Introduction to Syndemics E-Book

Merrill Singer

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 656

Veröffentlichungsjahr: 2009

Beschreibung

This book explains the growing field of syndemic theory and research, a framework for the analysis and prevention of disease interactions that addresses underlying social and environmental causes. This perspective complements single-issue prevention strategies, which can be effective for discrete problems, but often are mismatched to the goal of protecting the public's health in its widest sense.

"Merrill Singer has astutely described why health problems should not be seen in isolation, but rather in the context of other diseases and the social and economic inequities that fuel them. An important read for public health and social scientists."
—Michael H. Merson, director, Duke Global Health Institute

"Not only does this book provide a persuasive theoretical biosocial model of syndemics, but it also illustrates the model with a wide variety of fascinating historical and contemporary examples."
—Peter J. Brown, professor of Anthropology and Global Health and director, Center for Health, Culture, and Society, Emory University

"The concept of syndemics is Singer's most important contribution to critical medical anthropology as it interfaces with an ecosocial approach to epidemiology."
—Mark Nichter, Regents Professor, Department of Anthropology, University of Arizona

"Merrill Singer offers the public the most comprehensive work ever written on this key area of research and policy making."
—Francisco I. Bastos, chairman of the graduate studies on epidemiology, Fundacao Oswaldo Cruz

"Exquisitely describes how this new approach is a critical tool that brings together veterinary, medical, and social sciences to solve emerging infectious and non-infectious diseases of today's world."
—Bonnie Buntain, MS, DVM, diplomate, American College of Veterinary Preventive Medicine

"For too long the great integrative perspectives on modern biomedicine and public health disease ecology and social medicine-have remained more or less separate. In this innovative and provocative book, Merrill Singer develops a valuable synthesis that will reshape the way we think about health and disease."
—Warwick H. Anderson, MD, PhD, professorial research fellow, Department of History and Centre for Values, Ethics, and the Law in Medicine, University of Sidney

