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With the revised IHR there is now a formal framework for proactive international surveillance and response to any epidemic that begins to spread internationally. And, in particular, the revised IHR which will come into full legal force in June will guide responses to any future flu pandemic. At the World Health Assembly in May , WHO was asked to coordinate immediate voluntary implementation of all provisions in the revised IHR relevant to the current avian influenza situation and the related threat of a pandemic.

An emergency Influenza Pandemic Task Force has been established for this purpose, and it held its first meeting in Geneva on September 25, During that meeting, the experts considered the criteria for declaring the start of an influenza pandemic and asked whether the current pandemic alert should be raised to a higher level.

Given the current situation—a novel influenza virus is causing sporadic human cases but remains poorly adapted to humans—the experts decided that there is no need to alter the present level of alert. The group also examined a variety of other issues, including ways to improve the sharing of H5N1 influenza virus isolates and information on genetic sequences, the updating of diagnostic reagents and test kits, the development of a pandemic vaccine, and the monitoring for virus strains resistant to currently available antiviral drugs. These activities form part of the strengthened mechanisms by which WHO and its many partners maintain vigilance for emerging microbial threats and activate defense mechanisms that protect the international community from threats to its health and shocks to societies and economies.

Although my initial charge for this workshop was to discuss and review the history of the influenza pandemic, I suspect that that most of you have heard or read that story many times, especially over the last few years. Instead, I propose to widen the dialogue so that we may consider the broader—and I think richer—history of epidemics and pandemics in the American experience. After all, epidemics are hardly quiet occasions; they are experienced and responded to in real time by the affected community and then later discovered, heralded, and explained by historians like me.

As a result, the historical record of these events is especially rich and provocative Briggs, ; Rosenberg, ; Rosenberg and Golden, In what follows I will link some of the lessons learned from pandemics past to the quandaries that policymakers are grappling with today in response to a potential influenza pandemic and other microbial threats.

And, given that we simply do not have that much solid data on the means of mitigating or containing worst-case scenario influenza pandemics in our modern era, I will discuss why exploring the historical record of the — pandemic may help uncover a body of clues and suggestions. What makes that record so compelling to me as a historian of infectious diseases is that the — American influenza experience constitutes one of the largest databases ever assembled in the modern, post-germ-theory era on the use of non-pharmaceutical interventions to mitigate pandemic influenza in urban centers.

Policy makers, on the other hand, may find it more compelling that the record allows them to have the chance to observe how large numbers of people respond when a pandemic appears but vaccines and antivirals are neither effective nor widely available. History suggests that when faced with such a crisis, many Americans—and more formally, American communities—will adopt, in some form or another, what they perceive to be effective social-distancing measures and other nonpharmaceutical interventions NPI.

This is precisely what the nation did in —, resulting in a wide spectrum of results and outcomes. A critical question is, Can we make sense of and exploit this historical data to inform decisions today on how best to employ or discard various NPI strategies? And, if so, can we evaluate their costs and benefits in a manner that includes a polished set of social, legal, and ethical lenses? No one can claim that history provides some magical oracle of what to expect in the future.

Human history simply does not work that way. It may move in distinct and recognizable patterns, but this is quite different than repeating itself in predictive cycles. Yet despite those limitations, historians, since at least the days of Thucydides, have contributed nuanced and contextualized views of how past dilemmas emerged or evolved and have offered useful models of the resolution of those dilemmas.

These views and models merit our attention. In particular, historians have been trying for millennia to make sense of epidemics, and we can learn much from studying their conclusions. What follows are but two of the many useful models that historians have developed for analyzing the structure of epidemics. When considering the broad scheme of an epidemic or pandemic as a social phenomenon, perhaps the best study that I know of is not a study at all but is rather the remarkable novel by Albert Camus, The Plague —a text I routinely assign to all my students hoping to learn anything about epidemics.

From these considerations Rosenberg characterizes the unfolding of an epidemic as a dramaturgic event, usually in four acts, with a distinct but somewhat predictable narrative plot line:. When leaving his surgery on the morning of April 16, Dr. Bernard Rieux felt something soft under his foot. It was a dead rat lying in the middle of the landing. On the spur of the moment he kicked it to one side and without giving it a further thought, continued on his way downstairs. Only when he was stepping out onto the street did it occur to him that a dead rat had no business to be on his landing.

In the pages that follow Dr. This lethargic response is not restricted to the pages of fiction. Slow acceptance and delayed courses of action in the face of contagious threats are common features in the history of human epidemics. More often the delayed acknowledgment of an epidemic can be explained by the fact that acknowledging it would threaten various interests or strongly held beliefs, from the economic and institutional to the personal and emotional. This dichotomy in understanding deadly disease, with religion or morality on one hand and science on the other, was a hallmark of many societies in the past, and we should not discount the role that religious, spiritual and cultural beliefs and practices can play in mitigating, containing, or inflaming an epidemic in our own era.

The history of epidemics is littered with tales demonstrating the importance of bold, decisive leadership and the costs of ineffective or incompetent crisis management. Epidemics often end as ambiguously as they appear. Or, to lift a phrase from the poet T. A critical question, therefore, is how a community or government maintains credibility in its warning systems, maintains public support for costly preparedness planning, and keeps the public alert but not alarmed, panic-stricken, or completely disengaged.

This four-act model of epidemics is an excellent starting point for our contemplation of pandemics, but, of course, not all microbial threats will follow such a straightforward narrative structure. For that reason, many historians of epidemics have taken a different tack and set out to understand epidemics by identifying their major ingredients or features. This leads to a different model of the structure of epidemics and pandemics. In my own work over the past 16 years I have attempted to identify and describe critical leitmotivs that have appeared repeatedly in epidemics and pandemics across time.

Not all of the themes that I have identified in this work will appear in each epidemic or pandemic. Instead they should be viewed as major ingredients of an epidemic with the understanding that the precise mix of the themes can change from era to era and disease to disease. These leitmotivs include the following:. Thinking about epidemics is almost always framed and shaped—sometimes in useful ways, sometimes not—by how a given society understands a particular disease to travel and infect its victims. People living in eras when microbes were not considered to be the cause of epidemic diseases responded to these threats differently from people living in eras when the role of microbes was understood.

Well into the nineteenth century, for example, experts and lay people alike believed that many epidemics and contagious diseases were spread through polluted air—or miasma, from the Greek word for defilement of the air or pollution. The miasmatic theory of disease held that toxic emanations emerged from the soil or from rotting organic material or waste products and caused specific epidemic diseases such as cholera, typhus, and malaria.

