by Sonia Shah
But that early detection made no difference in the course of the disease. There was no early containment effort that could have shortcircuited the outbreak in Belle-Anse. On the contrary, cholera killed people there at a rate four times higher than the rest of the country. By the time I visited, the sole NGO that had set up a cholera treatment center in the town center had already left, and people who fell ill in the hills above the town were being found dead along the three-mile-long descent into town. The local authorities could do little more than send body bags.43
Ironically, this wasn’t due to the village’s remoteness or to a lack of foreign aid. In fact, it was an aid project and a nascent transportation network that had made the people of Belle-Anse vulnerable to cholera in the first place. Due to a failing water supply system, built in the mid-1980s by the Belgian government, the people of Belle-Anse had very little access to clean fresh water. The system involved a pipe that had been laid across a high, long ridge, which carried fresh water from the hills into the town. The Belgians apparently hadn’t considered Haitian geography, climate, or the ability of locals to maintain the system when they installed it. Because of Haiti’s eroding hillsides and tropical storms, every year the pipe slipped off the ridge toward the beach. Today, it rests just inches above the turquoise waves, vulnerable to the force of hurricanes and peppered with holes. Locals don’t have the right tools to fix the pipe or sufficient resources to get them, so they wrap the holes with cloth bandages secured with elastic. They leak nonetheless. Only a trickle of fresh water arrives in the village as a result, necessitating all the shortcuts that diminish people’s ability to avoid filth and its pathogens.44
Just as ill-conceived aid had exposed Belle-Anse to pathogens, so had a partially functional, inaccessible transportation system. On one hand, Belle-Anse was viscerally connected to the world of commerce and disease around it. It was because Belle-Anse was connected to the rest of the country that cholera had arrived, after all. On the other hand, while the transportation system was sufficient to bring in the disease, it couldn’t bring in sufficient aid or resources to stanch it, and it couldn’t carry away to safety those who wanted to leave, either. Three days before we’d arrived in Belle-Anse, some residents desperate to escape had stolen a skiff like the one we rode over in. But unlike us, they didn’t have access to life jackets. When the overloaded boat capsized on the crossing, four drowned. On our boat ride back out of Belle-Anse, we saw the swollen body of one of the would-be escapees, a three-year-old girl dressed in pink leggings, bobbing in the sea. There was no room in our boat to take her corpse with us. We cut the motor and silently swayed alongside her, while our skipper made some calls to report the location of her watery grave.
Many simple solutions and quick fixes have been sought to address the lack of governance and poverty that prevented Belle-Anse from protecting itself from cholera. The history of foreign aid is littered with them. But it seems that there are no easy answers. The first step, perhaps, is simply to accept that a sustained, multifaceted effort will be required.
* * *
I returned home from Haiti just as I had from other trips far afield, struck by the power of pathogens to transform society. Their disruptive force looms over all of us, although only some have felt it so far. And yet even as the next pandemic gains momentum, the identity of the pathogen that will cause it remains as obscure as ever. It could be a jungle pathogen like Ebola. It could be a marine creature like cholera. It could be something else entirely. Somehow we have to live with the fact of not knowing its name.
So I wondered one summer evening, en route to the Chesapeake Bay to escape the heat of the city. The opaque, brackish water was as warm as a bath and rich with life. There were schools of striped bass and bluefish, beds of seagrass with crabs tangled in their waving blades, and floating armies of plankton. There were vibrio bacteria in the water, too, I knew, including cholera. It lapped at the curved sides of the fiberglass boat onto which we’d clambered.
Still, while the water was warm, the air was warmer, and it felt lovely to slip off the side of the boat into its fluid embrace. The bay is not deep, but it took a while before I reached the soft silt blanketing its floor. Above, the cholera-rich waters displaced by my dive whirled around, glittering darkly.
GLOSSARY
antibiotic. A compound that either kills or slows the growth of bacteria, used in the treatment of bacterial infections.
antibodies. Proteins produced by the immune system to identify and neutralize pathogens.
bacteria (singular: bacterium). Microscopic single-celled organisms.
bacteriophage. A virus that infects bacteria.
basic reproductive number. The average number of susceptible people who are infected by a single infected person, in the absence of outside intervention.
Batrachochytrium dendrobatidis. The fungal pathogen responsible for widespread declines in amphibians around the world; also known as amphibian chytrid fungus.
Borrelia burgdorferi. The tickborne bacterium that causes Lyme disease.
contagion. An infectious disease that spreads through direct or indirect contact.
copepods. A group of tiny marine crustaceans that are often colonized by vibrio bacteria, including Vibrio cholerae.
coronaviruses. A genus that includes the virus that causes SARS and MERS.