Leseprobe

Table of Contents

Title Page

Copyright Page

Dedication

PREFACE

THE AUTHOR

Acknowledgements

PART 1 - INTRODUCING KEY CONCEPTS IN SYNDEMICS

CHAPTER 1 - LEARNING FROM LICHEN

ON NOT PLANTING CUT FLOWERS: THE WEIGHT OF HISTORY

GERM THEORY AND THE BIOMEDICAL CONCEPTION OF DISEASE

REVOLUTIONS IN BIOMEDICAL REALITIES

PROBLEMS WITH THE POSTULATES

CONFRONTING COMORBIDITY

TOWARD SYNDEMIC RECONCEPTUALIZATION

LOCAL KNOWLEDGE

CONNECTIONS: HUMAN AND NONHUMAN

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

PART 2 - SYNDEMIC CASES

CHAPTER 2 - TRUCKING BETWEEN THE BAILIWICKS

WHY MULTIDISCIPLINARITY

THE TERM SYNDEMIC

THE SAVA SYNDEMIC

SAVA AMONG VICTIMS OF DOMESTIC VIOLENCE

SAVA AMONG MSM

SAVA AMONG STREET DRUG USERS

SAVA AMONG COMMERCIAL SEX WORKERS

SAVA AND PUBLIC HEALTH

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

CHAPTER 3 - EXEMPLARS

SYLLABLES IN THE BIOLOGICAL MESSAGE

VARIETIES OF MICROLEVEL DISEASE INTERACTION

SYNDEMIC DIVERSITY

RENOCARDIAC SYNDEMIC

SARS-CHRONIC DISEASE SYNDEMIC

ASTHMA-INFLUENZA SYNDEMIC

DIABULIMIA SYNDEMIC

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

CHAPTER 4 - HIV/AIDS AND OTHER INFECTIONS

ASSESSING THE HIV/AIDS SYNDEMICS

OPPORTUNISTIC INFECTIONS AND HIV/AIDS

SEXUALLY TRANSMITTED DISEASE SYNDEMICS

HEPATITIS AND HIV/AIDS SYNDEMIC

TUBERCULOSIS AND HIV/AIDS SYNDEMIC

MALARIA AND HIV/AIDS SYNDEMIC

VL AND HIV/AIDS SYNDEMIC

HELMINTHS AND HIV/AIDS SYNDEMIC

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

CHAPTER 5 - BEYOND CONTAGION

AN AGING EPIDEMIC

INFECTIOUS AND CHRONIC DISEASE CONNECTIONS

KIDNEY DISEASE AND HIV

FOOD INSUFFICIENCY AND HIV

CARDIOVASCULAR DISEASES AND HIV/AIDS

EMOTIONAL AND COGNITIVE HEALTH AND HIV/AIDS

COUNTERSYNDEMICS

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

PART 3 - SOCIETY, HISTORY, AND THE ENVIRONMENT

CHAPTER 6 - INEQUITY AS A COFACTOR

DISEASE IN THE TIME OF DISPARITY

THE MAKING SOCIAL OF DISEASE

BIOLOGIZING EXPERIENCE

SUPERSYNDEMICS

HEALTH AND HUMAN RIGHTS

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

CHAPTER 7 - SYNDEMICS AND THE WORLDS THEY MADE

BEFORE NOW

IRISH FAMINE SYNDEMIC OF 1741

GIBRALTAR CHOLERA SYNDEMIC OF 1865

MASSACHUSETTS SCARLET FEVER SYNDEMIC OF THE 1800S

GLOBAL INFLUENZA SYNDEMIC OF 1918

SYNDEMICS AMONG NATIVE AMERICANS ON THE AMERICAN FRONTIER

SYNDEMICS OF THE MORMON MIGRATION

SYNDEMICS OF WAR

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

CHAPTER 8 - A WORLD OUT OF BALANCE

EMERGENT SYNDEMICS OF A TROUBLED WORLD

FROM EMERGENT INFECTION TO EMERGENT SYNDEMIC

REEMERGENT DISEASES AND EMERGENT SYNDEMICS

SUPERINFECTION: INTRAGENUS SYNDEMICS

IATROGENIC SYNDEMICS

UNINTENDED COUNTERSYNDEMICS

ECOSYNDEMICS AND THE ANTHROPOCENE

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

PART 4 - APPLICATIONS OF THE SYNDEMIC PERSPECTIVE

CHAPTER 9 - PRACTICAL UTILITY

WHY STUDY SYNDEMICS?

PUBLIC HEALTH AND SYNDEMIC PREVENTION

MEDICAL TREATMENT OF SYNDEMICS

MODELING SYNDEMICS

FUTURE SYNDEMICS

SUMMARY

KEY TERMS

QUESTIONS FOR DISCUSSION

GLOSSARY

REFERENCES

INDEX

Copyright © 2009 by John Wiley & Sons, Inc. All rights reserved.

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Library of Congress Cataloging-in-Publication Data

Singer, Merrill.

Includes bibliographical references and index.

eISBN : 978-0-470-48300-8

1. Epidemics. 2. Social medicine. 3. Poor—Health and hygiene. I. Title. [DNLM: 1. Health Status Disparities. 2. Ecology. 3. Healthcare Disparities.

4. Social Medicine. 5. Systems Theory. WA 300.1 S617i 2009]

RA652.S56 2009

362.1—dc22 2009008869

PB Printing

This book is devoted to my colleagues in the United States,Canada, New Zealand, and elsewhere who have taken an interestin and contributed to the body of work on syndemics. This bookis dedicated to Bruce Gould, associate dean for primary caremedicine, University of Connecticut Health Center, a role model,friend, and physician.

