be a recombinant between subgroups A, D, and It was first found in Cuba. G. Payne et al. argue that lowered virulence in South Africa is largely due to antiretroviral therapy. In a news piece, Cairns tries to reconcile the new reports on HIV virulence evolution. Knell offers evidence that there was an extremely rapid evolution of lower virulence in syphilis shortly after it was introduced to Europe in the 16th century. Pepperell et al. discuss natural selection in the human tuberculosis pathogen.

3b. Global warming and infectious disease(Weiman, 2015)†; (Patz et al., 2014); (Parmesan and Yohe, 2003); (Lindgren et al., 2012); (Gould and Higgs, 2009)*; (Hopp and Foley, 2001); (Hales et al., 2002); (Peterson et al., 2005)*; (Peterson, 2009); (Levine et al., 2004); (Tanser et al., 2003); (Danielova´ et al., 2008); (Lindgren and Gustafson, 2001); (Kovats et al., 2004)*; (Baker-Austin et al., 2010)†; (Vezzulli et al., 2013)†; (Lowen et al., 2007)*; (Siraj et al., 2014); (Zhou et al., 2008); (Ackerman, 2015)†.Weiman gives an overview of the effects of climate change on infectious diseases that affect plant pathogens of our crops, pathogens of marine animals that affect the seafood industry, marine Vibrio species that threaten human health, and on marine pathogens that threaten entire ecosystems†. (This just came out last week in Microbe magazine, and was not available for our discussion.) Patz et al. present an overview of the effects of climate change, including temperatures and precipitation patters on human health, including infectious disease consequences and beyond. Parmesan and Yohe provide a meta-analysis of changes in phenology and in geographic distribution of many species previously studied. The most important part of the paper, for our purposes, is Table 1 on changes in phenology and geographic distribution. Lindgren et al. discuss the emergence of various tropical diseases in Europe, as a result of

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both climate change and increased rates of transfer of diseases across continents. Gould and Higgs attribute many unexpected range expansions of tropical diseases into Europe to global warming and precipitate change. Hopp and Foley present a map of geographic distributions showing the huge geographic extent over which the dengue mosquito lives but where dengue is not yet present (including the Deep South of the US). They make a case that absolute humidity predicts the distribution of Aedes aegypti mosquitoes, and provide experimental evidence for increased survival of the mosquitoes at higher humidities. Hales et al. predict the future geographic distribution of Aedes aegypti assuming absolute humidity as the major determinant. Peterson et al. provide a more inclusive (i.e., more parameters included) model of dengue distribution in Mexico. In another paper, Peterson et al. predict the future geographical distribution of malaria in Africa. Levine et al. determine the physical parameters that most clearly predict the distribution of the predominant malaria vector. Danielova et al. present evidence for the appearance of TBEV at elevations above 1000 meters for the first time in the Czech Republic, and argue that this is due to global warming. Lindgren and Gustafson discuss the weather determinants for high incidence of TBEV in Sweden, and argue that global warming will increase the incidence of TBEV. Kovats et al. show how Salmonella-based food poisoning increases with temperature, and how the functional response of food poisoning rates to temperature varies across countries. Baker-Austin et al. and Vezzulli et al. present evidence that warming of the ocean is causing increased incidence of human Vibrio diseases. Lowen et al. provide a compelling argument for why influenza is transmitted at higher rates in cooler seasons, and gives us reason to cheer for one health-benefiting effect of global warming. Siraj et al. show that in the highlands of Ethiopia and Colombia, the distribution of malaria extends to higher altitudes in warmer years, and they predict that the altitudinal distribution of malaria will move upward with global warming. Zhou et al. predict movement northward in China of the tropical parasite causing schistosomiasis. Ackerman’s news article explains the ecology of cholera and why it is expected to be more of a global problem with raising temperatures (with thanks to Andrew).

Feb. 18

4a. Extreme storms and drought and infectious disease.

4a. Extreme storms and drought and infectious disease(Xu et al., 2014); (Stenseth et al., 2006)*; (Dearing and Dizney, 2010)*; (Yohe, 2012), URL: http://www.sbs.com.au/news/article/1706329/Hurricane-Sandy-the-new-normal ; (Curriero et al., 2001); (Hunter, 2003);

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4b. Globalization—local diseases go viral, in history and today

(Peeples, 2012), URL: http://www.huffingtonpost.com/2012/10/29/hurricane-sandy-flood-rats-disease-new-york_n_2041474.html; (Himsworth et al., 2013)*; (Chase and Knight, 2003); (Brown et al., 2014)*; (Cuevas et al., 2007)Xu et al. present an analysis of the most recent Plague epidemic in China, predicting that times of high rainfall cause outbreaks of Plague. In a study of more ancient Plague, Stenseth et al. identify the weather parameter values that predict high incidence of plague in Kazakhstan; this analysis, applied to tree ring data on historical weather patterns, predicts a high incidence of plague in Kazakhstan at the time of the 14th century Black Death and the 19th century Third Pandemic. Dearing and Dizney discuss the effects of increasing El Niño events (predicted with global climate change) on Hanta virus outbreaks, such as seen with the Sin Nombre virus outbreak in the Four Corners region of the US. Gary Yohe discusses why Hurricane Sandy should be considered the harbinger of weather to come, but argues that Sandy is not the new normal; weather will actually get much worse. Curriero et al. discuss how extreme precipitation events are associated with water-borne disease outbreaks in the US. Hunter et al. discuss the effects of extreme flooding on water-borne infectious disease, and present a nice review of all the pathogens that could be affected. The news article by Peeples discusses how rats are being displaced from their underground haunts by Hurricane Sandy and are infesting homes in New York. Himsworth et al. describe the huge number of known pathogens and microbes that are closely related to known pathogens among the rodents of New York City. Chase and Knight show how climate-change-induced drought could (counter-intuitively) increase mosquito-borne infectious disease. Brown et al. translate this drought effect into consequences for particular vector-borne diseases. Cuevas et al. set up a kind of ecological niche modeling for Neisseria-caused meningitis, and find an effect of drought on infection rates; they predict higher rates of infection into the future.

