Legionnaires’ Disease: Building a Better World for You

Legionnaires’ Disease: Building a Better World for You Abstract The emergent or newly reemerging disease model often relies on poverty as a contributing factor in the transmission of infectious diseases. But as Andrew Price-Smith has argued, affluence can also be a factor in the enhanced transmission of infection. Legionnaires’ disease, first identified in 1976 as the cause of a novel disease outbreak in Philadelphia, fits the model of such a disease of affluence. The Legionella bacteria readily finds niches in the equipment and systems of the modern-built environment designed to deliver and store fresh water for the comfort of its inhabitants. Ubiquitous in freshwater sources around the world, the built environment constitutes a “better” world for Legionella population increase and is likely to facilitate expanding outbreaks of Legionnaires’ disease. INTRODUCTION At the height of the summer of 2015, New York City public health officials announced that a respiratory illness had struck more than thirty citizens of the South Bronx, killing two of them.1 Health officials declared they were currently seeking the origin or origins of this ailment and gathering evidence about the scale and scope of the outbreak. The report predictably set off a feverish media response that tallied up the number of stricken and killed, closely tracked the investigation of the source or sources of the illness, and asked pointed questions about how the outbreak was allowed to occur and what health officials were doing to protect the public.2 In similar fashion the public fretted over their potential exposure and besieged their elected officials to ensure steps were taken both to end the current outbreak and prevent future reoccurrences. Although unfolding in the summer of 2015, in many respects the incident was an eerie echo of events that happened in another large northeastern American city just less then forty years previously. During the week of July 21–24, 1976, nearly five thousand Pennsylvania State American Legionnaires, family, and friends descended on the city of Philadelphia for their annual conference. The conventions combined a little business, the election of state officers and delegates, and a lot of fun; the Legion was notorious for its raucous meetings. The traditional reverie was further enhanced by the US bicentennial celebration. Unbeknownst to the conference attendees, however, was that the headquarters hotel (the venerable Bellevue Stratford) would soon serve as the epicenter of an explosive outbreak of a previously unknown illness. The affliction, dubbed Legionnaires’ disease in commemoration of its 29 unlucky fatal victims and their 153 stricken colleagues, struck suddenly and left the attending physicians mystified about its cause. The ensuing epidemiological investigation directed by personnel from the Centers for Disease Control and Prevention (CDC) would be conducted under harsh public scrutiny and amid dark conspiracy theories. As the weeks ticked by without a solution, the pressures on the CDC increased. Health officials could not explain what caused the outbreak, where it had come from, and whether it would appear again. Critics charged the investigators with being incompetent, malfeasant, or worse. Ultimately, in a research triumph, Joseph McDade and Charles Shepard, a pair of CDC scientists, identified the culprit that was a previously unknown genus of bacteria they named Legionella.3 In addition to determining that the organism was responsible for the Philadelphia outbreak, McDade and Shepard were also able to trace the bacteria to two previously unsolved disease outbreaks. Using samples stored at the CDC, the scientists demonstrated that in 1965, Legionella had sickened eighty-one patients at St. Elizabeth’s Hospital in Washington, D.C., ultimately killing fourteen before the outbreak ended as suddenly as it began. In 1968 a large outbreak of a respiratory ailment among employees, patients, and visitors at the Oakland County Public Health Department in Pontiac, Michigan, was also identified as Legionella. In the years since McDade and Shepard’s breakthrough, it has been determined that the organism is a ubiquitous inhabitant of the environment that comprises more than fifty species and seventy distinct serogroups described with more being discovered virtually every year. The bacterium has been recovered from standing and running freshwater courses, soil, and even from rainwater puddles.4 If one looks for it, one can find it. But although the bacteria can be easily recovered from samples around the world, it is the human-built environment that has provided an especially beneficial niche for the Legionella genus of bacteria. The transition of human occupation patterns to the built environment is not a new phenomenon. Indeed, the shift from nomadic to settled population is the story of human civilization, and we all are the inheritors of this transformational process. The farming communities and trading centers gave rise to towns and later cities increasing population size and density as well as being linked to other urban centers. As has been amply documented, both population growth and urbanization rates have expanded in the late twentieth and early twenty-first centuries.5 Increasingly, the global human population has become an urban creature inhabiting the built environment. And an expanding number of these urbanites are living and working in temperature-controlled environments. Changing human living patterns has also engendered changing relationships with the environment that oftentimes has an impact on human health. The transition from hunter-gatherer to farming lifestyle ultimately generated zoonotic transfers of animal pathogens to human diseases and the emergence of crowd diseases. The interconnection of population centers on the Eurasian and African continents created a large shared disease pool that became a global entity with the bridging of regions by the European empires. The scope and scale of transportation technological advances further tightened these global connections.6 Each changed relationship with the wider environment has presented new challenges for human health.7 The current transition to the temperature-controlled built environment is no different. In the case of Legionnaires’ disease, the built environment has created conditions supremely suited for the bacteria’s flourishing. Modern human habitations include a number of systems that transport and store fresh water for the purposes of drinking, bathing, cooling, soothing, and moisturizing the world they inhabit. In addition to creating a more comfortable and clean living arrangement, these conveniences have also brought larger human populations into ever-closer contact with the Legionella organism. This combination of events has prompted sickness and death from Legionnaires’ disease among untold numbers of people globally. The Legionella family of bacteria, and the disease it prompts, is generally grouped in the category of “emergent diseases” that are new, newly discovered, or resurgent organisms that are causing illness. Implicit in this definition is that these disease-causing entities, either because they are new or new to this population, represent a threat of epidemic or pandemic spread. The concept of emerging diseases, famously promoted by Stephen Morse and Joshua Lederberg, was the subject of an influential Institute of Medicine report in 1992.8 The report sought to document the relationship between human populations and potential disease-causing agents. Rather than marking the dawn of a postinfectious disease age (as some public health theorists hoped), the late twentieth century created conditions ripe for global spread of both novel and resurgent infectious entities. The combination of expanded encroachment of human populations into previously inaccessible areas; constantly evolving viral, bacterial, and parasitic organisms; and changing living patterns and social and cultural norms, tied together with accelerating transportation linkages and booming global trade, allowed previously local, controlled, or new disease-causing organisms to become global health threats. The discussion of emergent microbial threats has frequently carried with it notions that impoverished circumstances underlay these new ailments. A typical example cites the conditions of the desperate slums that surround the fast-growing megacities of the world. These urban areas have served as magnets for migrants from rural areas, crowded together in neighborhoods that have outstripped the capacity for basic water, sewerage, and sanitation infrastructure and linked to a wider world by high-speed jet, train, or highway travel. Such a tacit assumption of the links between poverty and disease obscures the fact that new or newly modified health threats can arise in conditions other than deprivation. For example, Andrew Price-Smith referred to certain new diseases as examples of a phenomenon he dubbed “plagues of affluence.”9 Although the term affluence is mildly imprecise (what exactly marks a society as affluent?), Legionnaires’ disease does fit the organizing principle as proposed by Price-Smith. The built environment has generated a series of niches that allows Legionella to multiply, and these mushrooming populations have been brought in very close contact with human populations. The outcome has been a series of increased, and apparently increasing, number of Legionnaires’ disease outbreaks. The constructed world that now surrounds the majority of the human population constitutes an environment that the Legionella family of bacteria finds quite to its liking. Underpinning both the concepts of emergent disease and plagues of affluence is the idea that human-induced changes have altered the environmental balance of the system. These new plagues, then, are a consequence of ecological change. Some writers have posited that these human-wrought changes are of such magnitude that they constitute a new era in earth’s history that they have dubbed the Anthropocene epoch. Most clearly manifested in the greatly accelerated rate of species extinction, according to this model the surging human population and its consumption patterns are altering the ecosystem planet-wide.10 While the paradigm that human-induced ecological changes constitutes a new epoch in the planet’s life span may be a matter of academic debate—when to date the epoch’s onset; how to measure the scale of humankind’s impact; and even if recent ecological changes truly represent a new epoch—examining the changes set in motion by human activity is not a recent academic innovation. Identifying the unintended effects of human decision making and actions has long been a staple in historical research, especially in the field of environmental history where it is sometimes referred to as the law of unintended consequences. Examples of this type include the effects of exterminating keystone species as nuisances in an environment, the role of fashion choices on fur and feather-bearing species, or the impact of introducing novel species to parasitize pests or other functions. Similar inadvertent outcomes are described in examining diseases in human history whereby changes in living patterns facilitated the embedding of malarial parasites in a population, the Atlantic slave trade’s role in delivering yellow fever to the Americas, or the role of trade routes in the dissemination of plague during the Black Death.11 Legionnaires’ disease fits easily into this paradigm. In general, discussion of disease impact in human history has often revolved around the introduction of infections to new regions, a wider environment for the infectious agent. But the case of Legionnaires’ disease (or legionellosis) is a little more unusual in that the modern-built environment constitutes a “better” or more ideal environment for Legionella to flourish. If we limit our definition of better to species reproductive success and demographic increase, human-wrought changes have created a number of winners and losers. Some of these winners were purposefully selected by humans—the number of cattle on the planet dwarfs the number of wild auroch populations that could be sustained while others have been quite accidental—the rise of the city in history has led inadvertently to the rise of the rat. Viewing it from the angle of increased numbers, Legionella would be in the rat category of success. For while the organism can generally be found in a variety of environments around the globe, only rarely is it found in highly dense concentrations.12 The overall effect of the human-caused changes has been to take a ubiquitous organism in which the circumstances for causing human illness only rarely aligned, and turn it into an organism that is frequently brought into human contact in an environment that favors colony formation and rapid growth. Human infection is far more likely when there is dense concentration of the organism and it is delivered in a way optimum for inhalation. Even though the organism can be found in the wider environment and has been found to cause illness, Legionnaires’ disease is more an example of a human-built threat to health then the consequence of a natural infection. An expanding number of humans work and live in units with mechanically controlled temperatures. This occupation pattern represents a novel living arrangement for the human species. These climate-controlled systems represent a changed interaction with the natural world and encompass new niches for micro- and macroscopic entities to inhabit. This intersection constitutes the latest chapter in the human story. THE ORGANISM AND INFECTION Legionella are intracellular parasites of freshwater protozoa and amoeba found in a variety of freshwater sources around the world.13Legionella induce these organisms to draw the bacteria inside where they utilize the nutrients of the amoeba and protozoa to replicate. As the bacteria begin to deplete the resources of their hosts, they are released into the aquatic environment, in some cases as a vesicle teeming with bacteria and enclosed by a membrane.14 The Legionella family was detected in 40 percent of random water samples by culturing and in more than 80 percent of samples measured by genetic recovery methods (polymerase chain reaction [PCR]). Since Legionella are comparatively difficult to culture, the PCR method of detection is a surer measure that the bacteria is, or has recently been, present in the water sample. The organism is acid tolerant and can be found in water temperatures ranging from 25 to 60°C (77–150.8 °F), but they are destroyed almost instantly when the temperature ranges above 70°C (158 °F). Their optimal growth range is from 35 to 45°C (95–113 °F), which has important implications for conditions created by modern human settlement components. Provided with single-cell organisms to invade and replicate in, nutrients to feed the growth of these organisms, and water with the right temperature ranges, Legionella are usually present. If the conditions are perfect, ideally with water temperatures in that magic 35 to 45°C (95–113 °F) band, Legionella will proliferate; or as the epidemiologists prefer to call it, amplify. Although there are more than fifty species of Legionella with at least seventy serogroup types, close to 90 percent of all human infections are associated with the type first discovered at the Bellevue Stratford in Philadelphia (although it should be noted that this percentage may be artificially inflated since most medical tests for Legionella are designed to detect this particular species of the genus). Since first characterized, Legionnaires’ disease outbreaks have been detected around the globe, and it is certain even more went unidentified. That first strain, named Legionella pneumophila (small [ella] army [legion] of organisms that love [phila] the lung [pneumo]), appears to be the most virulent.15 Legionnaires’ disease rarely, if ever, passes from person to person.16 This general inability to transit from person to person makes legionellosis an environment source infection, meaning a person has to be exposed to the organism in the environment in order to contract the ailment. Typically, Legionella invades the human