Given the foul odor that pervaded every urban center of this era, the belief that it was an unhealthy force makes a good deal of sense, but when this theory was in vogue it led to public-health approaches that were very different from those taken today. Aside from calls for quarantine, most attempts to manage an epidemic centered on cleaning up and disinfecting streets, sewers, privies, and other dirty parts of the urban environment.

This trend changed markedly in the mid-to-late nineteenth century with the advent of the germ theory of disease, and it continues to be revised, refined, and fine-tuned today as we learn more and more about microbial ecology, evolution and genomics. Still, old ideas about contagion are often slow to die and, like fevers of unknown origin, have the power to recrudesce; as a result, many people today have ideas about the cause and spread of particular infectious diseases that are markedly different than the principles we teach in the medical school classroom Duffy, An order of quarantine, which closes a port or a city to foreign travelers or goods, costs communities a great deal of money and creates great hardships for individuals.

It is not surprising, then, that during the international sanitary conferences of the mid-nineteenth century, merchants were often vocal opponents of any efforts to prevent or contain disease that might have had the effect of impeding commercial enterprises and the flow of capital. There are two sides to this equation however. While increased global commerce can certainly contribute to the spread of a pandemic, it also sets up conditions that encourage more effective responses to a pandemic.

Epidemics cost the business community a lot of money, and, in particular, the cost of a human-to-human avian influenza pandemic would be, according to all reliable projections, simply staggering. The threat of such losses could therefore encourage developing nations faced with a brewing epidemic to communicate more openly with Western nations in the hope that their greater financial resources could help them rapidly contain or mitigate the outbreak Stern and Markel, The movements of people and goods and the speed of travel are major factors in the spread of pandemic disease.

It is no coincidence that the rise of bubonic plague pandemics during the Middle Ages as well as the invention of the formal concept of quarantine coincided with the advent of ocean travel and imperial conquest.

As humans traveled in wider and wider circles, so too did the germs that inhabited them. During the nineteenth century, four devastating cholera pandemics were aided and abetted by the transoceanic steamship travel of millions of people. By the close of the 19th century, journeys from Europe or Asia to North America required a travel time of 7 to 21 days, which gave most infectious diseases ample incubation periods and facilitated their recognition by health officers at the point of debarkation. It is quite different today, when the main mode of international travel, commercial jet planes, allow people to travel anywhere in the world in less than a day.

Indeed, a recent study in PLoS Medicine details how seasonal influenza can mirror peaks and valleys in air travel Brownstein et al. Yet while the natural response to a pandemic might be to limit air travel, either by an international edict or by the natural response of people to avoid travel by commercial airliner during such a crisis, such a response would pose a new set of troubling and potentially damaging consequences.

Our fascination with the suddenly appearing microbe that kills relatively few in spectacular fashion too often trumps our approach to infectious scourges that patiently kill millions every year.

Preparing for an Influenza Pandemic, A CDC Perspective

An even more egregious example is the lack of widespread attention to the common scourges of lower respiratory tract infections and diarrheal diseases, which kill millions on an annual basis Markel and Doyle, ; Achenbach, Unfortunately, it will be impossible to know until long after the money and resources have been committed—and perhaps only after a flu pandemic has actually occurred—whether influenza was the right microbe to focus upon instead of one of the host of other emerging and re-emerging infectious threats that we face.

Perhaps the more salient question for our discussion today is how we can apply the lessons of SARS, influenza, AIDS, bioterrorism, and other microbial threats to develop a comprehensive and global plan against contagion. Widespread media coverage of epidemics is hardly new and is an essential part of any epidemic. The media has the power both to inform and to misinform. In the early twentieth century, for instance, American consumers relied heavily on an extensive print media, whereas consumers today can turn to a panoply of newspapers, magazines, television, radio, cable, Internet sites, Web logs, and discussion groups.

That does not mean that Americans today are better informed. In the early twentieth century there were multiple daily editions of newspapers in every major city and large town and a great deal of superb reporting on epidemic threats, allowing a majority of Americans to be well-informed on a wide swathe of scientific issues as they were understood at the time. It is hardly a new phenomenon how physicians, public-health officials, and others simultaneously accommodate, inform, and, at times, correct the press.

Nonetheless there is no question that the breadth of media genres—and the demographics of their consumers—is far greater today than in previous eras, and there is no doubt that the media has a far greater ability to provide consumers with both useful information and misinformation. A dangerous theme of epidemics past is the concealment of the problem from the world at large. Across time many nations or states have concealed news of an epidemic to protect economic assets and trade.

At other times concealment efforts have been motivated by nationalistic bias, pride, or politics, as was the case with South Africa and HIV in the s, China during the first months of the SARS epidemic of , and, over the past few years, Indonesia and avian influenza IOM, , Regardless of the reasons for concealment of a public-health crisis, from the political to the purely mercenary, secrecy has almost always contributed to the further spread of a pandemic and hindered public health management.

One of the saddest themes of epidemics throughout history has been the tendency to blame or scapegoat particular social groups. At many points in American history, especially during the nineteenth and early twentieth centuries, the implicit assumption that social undesirability was somehow correlated with increased risk of contagion has led to the development of harsh policies aimed at the scapegoats rather than the containment of a particular infectious microbe. There are many examples of scapegoating across time, such as the widespread American assumption during the cholera pandemic of that any case of cholera discovered in the United States had been brought from Eastern Europe in the bodies of impoverished Jewish immigrants, the demonization of the Chinese in the bubonic plague outbreak in San Francisco, and, more recently, the stigmatization of gay men and Haitians during the early years of the AIDS epidemic in the United States Markel, , ; Kraut, ; Grmek, Public-health policies that place blame on victims or, worse, on perceived victims can have many negative consequences, including the misdiagnosis of the healthy and isolating or quarantining them with unhealthy people; social unrest, legal entanglements, and infringements of civil liberties; and extremely counterproductive behaviors by those targeted as diseased.

Such negative results have the potential to detract in a major way from efforts to contain or mitigate a contagious disease. Ultimately, however, the Rosenberg model works best for a single-phase epidemic rather than a multiphasic pandemic such as the entire four-wave flu pandemic of — The leitmotiv model can also be a useful lens through which to view the pandemic, but with one key exception: the social scapegoating leitmotiv was not all that loud. I suggest that this was because the pandemic spread so rapidly and ubiquitously among all sectors of American society especially among those 20—45 years of age.