4b. Globalization—local diseases go viral, in history and today(Thucydides, 1972), pp. 151-156; (Papagrigorakis et al., 2006); (Rosen, 2007), pp. 1-11, 185-223; (Wagner et al., 2014)*; (Harbeck et al., 2013)*; (Haensch et al., 2010); (Morelli et al., 2010)*; (Diamond, 1997), Chapter 11; (Corum, 2014); (Morens and Fauci, 2014); (Staples and Fischer, 2014); (Johansson et al., 2014); (Zimmer, 2011), p. 64-69; (Lanciotti et al., 1999);

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(Kilpatrick, 2011)*; (Kilpatrick et al., 2006)†; (Davis et al., 2005)†

From Biblical times until the Justinian Plague in the 6th century CE, Mediterranean civilization was bombarded by one epidemic after another, presumably due to the global spread of local diseases. Thucydides provided a contemporary account of the Plague of Athens. Papagrigorakis et al. present an analysis of fossil DNA from the mass burials of the Plague of Athens to identify the microbe responsible. Rosen explains the role of Plague in bringing the collapse of the Roman Empire in the 6th century, also why the Plague was limited to the Mediterranean region. Wagner et al. and Harbeck et al. perform a phylogenetic analysis on the Plague bacteria isolated from victims of Justinian’s Plague of the 6th century. Interestingly, there are no known descendants of these organisms, including in humans who died in the 14th century and 19th century epidemics. Haensch et al. obtained DNA from human skeletons from 14th century Black Death burials, and mapped the Plague bacteria to the phylogeny of currently existing Plague organisms, establishing a route of geographic spread. The Morelli article is a genomic analysis reconstructing the history of the Black Death of the 14th century, including the source region and transmission routes. Pay particularly close attention to Figure 2 (from which the order of geographic spread was determined) and Table 1 (which associates each step of spread with a known historical event). Diamond discusses the devastation brought about by the introduction of Old World diseases into the New World, and why the effects of disease were so asymmetrical.

Modern instances of globalization. Corum explains the factors that promote and hinder spread of Ebola, and why this last epidemic is so much more difficult to control. Morens and Fauci discuss how Chikungunya has made it to the Caribbean from Africa and is threatening the US; Staples and Fischer discuss the problem that there is no resistance to Chikungunya in the W. hemisphere. Johansson describe an effort toward “nowcasting” of predicted importation of Chikungunya to various cities and regions. The Zimmer chapter give an introduction to the spread of West Nile Virus from North Africa to a pandemic across the entire North American continent. Lanciotti et al. provide the phylogenetic evidence for the geographic source of WNV in the western hemisphere. Kilpatrick discusses the ecological and evolutionary changes that have occurred in WNV in its brief time in the New World. Kilpatrick et al. show why the robin has been

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such an efficient host of WNV. Davis et al. provide evidence for a novel WNV genotype taking over in North America.

Feb. 25

5a. Infectious diseases caused by poverty, neglect, greed, and war in modern times.

5b. Antibiotics and human health.

5a. Infectious diseases caused by poverty, neglect, greed, and war in modern times.(Farmer, 2013)*; (Firth et al., 2014)*; (Himsworth et al., 2013)*; (Harris, 2014, Bonner et al., 2007); (Bonner et al., 2007)†; (Kjetland et al., 2014); (Leaning and Guha-Sapir, 2013)*; (Gayer et al., 2007); (Cirillo, 2009)Farmer discusses the gap between what infectious diseases we can cure, and what we cannot, owing to poverty and a lack of will. Firth et al. surveyed the diversity of pathogens infecting the Norway rat population in New York City. They found a number of known pathogens, plus bacteria and viruses that are related to known pathogens but are not yet characterized. Himsworth et al. has more generally reviewed the reservoir of pathogens found in urban rodents. Bonner et al. discuss the effects of poor housing on infection from rodents of Lassa fever virus in West Africa.Harris describes how in India, where outdoor defecation is common, poor sanitation (and infectious disease) cause severe malnutrition even in well-fed children. Kjetland et al. show how women in South Africa become more susceptible to infection by HIV because of the genital schistosomiasis they pick up washing clothes in open water. Leaning and Gupa-Sapir discuss the effects of war on infectious disease. Gayer discusses the problem of war in infectious disease, including the effects of collapsed infrastructure. Note that this problem may be particularly acute if a new spillover disease emerges in a war-torn region. Cirillo discusses the effect of a 19th century war on infectious disease—that dysentery caused more US soldier deaths in the war with Mexico than gunshot.