organism when it is inhaled, although there have been cases of infection contracted from ingesting Legionella-contaminated water and even cases of infection when Legionella-contaminated water was used to irrigate a wound.17 These unusual cases of infection have been limited to hospitals and long-term care facilities where the victims tended to be in an immunocompromised state. The normal route of infection with the bacteria is when a person breathes in Legionella-laden water that has aerosolized from a contaminated source. Aerosolization can occur in many ways, but the most common fashion is through mechanical processes. Droplets in the 1 to 5 micron range are the most dangerous because these are the type that can be inhaled most deeply into the lungs. When this event occurs, there is a chance the individual will contract the disease, but infection is not certain. Legionnaires’ disease is dose dependent, meaning the greater the dose, the greater the likelihood of infection. When the bacterium becomes lodged in the lungs, it has entered the new harsher environment of the human body and is now subject to the ferocious and effective immune system. The human immune system is supremely adapted to detect and eradicate alien material that enters the body. Special cells identify nonself entities for rapid elimination. The Legionella organism, however, has an ingenious trick to evade the eradication efforts of the human immune system first responders. When the bacterium comes in contact with a phagocyte (commonly called a white blood cell), the bacterium is able to induce the white blood cell to transport it inside the cell rather than be engulfed and destroyed like other foreign matter the patrolling phagocyte encounters. In the interior of the cell it is ensconced in a vacuole that does not come in contact with the powerful enzymes the cell uses to digest alien invaders. Remarkably, once inside the white blood cell, the Legionella bacterium is able to use the cell as it does protozoa and amoebas—it recruits the cell for bacterial replication. In addition to avoiding the body’s natural defense of white blood cells, the bacteria actually weakens the immune protection of the individual. Legionella uses up the resources of the phagocyte causing the death of the cell while simultaneously generating many more copies of itself. This ability not only to circumvent a key component of first-line immune defense, but to use that element of the immune system to replicate, gives the bacterium a leg up on colonizing the human organism. After infection, an incubation period ranging from two to ten days ensues (although classically, the majority of cases manifest themselves four to five days after infection). Initial symptoms are categorized as flulike with a low-grade fever, headache, and fatigue. Intestinal complaints sometimes follow. Subsequently, the infection worsens and the patient spikes a high fever of 40°C (104 °F) with chills, a deep cough (both productive and nonproductive), difficulty breathing, and in the worst cases, delirium and kidney damage. Frequently, the illness deepens and develops into pneumonia. Left untreated, Legionnaires’ disease outbreaks have had mortality rates ranging from 5 to 30 percent of the infected. Fortunately, the bacteria are susceptible to certain categories of antibiotics. The current regime calls for the 4-quinolone group, generally consisting of levofloxacin and moxifloxacin, but azithromycin was also found to be effective.18 If treatment is provided early in the course of infection, the recovery rate is favorable. But survival and recovery rates are subject to a number of factors including the underlying health of the patient. Fortunately, one or more of the effective antibiotics are standard in the broad-spectrum treatment of pneumonia patients. But, as we shall see, this treatment practice serves to obscure the true burden of Legionnaires’ disease in the population and is a hindrance to surveillance efforts to enumerate and track the ailment. Exposure to the bacteria does not guarantee infection. Indeed, the vast majority (generally well above 90 percent) of people who come in contact with Legionella do not contract the illness or the course of infection is so mild that the individual is asymptomatic. There are certain risk factors that have been associated with a greater chance of becoming sick when encountering the bacteria. These factors include cigarette smoking, alcohol abuse, age, and underlying conditions that leave a person in an immunocompromised state. Many nations, especially the more economically developed nations of Eurasia, have populations that have increasing numbers of the elderly whose immune systems are less robust in fending off disease. That said, even healthy people may become sick and die after exposure and as is always the case when dealing with a biological organism, there is quite a bit of unpredictable randomness in determining the outcome. Further muddying the waters in evaluating the impact of Legionella infections is that the same organism responsible for the deadly outbreak in Philadelphia—Legionella pneumophila—can prompt a highly infectious, but not deadly infection known as Pontiac fever. The 1968 outbreak at the Oakland (Michigan) County Health Department (which gave the condition its name) struck 95 of 100 employees, 49 of 170 patients and visitors, and even 7 of 20 CDC investigators. The ailment sickened the victims with acute onset of fever, chills, headache, and malaise, but the course of infection was generally only three or four days, and the symptoms were neither as severe as Legionnaires’ disease nor the outcome as deadly. In fact, every single victim of Pontiac fever recovered with few lasting effects. Tellingly, in this 1968 case, the source of the infection was linked to the air-conditioning unit. Only the CDC investigators who were working on site when the unit was turned on after several days of shutdown were struck by Pontiac fever.19 The agent responsible for this outbreak remained a mystery until the CDC discovery of the bacteria for Legionnaires’ disease that enabled the scientists to test reagents against stored samples from the Pontiac facility. BUILT ENVIRONMENT Legionella inhabit a variety of niches around the globe, and they have likely caused some infection and death for an unknowable amount of time. Indeed, if the conditions are right, the organism can produce outbreaks with a multitude of victims without the congenial conditions of the human-built environment as the following two examples attest.20 In 1965 CDC epidemiologists investigated a mysterious pneumonia outbreak at St. Elizabeth’s Hospital in Washington, D.C.21 A statistical association was detected in which the eighty-one patients stricken with the ailment were likely to have either roamed the grounds or had beds near the window of their rooms. In fact, those who contracted the illness were ten times more likely to have such access to the outside. In their investigation, CDC researchers determined that while the psychiatric hospital had recently undergone excavation to install a new sprinkler system, no causative agent was discovered to account for the outbreak. In 1942 an unidentified agent hospitalized forty men from Fort Bragg with symptoms of high fever, chills, malaise, and headaches. The cases came from a cluster of base housing located in a remote corner of the camp with a small stream that flowed behind the barracks. Despite an exhaustive investigation, no culprit for the illnesses was detected. Both cases remained unsolved until stored samples were tested against Legionella reagents. In retrospect, it appears that the Fort Bragg cases were generated by Legionella that had aerosolized from the running stream and that the excavation at St. Elizabeth’s had stirred up dust particles laden with Legionella that the victims had inhaled. Although not the usual place the bacteria can be found, Legionella can occasionally be cultured from the soil.22 Both cases suggest that outbreaks of Legionnaires’ disease can occur without mechanical stimulus. While these examples suggest that Legionella outbreaks occur without the assistance of the built environment, it is the conditions created by the modern world that have truly turned this organism into a serious human health threat. A dizzying array of modern conveniences have been linked with Legionella outbreaks including cooling towers, evaporative condensers, steam turbines, showers, hot tubs, humidifiers, decorative fountains, and even a grocery store produce mister.23 In hospitals, where the patients are particularly vulnerable, infections have been detected through the usual cooling and water and shower mechanisms, but also through aspirators, lavages, and even drinking water. The bacterium has also demonstrated unusual persistence. For example, a Spanish hotel intermittently infected British tourists for over seven years (1973–80) before it was detected. In an outbreak at the Veterans Affairs Hospital in Oakland (Pittsburgh, Pennsylvania), a strain that killed five patients in 2013 was a genetic descendant of a strain first identified in the facility in 1982. In addition, the bacteria have shown the ability to infect a multitude of people in one site. In 1999 a Jacuzzi on display at a Dutch flower show harbored the bacteria and exposed 188 attendees to the disease, and in Melbourne, Australia, 125 visitors to the aquarium were infected from the air-conditioning unit.24 The common element in all these cases is that the human-built environment allowed Legionella bacteria to thrive and survive. The key element in devices linked to Legionnaires’ disease outbreaks is water, and in the twentieth century water was an essential component of new technologies to cool, and to a lesser degree, heat the indoor environment. In the early decades of the twentieth century, engineers and technicians had formulated systems to generate the self-proclaimed optimal conditions for comfortable working and living indoors. It is telling that the early pioneers in “air-conditioning” expressed their desire to “control the weather.” Indeed, the Carrier Corporation called their unit designed for the residential market the “Weathermaker.”25 Although various formulas were used to supercool the air—ammonia, carbon dioxide, and ultimately Freon—water was a ubiquitous component of the process. Sometimes water came in the form of condensation from the cooling and humidity control aspects of the units; in larger units the water facilitated heat transfer that allowed the cooling process to work most effectively. Initially focusing on creating desired humidity levels for certain factory products such as textiles or food manufacturing, air-conditioning manufacturers soon promoted the benefits of increased productivity of workers in factories and office buildings from controlled temperatures and humidity. Air-conditioning was heralded as the wave of the future maintaining productivity, cleanliness, beneficial health, and good-humor.26 Productivity was not limited to merely the factory floor according to a Saturday Evening Post story. In referring to one of the effects of the energy-hungry air-conditioning system, the aptly named Professor Watt observed that his studies recorded that “the rate of pregnancy in the air-conditioned houses showed a significant increase above that in the non air-conditioned.”27 By the end of World War II, the advocates who touted the benefits of climate control had won out over the fresh-air crowd. In line with other postwar ideas of human mastery of the environment, air-conditioning manufacturing and installation boomed in postwar America, soon to be exported with other American cultural ideals.28 While the proponents of controlled environments were certain of its superiority, the changing living conditions altered the relationship between humans and their environments—many times in unexpected and unforeseen ways. For example, the built environment creates conditions that are extraordinarily well suited to the flourishing and propagation of bacteria. Cooling towers, as was the likely culprit at the Bellevue Stratford in Philadelphia and in the 2015 Bronx cases, serve as watery heat exchangers that operate at temperatures ideally suited for Legionella growth. The normal functioning of the unit—heated water from the building is sprayed across a system of pipes and veins that cool the water through evaporation and that cooled water is collected at the bottom while heated water vapor is vented out through fans—serves to broadcast Legionella-contaminated droplets into the wider environment. Such a system is tailormade for Legionella amplification. The water temperature in the exchanger is generally in the 29 to 35°C (85–95 °F) range, openings to the outside environment allow dust and debris to enter and provide nutrients for the growth of single-cell organisms in which the bacteria replicate, and the water is circulated (figure 1). Combined with the aerosol properties of the water spraying and the fan blowing, it is no surprise that cooling towers have been repeatedly linked with legionellosis.29 Figure 1. View largeDownload slide Drawing number one from “injector type indirect evaporative condensers,” patent number 3800553 by John Engalitcheff Jr. Source: US Patent and Trademark Office. Figure 1. View largeDownload slide Drawing number one from “injector type indirect evaporative condensers,” patent number 3800553 by John Engalitcheff Jr. Source: US Patent and Trademark Office. The dangers of these systems for the transmission of Legionella are heightened when a structure that has been dormant for a period of time—as in the winter months—is switched on without proper disinfection. The Legionella bacterium, which has had a period of time to colonize in the stagnant water, is then aerosolized when the infrequently used source is put into service. So, for example, a showerhead that has been idled for a period of time will suddenly emit a dense concentration of bacteria when put into use. The stagnation period allows the protozoa and amoebas that Legionella parasitize to form a biofilm or slime layer on the surface of pipes and equipment. Poorly maintained or ineffectively disinfected systems make it more likely that the bacteria will flourish. But even well-maintained water systems may harbor Legionella bacteria. The organism is moderately tolerant of chlorine and other disinfectants, so it is likely that some members of the bacteria’s family will survive the standard municipal water treatment processes. Indeed, it is most likely from municipal water systems that the bacteria are introduced into building water pipes. Even the most diligent maintenance and sanitation schedule will not prevent the introduction of Legionella. PREVENTION AND SURVEILLANCE From the account just described, the question naturally arises of how people can protect themselves and the public from the threat of Legionnaires’ disease. The simple answer is through prevention and surveillance. But of course to achieve these goals is not so simple. Prevention would seem to be a straightforward proposition. If Legionella replicate in water systems, then ensuring that the water systems are disinfected should destroy the organism. And in theory, that notion is true. However, in practice, building systems and their pipes tend to be a complex maze of linkages, especially in older buildings that have been remodeled and changed over the years. Therefore, it is difficult to ensure that every link receives the proper quantity of disinfecting chemical (such as chlorine) or that every stretch of pipe reaches above 70°C (158 °F) when superheating the system to kill Legionella (a common emergency health response to building outbreaks). And even if eradicating the bacteria in the system is successful, there is no guarantee that the structure is permanently protected. Potable water that meets every quality standard still may have Legionella bacteria, and systems that are open to the environment (like cooling systems) can never prevent bacteria from drifting into the process. If the disinfection regime relaxes or fails at any point, Legionella can recolonize the network. Another problem in controlling Legionella is related to evolution. Altering the environment through chemical