That does not mean, however, that we should assume that this unsavory feature of epidemic disease could not rear its head in the present or future. One has only to recall the SARS epidemic of and the short-lived but well-publicized ban on all Asian exchange students at the University of California at Berkeley, to name one recent example, to realize that it can still happen here.

All of the other leitmotivs described above did feature prominently in the influenza pandemic. For example, during the pandemic it was very common for local business owners to oppose nonpharmaceutical interventions that seriously affected their economic health. School and business closings, restrictions on travel, and even the use of face masks often proved to be quite contentious issues.

Furthermore, many warnings of an influenza pandemic in the early summer of went unheeded; indeed, the stacks of medical libraries are filled with rarely read public health reports published in the years before the flu pandemic that urged the creation of more hospital beds and isolation wards as well the development of better diseases surveillance and containment strategies Markel, And once the flu crisis was over, little was done to rectify public health administrative problems that were exposed by the —20 pandemic.

Other leitmotivs that played significant roles in the pandemic include how the media interpreted the contagious spread of influenza and reported on these events; the role public health risk communications played in containing or mitigating the spread; the internecine rivalries between local, state, and federal health agencies and political leaders; suppression of reporting of cases in , this was often because privately practicing physicians did not want to lose control of—and remuneration from—their paying patients by reporting and referring them over to public health departments ; the unclear etiology of influenza; ineffective vaccines against the wrong organism; and, of course, issues of travel, particularly the mass movements of soldiers around the country and then to the European theater of what we now refer to as World War I.

Although historians by nature are hesitant to predict the future, I feel quite comfortable in suggesting that most or all of these themes will again be part of whatever emerging infectious disease crises we face in years to come. And while I cannot tell you what the exact proportion or precise mix of ingredients in this recipe will be, I do think history provides us with many thought-provoking, broad-brush strokes with which to think about pandemics.

To investigate how historical inquiry can inform the planning of pandemic mitigation strategies, one must first be aware of the limits of this approach. A good way to think about archival research is to imagine your life being recorded by a historian. Every day the scholar would file a report and store that document in a bank of file cabinets that, by the end of your life, would presumably hold many reams of paper.

Imagine, then, that a fire destroys most of that room, with only occasional file folders from discrete periods of your life surviving. With few exceptions, such spotty records are what historians deal with in their inquiries, and much of our knowledge of the past depends on the supporting archival materials that were actually saved. Furthermore, some archival materials may not be entirely reliable or may simply be unavailable, and sometimes historians may misinterpret the materials, creating yet more problems.

Many times, lacunae in the historical record are so great that we can only hypothesize or speculate about what may actually have occurred. Moreover, when one studies the history of epidemic disease, a whole new set of highly specialized records becomes important. For the — influenza pandemic there are many cases where critical numerical population and case-incidence data were not recorded or were recorded in a manner less consistent than we would demand of a prospective study conducted today.

Such gaps constitute significant challenges and even roadblocks in any historical study. One also needs to be familiar with the social, cultural, and intellectual history of the region under study and to know its differences from and similarities to our contemporary era. For example, someone studying the flu epidemic should know that the United States of that time had many similar features to the modern era: rapid transportation in the form of trains and also automobiles, although certainly many fewer automobiles than we have today; rapid means of communication in the form of telegraph and telephone; large, heterogeneous populations with substantial urban concentrations although many more Americans lived in rural environments in as compared to the present ; a news and information system that was able to circulate information on the pandemic widely; and a broad spectrum of public health agencies at various levels of government.

Conversely, there are also many striking contrasts between that era and our own. For example, the legal understanding of privacy and of civil and constitutional rights as they relate to public health and governmentally directed measures such as mass vaccination programs or medications has changed markedly over the past eight decades.

Furthermore, public support of and trust in these measures—along with trust in the medical profession in general—has changed significantly over this time, especially with regard to vaccines and medications. This can be seen, for example, in the recent spate of lawsuits filed because of vaccine failures or because of perceptions that vaccines may have significant and dangerous side effects.

Other features of the modern world that need to be considered when studying the historical record of the pandemic in order to inform contemporary policymaking include the speed and mode of travel, particularly the development of high-volume commercial aviation; immediate access to information via the Internet and personal computers; a baseline understanding among the general educated population that the etiological agents of infectious diseases are microbial; and advances in medical technology and therapeutics which have vastly changed the options available for dealing with a pandemic.

Another important aspect of American society circa that was markedly different from the present is how daily commercial transactions are carried out. In there were no supermarkets, refrigeration was primitive, and a limited variety of preserved foods were available for purchase. Consequently, consumers often needed to shop daily at multiple locations, such as grocers, produce vendors, bakeries, and butchers. Moreover, there were no credit cards, and personal checking accounts were typically employed only by the affluent, so frequent visits to banks for cash were not uncommon.

Indeed, for ordinary citizens in the United States was almost entirely a cash economy. So while the closure of a bank during an epidemic in might be explained as a public health measure, for the many Americans who had lived through the Depression of as well as other boom and bust cycles, such an action might well be misconstrued as a failure of the bank itself, and, as such, it had the potential to create civil unrest. As a result, the last public spaces to close during the pandemic—after theaters, schools, churches, restaurants, and saloons—were often banks and other financial institutions.

Today, on the other hand, a number of daily functions of life can be accomplished with little or no human interaction—provided you have the economic and educational resources to carry them out. Banking and credit transactions, the ordering and delivery of food via the Internet, entertainment, and personal and business communication, to name just a few, can all be carried out by large numbers of Americans in a way that can allow them to minimize human contact and thus shield themselves somewhat from the spread of contagious disease Germain, ; Chandler, ; Blackford, ; Rothbard, Nevertheless, as recent disasters have shown, many Americans have little in the way of an economic safety net, and their restricted access to financial resources and even basic needs of living could have a deleterious affect on disaster-containment strategies.

The overwhelming majority of histories of the influenza pandemic focus on its widespread carnage. Consequently, our research group was surprised to uncover the archival remnants of a handful of American towns or institutions that emerged from the virulent second wave of the pandemic—September to December —with relatively few influenza cases and no deaths.

The crucial question we were being asked was if the historical experiences of these escape communities might reveal some strategy to keep a small, but specific, sector of the population—the U. Armed Forces—completely free of influenza. The results of this year-long, in-depth archival study proved somewhat vexing. Some of these so-called escape communities that we studied, such as the village of Fletcher, Vermont population were too small to suggest that their success resulted from anything more than remote location, the uneven attack rates of the virus, and good fortune.