5b. Antibiotics and human health(Levy, 1992), Chs. 1-2; (Groopman, 2012); (Sommer et al., 2009)*; (Nesme et al., 2014)*; (Nichols et al., 2010); (Ling et al., 2015)*; (Hollis and Ahmed, 2013); (Harrison et al., 2013); (White-House, 2015) https://www.whitehouse.gov/the-press-office/2015/01/27/fact-sheet-president-s-2016-budget-proposes-historic-investment-combat-a ; (Zimmer, 2011), “The enemy of my enemy”; (Synnott et al., 2009)*Levy’s chapters give an introduction to antibiotics and the promise that they once showed for solving all problems with bacterial infections. Groopman’s New Yorker article is a chilling account of what has happened to antibiotic therapy in recent

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decades, owing to bacterial evolution of antibiotic resistance. The Sommer et al. and the Nesme et al. articles are recent studies showing that antibiotic resistance genes are everywhere—in our own guts and in every environment, no matter how remote. Nichols et al. provide a novel high-throughput approach to isolating previously uncultivable bacteria, and Ling et al. use the approach for discovering antibiotics in a time after the low-hanging fruit have already been gathered—by cultivating the previously uncultivable bacteria. Hollis and Ahmed discuss strategies for preserving the efficacy of antibiotics. Yes, antibiotic resistance in human pathogens really does emerge from agricultural animals (Harrison et al.). In a press release, the White House describes President Obama’s initiative to preserve the efficacy of antibiotics. So, all this leads us to a search for alternative therapies …. Zimmer’s chapter on phage therapy is a great introduction to phage therapy to a general audience, and should prepare you for the more technical accounts that follow (in the next lecture). Synnott et al. illustrate how the phage infecting a given bacterial strain can be isolated.

Mar. 4 6a. Global change and the human microbiome. 6b. Forest fragmentation, change in land use, and infectious disease

6a. (Blaser, 2014); (Ali, 2015)†; (Velasquez-Manoff, 2012); (Pollan, 2013); (Buffie and Pamer, 2013)*; (Suez et al., 2014); (Ridaura et al., 2013); (van Nood et al., 2013)*; (Mathur et al., 2013); (Xu et al., 2015)†; (Wang et al., 2015)†; (Yano et al., 2015)†; (Clemente, 2015)†.Martin Blaser’s book emphasizes the importance of antibiotic abuse in ruining our microbiomes. Although Dr. Blaser (that is, Dr. Blaser MD) talks in his book about the pressures of mothers demanding inappropriate antibiotics for their children, that patients put pressure on doctors for antibiotics appears to be a myth (http://theincidentaleconomist.com/wordpress/healthcare-triage-news-patients-bossing-doctors-around-its-a-myth/ , with thanks to Lars Berg for pointing this out). The chapters provided discuss Helicobacter (the ulcer bacterium) being necessary to regulate our stomachs’ acidity, as well as the role of antibiotics in producing the obesity epidemic. Blaser’s book is reviewed by Ali. Velasquez-Manoff’s book emphasizes changes in environmental exposures to bacteria. (I haven’t assigned any particular chapters, as I have not yet read the book.) Michael Pollan discusses both. Many changes in diet have led to changes in the gut microbiome. Buffie and Pamer discuss how a denuded gut microbiome is less effective in resisting infection by a gut pathogen. Van Nood show the efficacy of fecal microbiota transplants to help defend against Clostridium difficile infection.

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Ridaura et al. perform fecal transplants from discordant human twins with very different body masses to show the effect of gut microbes on mouse metabolism and weight. Cho et al. show that subtherapeutic antibiotic dosages can have lasting effects on the microbiome and on adiposity. Mathur et al. show that Methanobrevibacter smithii is one gut bacterium that looks to have an effect on obesity. Suez et al. discuss how artificial sweeteners have been shown to cause glucose intolerance, and this is brought about by changes in the gut microbiome. I’ve mentioned Liping Zhao of Shanghai Jiao Tong University as an advocate of Chinese herbal medicine in engineering our microbiomes toward greater human health. He and his group (Xu et al.) recently published a provocative piece on the role of berberine in ameliorating type 2 diabetes in humans and in changing the contents of the gut microbiome toward having more microbes known to be healthful, such as Faecalibacterium species. Also from Liping Zhao is a study showing that use of any of three probiotic strains decreased weight gain in mice given a high-fat diet, and that any of these three strains has an impact on moving the gut microbiome toward that of a lean mouse (Wang et al.). Very recently, Yano et al. discovered that the spore-forming bacteria in the gut regulate serotonin synthesis (with possible positive repercussions on mental health). Clemente et al. contrast the western microbiome to the microbiome of previously uncontacted Yanomami Amerindians.

6b. (Hansen et al., 2013); (Walters, 2003); (Keesing et al., 2010)*; (Keesing et al., 2009); (Allan et al., 2003); (Guerra et al., 2006); (Dearing and Dizney, 2010); (Goodyear, 2014)*; (Brown et al., 2013); (Kuo et al., 2012)*Hansen et al. present a fine-detail (at 30-meter resolution) picture of worldwide forest losses and gains. The Walters chapter gives an extremely accessible account of Richard Ostfeld’s work on why Lyme disease is such a problem now, owing to changes in land use (in particular, forest fragmentation). Keesing et al. discuss the effects of biodiversity (often caused by changes in landscape) on disease transmission. Their earlier work showed how lowered small-mammal diversity increases the rate of Lyme disease transmission in the US northeast (Keesing et al. 2009 and Allan et al. 2003). In 2009, Keesing et al. show that most of the small mammals tend to reduce the tick population by efficiently grooming themselves, while the Peromyscus mice tends to increase the tick population (Keesing et al., 2009).

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Guerra et al. analyze worldwide how deforestation influences the rate of malaria transmission.