PREFACE

In ancient Greek the term µθοδοζ (methodos) was used to refer to the pursuit of knowledge and the approach taken for conducting such inquiry. Although the opening syllable conveys the notion of being in the midst of something (metha), the remainder of the word (odos) refers to an approach or journey. This book, the product of a personal and professional journey that began over twenty-five years ago, provides an introduction to the emergent concept of syndemics, which I developed as part of an ongoing effort to rethink the public health and social scientific understanding of disease so that it focused attention on the multifaceted interactions that occur among the health of a community, political and economic structures, and the encompassing physical and social environment. This reconceptualization developed specifically out of many years of work on the health challenges associated with social disparity, especially in the context of the human immunodeficiency virus and the acquired immunodeficiency syndrome (HIV/AIDS) epidemic (Singer, 1994; Singer & Snipes, 1992).

Employed for over twenty-five years as an applied medical anthropology researcher in a community-based, direct service, and research organization located in a primarily Latino and African American inner-city neighborhood, I was made painfully and daily aware of the many health problems caused by being poor and marginalized in American society. Poverty is well known to bring about regular exposure to diverse biological stressors, including social discrimination, food insufficiency and malnutrition, diverse infectious pathogens, toxic substances in the living and working environment, and climatic extremes owing to inadequacies of clothing and shelter. As summarized by the Prevention Institute (2002), “The chief underlying cause of health disparities is increasingly understood to be social and economic inequality; i.e., social bias and institutional racism, limited education, poverty, and related environmental conditions that either directly produce ill health or promote unhealthy behaviors that lead to poor health” (p. 3). More pointedly, Harvard public health researcher Nancy Krieger, who has produced an impressive body of work on these issues, asserts: “Social inequality kills. It deprives individuals and communities of a healthy start in life, increases their burden of disability and disease, and brings early death. Poverty and discrimination, inadequate medical care, and violation of human rights all act as powerful social determinants of who lives and who dies, at what age, and with what degree of suffering” (2005, p. 15).

Generally speaking, in short, health and wealth go hand in hand, and as a result the poor have worse health than the more affluent social groups. Consequently, many of the people and my coworkers and I studied and provided with health and social support services suffered from multiple diseases and multiple social problems, making it difficult often to know where to begin in addressing their myriad needs. Although the historical tendency has been to start with a specific health problem (consider for example the traditional argument in the substance abuse treatment field that you have to concentrate initially on a person’s substance abuse issues before addressing his or her other challenges), over the years it became increasingly apparent to me that to be effective in creating change a new, more holistic way of thinking was needed about health and illness in health disparity populations.

Rather than starting with the part (with this disease or that social condition), why not look at the whole (the full array of the health and social problems suffered by an individual or a community) and assess the nature of the interconnections among the parts, including the intricate ways in which they promote and reinforce each other and thereby create a complex and burdensome web of entwined health and social problems? With the emergence of HIV/AIDS and its rapid spread among the inner-city poor (a process that was occurring while the assumption among public health officials was that HIV/AIDS was a disease limited primarily to multipartnered gay men), it became apparent that studying this disease and responding to it with public health initiatives as though it were separate from other diseases and conditions also prevalent in the community was a distortion. Indeed, it became clear that even the public health term epidemic, which had quickly come to be used to describe the sudden spread of HIV/AIDS, did not sufficiently describe the growing (and several decades later still intense) inner-city HIV/AIDS crisis, which involved the transmission of this disease in close conjunction with a set of other health conditions (such as tuberculosis [TB], sexually transmitted diseases [STDs], hepatitis, cirrhosis, infant mortality, drug abuse, suicide, homicide, and so forth), all of which were intertwined and strongly influenced and sustained by broader political, economic, and social factors. In this process of rethinking the concept of syndemics was born. From the syndemics perspective, contemporary threats to the health of the poor, including violence, substance abuse, malnutrition, and HIV/AIDS, are not concurrent epidemics in that they are not completely separable phenomena. Rather they emerge among the poor as closely intertwined threads in the often tattered fabric of their daily lives.