Two communities, the U. Naval base at Yerba Buena Island, one mile from the busy port of San Francisco, and the mining town of Gunnison, Colorado not only escaped the pandemic, they also had carried out a particularly extensive menu of restrictive public health measures i. Under the bold, decisive direction of astute public health officers, the still-healthy island and mountain towns essentially cut off all contact with the outside world to shield themselves from the incursion of influenza before it arrived in their vicinity, a measure we termed protective sequestration.

In a nation besieged by flu, Yerba Buena and Gunnison boasted zero mortality and almost no cases of infection over a lengthy time period. When planning for pandemics, it is tempting to focus on the apparent success of protective sequestration at Yerba Buena and Gunnison. But lest we be too eager to adopt such measures widely today, we must recall that one of these communities was literally an island directed by the bold, iron hand of a naval commander who could isolate his men from flu-ridden San Francisco.

The other was a small, homogeneous, and well-run mining town situated high in the Rockies that could barricade its roads and regulate its railways. Historical analysis of the few communities around the world that did manage to escape the influenza pandemic including Australia and American Samoa reveals an obvious but admittedly not terribly practical prescription: live in a remote area, preferably an island or mountain community, that can wall itself off from human contact.

On the other hand, there are tantalizing suggestions that all these escape communities experienced much milder third waves of the pandemic when compared to neighboring communities. During the pandemic, a broad menu of NPI was executed in different American cities that have captured our attention including making influenza a reportable disease; isolation of the ill; quarantine of suspect cases and families of the ill; closing schools; protective sequestration measures; closing worship services; closing entertainment venues and other public areas; staggered work schedules; face-mask recommendations or laws; reducing or shutting down public transportation services; restrictions on funerals, parties, and weddings; restrictions on door-to-door sales; curfews and business closures; social-distancing strategies for those encountering others during the crisis; public-health education measures; and declarations of public health emergencies.

The motive, of course, was to help mitigate community transmission of influenza. Over the next twelve months we will endeavor an historical epidemiological analysis of the application of NPIs in these communities during — with the goal of informing the potential use of NPIs in future pandemics. At present, no rigrous, systematic historical and epidemiological study exists on the relationship, positive or negative, between influenza case incidence and death rates during the pandemic and the NPIs taken at different points of time by the most-populated urban centers in the United States.

Our principal aim is to fill this intriguing and pertinent lacuna. Working with a team of epidemiologists, historians, and statisticians, based both at Michigan and the CDC , we are now engaged in the rather arduous task of digging up every municipal report from the 43 large cities in the continental United States during the — pandemic—many of which reside in dusty unmarked boxes or storage units of libraries that have rarely if ever been consulted in the secondary historical literature on the pandemic.

Further, we will analyze a wide body of U. When completed, the final report and its supplementary Web-based influenza archive will constitute a widely accessible version of the largest single collection of nonpharmaceutical intervention data taken in the United States during the — influenza pandemic. Every detail, whether it is the number of the dead in a particular city for a particular week or the political battles being reported in the press, will be compared with at least two other sources for verification.

Similarly, in each of the cities studied we will consult at least two newspapers that have been identified in terms of political party affiliation, editorial policy, and circulation figures. We do not promise any oracular commandments for pandemic preparedness, but we are confident that our fine-grained, rigorous, and scholarly historical epidemiological analysis of these American cities will significantly inform those who are considering the application, utility, policies, and design of nonpharmaceutical interventions today.

When contemplating pandemics it is clear that precise shapes and contours of the next influenza pandemic will be strikingly different from those of the past. But there is a positive side to this change over time. Specifically, this is essentially the first pandemic in human history where we will have had some semblance of advance warning—and hence, the opportunity to prepare.

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As such, I am historically optimistic that lessons from both the past and present can help us devise effective and also ethically and socially appropriate strategies to mitigate the microbial threats that inevitably loom on our horizon. View in own window. For more information on the evolution of the International Health Regulations see Annex , pages 59— George E. Wantz M.

For a broader look at the history of quarantine, infectious diseases and public health, particularly as they pertain to influenza, see: Mullet CF. A century of English quarantine, — The history of quarantine in Britain during the 19th century. Bulletin of the History of Medicine 25 1 —44; Hardy A. Cholera, quarantine and the English preventive system, — Medical History 37 3 —; Rosen G. A History of Public Health. International Quarantine. Epidemics and history: ecological perspectives and social responses. In Fee E, Fox D. The Great Epidemic. The Great Influenza. New York: Viking.

For more literary versions of the drama of epidemic disease and quarantine, see: Boccaccio G. The Decameron, Translated by J Payne. A Journal of the Plague Year. The Plague. Paris: Knopf. Ibsen H. An Enemy of the People. Translated by J McFarlane. Communities during the Second Wave of the — Influenza Pandemic. Defense Threat Reduction Agency: U. Department of Defense. To consult all of the primary source materials that comprised this report, see: The University of Michigan Center for the History of Medicine.

Nonpharmaceutical influenza mitigation strategies, U.

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Emerging Infectious Diseases 12 12 : — Turn recording back on. National Center for Biotechnology Information , U. Search term. David Heymann, M. Issues Between Governments: Infectious Disease and Commerce Humans have long transmitted diseases over great distances.

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Securing Equitable Access to Health-Care Resources Some epidemics recur year after year because the affected populations do not have access to the appropriate vaccines and drugs. Public Health Measures: Balancing Individual Rights and the Common Good During the smallpox eradication campaign, vaccines were offered to targeted populations using a ring vaccination strategy: vaccinating all households around that of the infected person and vaccinating any contacts that could be traced.

Global Alert and Containment On February 26, , the WHO office in Hanoi reported the case of a year-old businessman with high fever, atypical pneumonia, and respiratory failure who had recently traveled to China and Hong Kong. Revision of the International Health Regulations Within four months of beginning containment activities, and without the use of novel drugs or vaccines, all chains of human-to-human transmission were broken, the SARS virus was driven out of its new human host, and the outbreak was declared over.

The Four Acts Model of an Epidemic When considering the broad scheme of an epidemic or pandemic as a social phenomenon, perhaps the best study that I know of is not a study at all but is rather the remarkable novel by Albert Camus, The Plague —a text I routinely assign to all my students hoping to learn anything about epidemics. Major Leitmotivs of Pandemics In my own work over the past 16 years I have attempted to identify and describe critical leitmotivs that have appeared repeatedly in epidemics and pandemics across time. These leitmotivs include the following: Thinking about epidemics is almost always framed and shaped—sometimes in useful ways, sometimes not—by how a given society understands a particular disease to travel and infect its victims.