Dearing and Dizney (which we previously read in the context of climate changer) argue that agricultural development has led to high densities of some rodent populations that carry Hantaviruses.

Goodyear explains how human population migration to dry regions, as well as development of dry regions, can lead to increases in valley fever. Brown et al. give a technical account of the epidemiology of valley fever.

Kuo et al. demonstrate that abandonment of rice paddies in Taiwan increases opportunities for opportunities for transmission of disease through chiggers and ticks, an unexpected effect of economic globalization.

Mar. 25

Op-Ed piece due (see updated course requirements and information)

Apr. 1 7a. Infectious disease, extinction, and ecosystem functioning.

7b. What we can do to prevent future plagues.

7a. (Altizer et al., 2013)†; (Smith et al., 2009)*; (Mordecai, 2013); (Collinge et al., 2008)*; (Kupferschmidt, 2012); (Fisher et al., 2012); (King, 2012), Sept. 14, URL: http://news.sciencemag.org/sciencenow/2012/09/plight-of-the-bumblebee.html (G. Castanon); http://www.sfgate.com/science/article/Explosive-growth-in-sudden-oak-death-3934216.php (N. Kosman-Wiener); (Grünwald et al., 2012)*; (Weiman, 2015); (Kolbert, 2014).

Altizer et al. review the effects of climate change on biodiversity and ecosystem functions† . Smith et al. discuss various consequences when a major player of an ecosystem is struck by disease. Mordecai has investigated the role of infectious diseases in increasing or decreasing host species diversity, in a plant system. Collinge et al. start with the concept of the keystone species, a species with a disproportionate effect on community stability, such that local extinction of the species would have catastrophic rippling effects through the community and ecosystem. They then discuss the possibilities of such extinctions through infectious disease. The Science news article by Kupferschmidt discusses the ability of some fungal pathogens to extinguish multiple species; Fisher focuses on the potential ecosystem effects of such extinctions. King discusses the pathogen that is ravaging through native bumblebee populations

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in North America. (The bumble bee plays a vital agricultural role in pollination of many crops and flowers.) The Grünwald article on Sudden Oak Death describes rapid spread of this disease across many trees of North America and Europe and describes the disease as a member of the eukaryotic group Chromalveolata (not a fungus). Weiman gives an overview of marine pathogens that threaten whole ecosystems, particularly work by Rita Colwell how effects of pathogens on corals are exacerbated by ocean warming. Kolbert explains in her book, The Sixth Extinction, how the entire ecosystem based on corals throughout the tropics is likely to disappear as a result of acidification of the oceans (by carbon dioxide emissions). The idea is that more energy is required to produce the calcium carbonate skeleton as calcium carbonate becomes more soluble in more acidic water; this stress causes corals become more susceptible to infectious diseases such as white-band disease, caused by bacteria.

7b. Note: I am not asterisking any of these. Please submit questions on any two. Be prepared for an open-ended discussion, perhaps drawing from your op-ed pieces.(Cohn, 2014); (Caplan, 2015b); (Azman et al., 2015); (Gostin and Friedman, 2015)†; (Rodin and Dahn, 2015)†; (Tomes, 1998); (Markel, 2014); (Glaeser, 2011); (Reimer et al., 2013); (5frogmargin, 2015); (Pike et al., 2010); (Medicine and Council, 2009); (White-House, 2015) https://www.whitehouse.gov/the-press-office/2015/01/27/fact-sheet-president-s-2016-budget-proposes-historic-investment-combat-a .

Improving hospital careCohn discusses why it is that all but one of Ebola patients in the US have survived, and asks why the same care cannot be given in West Africa. Caplan discusses how the ethics of treatment need to be changed in a time of Ebola epidemic. Azman et al. discuss how the threat of Ebola may hinder the inevitable need for a response to upcoming cholera epidemics; they urge for an upgrade of public health infrastructure. Gostin and Friedman reiterate what we’ve been discussing, that, yes, an effective WHO needs to be able to move in for severe emergencies in developing countries, but what we most need in these countries is an effective health care system for everyday issues. Rodin and Dahn, in their New York Times Op-Ed piece, celebrate the end of the Ebola outbreak in Liberia (but not alas in neighboring countries) but point to a lack of resilience in the Liberian health care system.

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Upgrading and securing water suppliesThe germ theory of disease led to both humanitarian and oppressive policies. Tomes describes how, on the one hand, there emerged a socialism of the microbe, that the health of anyone would help the health of everyone. Markel presents, on the other hand, how there emerged an incentive to persecute groups that were otherwise unwanted. Glaeser describes, on pages 97-101, what it took to heal cities of infectious disease.

Poor housingReimer et al. discuss the promise of (cheap!) insecticidal bed nets for control of malaria.

Poor hygiene practicesPike et al. recommend programs of behavior modification away from unsafe practices. The slide show by 5frogmargin displays an amusing set of billboards explicitly showing good health practices in cartoons (with thanks to Jordan) (http://imgur.com/a/Gq6Il ).

Mitigating and accommodating the dangers of bushmeat huntingWolfe et al. discuss how socioeconomic pressures have led to a need for bushmeat hunting and trade to meet nutritional needs. Can these pressures be dealt with to dissuade engagement in bushmeat hunting? Pike et al. describe a “healthy hunter” campaign that they instituted for Cameroonian bushmeat hunters.

Monitoring outbreaks of zoonotic diseases before they spreadPike et al. and the report by The Committee on Achieving Sustainable Global Capacity for Surveillance and Response to Emerging Diseases of Zoonotic Origin, convened by the Institute of Medicine and the National Research Council, make a case for world monitoring of new spillover diseases before the spread. They recommend that such surveillance would focus on humans with high exposure to animals and the animals to which these people are exposed.