E. coli (Escherichia coli). A bacterium found in the gut of warm-blooded animals.
emerging diseases. New diseases that have caused increasing numbers of cases in recent decades and are poised to continue to do so.
epidemic. An unusual increase in the occurrence of a disease in a particular locality, often caused by contagion.
excreta. Matter that is excreted from the body, such as urine, feces, and saliva.
gene. A segment of DNA that is the basic unit of heredity.
H1N1. A subtype of influenza that caused the 1918 influenza pandemic and the 2009 “swine flu” pandemic.
H5N1. Also known as “bird flu,” a subtype of avian influenza that first emerged in 1996 and is highly virulent in humans.
hemorrhagic fever. Fever caused by a viral infection, accompanied by heightened susceptibility to bleeding.
highly pathogenic avian influenza. Strains of avian influenza that are highly pathogenic, such as H5N1.
horizontal gene transfer. A method of transferring genes laterally, common in single-celled organisms.
MERS (Middle East respiratory syndrome). An emerging infectious disease first reported in 2012, caused by a coronavirus.
microbe. Any organism too small to be seen with the naked eye.
monkeypox. A virus, related to smallpox, that lives in rodents and causes a disease clinically indistinguishable from smallpox in humans.
MRSA (methicillin-resistant Staphylococcus aureus). A bacterium that causes a range of difficult-to-treat infections in humans.
NDM-1 (New Delhi metallo-beta-lactamase 1). A plasmid that enables bacteria to resist fourteen classes of antibiotics.
Nipah virus. A virus of bats first reported in humans in 1999.
outbreak. A sudden increase in or eruption of disease.
pandemic. An infectious disease that spreads out of a particular locality to infect populations across regions or continents.
pathogen. Any disease-causing organism.
Phythophthora infestans. Fungal pathogen that causes potato blight and was the causative agent of the 1845 Irish potato famine.
plankton. A diverse range of marine organisms that float in the water column and cannot swim.
plasmid. A fragment of DNA within cells that can spread and replicate independently.
Plasmodium falciparum. A parasitic pathogen that causes a deadly strain of malaria in humans.
Pseudogymnoascus destructans. The fungal pathogen that causes white-nose syndrome in bats.
quarantine. Isolation to prevent the spread of infectious disease.
reemerging disease. An old disease causing increasing numbers of
cases or spreading into new areas.
SARS (severe acute respiratory syndrome). An infectious disease first reported in 2003, which is caused by a novel coronavirus.
spillover. The process by which a microbe in one species starts infecting a different species.
STEC (Shiga toxin–producing E. coli). A strain of E. coli found in some cattle, which causes virulent disease in humans.
vectorborne pathogens. Pathogens carried from one host to another via a vector, such as an insect.
vibrio. Any of the bacteria from the genus Vibrio.
vibrio bacteria. A genus of marine bacteria that includes both pathogenic and nonpathogenic species.
Vibrio cholerae. The bacterial pathogen that is the causative agent of cholera.
virion. A single virus particle.
virulence. A measure of a pathogen’s ability to cause disease.
virus. Microscopic agents that replicate inside the living cells of other organisms.
zoonosis. An infectious disease of animals that can infect humans.
zooplankton. Animal-like plankton.
NOTES
INTRODUCTION: CHOLERA’S CHILD
1. Rita Colwell, “Global Climate and Infectious Disease: The Cholera Paradigm,” Science 274, no. 5295 (1996): 2025–31.
2. M. Burnet, Natural History of Infectious Disease (Cambridge: Cambridge University Press, 1962), cited in Gerald B. Pier, “On the Greatly Exaggerated Reports of the Death of Infectious Diseases,” Clin Infectious Diseases 47, no. 8 (2008): 1113–14.
3. Madeline Drexler, Secret Agents: The Menace of Emerging Infections (Washington, DC: Joseph Henry Press, 2002), 6.
4. Kristin Harper and George Armelagos, “The Changing Disease-Scape in the Third Epidemiological Transition,” International Journal of Environmental Research and Public Health 7, no. 2 (2010): 675–97.