A syndemic, in short, involves a set of enmeshed and mutually enhancing health problems that, working together in a context of noxious social and physical conditions, can significantly affect the overall disease burden and health status of a population. For example, in the Multicenter AIDS Cohort Study conducted between 1994 and 2000, Thio et al. (2002) divided the individuals in their research sample into four groups: those with HIV only, those with hepatitis B only, those with both HIV and hepatitis B, and those who were free of either disease. These researchers found that liver disease-related deaths were highest in the dually infected subgroup and were especially high in those with low CD4 cell counts (a sign of advanced HIV infection). Men infected with hepatitis B and HIV were seventeen times more likely to die of liver disease than were those infected with just hepatitis B. Similarly, in January 2004, the World Health Organization (WHO) announced its decision to support expanded collaboration between tuberculosis and HIV/AIDS programs in order to curb the growing spread of TB and HIV coinfection. The new WHO policy guidelines defined the public health activities needed to address what the WHO referred to as “the dual epidemic of TB and HIV.” According to WHO director-general Lee Jong-wook, “TB/ HIV is a deadly combination and needs to be tackled with an approach treating the whole person” (WHO, 2004b, p. 1).

Defined as the concentration and deleterious interaction of two or more diseases or other health conditions in a population, especially as a consequence of social inequity and the unjust exercise of power, syndemics appear to have played an important role in human disease history (and hence in human history generally), are having a significant impact on diverse populations currently, and are likely to have consequential influence on the emergent health profile of the twenty-first century. As a result the syndemics concept is receiving a growing level of attention in the field of public health, among social scientists concerned with health, and also in other disciplines that focus on the health effects of social and environmental conditions.

In the various fields in which a syndemic understanding of disease has garnered interest, it is generally recognized that the traditional biomedical approach to disease, an approach that dominated thinking about health throughout the twentieth century, resulted from an effort to diagnostically isolate, closely study, and therapeutically treat individual cases of disease, as if each disease were a distinct entity that existed in nature separate from other diseases and independent of the biosocial contexts in which it was found. This approach proved useful in its time in focusing medical attention on the immediate causes and biological expressions of disease (seen as any harmful change that interferes with the normal form, structure, or function of the body or any of its parts or systems) and contributed to the emergence of diverse pharmaceutical, surgical, and other biomedical treatments for specific diseases, some of which have been enormously successful, especially for acute conditions.

Similarly, “research protocols, prevention programs, policy interventions, and other aspects of public health practice have focused on one disease at a time, leaving other health problems to be addressed by parallel enterprises” (Syndemics Prevention Network, 2005d). This traditional approach is seen, for example, in public health textbooks. To take but one instance, Kathryn Jacobsen’s (2008) very thorough epidemiological introduction to global health includes a chapter titled “HIV/AIDS, Malaria, and TB.” Each of these diseases is discussed in a separate section, with a clear description of the disease and its causes, its geographical distribution, and the strategies for its prevention and treatment. The section on AIDS discusses it as a source of opportunistic infections by other pathogens, and the section on TB notes that people “with HIV infection are more likely to develop active TB disease than people without HIV infection” and that “TB is a leading cause of death in people with AIDS” (p. 163). Moreover, the book’s discussion of influenza mentions the antigenic shift that occurs when “two different influenza viruses attack the same cell and the genetic material from both recombines to form a new type of influenza” (p. 175). Finally, in a discussion of the immune system, the book notes that “poor nutrition . . . can . . . cause immune system suppression and lead to other diseases” (p. 29). Even though there are these fleeting references to syndemic processes and consequences, overall the volume is guided by a conventional, one-disease-at-a-time orientation. Although promoting an appreciation of the complexities and unique features of each disease, this approach cannot offer an equally developed appreciation of the fact that in the real world a disease does not usually exist in isolation from other diseases and disorders and that synergistic interactions have considerable effect on disease course and consequence. Moreover, these interactions may play a critical role in treatment and outcome. A telling example of this is the account provided by Watt, Jongsakul, and Suttinot (2003) of a Thai woman patient who “presented with leptospirosis [a bacterial disease that can result in renal failure] and was treated appropriately with high-dose intravenous penicillin. Her condition deteriorated rapidly, however, and she died with adult respiratory distress syndrome, the most common cause of death from O. tsutsugamushi infection [also known as scrub typhus]. Perhaps a fatal outcome could have been avoided had antibiotics active against scrub typhus been administered. A mixed infection should be considered in patients with either leptospirosis or scrub typhus who are responding poorly to treatment” (p. 90).