Forest fragmentationPressures on forests may be mitigated by greater urbanization, including building up rather than out. Glaeser’s book explains the many benefits of urban living.

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AntibioticsIn a recent press release, the White House described President Obama’s initiative to preserve the efficacy of antibiotics.

Apr. 8 8. Report from the “Impact of Environmental Changes on Infectious Diseases” meeting, part 1

8. The talks I heard at the meeting were based on unpublished and published results. I am trying to find and assign some works already published on the most interesting and germane subjects. I feel I’ve learned enough at the meeting to teach an entire course. Here I’ve started to find articles related to the talks I’ve heard. There is so much more to provide you, and I’ll do my best.

For April 8, please read one article that looks the most interesting to you, and submit questions and a very brief project proposal concept.

Malaria(Baeza et al., 2013); (Siraj et al., 2014); (Mordecai et al., 2013)Baeza et al. discuss the problem of bringing irrigation to dry areas that are on the fringe of a malarial region, focusing on the semi-arid region of northwest India. The problem is that irrigation is needed for long-term agricultural development and eventual affluence and good health; however, in the short term, the irrigation increases exposure to malaria.Siraj et al. explore evidence for whether global warming is likely to result in malaria moving up the highlands of Colombia and Ethiopia. Their approach was to determine whether in warm years malaria was found at higher elevations. They found a positive correlation, which suggests that with global warming, malaria will indeed move up the mountains. Mordecai et al. showed that the optimal temperature for malaria transmission is much lower than previously thought—it’s at 25 degrees and transmission falls rapidly above 28 degrees. Following this work, Courtney Murdock and Matthew Thomas (in unpublished work) wanted to find out if global warming would act to contract the geographical range of malaria from the African equatorial region if it became too hot for malaria. In experiments focusing on the effect of temperature on vector competence and biting rate in two Anopheles mosquito species. The authors predict an 85% reduction of malaria in some tropical areas, a silver lining to global warming.

Yellow fever and other Aedes-transmitted diseases(Arana-Guardia et al., 2014); (Manrique-Saide et al., 2013); (Mohammed and Chadee, 2011)Arana-Guardia et al. and Manrique-Saide et al. showed that

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Aedes aegyptii, the vector for Yellow fever, Dengue, and Chikungunya, is found frequently in stormwater drains. A presentation by David Chadee discussed how A. aegypii began in Africa as a mosquito developing as larvae in tree-hole puddles, and then evolved to develop in association with human structures, such as outdoor domestic water tanks and more recently the puddles in abandoned tires. He presented evidence that since the 1950’s, this mosquito has been evolving back toward tree-hole development and is frequently developing in underground habitats, such as stormwater drains. A recent paper by Mohammed and Chadee discusses how current tropical temperatures can make domestic water containers too warm for Aedes development. Vectors can adapt!

Tick-borne diseases(Lèger et al., 2013); (Jaenson et al., 2012); (Parola et al., 2008); (Mannelli et al., 2012)Lèger et al. discuss how both climate warming and land use changes have affected the distributions of ticks and the diseases they carry. Expansion of the range of Ixodes ricinus, which carries Lyme and TBEV, has moved northward in Sweden, owing to climate warming and to a loss of deer, particularly around urban areas, owing to reduced hunting by red fox and lynx. Parola et al. give evidence that in warmer weather, the dog tick (which carries Rickettsial diseases) tends to be more aggressive and increases affinity or biting humans. Mannelli et al. show how a particular host organism, in a multi-host system such as Lyme Borelliosis, can either increase or decrease disease transmission, and that even if the host cannot transmit the disease, its presence can decrease disease transmission.

Climate change and West Nile Virus(Wimberly et al., 2014)Michael Wimberly of South Dakota State University presented an ecological niche model to try to understand why his state has such a horrendous rate of human WNV cases, and to understand variation over time in prevalence of the disease. He found that warm temperature anomalies yielded much higher rates of human infection, where warm winters (favoring mosquito and virus survival over the winter) and springs (favoring higher virus amplification in spring) yielded higher rates of infection in August. Thus, higher rates of infection are expected with global warming. Also, eastern South Dakota has traditionally been dryland agriculture (without irrigation), but irrigation is being

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planned and implemented. This is expected to further exacerbate WNV in the future.

Community and ecosystem effects of single species (could be a pathogen)(Middleton, 2014); (Morell, 2015); (Ripple et al., 2014)There is a famous ecology story about how re-introduction of the wolf had many amazing impacts on the community ecology, ecosystem functioning, and even the hydrology of Yellowstone. It is told in the film How Wolves Change Rivers (https://www.youtube.com/watch?v=ysa5OBhXz-Q ). (We were shown this film at the conference, with the idea that perhaps a single pathogen could have the same effect.) Here the re-introduction of the wolves is said to have changed the feeding behavior of elk and deer, restoring the riverine vegetation. However, the story is probably an oversimplification, as told by Middleton in the New York Times. The March 20 issue of Science has an article by Morell discussing the effect of cougars as part of the resurgence of willows and riverine vegetation. The article by Ripple et al. documents other cases where large mammalian carnivores have had major effects on ecosystems.