measures or other technologies applies natural selection pressures on the genome of the bacteria. Over time this selection pressure will select for organisms with increased tolerance to disinfectants or higher temperatures. More worrisome is that new genetic testing technology has revealed that the Legionella family actively engages in horizontal gene transfer of genetic material. Horizontal gene transfer, or recombination events, allows the exchange of portions of genetic code both within and between species. The ability to transfer genetic packages (plasmids) that facilitate enhanced survival and replication in different environments has been associated with the rapid development of antibiotic resistance across a variety of bacterial species. In the case of Legionella, the bio-slime layers that the organism thrives in constitute an excellent environment in which a multitude of bacterial species are brought into close proximity, potentially facilitating the transfer of genetic information.30 Since a 100 percent prevention of Legionella from entering the system is impossible, perhaps the answer lays in attacking the larger organisms that the bacteria needs to reproduce. A diligent schedule of cleaning, descaling, and disinfecting equipment can remove the buildup of organisms that facilitate bacterial growth. But even the most faithful maintenance program faces a daunting challenge. Wear and tear on machinery creates a more difficult surface area to clean, and even tactics that appear to be protective can inadvertently create conditions that favor organic growth. For example, hyperchlorination kills bacteria and other organisms. However, prolonged chlorine use actually corrodes and degrades the equipment and pipes creating niches and crevasses that can serve to shield the organism from the disinfecting chemicals and processes. Biofilms and slimes are many layers deep, and the outside layer exposed to the disinfecting substance can protect the organisms beneath, allowing for the persistence of the single-celled creatures and bacteria. If we cannot keep Legionella completely out of our system, nor can we ensure that the amoebas and protozoa the bacteria needs to replicate are excluded, perhaps we can keep the organism at a level that does not represent a risk of disease. Here lies the third challenge to the prevention effort. What exactly is that acceptable level? This topic has engendered much debate but no consensus. Legionella are generally measured as the number of colony-forming units per milliliter of water (cfu/ml). In the natural environment such as streams and ponds, the bacteria are measured at 1 cfu/ml. In the favorable conditions of the built environment, however, Legionella counts can get many thousands of times higher, even above 10,000 cfu/ml.31 It would seem, then, that taking aggressive action above a certain Legionella concentration point would mitigate the risk of infection. This approach is the one recommended by some epidemiologists and microbiologists. It is not, however, the one endorsed by the CDC. According to Lauri Hicks, epidemiologist assigned to Legionella outbreak investigations by the CDC, the problem with this idea of a threshold is that there is too much variation in bacterial strains to assess the risk of Legionella concentrations adequately. To begin with, the method of enumerating bacterial counts per milliliter is a difficult laboratory technique, so counts conducted by commercial laboratories may be unreliable. In addition, there are many examples where it was determined that the Legionella had indeed concentrated in great number, yet there was no disease. Conversely, systems with low levels of bacteria have recorded disease. As Hicks states it, “Actually, what’s more important [than concentration of bacteria] are the types of Legionella in the environment.”32 CDC officials fear that thresholds induce complacency with Legionella contamination. Rather than prospectively testing potential exposure sites and mechanisms, the CDC recommends regular maintenance and disinfection with testing and mitigation responses only undertaken after an outbreak has been confirmed.33 The waiting for an outbreak model is seen by some CDC critics as a backward approach to public health. J. Donald Millar, former director of the National Institute for Occupational Safety and Health, and a longtime administrator of public health, argued that this process puts the health of citizens at risk since people have to be sickened before an investigation or mitigation efforts ensue. Millar favored a “hazard analysis” approach in which potential Legionella infection sites are periodically tested and measured. Sites with high levels of colony-forming units per milliliter or ones where Legionella concentrations are rapidly escalating (or “blooming” in the terminology) are immediately treated to lower or eradicate the number of Legionella present. Although acknowledging such a testing system is an imprecise tool, it does have at its heart a plan to protect citizens from infections proactively.34 This preventive monitoring approach is also the method pursued by the European Working Group for Legionella Infections (EWGLI) as well as several Asian and Pacific states (Australia and Singapore among them).35 Surveillance is another aspect of Legionnaires’ disease that is fraught with controversy. The problem is that there is very little active surveillance for Legionella in the United States. Legionnaires’ disease is a reportable disease, meaning that when physicians detect a case of the illness, they are required to report this information to the local health department that ultimately reports that information to the CDC. These reports enable the organization to track outbreaks and to gather an estimate of disease activity. But this is a type of passive reporting that places the entire onus on the physician to identify and report the Legionella infection. Physicians generally encounter a patient with Legionnaires’ disease when they present with pneumonia, and pneumonia is a fairly common component of hospital caseloads. Unfortunately, only a small percentage of pneumonia cases are tested for Legionella, primarily because the standard broad-spectrum antibiotic course prescribed for pneumonia cases generally includes antibiotics that are used to treat Legionella. Physicians adopt a practical approach, thinking if the treatment is working, who cares what caused the illness? It is not as if the doctors need to do additional paperwork. The answer, of course, is that public health officials care because if a patient can be linked to a specific place or time when he or she was infected, steps can be taken to prevent others from being exposed and possibly sickened as well. There is also a more prosaic reason for the reluctance of physicians to test for Legionella in their patients, and it has to do with money. Hospitals, like any other business, are entities that can be acquired by others or are subject to the market demands of competition. The late twentieth and early twenty-first centuries were marked by a wave of consolidations and mergers in the hospital sector. Administrators sought to maximize efficiencies and cut costs either in the wake of a merger or as an attempt to make the hospital leaner and more competitive. One area frequently targeted for budgeting cutbacks was the in-house microbiology laboratories. It was deemed cheaper to send these samples out to commercial labs rather than maintain one inside the hospital. These decisions have a cost, and that cost is measured in time. Sending out samples to be tested results in a longer turnaround time to identify the results of the screening. For example, a large-scale study of sixty-two laboratories in Georgia that conducted Legionella identification tests revealed there was a median reporting time of three days in outside commercial labs. Hospitals that still had an in-house microbiology lab reported a median time of three-quarters of a day to report results.36 No physician would wait three days to begin treatment for a pneumonia case, especially since those hospitalized with Legionella-induced pneumonia tend to be very sick. In the United States, there are an estimated 8,000 to 18,000 reported cases of Legionella-caused pneumonia in which the person needs to be hospitalized each year. But few epidemiologists have much confidence in that estimate drawn from a single 1991 study of community-acquired pneumonia cases in two Ohio counties. Recognizing the paucity of surveillance data on the incidence of legionellosis, the CDC has recently embarked on a trial system of more proactive Legionella data collection. These new approaches are still in the preliminary phases at the present time.37 The accuracy of surveillance in the United States is problematic. To a certain degree this is a function of the structure of public health in the United States that places great authority for its practice in the hands of state and local health departments. In fact, technically the CDC has to be invited in to do an epidemiological investigation within any state. Without that request, the CDC has no legal authority for action in individual states. The limitations of this approach were exemplified in events in Flint, Michigan, in 2014–16. In the late winter of 2016, it was reported that the switch to municipal water from the Flint River may be associated with a Legionnaires’ outbreak as well as lead poisoning in the city of Flint. Flint’s home county of Genesee reported eighty-seven people as possible Legionnaires’ cases in the period of June 2014 through October 2015. Despite county health officials’ requests to the Michigan Department of Health and Human Services, the state health officials did not formally request CDC assistance until January 2016.38 By all accounts the more centralized European EWGLI group does a more effective surveillance job than the United States. The same can be said for Australia. The larger problem for assessing legionellosis is not the relative effectiveness of various systems, however; it is that the vast majority of states in the world conduct no or little Legionella detection at all. Therefore it is not possible to even hazard a guess as to the global burden of Legionnaires’ disease. Even absent a formal accounting of the prevalence of legionellosis, there are indications that the number of Legionella infections are on the rise. The CDC announced that the quantity of Legionnaires’ disease cases reported to public health services in the United States between 2000 and 2009 increased 217 percent. The CDC declined to speculate whether this increase was due to greater testing and reporting data or represented a real increase in the prevalence of infections. Others, however, were not so reticent. Ruth Berkelman, former deputy director of the National Center for Infectious Diseases at the CDC, wrote in a 2008 article drawn from the CDC data that she and her coauthor Karen Neil “found no evidence that changes in diagnostic testing were responsible for the increase after 2000” and that there was no evidence that new case reporting procedures were responsible for the increase either.39 A possible driver for increasing numbers of Legionella cases could be climate change. Average temperature increases provide a more suitable setting for Legionella replication in both the natural and built environments. Regions with increased rainfall and warmer temperatures due to climate change would likely also see an increase in Legionella propagation. Theoretically, these gains, driven by warmer, wetter weather, should be counterbalanced by regions that are more drought prone due to climate change. There are indications, however, that drought conditions do not have a strong dampening effect on Legionnaires’ disease cases.40 Like many predictions based on the impact of climate change, these projections can only be tentative. CONCLUSION Legionnaires’ disease is an undercounted, underestimated, and underappreciated global threat to human health. If there is no clear consensus on how many cases there are, or whether the number of cases is increasing, it is generally agreed that the number of people stricken by the infection each year is significantly higher than reported. It seems likely that the number of people exposed to Legionella will increase, partly as a factor of increasing urbanization rates, partly due to greater access to climate control and water distribution systems tied with a global rise in standards of living, and perhaps as a result of a warming planet. We can also posit that the number of those who succumb to Legionnaires’ disease will increase as well. In addition to increased numbers of people who are able to survive in an immunocompromised state due to medical advances, the number and percentage of the elderly population continues to increase in a number of nations. Legionella-induced pneumonia taxes even the most sophisticated health systems requiring access to powerful antibiotic treatments and to the ministrations of intensive care units. Despite these services, somewhere between 10 and 20 percent of people hospitalized with Legionnaires’ disease will die.41 It is almost certain that the mortality rate in places without these amenities is higher. In some ways, the Legionella story is of a standard type of environmental and disease narrative. As the development of farming lifestyles led to settled populations that fed increasing concentrations of mosquitoes ensuring the continued transmission of malaria, or the development of speedy ships and trains allowed cholera-stricken patients to reach further destinations ultimately serving to create the pandemic waves of cholera in the nineteenth and twentieth centuries, so too did technologies to cool the air facilitate conditions ripe for explosive growth of Legionella. Legionellosis is just another example of the law of unintended consequences impacting human health. But in some fashion the Legionella example is unusual. In many ways the modern-built environment constitutes a better world for the organism and not just a wider world. Safely ensconced in its warm bath, the bacteria remain inured to dramatic temperature changes and perhaps could even benefit as rising temperatures from a warming planet elevate the clime of its watery home. With its trusty single-celled organisms sharing its shelter, the bacteria can go on happily multiplying. If harsh disinfecting chemicals disturb its Eden or its vital biofilms and slimes are swept away by diligent cleaning, it is certain that another of its kind will drift in and renew the colonization of this bacterial paradise. Further, an increasing percentage of people are living and working exclusively in climate-controlled environments. Those water systems that constitute a vital part of environment control represent a large new niche for watery microbiota. When examining the historical trajectory of threats to public health, there is often a tendency to look for lessons to take from the research that will apply to other cases. An obvious conclusion to take from this overview of legionellosis is that we need to know a whole lot more about this organism. Many basic questions about the bacteria—how prevalent is Legionella; how many cases of Legionnaires’ disease does it cause each year; are the infections increasing, decreasing, or steady; what is its geographic reach among them—remain unknown or incomplete. In short, a lot more surveillance and epidemiological work needs to be done on the local, national, and global level. To some extent, getting this information is more pressing than medical advances to treat the disease. While it is important to save those who Legionella has infected, ultimately it is more useful to prevent those infections in the first place. Legionella and the niches it inhabits are micro versions of a larger and accelerating process of human-wrought ecological changes. Whether these changes constitute a new epoch in the earth’s history is a matter of some debate. But we can state confidently that human history is marked by the propensity to alter the environment to suit its needs. Human action, whether planned or inadvertent, has rippled through its ecological surroundings. The built environment constitutes a continuation of this human pattern both destroying some ecological niches and generating a number of new and changed ones. If our gaze is drawn (and rightfully so) to large-scale ecological changes such as deforestation and climate change, we should not overlook the changing world at the micro level. Building a “better” world for human populations may inadvertently build a “better” world for something else as well. George Dehner is an associate professor in the Department of History at Wichita State University where he teaches courses in world, environmental, and USS history. He is the author of Influenza: A Century of Science and Public Health Response (University of Pittsburgh Press, 2012) and Global Flu and You: A History of Influenza (Reaktion Press, 2012). Footnotes I would like to gratefully acknowledge the assistance of Guy Hall and the staff at the National Archives and Records Administration, Southeast Region, Mary Hilpertshauser at the David J. Sencer CDC Museum, the staff at the Stephen B. Thacker CDC Library, the interlibrary staff at Ablah Library, Wichita State University, for archival and library material, and Nan Myers’s aid in tracking down the patent image used; Ruth Berkelman, Lauri Hicks, Claressa Lucas, Brian Shelton, and the late J. Donald Millar for making themselves available for interviews; the panel and audience at the “Intersections of Human Disease and Environment” at the 23rd Annual World History Conference, Costa Rica, for their questions and comments; and Day Radebaugh and the students in the Honors “Epidemics and World History Course” (Fall 2016 and Fall 2017 Wichita State University) for their comments on a draft of this article. I appreciate the funding of an Award for Research/Creative Projects in Summer (2013) from Wichita State University that supported a research trip to Atlanta. I would also like to acknowledge the editorial comments from Lisa M. Brady and two anonymous referees at Environmental History who substantially helped sharpen the manuscript and editor Brady’s assistance in uploading the image used in this article. Omissions and errors remain mine alone. 