Finally, the traditional biomedical approach tends to pay little attention to the fact that the social environments of people with diseases are critical to understanding the clustering and spread of diseases within and between populations, disease expression through bodily signs and symptoms, and the added burden of intertwined diseases at the individual and population levels.

The purpose of this book, then, is to draw attention to the developing field of syndemic theory and research and to provide a framework for the analysis of disease interactions, including their origins and the threat they present to human life and well-being, and for the prevention of damaging disease interactions by addressing underlying social and environmental causes. As Julie Gerberding (2005), the former head of the Centers for Disease Control and Prevention (CDC), has stated, the “application of complex systems theories or syndemic science to health protection challenges is in its infancy” (p. 1405). Nonetheless, it is the CDC’s position that this line of attack represents a “promising new frontier for public health action in response to the critical challenges of our time” (Leischow & Milstein, 2006, p. 405). Further, the CDC has heralded the syndemic orientation as offering an approach for “establishing new theories of change, new alliances among interest groups, new funding policies, and new levels of achievement in protecting the public’s health” (Syndemics Prevention Network, 2005a).

Syndemic theory extends the work of other health researchers who have long recognized the critical importance of disease interaction in a social context. In an important series of papers on health in New York City, for example, Rodrick Wallace and Deborah Wallace (Wallace, 1988, 1990; Wallace & Wallace, 1998) drew attention to the “synergism of plagues” produced by public policies designed to restrict municipal services in low-income neighborhoods as a way of getting people to move away, thus freeing up the land for profitable economic development. The tragic result was a mass movement of people to new (also poor) areas, overcrowding, and an unraveling of community relationships and support structures, as well as a set of linked epidemics of tuberculosis, measles, substance abuse, AIDS, low-weight births, and street violence. Examining these health issues by separating them, overlooking the ways in which they are intimately linked and mutually enhancing, and ignoring the underlying social and biological processes involved in their development and expression does not lead to insight born of fine-grained analysis. Rather it distorts on-the-ground and in-the-body realities and obscures the nature of the connections between the health of physical bodies and the health of social bodies. The syndemics perspective is intended to capture, analyze, and respond to these complex realities. As an approach to addressing community health issues, it “complements single-issue prevention strategies that may be effective in controlling discrete problems but often are mismatched to the goal of improving community health in its widest sense” (Syndemics Prevention Network, 2005a).

The appeal of this new conception is seen in the rising number of recent scholarly publications in public health, biomedicine, and dentistry (for example, Freudenberg, Fahs, Galea, & Greenberg, 2006; Hein & Small, 2007; Milstein, 2008), biology (for example, Herring & Sattenspiel, 2007), and the health-related social sciences (for example, Marshall, 2005; Singer, 2006a; Singer & Clair, 2003; Singer, Erickson, et al., 2006) that have adopted a syndemic approach. It is being used in accounting for health patterns and developing community-based prevention initiatives (as seen, for example, in the work on diabetes prevention among Native Americans by Bachar et al., 2006). There are efforts under way within the CDC to build a national syndemics prevention strategy and online prevention community (see Syndemics Prevention Network, 2008a). Moreover, the concept is appearing in national (see, for example, National Institutes of Health, Office of AIDS Research, 2006) and international health reports (for example, Laserson & Wells, 2007). It is being discussed at international health conferences (for example, by Prince Charles in a speech at the 2006 Enhancing the Healing Environment conference, St James’s Palace, London), in dictionaries and encyclopedias (for example, Easton, 2004; MacQueen, 2002; Milstein, 2005; Ragsdale, 2008; Singer, 2004a, 2008), in book chapters (for example, Nichter, 2008; Singer, 2009; Stall, Friedman, & Catania, 2007), in the mass media (for example, Specter, 2005), in student graduate theses (for example, Erstad, 2006), and in the classroom (American Association of Public Health Physicians, 2006).