Data sets for analysis of emerging infectious diseasesChia-Yi Hou of Imperial College London presented a nice set of databases that you might find useful for studies of emerging infectious diseases:Livestock Geo-Wiki (http://livestock.geo-wiki.org/ )FAO Forest Resource Assessment (http://faostat.fao.org/ )

The next group comes from an article by Jenkins on mapping patterns of vertebrate diversity (Jenkins et al., 2013):BirdLife International (www.birdlife.org )International Union for the Conservation of Nature (www.iucn.org )Hotspots Revisited (available at www.conservation.org )

A talk by Kris Murray discussed use of Gideon, a web site that gives incidence of human diseases in each country:(http://www.gideononline.com/ )

Predictors of emerging infectious diseases in AfricaChia-You Hou stated that the best predictors for the incidence of emerging infectious diseases in Africa were the local density of pigs and the local diversity of mammals.

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The untold story of Leishmaniasis (a “neglected tropical disease”) marching up through Texas and now into OklahomaStavana Strutz (a student of Camille Parmesan at U. Texas) has been investigating the movement of cutaneous Leishmaniasis throughout Texas and now Oklahoma (not yet published). Leishmaniasis mexicana is the protist that causes cutaneous Leishmaniasis, the mildest form of the disease, and was previously thought to be limited to tropical areas. She has worked to map the climatic variables and landcover variables that best predict incidence of human disease. While this disease is transmitted by a sandfly, which develops in moist soils, lower precipitation tends to increase habitat suitability.

Ebola(Talbot, 2014)Z. Song of Stanford discussed how the fundamental parameter of transmission, R0, can vary greatly between countries and cultures. In particular, an optimistic value of R0 based on Guinea gave a tragic underestimate of disease transmission in Liberia and Sierra Leone. He discussed how Flowminder (http://www.flowminder.org/ ) has used cell phone data to track mobility of people at various geographical scales to predict spread of disease. He discussed how human-to-human transmission depends on population density, hygiene, social culture, health conditions, and enhanced connectivity of human populations (explained by the Talbot article).

Pollution and infectious diseases of fish(Lafferty and Kuris, 1999)Kevin Lafferty of USGS discussed how various forms of pollution (eutrophication with pulp-mill runoff, crude oil, and industrial effluent) are contributing to infectious disease in fish populations.

Loss of diversity among trematode parasites(Thomas et al., 2004)Starting with the prediction (Thomas et al.) of massive extinctions of vertebrates by 2050, Kevin Lafferty predicted massive extinctions of species-specific trematode parasites. Is anyone crying for their loss?

Biocontrol for schistosomiasisLafferty discussed introducing the predatory river prawn to eat

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the Biomphalaria snails that host the schistosome parasite. The rates of new infections and re-infections plummeted through this biocontrol (an article by Sokolow and Lafferty, which is in revision for a journal). There are plans to build prawn ladders to allow prawns to migrate past a dam.

Changing pathogen diversity in the arctic region(Kutz et al., 2013)Susan Kutz of the University of Calgary investigated how changes in air temperature, sea temperature, ice melt, and socioeconomic and political changes are affecting the geographic ranges of pathogens in Canada’s far north. She explained how in 24-hour sun, the soil temperatures can be much warmer than the air (e.g., soil reaching 33 C while the air is 14 C). She notes that the sea ice decline has prevented caribou from reaching many islands. The new northwest passage has allowed for movement of pathogens between the Atlantic and Pacific. She described two emerging infectious diseases in muskox and caribou. The muskox becomes infected by protostrongylid lungworms by eating the slug that harbors the parasite along with their vegetation. Both the muskox and caribou are newly infected by varestrongylid lungworms, which also are harbored by gastropods that the herbivores inadvertently consume. There has been very rapid range expansion of both parasites northward, to Victoria Island. Whereas in 1980-1985 there were not enough degree days to support lungworm development, by 2013 the lungworms were able to develop on most of Victoria Island. She also presented evidence for a new bacterial infection among far-north mammals from the genus Erysipelothrix, and that this is the first time this pathogen has been seen in the Arctic. She found that, at the whole-genome level of resolution, there is almost no variation among the Erysipelothrix population, indicating that it is a newly emerging pathogen in this region.

Biosignatures for climate change(Parmesan and Yohe, 2003); (Burrows et al., 2011); (Poloczanska, 2013); (Rosenzweig et al., 2008)Camille Parmesan, now of Plymouth University in the UK, published the original meta-analysis of changes in geographic ranges and in phenology, providing biological evidence for climate change (with Wesleyan’s Gary Yohe in 2003). In her talk she provided some updates of this idea, including an article by Burrows et al., Poloczanska et al., and Rosenzweig. Burrows et al. and Poloczanska et al. (both including Parmesan) showed that

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the rate of geographical shift was much higher in marine than in terrestrial organisms. 83% of species studied showed a geographical change in the direction consistent with global warming. The high Arctic has shown extremely rapid geographical shifts, while changes in the boreal forest have been much slower; also, tropical species are moving very quickly. The average rate of shift for terrestrial animals if 6.1-17 km/decade, but marine animals have shifted 54-75 km/decade! In the Andes, frogs and fungi have moved 400 m upward over 70 years (Seimon, 2007). Parmesan has argued, however, that to attribute change in geographical range of a given species to one factor is often difficult (Parmesan et al., 2013). She also gave examples of diseases that have moved poleward: an oyster parasite, a brown trout kidney pathogen, avian malaria, chytrid fungus, and cutaneous Leishmaniasis.