The Power and Limits of Historical Inquiry To investigate how historical inquiry can inform the planning of pandemic mitigation strategies, one must first be aware of the limits of this approach. Conclusion When contemplating pandemics it is clear that precise shapes and contours of the next influenza pandemic will be strikingly different from those of the past. Can we stop the next killer flu? Washington Post. Dec 7, Blackford MG. A History of Small Business in America.

Briggs A.

1. Introduction

Cholera and society in the nineteenth century. Past and Present. Figure Haskell County, Kansas. America had already entered World War 1. And though consensus has it that the lethal epidemic of began in Camp Funston, Kansas as early as January, physician Dr. Loring liked to drink. But soon, a string of deadly events were about to happen that would sober-up even Loring Miner.

Suddenly frantic townspeople were hunting him down at all hours of the day and night, reporting that members of their family would wake up one day feeling fine, have a severe headache by noon, be bedridden by late afternoon, with many of them lying dead by the following morning. The situation was bizarre.

Loring Miner. By , Haskell County was one of the poorest areas in America. The spirit of invention and change that had swept America for decades, bringing with it the railroad, the telegraph, and now electricity, had mostly passed Haskell by. Its inhabitants, mostly farmers, grew grain, and raised poultry, hogs, and cattle. Its dominant building material was sod —topsoil held together by the roots of foliage. Even the Haskell post office, built in , was sod. So you might just say that Haskell was just a place where people, hogs, poultry, earthen sod houses, cattle, and manure melded into one.

Figure The sod hut-house of a Haskell Kansas farmer. Miner would try to see to it that this small rural epidemic got national attention, through the April issue of what today is called The Morbidity and Mortality Weekly Report [68]. He noted that the disease appeared to be associated with farms. So while the Haskell epidemic ended as abruptly as it had begun, soon disease spread to Army barracks in nearby Funston. Many of Haskell counties young farmers had been incorporated into Camp Funston. Colonel Warren T. Figure Camp Funston, Kansas, Because the country was at war, farm boys from isolated communities such as Haskell County were on the move.

During the spring, a soldier from Haskell County probably brought this new and virulent form of influenza to Camp Funston, a military camp in Kansas. These men had previously been so free from signs of their tuberculosis, as to be accepted for military service as healthy individuals.

Vaughan, MD. Whatever the agent responsible for influenza, concluded Vaughan, whether viral or bacterial, many individuals with pulmonary tuberculosis did get influenza, and that this disease, having been contracted, in many cases hastened fatal termination of both the tubercular process and the patient. Fort Riley, Kansas was a sprawling establishment housing 26, men and encompassing an entire camp, Camp Funston.

Soldiers there often complained about the inhospitable weather: bone-chilling winters and sweltering summers. Squeezed between these extremes were the blinding dust storms. Within the camp, thousands of horses, hogs, mules and chickens produced in excess of a stifling nine tons of manure each month. And the accepted method for its disposal was to burn it, even against driving wind. State Veterinarian W. And so on Saturday, the 9 th of March, , a threatening black sky forecast the coming of a major dust storm.

When this storm combined with the ashes of over 9 tons of burning manure, a stinking, stinging yellow haze resulted. The sun was said to have gone black in Kansas that day. Among his symptoms were a headache, a sore throat, muscle aches, chills and fever. He also reported cleaning pig pens on March 4 th , one week before feeling sick. Gitchell would never recover from this, his last illness.

And by noon of March 4 th , a hundred men joined him at the Army infirmary he had walked into. Within a month 1, men were sick and approximately 50 dead [71]. Camp Funston was having a deadly epidemic. These deaths were highly unusual, but nothing like what would return in the fall, when the disease would come back with a vengeance, seeming to gain strength through human passage. Camp Funston in March, Camp Devens in September, then across the country and the world, leaving an estimated million dead globally, at least , to a million of them American, in the span of less than a year —the most destructive plague that man had ever witnessed.

Figure Army training camps in the U. Source: War Department US. Annual report, Washington: Government Printing Office; Kansas might have been situated in the middle of the United States, but it also found itself a state with a fairly high incidence of TB, sandwiched between states with some of the highest incidence of tuberculosis in the United States [Figure 20]:. Figure Kansas on a US Map. Figure Map of the United States, circa , showing by States the varying incidence of pulmonary tuberculosis as found at mobilization camps in the first million men drafted.

The highest incidence is in the blacked-out and darkened-grid designated States, most of them Southern.

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Note that Kansas, were Fort Funston was located and the Influenza epidemic initially broke out, is squarely sandwiched between some of the States, marked in solid black, with the highest incidence of tuberculosis in the US. Hall, M. Pneumonia is what killed in But pneumonia from what? Similarly, by , tubercular deaths had spiked around the world, including such places as Japan and Australia. In , Flick had already concluded that one-fifth of all tubercular patients gave previous histories of pneumonia [75], something which Baum and Amberson pursued in their discussion of how non-tuberculous pneumonias could and did often complicate the pneumonia of pulmonary tuberculosis [76].

Farber and Clarke reported cases which were admitted to a general hospital for non-tuberculous pneumonia, which were found to be of a tubercular cause [78]. Warfield T. Longcope appeared in Medical Clinics of North America in November of in an article dealing with deadly acute tuberculosis, an underlying consideration in any pneumonia or empyema during the Great Pandemic.

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Longcope, faced with the classic dilemma of finding hemolytic streptococcus in the sputum of a patient that also had tuberculosis, asked his student resident during clinical rounds what he thought came first in a situation in which streptococcus or for that matter pneumococcus were found with a pneumonia showing TB in the sputum. Without further examination one might be tempted to assume that this patient was suffering from pneumonia caused by Streptococcus haemolyticus.

Smears of the sputum as well as cultures were examined. It is well known, however, that such a series of events exist almost exclusively in the conceit of the physician and not in the workings of nature, and that tuberculous pneumonia is tuberculous from the start and not secondary to a pneumonia caused by some other organism. It is, of course, possible for a tuberculous patient to have an acute lobar pneumonia caused by the pneumococcus, but in the vast majority of cases signs of lobar pneumonia and symptoms of acute infection in cases of chronic tuberculosis are caused by an acute tuberculous process involving the lungs.