1 The following account is drawn from New York Times coverage from July 30, 2015, to August 28, 2015, available at www.nytimes.com unless otherwise noted. The public health announcement is from Winnie Hu, “Legionnaires’ Disease Kills 2 in the Bronx,” July 30, 2015, from nytimes.com. 2 Ultimately reported as claiming 12 lives and sickening an additional 120 more. Winnie Hu, “Legionnaires’ Outbreak Over, Officials Say,” August 21, 2015, www.nytimes.com. 3 This information is drawn from David Fraser et al., “Legionnaires’ Disease: Description of an Epidemic of Pneumonia,” New England Journal of Medicine 297, no. 22 (December 1, 1977): 1189–97; Joseph McDade, Charles Shepard, David Fraser, Theodore R. Tsai, Martha A. Redus, Walter R. Dowdle, and the Laboratory Investigation Team, “Legionnaires’ Disease: Isolation of a Bacterium and Demonstration of Its Role in Other Respiratory Disease,” New England Journal of Medicine 297, no. 22 (December 1, 1977): 1197–1203; and Barry S. Fields, Robert F. Benson, and Richard E. Besser, “Legionella and Legionnaires’ Disease: 25 Years of Investigation,” Clinical Microbiology Reviews 15, no. 3 (July 2002): 506. 4 For connection to 1965 (St. Elizabeth) and 1968 (Pontiac) outbreaks, see Fraser et al., “Legionnaires’ Disease,” 1196; McDade et al., “Legionnaires’ Disease,” 1201; and David W. Fraser and Joseph E. McDade, “Legionellosis,” Scientific American 241, no. 4 (October 1979): 88. For numbers of Legionella species and serotypes, see Jamie Bartram, Yves Chartier, John V. Lee, Kathy Pond, and Susanne Surman-Lee, eds., Legionella and the Prevention of Legionellosis (Geneva: World Health Organization, 2007), 19. For locations of recovered Legionella bacteria in the natural environment, see E. van Heijnsbergen et al., “Viable Legionella Pneumophila Bacteria in Natural Soil and Rainwater Puddles,” Journal of Applied Microbiology 117, no. 3 (September 2014): 882–90. 5 According to the United Nations, the global population as of mid-2015 stood at 7.3 billion people. See “World Population Prospects: Volume I: Comprehensive Tables (2015 Revision),” https://esa.un.org/unpd/wpp/Publications/Files/WPP2015_Volume-I_Comprehensive-Tables.pdf. A total of 54 percent of the population resides in urban areas as of 2014 with the urbanization rate increasing. See “World Urbanization Prospects [Highlights],” https://esa.un.org/unpd/wup/Publications/Files/WUP2014-Highlights.pdf. Both reports accessed June 8, 2017. 6 Classic works that tell these tales include Jared Diamond, Guns, Germs, and Steel: The Fates of Human Societies (New York: Norton, 1997); William H. McNeill, Plagues and Peoples (New York: Anchor Books Doubleday, 1976); Alfred W. Crosby, The Columbian Exchange: Biological and Cultural Consequences of 1492 (Westport: Greenwood Press, 1972); and J. N. Hays, The Burdens of Disease: Epidemics and Human Response in Western History (New Brunswick: Rutgers University Press, 2000). 7 For a collection of essays that seek to bring together the once separate histories of health and environment, see Gregg Mitman, Michelle Murphy, and Christopher Sellers, eds., Landscape of Exposure: Knowledge and Illness in Modern Environments, in Osiris, Vol. 19 (Chicago: University of Chicago Press, 2004). 8 See Institute of Medicine, Emerging Infections: Microbial Threats to Health in the United States (Washington, DC: National Academies, 1992); Stephen S. Morse, ed., Emerging Viruses (New York: Oxford University Press, 1993); and Stephen S. Morse, The Evolutionary Biology of Viruses (New York: Raven, 1994). 9 Andrew Price Smith, “The Plagues of Affluence: Human Ecology and the Case of the SARS Epidemic,” Environmental History 20, no. 4 (October 2015): 765–78. 10 For an overview of this concept, see Will Steffen, Jacques Grinevald, Paul Crutzen, and John McNeill, “The Anthropocene: Conceptual and Historical Perspectives,” Philosophical Transactions: Mathematical, Physical and Engineering Sciences 369, no. 1938 (March 2011): 842–67. 11 See Thomas Dunlap, “Values for Varmints: Predator Control and Environmental Ideas, 1920–1939,” Pacific Historical Review 53, no. 2 (May 1984): 141–61; Anthony N. Penna, Nature’s Bounty: Historical and Modern Environmental Perspectives (Armonk: M. E. Sharpe, 1999); J. R. McNeill, Something New Under the Sun: An Environmental History of the Twentieth-Century World (New York: Norton, 2000); James L. A. Webb Jr., Humanity’s Burden: A Global History of Malaria (Cambridge: Cambridge University Press, 2009); Philip Curtin, “Epidemiology and the Slave Trade,” Political Science Quarterly 82 (June 2, 1968): 94–110; and John Aberth, The Black Death: The Great Mortality of 1348–1350, A Brief History with Documents, 2nd ed. (Boston: Bedford/St. Martin’s, 2017). 12 Interestingly, one of those occasions is in watercourses and bodies near recently erupted volcanoes. These disturbed environments apparently favor Legionella blooming, particularly near thermal seeps. See, for example, David L. Tison, John A Baross, and Ramon J. Seidler, “Legionella in Aquatic Habitats in the Mount Saint Helens Blast Zone,” Current Microbiology 9 (1983): 345–48, and Douglas Larson, “The Recovery of Spirit Lake,” American Scientist 81, no. 2 (March-April 1993): 166–77. 13 The following description of Legionella is drawn from Bartram et al., Legionella, 29–38; Lisa A. Beltz, Emerging Infectious Diseases: A Guide to Diseases, Causative Agents, and Surveillance (San Francisco: Jossey-Bass, 2011), 186–94; and Fields et al., “Legionella and Legionnaires’ Disease,” 506–17, unless otherwise noted. 14 For a summary of the literature on the parasitic lifestyle of the Legionella family, see Atac Uzel and E. Esin Hames-Kocabas, Legionella Pneumophila: From Environment to Disease (New York: Nova Biomedical Books, 2010), 5–12, 31–32. 15 John G. Barlett, “Legionnaires’ Disease: Overtreated, Underdiagnosed,” Journal of Critical Illness 8, no. 7 (July 1993): 755. 16 Strong evidence supports an isolated case of human transmission in a Portuguese outbreak. See correspondence from Ana M. Correia et al., “Probable Person-to-Person Transmission of Legionnaires’ Disease,” New England Journal of Medicine 374, no. 5 (February 4, 2016): 497–98, and Victor Borges et al., “Legionella Pneumophila Strain Associated with the First Evidence of Person-to-Person Transmission of Legionnaires’ Disease: A Unique Mosaic Genetic Backbone,” Scientific Reports 6, no. 26261 (May 19, 2016): 1–11. 17 The following information about human infection is drawn from Fields et al., “Legionnaires’ Disease,” 508–10; Bartram et al., Legionella, 1–18; Beltz, Emerging Infectious Diseases, 185–90; and my interview with Brian Shelton, president and CEO of PathCon, July 9, 2013. 18 My interview with Lauri Hicks (CDC epidemiologist assigned to Legionella group) and Claressa Lucas (CDC microbiologist in the Legionella laboratory), July 11, 2013. 19 Memorandum to “Director, National Communicable Disease Center,” from “Viral Diseases Branch Epidemiology Program,” subject “Pontiac Fever: An Epidemic of Obscure Etiology in a Health Department,” dated July 31, 1969, from Box 10 of 18, folder: “EPI Aids 1968-68-84 through 1969-69-1 through 24,” RG 442-83-0042, National Archives and Record Administration, Southeast Region. 20 The description of the St. Elizabeth outbreak comes from S. B. Thacker et al., “An Outbreak in 1965 of Severe Respiratory Illness Caused by the Legionnaires’ Disease Bacterium,” Journal of Infectious Diseases 138, no. 4 (October 1978): 512–19; for the Fort Bragg case, see Lieutenant Colonel Worth B. Daniels and Captain H. Arthur Grennan, “Pretibial Fever: An Obscure Disease,” Journal of the American Medical Association 122, no. 6 (June 5, 1943): 361–65; and Hugh Tatlock, “A Rickettsia-like Organism Recovered from Guinea Pigs,” Proceedings of the Society for Experimental Biology and Medicine 57 (October-December 1944): 95–99, unless otherwise noted. 21 These investigations by the CDC are termed “EPI Aids,” and the reports are collected and available for all CDC researchers to use. 22 The strain at Fort Bragg was L. micdadei. See Paul H. Edelstein, “Legionnaires’ Disease: History and Clinical Findings,” in Klaus Heuner and Michele Swanson, eds., Legionella: Molecular Microbiology (Norfolk: Caister Academic Press, 2008), 6. 23 The list is adapted from ASHRAE Guideline 12-2000, “ASHRAE Standard: Minimizing the Risk of Legionellosis Associated with Building Water Systems” (American Society of Heating, Refrigerating and Air Conditioning Engineers, Inc., 2000): 3. In my possession. 24 For Spain, see Edelstein, “Legionnaires’ Disease,” 3; for Veterans Administration, see Adam Smeltz, Luis Fabregas, and Mike Wereschagin, “Legionnaires’ Bacteria in VA Water System Tracked to 1982,” Tribune-Review (Pittsburgh), collected from triblive.com, accessed June 18, 2014; for flower show, see Jeroen W. Den Boer et al., “A Large Outbreak of Legionnaires’ Disease at a Flower Show, the Netherlands, 1999,” Emerging Infectious Diseases 8, no. 1 (January 2002): 37–43; for aquarium, see Jane E. Greig et al., “An Outbreak of Legionnaires’ Disease at the Melbourne Aquarium, April 2000: Investigation and Case-Control Studies,” Medical Journal of Australia 180 (June 7, 2004): 566–72. 25 Stuart Cramer, an engineer at a North Carolina textile mill serviced by a dehumidifying machine, coined the term “air-conditioning” in 1906. See Gail Cooper, Air-Conditioning America: Engineers and the Controlled Environment, 1900–1960 (Baltimore and London: The Johns Hopkins University Press, 1998), 19 and 114 for “Weathermaker.” 26 For history of air-conditioning, see Cooper, Air-Conditioning America; Marsha E. Ackermann, Cool Comfort: America’s Romance with Air-Conditioning (Washington, DC, and London: Smithsonian Institution Press, 2002), and Raymond Arsenault, “The End of the Long Hot Summer: The Air Conditioner and Southern Culture,” Journal of Southern History 50, no. 4 (November 1984): 597–628. 27 Professor Watt as quoted in John Reese, “The Air-Conditioning Revolution,” Saturday Evening Post, July 9, 1960, 97. Professor Watt’s sample size was only twenty-two air-conditioned homes, however. 28 The literature on this discussion is voluminous. A good place to start for an overview is James T. Patterson, Grand Expectations: The United States, 1945–1974 (New York: Oxford University Press, 1996). 29 Indeed, Legionella bacteria in cooling tower aerosols have been detected two miles downwind in certain climatic conditions. See ASHRAE Guidelines 12-2000, in my possession. 30 See Mireia Coscolla, Inaki Comas, and Fernando Gonzalez-Candelas, “Quantifying Nonvertical Inheritance in the Evolution of Legionella Pneumophila,” Molecular Biological Evolution 28, no. 2 (February 2011): 985–1001, and Borges et al., “Legionella Pneumophila Strain Associated with the First Evidence of Person-to-Person Transmission of Legionnaires’ Disease,” 1–11. For a paradigmatic discussion of anthropogenic evolution and human history, see Edmund Russell, Evolutionary History: Using History and Biology to Understand Life on Earth (Cambridge University Press, 2011). 31 See Brian G. Shelton, W. Dana Flanders, and George K. Morris, “Legionnaires’ Disease Outbreaks and Cooling Towers with Amplified Legionella Concentrations,” Current Microbiology 28 (1994): 359–63. 32 Interview with Lauri Hicks, July 11, 2013. 33 The CDC has set a low bar for declaring an outbreak. In its categorization scheme, two or more cases associated with a location over a period of six months meets the definition. Interview with Claressa Lucas, July 11, 2013. 34 Interview with J. Donald Millar, May 22, 2007. 35 The United Kingdom standard is quite high in comparison to US standards. The ideal testing range for Legionella detection ranges from zero to 100 colony-forming units per liter (a significantly lower level of toleration than a milliliter). Levels detected above 1000 cfu/liter call for immediate disinfective action. See Health and Safety Executive, “Legionnaires’ Disease: Technical Guidance: Part 1, The Control of Legionella Bacteria in Evaporative Cooling Systems,” Table 1.10. Available from www.hse.gov.uk/pubns/books/hsg274.htm; in my possession. 36 Amanda K. Brzozowski, Benjamin J. Silk, Ruth L. Berkelman, Deborah A. Loveys, and Angela M. Caliendo, “Use, Location, and Timeliness of Clinical Microbiology Testing in Georgia for Select Infectious Diseases,” Journal of Public Health Management Practice 18, no. 4 (2012): E4–E10. 37 For the Ohio Study, see Barbara J. Marston et al., “Incidence of Community-Acquired Pneumonia Requiring Hospitalization,” Archives of Internal Medicine 157 (August 11/25, 1997): 1709–18; for CDC programs, see interview with Lauri Hicks, July 11, 2013. 38 Abby Goodnough, “Flint Outbreak Was Treated with Silence,” New York Times, February 23, 2016, available at www.nytimes.com. 39 For CDC data, see Lauri A. Hicks, Laurel E. Garrison, George E. Nelson, and Lee M. Hampton, “Legionellosis: United States, 2000–2009,” Morbidity and Mortality Weekly Report 60, no. 32 (August 19, 2011): 1083–86; and Karen Neil and Ruth Berkelman, “Increasing Incidence of Legionellosis in the United States, 1990–2005: Changing Epidemiologic Trends,” Clinical Infectious Diseases 47 (September 1, 2008): 594. 40 For association with increases in Legionella growth in warmer, wetter weather, see David N Fisman et al., “It’s Not the Heat, It’s the Humidity: Wet Weather Increases Legionellosis Risk in the Greater Philadelphia Metropolitan Area,” Journal of Infectious Diseases 192 (December 15, 2005): 2066–73, which reported a 2.5-fold increase in cases during wet and warm summers; for drought not affecting legionellosis, see Neil and Berkelman, “Increasing Incidence of Legionellosis,” 595, which reported that case reports increased in the South Atlantic states of the United States despite the 2006 drought in the region. 41 Fisman et al., “It’s Not the Heat,” 2066. © The Author(s) 2018. Published by Oxford University Press on behalf of the American Society for Environmental History and the Forest History Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Environmental History Oxford University Press

Legionnaires’ Disease: Building a Better World for You

Environmental History , Volume Advance Article (3) – May 17, 2018