A resource-based approach to ecological niche modeling(Li et al., 2012)Sophie Vanwambeke of Catholic University of Louvain, Belgium, presented a resource-based approach to ENM. This takes into account all the different resources that a host and a vector require throughout their lifetimes; suitability of a habitat requires that all the various resources be within mobility range. For example, the midges that transmit Bluetongue Virus require at different times of their life cycle: nectar, blood, forest trees (for resting), and others. Her group previously published a paper on this approach regarding Lyme disease (Li et al.)

Apr. 15

9. Report from the “Impact of Environmental Changes on Infectious Diseases” meeting, part 2

For April 15, please choose one article to read, and submit questions and a proposal based on the article.

Avian malaria in Alaska(Loiseau et al., 2012a)Ravinder Sehgal of San Francisco State University presented a talk on the first observation of avian malaria in the far north, up to 64 degrees north in Alaska, and he and his colleagues have predicted the further northward spread of this disease. One question is whether further northward spread is limited by the mosquito (as yet unidentified) or the parasite.

Evolution in Plasmodium of generalists and specialists(Loiseau et al., 2012b)Also in his talk Sehgal gave phylogenetic evidence for generalist avian malaria species evolving into specialists (narrow host range) at a rate four times greater than the reverse (Loiseau et

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al. 2012). Also, African lowland forests have a greater diversity, composed largely of Plasmodium specialists, compared to less diverse highland forests composed of generalists.

Climate change and diarrhea(Kolstad and Johansson, 2011); (Hashizume et al., 2008); (Milojevic et al., 2012); (Cash et al., 2014)In his talk, Masahiro Hashizume featured work by Kolstad and Johansson on the effect of future climate warming on diarrhea cases. Hashizume discussed how extreme flooding in Dhaka, Bangladesh severely increased diarrhea rates, but primarily among poor people. In a more rigorous, comparative study in Matlab, India, Hashizume and colleagues contrasted a set of flooded areas to a set of non-flooded areas (Milojevic et al.). Cash et al. also studied the correlation between climate warming and incidence of cholera and shigellosis in Dhaka.

How drought can lead to diarrhea(Lloyd et al., 2007)Jordan Emont of Yale presented his study on the health effects of severe drought on the South Pacific island of Tuvalu. He found that diarrhea rates increased during the drought because people were less likely to use precious water to wash their hands. While he hasn’t yet published his study, he suggested an article by Lloyd.

Estimating the public health dangers of global travel(Bogoch et al., 2015); (Semenza et al., 2014); (Khan et al., 2013)Kamran Khan of the University of Toronto compared countries along a plot of international travel per person versus domestic health care per person. The problem for international public health, he says, stems from countries like China with lots of travel but poor health care. He has published many interesting articles on the risk of spread of Ebola, MERS, Dengue, and influenza.

Using cell phones to estimate human mobility during an epidemic (Ebola and beyond )(Bharti et al., 2015); (Bharti et al., 2011); (Tatem et al., 2012b); (Bradley et al., 2015)Andy Tatem of the University of Southampton presented how epidemiologists can see travel through cell phone calls Bharti et al. 2015). Also, as a proxy he showed how satellite images at night can predict the extent of travel (i.e., compare North and

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South Korea at night). In his Bharti et al. paper of 2011, he shows how measles epidemics in Niger can be predicted from seasonal changes in population density, as measured by night-time satellite imagery. He has developed Vector-Borne Disease Airline Importation Risk (VBD-Air), which predicts the danger of importation of various diseases across the seasons (Tatem et al. 2012). Tatem also mentioned a paper by Bradley showing that the probability of becoming infected by an imported disease is higher in people who travel, but also in non-travelers who live in a neighborhood with lots of travelers. He also discussed how, despite our global travel, there are whole regions (e.g., southeast Africa) that have their own endemic clusters of HIV (Tatem et al., 2012a).

The origin of urinary schistosomiasis in Corsica(Berry et al., 2014)J. Boissier of Perpignan’s Centre National de la Recherche Scientifique gave a talk on the recent discovery of schistosomiasis on the Mediterranean island of Corsica. The Cavo River of Corsica is a bathing site for thousands of tourists, daily, and now it is known to be contaminated with the worm Schistosoma haemotobium, which causes urinary schistosomiasis. The intermediate host species, a snail called Bulinus, was known to be in Corsica for the last 50 years, but the schistosome is newly arrived. The authors deal with the possibility of invasion of southern Europe.

Global biogeography of human infectious diseases(Just et al., 2014)Kris Murray of Imperial College London presented an extremely interesting story on global biogeography of human infectious diseases. The issue is whether there are biogeographical regions for human infectious diseases, much like there are such regions for animals and plants, for both vector-borne and directly transmitted diseases. He found that there are indeed such biogeographical regions, especially for vector-borne diseases and to a lesser extent for directly transmitted diseases. This study took advantage of the Gideon database providing the list of infectious diseases found in each country (a rather coarse scale set). After his talk, at lunch, I told him how much I liked his paper when it first came out in November; he said he hadn’t submitted it yet. Oops. I’ve provided the article by Just et al, which scooped him.