TB often does not surface in the sputum. Evidence of chronic tuberculous changes is found in some cases of pulmonary tuberculosis with acutely fatal termination. That they are not found in all such cases which occur in civilized man is largely accounted for by the difficulties of the search. Even Nigeli in his classical investigations which finally resulted in finding tuberculous changes present in 97 to 98 per cent of autopsies, at the beginning found only 40 per cent.

He was in the Philippines during the Filipino-American war, where some of the greatest atrocities, on both sides, were committed in the history of warfare. And while there, Ireland saw direct field action, participating in a dozen engagements in the provinces of Cavite, Camarines, and Albay in southern Luzon. While at Funston, Ireland took direct charge of the first company for instruction of the Hospital Corps organized by Captain Hoff. Surgeon General Ireland, as Gorgas before him, both knew that the army had a tubercular problem on its hands. They also knew that it could only get worse.

War and tuberculosis simply fed off of one another. As early as , the tubercular death rate had not only increased in all countries at war, but even in some, like the United States, that had not yet taken direct action in the conflict. And as the global conflict mushroomed, it became more and more obvious that war was increasingly and commonly spawning deadly forms of tuberculosis with a rapid course and without any tendency towards healing. There was no cavitation of the lungs or fibrotic reactions.

There was not enough time to form them. And in too many cases, the diagnostic path of least resistance, was that their patient had a bad case of influenza. At the time S. Adolphus Knopf estimated that , in the US army of were either already tubercular or were strongly predisposed to developing or contracting the disease [81].

And so as soon as war was declared Surgeon General Gorgas, and then Ireland after him , moved to expand a single bed TB facility at Fort Bayard, New Mexico into a 10, bed chain of tubercular hospitals around the country. Never had any nation, in so short a time, constructed, equipped and made operational such an efficient chain of TB hospitals for its military personnel.

Nor was there a wasted bed.

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The State of the south wind was an accurate enough description for Kansas, as there was certainly enough wind and dust storms to go around. The state found itself in a transition zone between the cool, dry air from Canada and the hot, humid air from the Gulf of Mexico. In addition an undulating jet stream from west to east flows over the US, carrying an alternating pulse of low pressure systems from the West which when intermingling with the opposing north-south air masses generated steady winds mixed with violent thunderstorms and tornadoes. Pandemic physician Fishberg seemed aware that the inhalation of dust is a strong predisposing factor in the instigation of tubercular lung disease, lowering the resisting powers of the invaded lung, and preparing the soil for the deposit of tubercular bacilli to thrive on inflamed, dust damaged tissue [82].

Kansas itself was home to many American Indians, including in Haskell County, which Fort Funston found itself close to. In fact many American Indians who were inducted or volunteered to be in the Army found themselves at Fort Funston, including the Lakota Sioux. Merritte Weber Ireland knew that the War Department looked at American Indians as its secret weapon —a group with little fear of the enemy and an almost inborn ability when it came to scouting, reconnaissance, the ability to plan accurate and unexpected attacks —and an uncanny marksmanship.

Thousands of American Indian from various tribes had been moved to the area that is now Kansas from the eastern United States and Great Lakes area. And by the time of the Great Pandemic, four American Indian tribes still retained reservations there. When war became imminent, Congress quickly established a draft, and more than 4, Selective Service draft boards screened 10 million men to find the strongest and most fit among them, including 12, American Indians, some from the Lakota Sioux [83].

What was known is that at least one multi-tribal group of Indians enlisted at Lawrence, Kansas, from the Haskell Indian School and trained at Funston. The American Indians, once removed from their native habitat and shoved onto reservations, where no strangers to killer epidemics.

Ireland had witnessed some of these himself. Nor was it just the Sioux or just those in barracks. What happened to the Sioux was being seen in Indian reservations across the country, including those of the Navaho. In fact it was on such reservations that Indian tubercular mortality rate reached the highest rate anywhere at any time [84]. Because of their sheer number and the burden placed on the Medical Corps, the process was of necessity so fast that some men took their mandatory oath of loyalty before the physician had completed his examination, leaving half-dressed young soldiers to pledge their allegiance to the country [85].

There was much emphasis in the Medical Corps towards simply detecting TB through auscultation of the chest with a stethoscope. As is the case today, the tuberculin skin test could and often was negative even with active tuberculosis —the immunosuppression of the disease itself not allowing the person being tested to muster a skin reaction to the test. Also known was that TB frequently did not show up on x-rays, which rely on differentials in density to portray the disease. In a film with homogenous distribution, TB was unlikely to be diagnosed. William Hallock Park.

Along with collaborators, including bacteriologist Anna Williams, Park co-authored the important teaching text, Pathogenic Microorganisms [86]. But flustered by the secondary infections and lack of consistency in other labs in isolating Pfeiffer's, Park flip-flopped, cautioning against attributing the pandemic solely to Pfeiffer's.

By the same token, Park felt uncomfortable with the muzzling of the media and medical corps by the Wilson administration regarding the ferocity of the American epidemic in general —that is, until it was too late to deny its viciousness. So although Pfeiffer's influenza bacillus, also known as Mycobacterium influenzae , was no longer at the top of his choices for the causal agent of the pandemic, it was its association with another mycobacterium, tuberculosis, which bothered Park the most.

He had just re-read Flick's account of what preceded both Great Pandemics. By , physician Lawrence Flick, citing US census reports leading into the two greatest world "influenza" pandemics in history, reported that out of every 1,, deaths, , males and , females died of tuberculosis. This was for all nationalities and colors. Specific subsets within these statistics revealed that among African Americans, every million deaths represented , males and , females having died of tuberculosis. Among people of Irish parentage, , males and , females died of TB for every million deaths.

And among people of German parentage, its victims numbered , males and , females for every one million deaths [87]. In , with "flu" victims dropping all around them, John B. Figure Influenza. Death was all around in Tufts pulmonologist Edward O. Otis also caught Park's attention. Otis not only mirrored Hawes and Cabot's view, he went a step further: " Often a patient gives the history of a previous attack of influenza which may have been an active outbreak of a latent tuberculous focus, which later again became inactive.

Back in , an editorial in the Journal of the American Medical Association specifically cited Liverpool physician R. Buchanan: " Dr. Buchanan makes the not improbable suggestion that many of the so-called sporadic cases of influenza are really symptomatic of the initial infection of tuberculosis, or possibly an exacerbation of a latent tuberculosis previously unsuspected or undetected. Lindley on Buchanan: " The author, impressed by the large number of instances in which patients have referred the commencement of their ill-health to an attack of so-called influenza, conceives that many of the so-called sporadic cases of influenza are really symptomatic of the initial infection of tuberculosis or possibly an exacerbation of a latent tuberculosis.