5. Peter Washer, Emerging Infectious Diseases and Society (New York: Palgrave Macmillan, 2010), 47.
6. Kate E. Jones et al., “Global Trends in Emerging Infectious Diseases,” Nature 451, no. 7181 (2008): 990–93.
7. Stephen Morse, plenary address, International Society for Disease Surveillance, Atlanta, GA, Dec. 7–8, 2011.
8. Burnet, Natural History of Infectious Disease.
9. Jones, “Global Trends in Emerging Infectious Diseases.”
10. Paul W. Ewald and Gregory M. Cochran, “Chlamydia pneumoniae and Cardiovascular Disease: An Evolutionary Perspective on Infectious Causation and Antibiotic Treatment,” The Journal of Infectious Diseases 181, supp. 3 (2000): S394–S401.
11. Brad Spellberg, “Antimicrobial Resistance: Policy Recommendations to Save Lives,” International Conference on Emerging Infectious Diseases, Atlanta, GA, March 13, 2012.
12. Drexler, Secret Agents, 7.
13. Wändi Bruine de Bruin et al., “Expert Judgments of Pandemic Influenza Risks,” Global Public Health 1, no. 2 (2006): 179–94.
14. Fatimah S. Dawood et al., “Estimated Global Mortality Associated with the First 12 Months of 2009 Pandemic Influenza A H1N1 Virus Circulation: A Modelling Study,” The Lancet Infectious Diseases 12, no. 9 (2012): 687–95.
15. Ronald Barrett et al., “Emerging and Re-emerging Infectious Diseases: The Third Epidemiologic Transition,” Annual Review of Anthropology 27 (1998): 247–71.
16. World Health Organization, “Ebola Response Roadmap—Situation Report,” May 6, 2015; “UN Says Nearly $1.26 Billion Needed to Fight Ebola Outbreak,” The Straits Times, Sept. 16, 2014; Daniel Schwartz, “Worst-ever Ebola Outbreak Getting Even Worse: By the Numbers,” CBCnews, CBC/Radio-Canada, Sept. 16, 2014; Denise Grady, “U.S. Scientists See Long Fight Against Ebola,” The New York Times, Sept. 12, 2014.
17. CDC, “U.S. Multi-State Measles Outbreak 2014–2015,” Feb. 12, 2015; CDC, “Notes from the Field: Measles Outbreak—Indiana, June–July 2011,” MMWR, Sept. 2, 2011.
18. Maryn McKenna, Superbug: The Fatal Menace of MRSA (New York: Free Press, 2010), 34; Andrew Pollack, “Looking for a Superbug Killer,” The New York Times, Nov. 6, 2010.
19. N. Cimolai, “MRSA and the Environment: Implications for Comprehensive Control Measures,” European Journal of Clinical Microbiology & Infectious Diseases 27, no. 7 (2008): 481–93.
20. Interview with Rita Colwell, Sept. 23, 2011.
21. Dawood, “Estimated Global Mortality”; Cecile Viboud et al., “Preliminary Estimates of Mortality and Years of Life Lost Associated with the 2009 A/H1N1 Pandemic in the US and Comparison with Past Influenza Seasons,” PLoS Currents 2 (March 2010).
1. THE JUMP
1. Rachel M. Wasser and Priscilla Bei Jiao, “Understanding the Motivations: The First Step Toward Influencing China’s Unsustainable Wildlife Consumption,” TRAFFIC East Asia, Jan. 2010.
2. Y. Guan, et al., “Isolation and Characterization of Viruses Related to the SARS Coronavirus from Animals in Southern China,” Science 302, no. 5643 (2003): 276–78.
3. Tomoki Yoshikawa et al., “Severe Acute Respiratory Syndrome (SARS) Coronavirus-Induced Lung Epithelial Cytokines Exacerbate SARS Pathogenesis by Modulating Intrinsic Functions of Monocyte-Derived Macrophages and Dendritic Cells,” Journal of Virology 83, no. 7 (April 2009): 3039–48.
4. Guillaume Constantin de Magny et al., “Role of Zooplankton Diversity in Vibrio cholerae Population Dynamics and in the Incidence of Cholera in the Bangladesh Sundarbans,” Applied and Environmental Microbiology 77, no. 17 (Sept. 2011).
5. Arthur G. Humes, “How Many Copepods?” Hydrobiologia 292/293, no. 1–7 (1994).
6. C. Yu et al., “Chitin Utilization by Marine Bacteria. A Physiological Function for Bacterial Adhesion to Immobilized Carbohydrates,” The Journal of Biological Chemistry 266 (1991): 24260–67; Carla Pruzzo, Luigi Vezzulli, and Rita R. Colwell, “Global Impact of Vibrio cholerae Interactions with Chitin,” Environmental Microbiology 10, no. 6 (2008): 1400–10.