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How agriculture is driving expansion of the bacterial resistome(You and Silbergeld, 2014)Ellen Silbergeld of Johns Hopkins gave a fabulous talk on the role of agricultural abuse of antibiotics in expanding the resistome available to all pathogens. The You and Silbergeld article pretty much cover her talk. Highlights included the fact that chickens spend their entire lives with their poops beneath them, and that there are huge fans cooling the super-coops but also spreading pathogens from one chicken to another. She says there is nothing contained about this farming, even to the extent of transporting chickens from farm to slaughterhouse. In one episode of this story, she followed a chicken truck sampling for antibiotic resistant bacteria in the air behind the truck, and she obtained lots of resistant bacteria that way! She notes that some major factory farms are just outside of suburbs, so the antibiotic resistant bacteria are very likely to enter water encountered by humans through waste water from the farms. Being vegan doesn’t protect you from being exposed to the resistance-bearing bacterial effluent of farms. She emphasizes that our antibiotic resistance problem is almost entirely due to agricultural abuse and almost not at all to mothers brow-beating doctors. She also mentions that using second-tier drugs does not protect the efficacy of our urgently needed antibiotics, since resistance is often on multiply-resistant plasmids.

Climate signatures of disease transmission(Rodó et al., 2013)Xavier Rodó of the Institució Catalana de Recerca i Estudis Avançats in Barcelona presented his work on trying to predict the transmission rates of many diseases based on climate and weather patterns. I’ve assigned a review article that covers much of his talk.

Apr. 22

10. Global warming, ocean acidification, and urbanization as challenges to non-pathogenic bacteria

10.For the April 22 meeting, please choose four articles for your homework.

The evolutionary challenges brought by rapid environmental change(Storch et al., 2014)*Storch et al. discuss the relationship between organism complexity and intolerance to environmental change. They predict that the lower complexity of Archaea and Bacteria will allow them to colonize extremely hot tropical oceans in a globally warmed world, while animals and plants will fail in this

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climate.

Marine acidification caused by increased CO2 levels(Schaum and Collins, 2014); (Collins et al., 2014); (Morrow et al., 2015)*Schaum and Collins study evolution of marine green algae of the genus Ostreococcus in the laboratory to test how plasticity affects the potential for evolutionary response, in this case to marine acidification. In related work, Collins et al. show how the ability to evolve tolerance to increased acidification varies greatly among taxa of marine algae. Morrow et al. have taken advantage of a natural volcanic seep, leaking carbon dioxide, in the ocean near Papua New Guinea to measure the effects of increased acidification on the microbiomes of corals and sponges.

Global warming(Sun et al., 2012)*; (Clarkson et al., 2015)†; (García-Palacios et al., 2015); (Lokmer and Wegner, 2015); (Tu et al., 2014)*; (Deng et al., 2015)*Just to give an extreme case of what could potentially happen with global warming, I’m introducing you to the paper by Sun et al. on the extreme greenhouse climate of the Permian extinction. The Permian extinction has long been attributed to extreme levels of greenhouse gases and extreme temperatures. The paper by Sun et al. makes a case that the tropics became nearly devoid of all plants and animals in this time. However, Clarkson et al., in a very recent paper in Science, provide evidence, using Boron-11 isotope data, that the extinction (at least the second pulse of the extinction) was caused by extreme acidification. García-Palacios et al. present a meta-analysis of 75 research articles to identify responses of microbes to various drivers of ecological change, including warming and increasing carbon dioxide levels. Lokmer and Wegner have explored the effects of predicted warm temperatures and infection by a pathogen on the hemolymph microbiome of oysters. They found a large effect of temperature on the microbiome at the species level, but not at higher taxon levels. Tu et al. 2014 introduce a new “GeoChip” (version 4, a microarray approach) for characterizing the physiological functions coded in the genomes of a community; they used it to assess the changes in the functions of a soil community with long-term warming. Deng et al. have investigated the effects of thawing of permafrost in the far north on microbial communities, with a focus on the effects on

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methane production and consumption.

Interaction of acidification and warming effects(Lindh et al., 2013)Lindh et al. tested the effects of acidification and warming, together and separately, on the bacterial plankton in the Baltic Sea, and found that temperature was much more important as a driver of change. However, mixed with acidification, temperature had much greater effects.

Apr. 29

Six student presentations

Katie and DaraJerry and KaylaTravis and LaurenWilsonEva and LarsJake and Jacob

May 6 Six student presentations

NatalieGabeAndrew and HannahZack and ThomasJordan and GregEli and Mollie

Bonus Eradication of diseases

(Bray and Buller, 2004); (Mundel and Orenstein, 2013); (Klepac et al., 2013); (Bray and Babiuk, 2011)Bray and Buller look back at the origins and eradication of smallpox. Mundel and Orenstein present the importance of global eradication of diseases such as polio. Klepac et al. discuss the challenges of the endgame in eliminating an infectious disease. How to plan a new world eradication program? Bray and Babiuk consider the possible global eradication of camelpox, the pathogen that evolved into smallpox.

Medical ethics—development of a vaccine in Nazi Germany’s concentration camps

(Caplan, 2015a)Arthur Caplan reviews a new book by Arthur Allen, The Fantastic Laboratory of Dr. Weigl. This tells of Dr. Weigl’s research in developing a typhus vaccine in Nazi concentration camps, using vulnerable prisoners as test patients. Dr. Weigl and his team ended up constructing an effective vaccine. The twist is that he shipped off to the Wehrmacht’s Eastern Front a useless vaccine but made available to the concentration camps the fully active vaccine. You decide.

Health care reform in the US—ACA at five years

(Blumenthal et al., 2015)†Blumenthal et al. analyze the successes and failures of the Affordable Care Act at five years. I include this because the socialism of the microbe may be an extremely important health strategy in times of future plagues brought about by global

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change.

* Starting with the February 11 discussion, choose the two articles to read and comment on from those that are asterisked. The other articles are there as resources for you and could be part of our discussions.

† These articles were listed after we had our class discussion.

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