Every ache and pain, no matter where located and whether accompanied by fever or not, is at once put down as 'influenza'; every headache, every coryza [nasal congestion, common cold], every sore-throat, every attack of gastroenteritis, from whatever cause, is promptly self-diagnosed as 'influenza', and when the practitioner arrives upon the scene he will be expected to fall in with this view, and there is a great temptation to do so.

Hendrickson, who practiced during the Great Pandemic of —19, spoke even more bluntly:. Of more vital interest, even in the cases of dormant, healed TB in which the individual has contracted the disease in childhood, he quotes Osler on influenza being "an important exciting cause" of latent tuberculosis. At the same time, Hendrickson clarifies why in certain US Army barracks in , measles-in marked analogy to influenza-could also cause the reactivation and rapid spread of dormant tuberculosis.

Hendrickson, in , therefore told American science all it needed to know about the pandemic, but it just wasn't listening. Epidemic measles had kicked things off in Army barracks before the influenza epidemic, during the bitterly cold winter of — But unlike childhood measles, it was deadly, racking its victims with high fever, intractable cough, savage earaches and even brain inflammation. As with tuberculosis, the measles didn't kill by itself; rather, it killed by the very same secondary bacterial infections that dogged TB-infested lungs. Figure Two nurses watching as a pandemic patient dies.

So, even prior to Pfeiffer's bacillus becoming the focus of national attention in the "influenza" epidemic, upwards of 5, out of approximately 30, barracks soldiers died of measles "complications" on American soil. At Camp Shelby, Mississippi, alone, almost half of the deaths from all reportable causes were linked to pneumonia secondary to the measles. American newspapers began to headline a measles fiasco, and Army Surgeon General William Gorgas was called to task.

Hendrickson warned American medicine that both measles and then Pfeiffer's bacillus were nothing but red herrings landing on an underlying tubercular infection. In , with the killing fields of —19 laid out clearly before him, British physician Marcus Paterson took yet another jab at the "flu" epidemic [94]. He wrote: " During the time I was Resident Medical Officer at Brompton, it was usual to classify a rise of temperature in an ordinary case of 'chronic' pulmonary tuberculosis as influenza, even when there was no epidemic.

They are not, simply because they denote not a particular disease, but a toxemia due to bacterial action. Paterson's reference to clinicians confusion of sorting out influenza from TB was pointed: " Surely there is no more emphatic testimony to the clinical difficulties of a differentiation between the two diseases when one group of clinicians describes a rise of temperature in a proven case of tuberculosis to be influenza, and another section terms an arrested case of tuberculosis with pyrexia [fever] an active case of tuberculosis.

Writing in , after the greatest pound-for-pound health catastrophe ever, Paterson said what every physician still learns as a resident: " Before the war, it was usual to classify a sudden onset of acute symptoms as influenza, and it is very easy to appreciate the reason. When a person is taken ill, the patient's friends demand to know at once what the ailment is: hence it must be given a name, and 'influenza' is a good enough term for the moment.

What Paterson left out, as a given, was the hysteria in the family and immediate community that would intrude were the diagnosis of tuberculosis rendered. Instead, he stated that he knew of no physician who could differentiate clinically between tuberculosis and influenza. And he said that he "shudders to think" of the number of times that "tubercle bacillus have been classified as influenza without further investigation". To Paterson, this represented countless opportunities to cure the real cause, masked under the designation "influenza".

His conclusion: " There is no research required here. It is a known fact that what is at present called influenza is often tuberculosis. But the knowledge is not practically applied. It is information of inappreciable value lying idle. It is no new discovery, or its import would ring throughout the world. Shope, based in the Department of Animal Pathology at the Rockefeller Institute , was in direct communication with British investigators Smith, Andrewes and Laidlaw at Mill Hill, England, and sent samples of his flu virus and Pfeiffer's bacillus.

But the British group, in return, wasn't being per cent supportive. Patrick Playfair Laidlaw. Virologists like Shope and Laidlaw saw a great opportunity for virology provided by the — pandemic. Shope began the first salvo on swine "influenza", again falling back on the stale conception that the mild disease and flu-like symptoms were created in pigs by what he believed to be a "filterable virus"[96].

Shope had the singular advantage of realizing that since , pigs had been coming down with the same "influenza" each year. Having lived in Iowa, he had grown up with the knowledge. But beginning his investigations in earnest, Shope became perplexed. Not a virus but a bacterium kept cropping up in swine mucous secretions, and it resembled Pfeiffer's bacillus or Haemophilus influenzae H.

The problem was that he couldn't infect most of his subjects with the bacterium. So he took the mucous secretions of sick pigs and put them through a filter which he thought would only yield a virus. However, incredibly, even the filtrate from the discharge just gave low-grade symptoms. So if it wasn't a "virus" that had caused the deadly strains of flu, and if it wasn't a bacterium present in most malignant "flu", what could it be? In , he introduced both the "virus" and Pfeiffer's bacillus into animals [97], which subsequently came down with just the deadly "flu" complicated with pneumonia that killed between 50 and million people in — There is no evidence in the literature that Shope even knew about the filterable forms of H.

As late as , Shope still was insisting that the pandemic influenza was this meld of "virus" plus Pfeiffer's bacillus [98]. But as opposed to what's written in today's revisionist history, the idea wasn't really his. Not only could such viral bacteriophages alter the shape of a bacteria [or mycobacteria in the case of mycobacteriophages], causing cell-wall-deficient forms, but such phages could also change a microbes staining characteristics and moreover, its virulence.

Therefore an individual with a latent case of TB could potentially be at risk for the reactivation of previously quiescent infection when another mycobacterial infection [ M. Actually, it was only sometime after joining Rockefeller in , had Richard Shope switched his interest from tuberculosis to virology. To accept Shope's conclusion, an exception had to be made. There wasn't a single cause behind the — pandemic, but two: a virus and a bacterium.

As far back as , the MRC purchased this 40 acre agricultural site, then part of Rhodes Farm, to breed experimental animals at and do studies in. The only problem was, that the vast weight of evidence was pointed in an entirely different direction, towards the fact that canine distemper was caused by a filterable bacterial bacillus, and not a virus. Nor was the fact lost on many that Patrick Playfair Laidlaw's team seemed to fly directly in the face of Shope's multifactorial conclusion, which said that both a virus and Pfeiffer's bacillus from swine were necessary to acquire the flu.