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Abstract

Abstract The emergent or newly reemerging disease model often relies on poverty as a contributing factor in the transmission of infectious diseases. But as Andrew Price-Smith has argued, affluence can also be a factor in the enhanced transmission of infection. Legionnaires’ disease, first identified in 1976 as the cause of a novel disease outbreak in Philadelphia, fits the model of such a disease of affluence. The Legionella bacteria readily finds niches in the equipment and systems of the modern-built environment designed to deliver and store fresh water for the comfort of its inhabitants. Ubiquitous in freshwater sources around the world, the built environment constitutes a “better” world for Legionella population increase and is likely to facilitate expanding outbreaks of Legionnaires’ disease. INTRODUCTION At the height of the summer of 2015, New York City public health officials announced that a respiratory illness had struck more than thirty citizens of the South Bronx, killing two of them.1 Health officials declared they were currently seeking the origin or origins of this ailment and gathering evidence about the scale and scope of the outbreak. The report predictably set off a feverish media response that tallied up the number of stricken and killed, closely tracked the investigation of the source or sources of the illness, and asked pointed questions about how the outbreak was allowed to occur and what health officials were doing to protect the public.2 In similar fashion the public fretted over their potential exposure and besieged their elected officials to ensure steps were taken both to end the current outbreak and prevent future reoccurrences. Although unfolding in the summer of 2015, in many respects the incident was an eerie echo of events that happened in another large northeastern American city just less then forty years previously. During the week of July 21–24, 1976, nearly five thousand Pennsylvania State American Legionnaires, family, and friends descended on the city of Philadelphia for their annual conference. The conventions combined a little business, the election of state officers and delegates, and a lot of fun; the Legion was notorious for its raucous meetings. The traditional reverie was further enhanced by the US bicentennial celebration. Unbeknownst to the conference attendees, however, was that the headquarters hotel (the venerable Bellevue Stratford) would soon serve as the epicenter of an explosive outbreak of a previously unknown illness. The affliction, dubbed Legionnaires’ disease in commemoration of its 29 unlucky fatal victims and their 153 stricken colleagues, struck suddenly and left the attending physicians mystified about its cause. The ensuing epidemiological investigation directed by personnel from the Centers for Disease Control and Prevention (CDC) would be conducted under harsh public scrutiny and amid dark conspiracy theories. As the weeks ticked by without a solution, the pressures on the CDC increased. Health officials could not explain what caused the outbreak, where it had come from, and whether it would appear again. Critics charged the investigators with being incompetent, malfeasant, or worse. Ultimately, in a research triumph, Joseph McDade and Charles Shepard, a pair of CDC scientists, identified the culprit that was a previously unknown genus of bacteria they named Legionella.3 In addition to determining that the organism was responsible for the Philadelphia outbreak, McDade and Shepard were also able to trace the bacteria to two previously unsolved disease outbreaks. Using samples stored at the CDC, the scientists demonstrated that in 1965, Legionella had sickened eighty-one patients at St. Elizabeth’s Hospital in Washington, D.C., ultimately killing fourteen before the outbreak ended as suddenly as it began. In 1968 a large outbreak of a respiratory ailment among employees, patients, and visitors at the Oakland County Public Health Department in Pontiac, Michigan, was also identified as Legionella. In the years since McDade and Shepard’s breakthrough, it has been determined that the organism is a ubiquitous inhabitant of the environment that comprises more than fifty species and seventy distinct serogroups described with more being discovered virtually every year. The bacterium has been recovered from standing and running freshwater courses, soil, and even from rainwater puddles.4 If one looks for it, one can find it. But although the bacteria can be easily recovered from samples around the world, it is the human-built environment that has provided an especially beneficial niche for the Legionella genus of bacteria. The transition of human occupation patterns to the built environment is not a new phenomenon. Indeed, the shift from nomadic to settled population is the story of human civilization, and we all are the inheritors of this transformational process. The farming communities and trading centers gave rise to towns and later cities increasing population size and density as well as being linked to other urban centers. As has been amply documented, both population growth and urbanization rates have expanded in the late twentieth and early twenty-first centuries.5 Increasingly, the global human population has become an urban creature inhabiting the built environment. And an expanding number of these urbanites are living and working in temperature-controlled environments. Changing human living patterns has also engendered changing relationships with the environment that oftentimes has an impact on human health. The transition from hunter-gatherer to farming lifestyle ultimately generated zoonotic transfers of animal pathogens to human diseases and the emergence of crowd diseases. The interconnection of population centers on the Eurasian and African continents created a large shared disease pool that became a global entity with the bridging of regions by the European empires. The scope and scale of transportation technological advances further tightened these global connections.6 Each changed relationship with the wider environment has presented new challenges for human health.7 The current transition to the temperature-controlled built environment is no different. In the case of Legionnaires’ disease, the built environment has created conditions supremely suited for the bacteria’s flourishing. Modern human habitations include a number of systems that transport and store fresh water for the purposes of drinking, bathing, cooling, soothing, and moisturizing the world they inhabit. In addition to creating a more comfortable and clean living arrangement, these conveniences have also brought larger human populations into ever-closer contact with the Legionella organism. This combination of events has prompted sickness and death from Legionnaires’ disease among untold numbers of people globally. The Legionella family of bacteria, and the disease it prompts, is generally grouped in the category of “emergent diseases” that are new, newly discovered, or resurgent organisms that are causing illness. Implicit in this definition is that these disease-causing entities, either because they are new or new to this population, represent a threat of epidemic or pandemic spread. The concept of emerging diseases, famously promoted by Stephen Morse and Joshua Lederberg, was the subject of an influential Institute of Medicine report in 1992.8 The report sought to document the relationship between human populations and potential disease-causing agents. Rather than marking the dawn of a postinfectious disease age (as some public health theorists hoped), the late twentieth century created conditions ripe for global spread of both novel and resurgent infectious entities. The combination of expanded encroachment of human populations into previously inaccessible areas; constantly evolving viral, bacterial, and parasitic organisms; and changing living patterns and social and cultural norms, tied together with accelerating transportation linkages and booming global trade, allowed previously local, controlled, or new disease-causing organisms to become global health threats. The discussion of emergent microbial threats has frequently carried with it notions that impoverished circumstances underlay these new ailments. A typical example cites the conditions of the desperate slums that surround the fast-growing megacities of the world. These urban areas have served as magnets for migrants from rural areas, crowded together in neighborhoods that have outstripped the capacity for basic water, sewerage, and sanitation infrastructure and linked to a wider world by high-speed jet, train, or highway travel. Such a tacit assumption of the links between poverty and disease obscures the fact that new or newly modified health threats can arise in conditions other than deprivation. For example, Andrew Price-Smith referred to certain new diseases as examples of a phenomenon he dubbed “plagues of affluence.”9 Although the term affluence is mildly imprecise (what exactly marks a society as affluent?), Legionnaires’ disease does fit the organizing principle as proposed by Price-Smith. The built environment has generated a series of niches that allows Legionella to multiply, and these mushrooming populations have been brought in very close contact with human populations. The outcome has been a series of increased, and apparently increasing, number of Legionnaires’ disease outbreaks. The constructed world that now surrounds the majority of the human population constitutes an environment that the Legionella family of bacteria finds quite to its liking. Underpinning both the concepts of emergent disease and plagues of affluence is the idea that human-induced changes have altered the environmental balance of the system. These new plagues, then, are a consequence of ecological change. Some writers have posited that these human-wrought changes are of such magnitude that they constitute a new era in earth’s history that they have dubbed the Anthropocene epoch. Most clearly manifested in the greatly accelerated rate of species extinction, according to this model the surging human population and its consumption patterns are altering the ecosystem planet-wide.10 While the paradigm that human-induced ecological changes constitutes a new epoch in the planet’s life span may be a matter of academic debate—when to date the epoch’s onset; how to measure the scale of humankind’s impact; and even if recent ecological changes truly represent a new epoch—examining the changes set in motion by human activity is not a recent academic innovation. Identifying the unintended effects of human decision making and actions has long been a staple in historical research, especially in the field of environmental history where it is sometimes referred to as the law of unintended consequences. Examples of this type include the effects of exterminating keystone species as nuisances in an environment, the role of fashion choices on fur and feather-bearing species, or the impact of introducing novel species to parasitize pests or other functions. Similar inadvertent outcomes are described in examining diseases in human history whereby changes in living patterns facilitated the embedding of malarial parasites in a population, the Atlantic slave trade’s role in delivering yellow fever to the Americas, or the role of trade routes in the dissemination of plague during the Black Death.11 Legionnaires’ disease fits easily into this paradigm. In general, discussion of disease impact in human history has often revolved around the introduction of infections to new regions, a wider environment for the infectious agent. But the case of Legionnaires’ disease (or legionellosis) is a little more unusual in that the modern-built environment constitutes a “better” or more ideal environment for Legionella to flourish. If we limit our definition of better to species reproductive success and demographic increase, human-wrought changes have created a number of winners and losers. Some of these winners were purposefully selected by humans—the number of cattle on the planet dwarfs the number of wild auroch populations that could be sustained while others have been quite accidental—the rise of the city in history has led inadvertently to the rise of the rat. Viewing it from the angle of increased numbers, Legionella would be in the rat category of success. For while the organism can generally be found in a variety of environments around the globe, only rarely is it found in highly dense concentrations.12 The overall effect of the human-caused changes has been to take a ubiquitous organism in which the circumstances for causing human illness only rarely aligned, and turn it into an organism that is frequently brought into human contact in an environment that favors colony formation and rapid growth. Human infection is far more likely when there is dense concentration of the organism and it is delivered in a way optimum for inhalation. Even though the organism can be found in the wider environment and has been found to cause illness, Legionnaires’ disease is more an example of a human-built threat to health then the consequence of a natural infection. An expanding number of humans work and live in units with mechanically controlled temperatures. This occupation pattern represents a novel living arrangement for the human species. These climate-controlled systems represent a changed interaction with the natural world and encompass new niches for micro- and macroscopic entities to inhabit. This intersection constitutes the latest chapter in the human story. THE ORGANISM AND INFECTION Legionella are intracellular parasites of freshwater protozoa and amoeba found in a variety of freshwater sources around the world.13Legionella induce these organisms to draw the bacteria inside where they utilize the nutrients of the amoeba and protozoa to replicate. As the bacteria begin to deplete the resources of their hosts, they are released into the aquatic environment, in some cases as a vesicle teeming with bacteria and enclosed by a membrane.14 The Legionella family was detected in 40 percent of random water samples by culturing and in more than 80 percent of samples measured by genetic recovery methods (polymerase chain reaction [PCR]). Since Legionella are comparatively difficult to culture, the PCR method of detection is a surer measure that the bacteria is, or has recently been, present in the water sample. The organism is acid tolerant and can be found in water temperatures ranging from 25 to 60°C (77–150.8 °F), but they are destroyed almost instantly when the temperature ranges above 70°C (158 °F). Their optimal growth range is from 35 to 45°C (95–113 °F), which has important implications for conditions created by modern human settlement components. Provided with single-cell organisms to invade and replicate in, nutrients to feed the growth of these organisms, and water with the right temperature ranges, Legionella are usually present. If the conditions are perfect, ideally with water temperatures in that magic 35 to 45°C (95–113 °F) band, Legionella will proliferate; or as the epidemiologists prefer to call it, amplify. Although there are more than fifty species of Legionella with at least seventy serogroup types, close to 90 percent of all human infections are associated with the type first discovered at the Bellevue Stratford in Philadelphia (although it should be noted that this percentage may be artificially inflated since most medical tests for Legionella are designed to detect this particular species of the genus). Since first characterized, Legionnaires’ disease outbreaks have been detected around the globe, and it is certain even more went unidentified. That first strain, named Legionella pneumophila (small [ella] army [legion] of organisms that love [phila] the lung [pneumo]), appears to be the most virulent.15 Legionnaires’ disease rarely, if ever, passes from person to person.16 This general inability to transit from person to person makes legionellosis an environment source infection, meaning a person has to be exposed to the organism in the environment in order to contract the ailment. Typically, Legionella invades the human organism when it is inhaled, although