7. Brij Gopal and Malavika Chauhan, “Biodiversity and Its Conservation in the Sundarban Mangrove Ecosystem,” Aquatic Sciences 68, no. 3 (Sept. 4, 2006): 338–54; Ranjan Chakrabarti, “Local People and the Global Tiger: An Environmental History of the Sundarbans,” Global Environment 3 (2009): 72–95; J. F. Richards and E. P. Flint, “Long-Term Transformations in the Sundarbans Wetlands Forests of Bengal,” Agriculture and Human Values 7, no. 2 (1990): 17–33; R. M. Eaton, “Human Settlement and Colonization in the Sundarbans, 1200–1750,” Agriculture and Human Values 7, no. 2 (1990): 6–16.
8. Paul Greenough, “Hunter’s Drowned Land: Wonderland Science in the Victorian Sundarbans,” in John Seidensticker et al., eds., The Commons in South Asia: Societal Pressures and Environmental Integrity in the Sundarbans of Bangladesh (Washington, DC: Smithsonian Institution, International Center, workshop, Nov. 20–21, 1987).
9. Eaton, “Human Settlement and Colonization in the Sundarbans”; Richards and Flint, “Long-Term Transformations in the Sundarbans Wetlands Forests of Bengal.”
10. Rita R. Colwell, “Oceans and Human Health: A Symbiotic Relationship Between People and the Sea,” American Society of Limnology and Oceanography and the Oceanographic Society, Ocean Research Conference, Honolulu, Feb. 16, 2004.
11. The filament is called the toxin coregulated pilus or TCP. Juliana Li et al., “Vibrio cholerae Toxin-Coregulated Pilus Structure Analyzed by Hydrogen/Deuterium Exchange Mass Spectrometry,” Structure 16, no. 1 (2008): 137–48.
12. Kerry Brandis, “Fluid Physiology,” Anaesthesia Education, www.anaesthesiaMCQ.com; Paul W. Ewald, Evolution of Infectious Disease (New York: Oxford University Press, 1994), 25.
13. Zindoga Mukandavire, David L. Smith, and J. Glenn Morris, Jr., “Cholera in Haiti: Reproductive Numbers and Vaccination Coverage Estimates,” Scientific Reports 3 (2013).
14. Ewald, Evolution of Infectious Disease, 25.
15. Dhiman Barua and William B. Greenough, eds.,
Cholera (New York: Plenum Publishing, 1992).
16. Jones, “Global Trends in Emerging Infectious Diseases.”
17. N. D. Wolfe, C. P. Dunavan, and J. Diamond, “Origins of Major Human Infectious Diseases, Nature 447, no. 7142 (2007): 279–83; Jared Diamond, Guns, Germs, and Steel: The Fates of Human Societies (New York: Norton, 1997), 207.
18. Interview with Peter Daszak, Oct. 28, 2011.
19. Lee Berger et al., “Chytridiomycosis Causes Amphibian Mortality Associated with Population Declines in the Rain Forests of Australia and Central America,” Proceedings of the National Academy of Sciences 95, no. 15 (1998): 9031–36.
20. Mark Woolhouse and Eleanor Gaunt, “Ecological Origins of Novel Human Pathogens,” Critical Reviews in Microbiology 33, no. 4 (2007): 231–42.
21. Keith Graham, “Atlanta and the World,” The Atlanta Journal-Constitution, Nov. 12, 1998.
22. “Restoring the Battered and Broken Environment of Liberia: One of the Keys to a New and Sustainable Future,” United Nations Environment Programme, Feb. 13, 2004.
23. “Sub-regional Overview,” Africa Environment Outlook 2, United Nations Environment Programme, 2006; “Deforestation in Guinea’s Parrot’s Beak Area: Image of the Day,” NASA, http://earthobservatory.nasa.gov/IOTD/view.php?id=6450.
24. P. M. Gorresen and M. R. Willig, “Landscape Responses of Bats to Habitat Fragmentation in Atlantic Forest of Paraguay,” Journal of Mammalogy 85 (2004): 688–97.
25. Charles H. Calisher et al., “Bats: Important Reservoir Hosts of Emerging Viruses,” Clinical Microbiology Reviews 19, no. 3 (2006): 531–45; Andrew P. Dobson, “What Links Bats to Emerging Infectious Diseases?” Science 310, no. 5748 (2005): 628–29; Dennis Normile et al., “Researchers Tie Deadly SARS Virus to Bats,” Science 309, no. 5744 (2005): 2154–55.