Just the "virus" itself was necessary, claimed the British trio []. Figure Sir Christopher Howard Andrewes. When that didn't pan out, and back in England, he, similar to Shope in America, put his efforts into the futile attempt to find a virus behind all cancers. Laidlaw and his colleague Wilson Smith. The MRC was originally founded as a consequence of the recommendations of the Royal Commission on Tuberculosis , but if Walter Fletcher had anything to say about it, it would now go viral.

So when influenza re-appeared in epidemic proportions during the autumn of , Andrewes and Smith executed an experimental outline planned long in advance by Laidlaw and designed to reveal their hypothetical virus. In the midst of this, Andrewes began to feel unwell with flu-like symptoms. Nothing happened immediately, but just afterwards Laidlaw was informed by the director of Wellcome laboratory, their reference lab, that some of their ferrets appeared to be suffering from influenza at the same time as the epidemic of influenza was raging among Wellcome's staff. Ferrets, traditionally used for rabbit hunting and in rat control, had never been used in medical research until Laidlaw and Dunkin used them in their dog distemper studies.

And it turned out that these Wellcome ferrets didn't have influenza but were suffering from distemper. In addition ferrets are extremely sensitive to tubercular mycobacteria as well, and Mycobacterium avium , M. In fact the very same techniques used by Andrews Smith and Laidlaw could easily have transmitted tubercular infection to their ferrets [].

But never mind, Smith had another idea and then inoculated several other ferrets through their nose with filtrates from Andrewes nasal secretions. Subsequently, Wilson Smith himself came down with a flu that the rest of the group suspected was from a ferret. From the filtrate of this strain, the infectious agent WS Wilson Smith was isolated. Figure Nasal injection of the ferret.

The ferret was anaesthetized with ether, to ease injection of the virus material. But as head of a government lab at that time, Dr. Nor did it have anything to do with "influenza". But to do so, he was using improved special-growth agents and a sufficiently high-powered microscope. Crofton's "moist-chamber method" kept his culture medium warm and moist. If the microbe wasn't kept warm, Crofton found, then it couldn't be isolated in every case. Pfeiffer's bacillus was clearly pleomorphic many forms with viral-like forms that could easily pass through a filter.

So, in , when Crofton was final able to corner Andrewes, who was presenting a paper before the Epidemiology Section of the Royal Society of Medicine, Crofton said this:. I told him that I had ascertained that Wilson Smith had, in fact, influenza, because he was swarming with [ bacterial or mycobacterial ] influenza bacilli. I asked him why no cultures on proper medium were made from the infected ferret to ascertain if the Pfeiffer bacillus could be grown, as it would have been inevitably if, in fact, influenza had been transmitted.

Andrewes replied not one word, and the authorities of the section would not publish my criticism. Neither did the rest of the world, which was forced to accept influenza as a virus. Christopher Andrewes, now flushed with victory, suggested with the help of Burnet and Bang that the term "myxovirus", meaning "mucous virus", be incorporated into a family name for the influenzas []. This, one imagines, was because the organism came from mucous secretions.

By May , another from this group, Patrick Playfair Laidlaw, who in his deceptive viral studies did anything but play fair, wrote "Epidemic Influenza: A Virus Disease" —an article seemingly titled to assure himself that this was the case. In this document, Laidlaw would give the only credence he saw fit to Crofton and the many scientists like Crofton who did not believe him, saying that although he thought that it was "gradually" being proven that a "filterable virus" was primarily responsible for epidemic influenza, "Pfeiffer's bacillus or Haemophilus influenzae is still regarded by many observers as the prime cause of the disease and many of its complications" [].

Crofton was convinced by the confirmation of scientists like Calmette at Pasteur regarding how certain forms of tuberculosis, appearing both minuscule and viral, could pass through the smallest of filters. Crofton himself then established that tuberculosis could disappear into tissues as viruses did, and then go through filters which stopped cold even most of those "now invariably called viral disease".

Flu with the TB it so often infected in coordination with, as historical and political momentum carried Laidlaw's study through for posterity. Pfeiffer's strongly resembled TB; it was just smaller. A great opportunity was missed to correct the record. The Name Game After the pandemic of —19, the name of Pfeiffer's bacillus, Mycobacterium influenzae , was officially changed to Haemophilus influenzae. American bacteriologist Margaret Pittman [] pinpointed the influenza bacillus's name change to a report by Charles-Edward A.

Winslow and colleagues for the Society of American Bacteriologists' nomenclature committee. By any stretch, C. Winslow was far from the ideal choice to head a panel to rename Mycobacterium influenzae to Haemophilus influenzae. Not only was he an avid one-form-only bacteriologist [], leaving very little room for a microbe which could appear in both fungal and bacterial forms, but his unique thought processes became obvious when, as Professor of Public Health at Yale, he said he believed that posture was a neglected cause of tuberculosis, a disease known since antiquity for its spine-bending changes.

Yet Winslow and his colleagues decided to ignore Pfeiffer's bacillus's previously documented fungal forms, concluding that, unlike the mycobacteria, it stained Gram-negative and liked hemoglobin. But neither was conclusive enough to warrant the name change that Winslow had in mind. Tuberculosis researcher Stephen J Maher of the Connecticut State Tuberculosis Commission wrote in "All non-acid coccal and bacillary derivatives of the tubercle bacillus are, strange to say, Gram-negative. The Gram stain, developed by Hans Christian Gram, separates bacteria based on their cell walls.

Like other bacilli, cultures of TB, on the other hand, could be Gram-positive when young but might become Gram-negative as they aged. Hans Much saw this in [], and Chandrasekhar reported it again in []. Furthermore, the organism was arbitrarily named Haemophilus influenzae from the Greek haemophilus , meaning blood-loving , but it grew on the same blood-based cultures on which Mycobacterium tuberculosis had long been known to thrive [].

To many in the lay and scientific communities, bacterial names and classifications are hallowed ground. Therefore, Sneath and Brenner said, bacterial lists and classifications called "taxonomy" are partly a matter of judgment and opinion, as is all science, and, until new information is available, different bacteriologists may legitimately hold different views.

In the same vein, George Fox and colleagues reminds us that even with regard to today's sacred 16S rRNA sequence identity as a criterion for species identification, 16S rRNA may not be sufficient alone to guarantee species identity []. We are not taught that Pfeiffer's bacillus itself has a virus-like cell-wall-deficient phase which goes right through a filter. Virology on the Ropes It was in that Cornelius P.