there have been cases of infection contracted from ingesting Legionella-contaminated water and even cases of infection when Legionella-contaminated water was used to irrigate a wound.17 These unusual cases of infection have been limited to hospitals and long-term care facilities where the victims tended to be in an immunocompromised state. The normal route of infection with the bacteria is when a person breathes in Legionella-laden water that has aerosolized from a contaminated source. Aerosolization can occur in many ways, but the most common fashion is through mechanical processes. Droplets in the 1 to 5 micron range are the most dangerous because these are the type that can be inhaled most deeply into the lungs. When this event occurs, there is a chance the individual will contract the disease, but infection is not certain. Legionnaires’ disease is dose dependent, meaning the greater the dose, the greater the likelihood of infection. When the bacterium becomes lodged in the lungs, it has entered the new harsher environment of the human body and is now subject to the ferocious and effective immune system. The human immune system is supremely adapted to detect and eradicate alien material that enters the body. Special cells identify nonself entities for rapid elimination. The Legionella organism, however, has an ingenious trick to evade the eradication efforts of the human immune system first responders. When the bacterium comes in contact with a phagocyte (commonly called a white blood cell), the bacterium is able to induce the white blood cell to transport it inside the cell rather than be engulfed and destroyed like other foreign matter the patrolling phagocyte encounters. In the interior of the cell it is ensconced in a vacuole that does not come in contact with the powerful enzymes the cell uses to digest alien invaders. Remarkably, once inside the white blood cell, the Legionella bacterium is able to use the cell as it does protozoa and amoebas—it recruits the cell for bacterial replication. In addition to avoiding the body’s natural defense of white blood cells, the bacteria actually weakens the immune protection of the individual. Legionella uses up the resources of the phagocyte causing the death of the cell while simultaneously generating many more copies of itself. This ability not only to circumvent a key component of first-line immune defense, but to use that element of the immune system to replicate, gives the bacterium a leg up on colonizing the human organism. After infection, an incubation period ranging from two to ten days ensues (although classically, the majority of cases manifest themselves four to five days after infection). Initial symptoms are categorized as flulike with a low-grade fever, headache, and fatigue. Intestinal complaints sometimes follow. Subsequently, the infection worsens and the patient spikes a high fever of 40°C (104 °F) with chills, a deep cough (both productive and nonproductive), difficulty breathing, and in the worst cases, delirium and kidney damage. Frequently, the illness deepens and develops into pneumonia. Left untreated, Legionnaires’ disease outbreaks have had mortality rates ranging from 5 to 30 percent of the infected. Fortunately, the bacteria are susceptible to certain categories of antibiotics. The current regime calls for the 4-quinolone group, generally consisting of levofloxacin and moxifloxacin, but azithromycin was also found to be effective.18 If treatment is provided early in the course of infection, the recovery rate is favorable. But survival and recovery rates are subject to a number of factors including the underlying health of the patient. Fortunately, one or more of the effective antibiotics are standard in the broad-spectrum treatment of pneumonia patients. But, as we shall see, this treatment practice serves to obscure the true burden of Legionnaires’ disease in the population and is a hindrance to surveillance efforts to enumerate and track the ailment. Exposure to the bacteria does not guarantee infection. Indeed, the vast majority (generally well above 90 percent) of people who come in contact with Legionella do not contract the illness or the course of infection is so mild that the individual is asymptomatic. There are certain risk factors that have been associated with a greater chance of becoming sick when encountering the bacteria. These factors include cigarette smoking, alcohol abuse, age, and underlying conditions that leave a person in an immunocompromised state. Many nations, especially the more economically developed nations of Eurasia, have populations that have increasing numbers of the elderly whose immune systems are less robust in fending off disease. That said, even healthy people may become sick and die after exposure and as is always the case when dealing with a biological organism, there is quite a bit of unpredictable randomness in determining the outcome. Further muddying the waters in evaluating the impact of Legionella infections is that the same organism responsible for the deadly outbreak in Philadelphia—Legionella pneumophila—can prompt a highly infectious, but not deadly infection known as Pontiac fever. The 1968 outbreak at the Oakland (Michigan) County Health Department (which gave the condition its name) struck 95 of 100 employees, 49 of 170 patients and visitors, and even 7 of 20 CDC investigators. The ailment sickened the victims with acute onset of fever, chills, headache, and malaise, but the course of infection was generally only three or four days, and the symptoms were neither as severe as Legionnaires’ disease nor the outcome as deadly. In fact, every single victim of Pontiac fever recovered with few lasting effects. Tellingly, in this 1968 case, the source of the infection was linked to the air-conditioning unit. Only the CDC investigators who were working on site when the unit was turned on after several days of shutdown were struck by Pontiac fever.19 The agent responsible for this outbreak remained a mystery until the CDC discovery of the bacteria for Legionnaires’ disease that enabled the scientists to test reagents against stored samples from the Pontiac facility. BUILT ENVIRONMENT Legionella inhabit a variety of niches around the globe, and they have likely caused some infection and death for an unknowable amount of time. Indeed, if the conditions are right, the organism can produce outbreaks with a multitude of victims without the congenial conditions of the human-built environment as the following two examples attest.20 In 1965 CDC epidemiologists investigated a mysterious pneumonia outbreak at St. Elizabeth’s Hospital in Washington, D.C.21 A statistical association was detected in which the eighty-one patients stricken with the ailment were likely to have either roamed the grounds or had beds near the window of their rooms. In fact, those who contracted the illness were ten times more likely to have such access to the outside. In their investigation, CDC researchers determined that while the psychiatric hospital had recently undergone excavation to install a new sprinkler system, no causative agent was discovered to account for the outbreak. In 1942 an unidentified agent hospitalized forty men from Fort Bragg with symptoms of high fever, chills, malaise, and headaches. The cases came from a cluster of base housing located in a remote corner of the camp with a small stream that flowed behind the barracks. Despite an exhaustive investigation, no culprit for the illnesses was detected. Both cases remained unsolved until stored samples were tested against Legionella reagents. In retrospect, it appears that the Fort Bragg cases were generated by Legionella that had aerosolized from the running stream and that the excavation at St. Elizabeth’s had stirred up dust particles laden with Legionella that the victims had inhaled. Although not the usual place the bacteria can be found, Legionella can occasionally be cultured from the soil.22 Both cases suggest that outbreaks of Legionnaires’ disease can occur without mechanical stimulus. While these examples suggest that Legionella outbreaks occur without the assistance of the built environment, it is the conditions created by the modern world that have truly turned this organism into a serious human health threat. A dizzying array of modern conveniences have been linked with Legionella outbreaks including cooling towers, evaporative condensers, steam turbines, showers, hot tubs, humidifiers, decorative fountains, and even a grocery store produce mister.23 In hospitals, where the patients are particularly vulnerable, infections have been detected through the usual cooling and water and shower mechanisms, but also through aspirators, lavages, and even drinking water. The bacterium has also demonstrated unusual persistence. For example, a Spanish hotel intermittently infected British tourists for over seven years (1973–80) before it was detected. In an outbreak at the Veterans Affairs Hospital in Oakland (Pittsburgh, Pennsylvania), a strain that killed five patients in 2013 was a genetic descendant of a strain first identified in the facility in 1982. In addition, the bacteria have shown the ability to infect a multitude of people in one site. In 1999 a Jacuzzi on display at a Dutch flower show harbored the bacteria and exposed 188 attendees to the disease, and in Melbourne, Australia, 125 visitors to the aquarium were infected from the air-conditioning unit.24 The common element in all these cases is that the human-built environment allowed Legionella bacteria to thrive and survive. The key element in devices linked to Legionnaires’ disease outbreaks is water, and in the twentieth century water was an essential component of new technologies to cool, and to a lesser degree, heat the indoor environment. In the early decades of the twentieth century, engineers and technicians had formulated systems to generate the self-proclaimed optimal conditions for comfortable working and living indoors. It is telling that the early pioneers in “air-conditioning” expressed their desire to “control the weather.” Indeed, the Carrier Corporation called their unit designed for the residential market the “Weathermaker.”25 Although various formulas were used to supercool the air—ammonia, carbon dioxide, and ultimately Freon—water was a ubiquitous component of the process. Sometimes water came in the form of condensation from the cooling and humidity control aspects of the units; in larger units the water facilitated heat transfer that allowed the cooling process to work most effectively. Initially focusing on creating desired humidity levels for certain factory products such as textiles or food manufacturing, air-conditioning manufacturers soon promoted the benefits of increased productivity of workers in factories and office buildings from controlled temperatures and humidity. Air-conditioning was heralded as the wave of the future maintaining productivity, cleanliness, beneficial health, and good-humor.26 Productivity was not limited to merely the factory floor according to a Saturday Evening Post story. In referring to one of the effects of the energy-hungry air-conditioning system, the aptly named Professor Watt observed that his studies recorded that “the rate of pregnancy in the air-conditioned houses showed a significant increase above that in the non air-conditioned.”27 By the end of World War II, the advocates who touted the benefits of climate control had won out over the fresh-air crowd. In line with other postwar ideas of human mastery of the environment, air-conditioning manufacturing and installation boomed in postwar America, soon to be exported with other American cultural ideals.28 While the proponents of controlled environments were certain of its superiority, the changing living conditions altered the relationship between humans and their environments—many times in unexpected and unforeseen ways. For example, the built environment creates conditions that are extraordinarily well suited to the flourishing and propagation of bacteria. Cooling towers, as was the likely culprit at the Bellevue Stratford in Philadelphia and in the 2015 Bronx cases, serve as watery heat exchangers that operate at temperatures ideally suited for Legionella growth. The normal functioning of the unit—heated water from the building is sprayed across a system of pipes and veins that cool the water through evaporation and that cooled water is collected at the bottom while heated water vapor is vented out through fans—serves to broadcast Legionella-contaminated droplets into the wider environment. Such a system is tailormade for Legionella amplification. The water temperature in the exchanger is generally in the 29 to 35°C (85–95 °F) range, openings to the outside environment allow dust and debris to enter and provide nutrients for the growth of single-cell organisms in which the bacteria replicate, and the water is circulated (figure 1). Combined with the aerosol properties of the water spraying and the fan blowing, it is no surprise that cooling towers have been repeatedly linked with legionellosis.29 Figure 1. View largeDownload slide Drawing number one from “injector type indirect evaporative condensers,” patent number 3800553 by John Engalitcheff Jr. Source: US Patent and Trademark Office. Figure 1. View largeDownload slide Drawing number one from “injector type indirect evaporative condensers,” patent number 3800553 by John Engalitcheff Jr. Source: US Patent and Trademark Office. The dangers of these systems for the transmission of Legionella are heightened when a structure that has been dormant for a period of time—as in the winter months—is switched on without proper disinfection. The Legionella bacterium, which has had a period of time to colonize in the stagnant water, is then aerosolized when the infrequently used source is put into service. So, for example, a showerhead that has been idled for a period of time will suddenly emit a dense concentration of bacteria when put into use. The stagnation period allows the protozoa and amoebas that Legionella parasitize to form a biofilm or slime layer on the surface of pipes and equipment. Poorly maintained or ineffectively disinfected systems make it more likely that the bacteria will flourish. But even well-maintained water systems may harbor Legionella bacteria. The organism is moderately tolerant of chlorine and other disinfectants, so it is likely that some members of the bacteria’s family will survive the standard municipal water treatment processes. Indeed, it is most likely from municipal water systems that the bacteria are introduced into building water pipes. Even the most diligent maintenance and sanitation schedule will not prevent the introduction of Legionella. PREVENTION AND SURVEILLANCE From the account just described, the question naturally arises of how people can protect themselves and the public from the threat of Legionnaires’ disease. The simple answer is through prevention and surveillance. But of course to achieve these goals is not so simple. Prevention would seem to be a straightforward proposition. If Legionella replicate in water systems, then ensuring that the water systems are disinfected should destroy the organism. And in theory, that notion is true. However, in practice, building systems and their pipes tend to be a complex maze of linkages, especially in older buildings that have been remodeled and changed over the years. Therefore, it is difficult to ensure that every link receives the proper quantity of disinfecting chemical (such as chlorine) or that every stretch of pipe reaches above 70°C (158 °F) when superheating the system to kill Legionella (a common emergency health response to building outbreaks). And even if eradicating the bacteria in the system is successful, there is no guarantee that the structure is permanently protected. Potable water that meets every quality standard still may have Legionella bacteria, and systems that are open to the environment (like cooling systems) can never prevent bacteria from drifting into the process. If the disinfection regime relaxes or fails at any point, Legionella can recolonize the network. Another problem in controlling Legionella is related to evolution. Altering the environment through chemical measures or other technologies applies natural selection pressures on the genome of the bacteria. Over time this selection pressure will select for organisms with increased tolerance to disinfectants or higher temperatures. More worrisome is that new genetic testing technology has revealed that the Legionella family actively engages in horizontal gene transfer of genetic material. Horizontal gene transfer, or recombination events, allows the exchange of portions of genetic code both within and between species. The ability to transfer genetic packages (plasmids) that facilitate enhanced survival and replication in different environments has been associated with the rapid development of antibiotic resistance across a variety of bacterial species. In the case of Legionella, the bio-slime layers that the organism thrives in constitute an excellent environment in which a multitude of bacterial species are brought into close proximity, potentially facilitating the transfer of genetic information.30 Since a 100 percent prevention of Legionella from entering the system is impossible, perhaps the answer lays in attacking the larger organisms that the bacteria needs to reproduce. A diligent schedule of cleaning, descaling, and disinfecting equipment can remove the buildup of organisms that facilitate bacterial growth. But even the most faithful maintenance program faces a daunting challenge. Wear and tear on machinery creates a more difficult surface area to clean, and even tactics that appear to be protective can inadvertently create conditions that favor organic growth. For example, hyperchlorination kills bacteria and other organisms. However, prolonged chlorine use actually corrodes and degrades the equipment and pipes creating niches and crevasses that can serve to shield the organism from the disinfecting chemicals and processes. Biofilms and slimes are many layers deep, and the outside layer exposed to the disinfecting substance can protect the organisms beneath, allowing for the persistence of the single-celled creatures and bacteria. If we cannot keep Legionella completely out of our system, nor can we ensure that the amoebas and protozoa the bacteria needs to replicate are excluded, perhaps we can keep the organism at a level that does not represent a risk of disease. Here lies the third challenge to the prevention effort. What exactly is that acceptable level? This topic has engendered much debate but no consensus. Legionella are generally measured as the number of colony-forming units per milliliter of water (cfu/ml). In the natural environment such as streams and ponds, the bacteria are measured at 1 cfu/ml. In the favorable conditions of the built environment, however, Legionella counts can get many thousands of times higher, even above 10,000 cfu/ml.31 It would seem, then, that taking aggressive action above a certain Legionella concentration point would mitigate the risk of infection. This approach is the one recommended by some epidemiologists and microbiologists. It is not, however, the one endorsed by the CDC. According to Lauri Hicks, epidemiologist assigned to Legionella outbreak investigations by the CDC, the problem with this idea of a threshold is that there is too much variation in bacterial strains to assess the risk of Legionella concentrations adequately. To begin with, the method of enumerating bacterial counts per milliliter is a difficult laboratory technique, so counts conducted by commercial laboratories may be unreliable. In addition, there are many examples where it was determined that the Legionella had indeed concentrated in great number, yet there was no disease. Conversely, systems with low levels of bacteria have recorded disease. As Hicks states it, “Actually, what’s more important [than concentration of bacteria] are the types of Legionella in the environment.”32 CDC officials fear that thresholds induce complacency with Legionella contamination. Rather than prospectively testing potential exposure sites and mechanisms, the CDC recommends regular maintenance and disinfection with testing and mitigation responses only undertaken after an outbreak has been confirmed.33 The waiting for an outbreak model is seen by some CDC critics as a backward approach to public health. J. Donald Millar, former director of the National Institute for Occupational Safety and Health, and a longtime administrator of public health, argued that this process puts the health of citizens at risk since people have to be sickened before an investigation or mitigation efforts ensue. Millar favored a “hazard analysis” approach in which potential Legionella infection sites are periodically tested and measured. Sites with high levels of colony-forming units per milliliter or ones where Legionella concentrations are rapidly escalating (or “blooming” in the terminology) are immediately treated to lower or eradicate the number of Legionella present. Although acknowledging such a testing system is an imprecise tool, it does have at its heart a plan to protect citizens from infections proactively.34 This preventive monitoring approach is also the method pursued by the European Working Group for Legionella Infections (EWGLI) as well as several Asian and Pacific states (Australia and Singapore among them).35 Surveillance is another aspect of Legionnaires’ disease that is fraught with controversy. The problem is that there is very little active surveillance for Legionella in the United States. Legionnaires’ disease is a reportable disease, meaning that when physicians detect a case of the illness, they are required to report this information to the local health department that ultimately reports that information to the CDC. These reports enable the organization to track outbreaks and to gather an estimate of disease activity. But this is a type of passive reporting that places the entire onus on the physician to identify and report the Legionella infection. Physicians generally encounter a patient with Legionnaires’ disease when they present with pneumonia, and pneumonia is a fairly common component of hospital caseloads. Unfortunately, only a small percentage of pneumonia cases are tested for Legionella, primarily because the standard broad-spectrum antibiotic course prescribed for pneumonia cases generally includes antibiotics that are used to treat Legionella. Physicians adopt a practical approach, thinking if the treatment is working, who cares what caused the illness? It is not as if the doctors need to do additional paperwork. The answer, of course, is that public health officials care because if a patient can be linked to a specific place or time when he or she was infected, steps can be taken to prevent others from being exposed and possibly sickened as well. There is also a more prosaic reason for the reluctance of physicians to test for Legionella in their patients, and it has to do with money. Hospitals, like any other business, are entities that can be acquired by others or are subject to the market demands of competition. The late twentieth and early twenty-first centuries were marked by a wave of consolidations and mergers in the hospital sector. Administrators sought to maximize efficiencies and cut costs either in the wake of a merger or as an attempt to make the hospital leaner and more competitive. One area frequently targeted for budgeting cutbacks was the in-house microbiology laboratories. It was deemed cheaper to send these samples out to commercial labs rather than maintain one inside the hospital. These decisions have a cost, and that cost is measured in time. Sending out samples to be tested results in a longer turnaround time to identify the results of the screening. For example, a large-scale study of sixty-two laboratories in Georgia that conducted Legionella identification tests revealed there was a median reporting time of three days in outside commercial labs. Hospitals that still had an in-house microbiology lab reported a median time of three-quarters of a day to report results.36 No physician would wait three days to begin treatment for a pneumonia case, especially since those hospitalized with Legionella-induced pneumonia tend to be very sick. In the United States, there are an estimated 8,000 to 18,000 reported cases of Legionella-caused pneumonia in which the person needs to be hospitalized each year. But few epidemiologists have much confidence in that estimate drawn from a single 1991 study of community-acquired pneumonia cases in two Ohio counties. Recognizing the paucity of surveillance data on the incidence of legionellosis, the CDC has recently embarked on a trial system of more proactive Legionella data collection. These new approaches are still in the preliminary phases at the present time.37 The accuracy of surveillance in the United States is problematic. To a certain degree this is a function of the structure of public health in the United States that places great authority for its practice in the hands of state and local health departments. In fact, technically the CDC has to be invited in to do an epidemiological investigation within any state. Without that request, the CDC has no legal authority for action in individual states. The limitations of this approach were exemplified in events in Flint, Michigan, in 2014–16. In the late winter of 2016, it was reported that the switch to municipal water from the Flint River may be associated with a Legionnaires’ outbreak as well as lead poisoning in the city of Flint. Flint’s home county of Genesee reported eighty-seven people as possible Legionnaires’ cases in the period of June 2014 through October 2015. Despite county health officials’ requests to the Michigan Department of Health and Human Services, the state health officials did not formally request CDC assistance until January 2016.38 By all accounts the more centralized European EWGLI group does a more effective surveillance job than the United States. The same can be said for Australia. The larger problem for assessing legionellosis is not the relative effectiveness of various systems, however; it is that the vast majority of states in the world conduct no or little Legionella detection at all. Therefore it is not possible to even hazard a guess as to the global burden of Legionnaires’ disease. Even absent a formal accounting of the prevalence of legionellosis, there are indications that the number of Legionella infections are on the rise. The CDC announced that the quantity of Legionnaires’ disease cases reported to public health services in the United States between 2000 and 2009 increased 217 percent. The CDC declined to speculate whether this increase was due to greater testing and reporting data or represented a real increase in the prevalence of infections. Others, however, were not so reticent. Ruth Berkelman, former deputy director of the National Center for Infectious Diseases at the CDC, wrote in a 2008 article drawn from the CDC data that she and her coauthor Karen Neil “found no evidence that changes in diagnostic testing were responsible for the increase after 2000” and that there was no evidence that new case reporting procedures were responsible for the increase either.39 A possible driver for increasing numbers of Legionella cases could be climate change. Average temperature increases provide a more suitable setting for Legionella replication in both the natural and built environments. Regions with increased rainfall and warmer temperatures due to climate change would likely also see an increase in Legionella propagation. Theoretically, these gains, driven by warmer, wetter weather, should be counterbalanced by regions that are more drought prone due to climate change. There are indications, however, that drought conditions do not have a strong dampening effect on Legionnaires’ disease cases.40 Like many predictions based on the impact of climate change, these projections can only be tentative. CONCLUSION Legionnaires’ disease is an undercounted, underestimated, and underappreciated global threat to human health. If there is no clear consensus on how many cases there are, or whether the number of cases is increasing, it is generally agreed that the number of people stricken by the infection each year is significantly higher than reported. It seems likely that the number of people exposed to Legionella will increase, partly as a factor of increasing urbanization rates, partly due to greater access to climate control and water distribution systems tied with a global rise in standards of living, and perhaps as a result of a warming planet. We can also posit that the number of those who succumb to Legionnaires’ disease will increase as well. In addition to increased numbers of people who are able to survive in an immunocompromised state due to medical advances, the number and percentage of the elderly population continues to increase in a number of nations. Legionella-induced pneumonia taxes even the most sophisticated health systems requiring access to powerful antibiotic treatments and to the ministrations of intensive care units. Despite these services, somewhere between 10 and 20 percent of people hospitalized with Legionnaires’ disease will die.41 It is almost certain that the mortality rate in places without these amenities is higher. In some ways, the Legionella story is of a standard type of environmental and disease narrative. As the development of farming lifestyles led to settled populations that fed increasing concentrations of mosquitoes ensuring the continued transmission of malaria, or the development of speedy ships and trains allowed cholera-stricken patients to reach further destinations ultimately serving to create the pandemic waves of cholera in the nineteenth and twentieth centuries, so too did technologies to cool the air facilitate conditions ripe for explosive growth of Legionella. Legionellosis is just another example of the law of unintended consequences impacting human health. But in some fashion the Legionella example is unusual. In many ways the modern-built environment constitutes a better world for the organism and not just a wider world. Safely ensconced in its warm bath, the bacteria remain inured to dramatic temperature changes and perhaps could even benefit as rising temperatures from a warming planet elevate the clime of its watery home. With its trusty single-celled organisms sharing its shelter, the bacteria can go on happily multiplying. If harsh disinfecting chemicals disturb its Eden or its vital biofilms and slimes are swept away by diligent cleaning, it is certain that another of its kind will drift in and renew the colonization of this bacterial paradise. Further, an increasing percentage of people are living and working exclusively in climate-controlled environments. Those water systems that constitute a vital part of environment control represent a large new niche for watery microbiota. When examining the historical trajectory of threats to public health, there is often a tendency to look for lessons to take from the research that will apply to other cases. An obvious conclusion to take from this overview of legionellosis is that we need to know a whole lot more about this organism. Many basic questions about the bacteria—how prevalent is Legionella; how many cases of Legionnaires’ disease does it cause each year; are the infections increasing, decreasing, or steady; what is its geographic reach among them—remain unknown or incomplete. In short, a lot more surveillance and epidemiological work needs to be done on the local, national, and global level. To some extent, getting this information is more pressing than medical advances to treat the disease. While it is important to save those who Legionella has infected, ultimately it is more useful to prevent those infections in the first place. Legionella and the niches it inhabits are micro versions of a larger and accelerating process of human-wrought ecological changes. Whether these changes constitute a new epoch in the earth’s history is a matter of some debate. But we can state confidently that human history is marked by the propensity to alter the environment to suit its needs. Human action, whether planned or inadvertent, has rippled through its ecological surroundings. The built environment constitutes a continuation of this human pattern both destroying some ecological niches and generating a number of new and changed ones. If our gaze is drawn (and rightfully so) to large-scale ecological changes such as deforestation and climate change, we should not overlook the changing world at the micro level. Building a “better” world for human populations may inadvertently build a “better” world for something else as well. George Dehner is an associate professor in the Department of History at Wichita State University where he teaches courses in world, environmental, and USS history. He is the author of Influenza: A Century of Science and Public Health Response (University of Pittsburgh Press, 2012) and Global Flu and You: A History of Influenza (Reaktion Press, 2012). Footnotes I would like to gratefully acknowledge the assistance of Guy Hall and the staff at the National Archives and Records Administration, Southeast Region, Mary Hilpertshauser at the David J. Sencer CDC Museum, the staff at the Stephen B. Thacker CDC Library, the interlibrary staff at Ablah Library, Wichita State University, for archival and library material, and Nan Myers’s aid in tracking down the patent image used; Ruth Berkelman, Lauri Hicks, Claressa Lucas, Brian Shelton, and the late J. Donald Millar for making themselves available for interviews; the panel and audience at the “Intersections of Human Disease and Environment” at the 23rd Annual World History Conference, Costa Rica, for their questions and comments; and Day Radebaugh and the students in the Honors “Epidemics and World History Course” (Fall 2016 and Fall 2017 Wichita State University) for their comments on a draft of this article. I appreciate the funding of an Award for Research/Creative Projects in Summer (2013) from Wichita State University that supported a research trip to Atlanta. I would also like to acknowledge the editorial comments from Lisa M. Brady and two anonymous referees at Environmental History who substantially helped sharpen the manuscript and editor Brady’s assistance in uploading the image used in this article. Omissions and errors remain mine alone. 1 The following account is drawn from New York Times coverage from July 30, 2015, to August 28, 2015, available at www.nytimes.com unless otherwise noted. The public health announcement is from Winnie Hu, “Legionnaires’ Disease Kills 2 in the Bronx,” July 30, 2015, from nytimes.com. 2 Ultimately reported as claiming 12 lives and sickening an additional 120 more. Winnie Hu, “Legionnaires’ Outbreak Over, Officials Say,” August 21, 2015, www.nytimes.com. 3 This information is drawn from David Fraser et al., “Legionnaires’ Disease: Description of an Epidemic of Pneumonia,” New England Journal of Medicine 297, no. 22 (December 1, 1977): 1189–97; Joseph McDade, Charles Shepard, David Fraser, Theodore R. Tsai, Martha A. Redus, Walter R. Dowdle, and the Laboratory Investigation Team, “Legionnaires’ Disease: Isolation of a Bacterium and Demonstration of Its Role in Other Respiratory Disease,” New England Journal of Medicine 297, no. 22 (December 1, 1977): 1197–1203; and Barry S. Fields, Robert F. Benson, and Richard E. Besser, “Legionella and Legionnaires’ Disease: 25 Years of Investigation,” Clinical Microbiology Reviews 15, no. 3 (July 2002): 506. 4 For connection to 1965 (St. Elizabeth) and 1968 (Pontiac) outbreaks, see Fraser et al., “Legionnaires’ Disease,” 1196; McDade et al., “Legionnaires’ Disease,” 1201; and David W. Fraser and Joseph E. McDade, “Legionellosis,” Scientific American 241, no. 4 (October 1979): 88. For numbers of Legionella species and serotypes, see Jamie Bartram, Yves Chartier, John V. Lee, Kathy Pond, and Susanne Surman-Lee, eds., Legionella and the Prevention of Legionellosis (Geneva: World Health Organization, 2007), 19. For locations of recovered Legionella bacteria in the natural environment, see E. van Heijnsbergen et al., “Viable Legionella Pneumophila Bacteria in Natural Soil and Rainwater Puddles,” Journal of Applied Microbiology 117, no. 3 (September 2014): 882–90. 5 According to the United Nations, the global population as of mid-2015 stood at 7.3 billion people. See “World Population Prospects: Volume I: Comprehensive Tables (2015 Revision),” https://esa.un.org/unpd/wpp/Publications/Files/WPP2015_Volume-I_Comprehensive-Tables.pdf. A total of 54 percent of the population resides in urban areas as of 2014 with the urbanization rate increasing. See “World Urbanization Prospects [Highlights],” https://esa.un.org/unpd/wup/Publications/Files/WUP2014-Highlights.pdf. Both reports accessed June 8, 2017. 6 Classic works that tell these tales include Jared Diamond, Guns, Germs, and Steel: The Fates of Human Societies (New York: Norton, 1997); William H. McNeill, Plagues and Peoples (New York: Anchor Books Doubleday, 1976); Alfred W. Crosby, The Columbian Exchange: Biological and Cultural Consequences of 1492 (Westport: Greenwood Press, 1972); and J. N. Hays, The Burdens of Disease: Epidemics and Human Response in Western History (New Brunswick: Rutgers University Press, 2000). 7 For a collection of essays that seek to bring together the once separate histories of health and environment, see Gregg Mitman, Michelle Murphy, and Christopher Sellers, eds., Landscape of Exposure: Knowledge and Illness in Modern Environments, in Osiris, Vol. 19 (Chicago: University of Chicago Press, 2004). 8 See Institute of Medicine, Emerging Infections: Microbial Threats to Health in the United States (Washington, DC: National Academies, 1992); Stephen S. Morse, ed., Emerging Viruses (New York: Oxford University Press, 1993); and Stephen S. Morse, The Evolutionary Biology of Viruses (New York: Raven, 1994). 9 Andrew Price Smith, “The Plagues of Affluence: Human Ecology and the Case of the SARS Epidemic,” Environmental History 20, no. 4 (October 2015): 765–78. 10 For an overview of this concept, see Will Steffen, Jacques Grinevald, Paul Crutzen, and John McNeill, “The Anthropocene: Conceptual and Historical Perspectives,” Philosophical Transactions: Mathematical, Physical and Engineering Sciences 369, no. 1938 (March 2011): 842–67. 11 See Thomas Dunlap, “Values for Varmints: Predator Control and Environmental Ideas, 1920–1939,” Pacific Historical Review 53, no. 2 (May 1984): 141–61; Anthony N. Penna, Nature’s Bounty: Historical and Modern Environmental Perspectives (Armonk: M. E. Sharpe, 1999); J. R. McNeill, Something New Under the Sun: An Environmental History of the Twentieth-Century World (New York: Norton, 2000); James L. A. Webb Jr., Humanity’s Burden: A Global History of Malaria (Cambridge: Cambridge University Press, 2009); Philip Curtin, “Epidemiology and the Slave Trade,” Political Science Quarterly 82 (June 2, 1968): 94–110; and John Aberth, The Black Death: The Great Mortality of 1348–1350, A Brief History with Documents, 2nd ed. (Boston: Bedford/St. Martin’s, 2017). 12 Interestingly, one of those occasions is in watercourses and bodies near recently erupted volcanoes. These disturbed environments apparently favor Legionella blooming, particularly near thermal seeps. See, for example, David L. Tison, John A Baross, and Ramon J. Seidler, “Legionella in Aquatic Habitats in the Mount Saint Helens Blast Zone,” Current Microbiology 9 (1983): 345–48, and Douglas Larson, “The Recovery of Spirit Lake,” American Scientist 81, no. 2 (March-April 1993): 166–77. 13 The following description of Legionella is drawn from Bartram et al., Legionella, 29–38; Lisa A. Beltz, Emerging Infectious Diseases: A Guide to Diseases, Causative Agents, and Surveillance (San Francisco: Jossey-Bass, 2011), 186–94; and Fields et al., “Legionella and Legionnaires’ Disease,” 506–17, unless otherwise noted. 14 For a summary of the literature on the parasitic lifestyle of the Legionella family, see Atac Uzel and E. Esin Hames-Kocabas, Legionella Pneumophila: From Environment to Disease (New York: Nova Biomedical Books, 2010), 5–12, 31–32. 15 John G. Barlett, “Legionnaires’ Disease: Overtreated, Underdiagnosed,” Journal of Critical Illness 8, no. 7 (July 1993): 755. 16 Strong evidence supports an isolated case of human transmission in a Portuguese outbreak. See correspondence from Ana M. Correia et al., “Probable Person-to-Person Transmission of Legionnaires’ Disease,” New England Journal of Medicine 374, no. 5 (February 4, 2016): 497–98, and Victor Borges et al., “Legionella Pneumophila Strain Associated with the First Evidence of Person-to-Person Transmission of Legionnaires’ Disease: A Unique Mosaic Genetic Backbone,” Scientific Reports 6, no. 26261 (May 19, 2016): 1–11. 17 The following information about human infection is drawn from Fields et al., “Legionnaires’ Disease,” 508–10; Bartram et al., Legionella, 1–18; Beltz, Emerging Infectious Diseases, 185–90; and my interview with Brian Shelton, president and CEO of PathCon, July 9, 2013. 18 My interview with Lauri Hicks (CDC epidemiologist assigned to Legionella group) and Claressa Lucas (CDC microbiologist in the Legionella laboratory), July 11, 2013. 19 Memorandum to “Director, National Communicable Disease Center,” from “Viral Diseases Branch Epidemiology Program,” subject “Pontiac Fever: An Epidemic of Obscure Etiology in a Health Department,” dated July 31, 1969, from Box 10 of 18, folder: “EPI Aids 1968-68-84 through 1969-69-1 through 24,” RG 442-83-0042, National Archives and Record Administration, Southeast Region. 20 The description of the St. Elizabeth outbreak comes from S. B. Thacker et al., “An Outbreak in 1965 of Severe Respiratory Illness Caused by the Legionnaires’ Disease Bacterium,” Journal of Infectious Diseases 138, no. 4 (October 1978): 512–19; for the Fort Bragg case, see Lieutenant Colonel Worth B. Daniels and Captain H. Arthur Grennan, “Pretibial Fever: An Obscure Disease,” Journal of the American Medical Association 122, no. 6 (June 5, 1943): 361–65; and Hugh Tatlock, “A Rickettsia-like Organism Recovered from Guinea Pigs,” Proceedings of the Society for Experimental Biology and Medicine 57 (October-December 1944): 95–99, unless otherwise noted. 21 These investigations by the CDC are termed “EPI Aids,” and the reports are collected and available for all CDC researchers to use. 22 The strain at Fort Bragg was L. micdadei. See Paul H. Edelstein, “Legionnaires’ Disease: History and Clinical Findings,” in Klaus Heuner and Michele Swanson, eds., Legionella: Molecular Microbiology (Norfolk: Caister Academic Press, 2008), 6. 23 The list is adapted from ASHRAE Guideline 12-2000, “ASHRAE Standard: Minimizing the Risk of Legionellosis Associated with Building Water Systems” (American Society of Heating, Refrigerating and Air Conditioning Engineers, Inc., 2000): 3. In my possession. 24 For Spain, see Edelstein, “Legionnaires’ Disease,” 3; for Veterans Administration, see Adam Smeltz, Luis Fabregas, and Mike Wereschagin, “Legionnaires’ Bacteria in VA Water System Tracked to 1982,” Tribune-Review (Pittsburgh), collected from triblive.com, accessed June 18, 2014; for flower show, see Jeroen W. Den Boer et al., “A Large Outbreak of Legionnaires’ Disease at a Flower Show, the Netherlands, 1999,” Emerging Infectious Diseases 8, no. 1 (January 2002): 37–43; for aquarium, see Jane E. Greig et al., “An Outbreak of Legionnaires’ Disease at the Melbourne Aquarium, April 2000: Investigation and Case-Control Studies,” Medical Journal of Australia 180 (June 7, 2004): 566–72. 25 Stuart Cramer, an engineer at a North Carolina textile mill serviced by a dehumidifying machine, coined the term “air-conditioning” in 1906. See Gail Cooper, Air-Conditioning America: Engineers and the Controlled Environment, 1900–1960 (Baltimore and London: The Johns Hopkins University Press, 1998), 19 and 114 for “Weathermaker.” 26 For history of air-conditioning, see Cooper, Air-Conditioning America; Marsha E. Ackermann, Cool Comfort: America’s Romance with Air-Conditioning (Washington, DC, and London: Smithsonian Institution Press, 2002), and Raymond Arsenault, “The End of the Long Hot Summer: The Air Conditioner and Southern Culture,” Journal of Southern History 50, no. 4 (November 1984): 597–628. 27 Professor Watt as quoted in John Reese, “The Air-Conditioning Revolution,” Saturday Evening Post, July 9, 1960, 97. Professor Watt’s sample size was only twenty-two air-conditioned homes, however. 28 The literature on this discussion is voluminous. A good place to start for an overview is James T. Patterson, Grand Expectations: The United States, 1945–1974 (New York: Oxford University Press, 1996). 29 Indeed, Legionella bacteria in cooling tower aerosols have been detected two miles downwind in certain climatic conditions. See ASHRAE Guidelines 12-2000, in my possession. 30 See Mireia Coscolla, Inaki Comas, and Fernando Gonzalez-Candelas, “Quantifying Nonvertical Inheritance in the Evolution of Legionella Pneumophila,” Molecular Biological Evolution 28, no. 2 (February 2011): 985–1001, and Borges et al., “Legionella Pneumophila Strain Associated with the First Evidence of Person-to-Person Transmission of Legionnaires’ Disease,” 1–11. For a paradigmatic discussion of anthropogenic evolution and human history, see Edmund Russell, Evolutionary History: Using History and Biology to Understand Life on Earth (Cambridge University Press, 2011). 31 See Brian G. Shelton, W. Dana Flanders, and George K. Morris, “Legionnaires’ Disease Outbreaks and Cooling Towers with Amplified Legionella Concentrations,” Current Microbiology 28 (1994): 359–63. 32 Interview with Lauri Hicks, July 11, 2013. 33 The CDC has set a low bar for declaring an outbreak. In its categorization scheme, two or more cases associated with a location over a period of six months meets the definition. Interview with Claressa Lucas, July 11, 2013. 34 Interview with J. Donald Millar, May 22, 2007. 35 The United Kingdom standard is quite high in comparison to US standards. The ideal testing range for Legionella detection ranges from zero to 100 colony-forming units per liter (a significantly lower level of toleration than a milliliter). Levels detected above 1000 cfu/liter call for immediate disinfective action. See Health and Safety Executive, “Legionnaires’ Disease: Technical Guidance: Part 1, The Control of Legionella Bacteria in Evaporative Cooling Systems,” Table 1.10. Available from www.hse.gov.uk/pubns/books/hsg274.htm; in my possession. 36 Amanda K. Brzozowski, Benjamin J. Silk, Ruth L. Berkelman, Deborah A. Loveys, and Angela M. Caliendo, “Use, Location, and Timeliness of Clinical Microbiology Testing in Georgia for Select Infectious Diseases,” Journal of Public Health Management Practice 18, no. 4 (2012): E4–E10. 37 For the Ohio Study, see Barbara J. Marston et al., “Incidence of Community-Acquired Pneumonia Requiring Hospitalization,” Archives of Internal Medicine 157 (August 11/25, 1997): 1709–18; for CDC programs, see interview with Lauri Hicks, July 11, 2013. 38 Abby Goodnough, “Flint Outbreak Was Treated with Silence,” New York Times, February 23, 2016, available at www.nytimes.com. 39 For CDC data, see Lauri A. Hicks, Laurel E. Garrison, George E. Nelson, and Lee M. Hampton, “Legionellosis: United States, 2000–2009,” Morbidity and Mortality Weekly Report 60, no. 32 (August 19, 2011): 1083–86; and Karen Neil and Ruth Berkelman, “Increasing Incidence of Legionellosis in the United States, 1990–2005: Changing Epidemiologic Trends,” Clinical Infectious Diseases 47 (September 1, 2008): 594. 40 For association with increases in Legionella growth in warmer, wetter weather, see David N Fisman et al., “It’s Not the Heat, It’s the Humidity: Wet Weather Increases Legionellosis Risk in the Greater Philadelphia Metropolitan Area,” Journal of Infectious Diseases 192 (December 15, 2005): 2066–73, which reported a 2.5-fold increase in cases during wet and warm summers; for drought not affecting legionellosis, see Neil and Berkelman, “Increasing Incidence of Legionellosis,” 595, which reported that case reports increased in the South Atlantic states of the United States despite the 2006 drought in the region. 41 Fisman et al., “It’s Not the Heat,” 2066. © The Author(s) 2018. Published by Oxford University Press on behalf of the American Society for Environmental History and the Forest History Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

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Environmental HistoryOxford University Press

Published: May 17, 2018

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