In light of the growing evidence for and recognition of the utility of the syndemics concept across various health disciplines, another way to state the purpose of this book is that it marks the coming of age of the syndemics methodos by assembling, assessing, and amplifying the key components of this approach to understanding and addressing human health as an intricate biosocial process.

THE AUTHOR

Merrill Singer, a cultural and medical anthropologist who earned his PhD degree from the University of Utah, holds a dual appointment as senior research scientist at the Center for Health, Intervention, and Prevention and professor of anthropology at the University of Connecticut. Additionally, he is affiliated with the Center for Interdisciplinary Research on AIDS (CIRA) at Yale University. He has authored, coauthored, or edited twenty books and over two hundred articles and book chapters on health and social issues. Active in the building of social science of health theory, the development of methods in qualitative health research, and the use of research in the development of community-based health promotion and intervention, he has been the recipient of the Rudolph Virchow Award from the Critical Anthropology of Health Caucus of the Society for Medical Anthropology, the George Foster Practicing Medical Anthropology Award from the Society for Medical Anthropology, the AIDS and Anthropology Prize Paper award from the AIDS and Anthropology Research Group, and the Prize for Distinguished Achievement in the Critical Study of North America from the Society for the Anthropology of North America. Since 1984 he has been the principal investigator on a continuous series of basic and applied federally funded health studies, and he has carried out health research in the United States, Brazil, China, and Haiti.

ACKNOWLEDGMENTS

This book is the product of work stretching well over a decade, and it has benefited from the inputs, insights, and support of many colleagues who warrant my gratitude and heartfelt appreciation, including Elizabeth Toledo, with whom I had my first conversations and coauthored my first conference presentation about syndemics; Jeremy Lauer, Larry Sawchuk, and Alan Swedlund, who read and commented on sections of the book; the Wenner-Gren Foundation, which provided a forum for the development of some of the ideas presented here, and also the participants in the foundation’s symposium “Plagues: Models and Metaphors in the Human ‘Struggle’ with Disease,” who offered their feedback; the School of Advanced Research (SAR) and Paul Farmer, Linda Whiteford, and Barbara Rylko-Bauer, who were the organizers of the SAR symposium “Global Health in the Time of Violence,” as well as all participants in the symposium who provided feedback on my syndemics and violence presentation at the symposium; Petra Rethmann and Ann Herring of McMaster University, Mary-Ellen Kelm, Craig Janes, and Kitty Corbett of Simon Frasier University, Alan and Josie Smart and Melanie Rock of the University of Calgary, Hans Baer of the University of Melbourne, and Judith Littlefield of Auckland University, who facilitated my visits to their respective universities to give presentations on syndemics and related topics; Al Mata, who facilitated my first publication on syndemics; Scott Clair and Pam Erickson, who collaborated on earlier publications that helped to advance my thinking about syndemics, and again, Pam Erickson, who supportively endured the demands that finishing a book imposes on an author and those nearby.

PART 1

INTRODUCING KEY CONCEPTS IN SYNDEMICS

Chapter One, “Learning from Lichen: Reconceptualizing Health and Disease,” which makes up Part One of this book, introduces the reader to the concept of syndemics and to the biosocial syndemic perspective on human health. Examining the syndemic perspective in a historical context, it describes the developing recognition that health and illness are shaped by multiple and complex factors, and it shows how the identification and study of syndemics has grown out of these far-reaching shifts in the ways that we conceptualize disease.

CHAPTER 1

LEARNING FROM LICHEN

Reconceptualizing Health and Disease

After studying this chapter, you should be able to

• Locate the syndemic perspective within the evolutionary history of the scientific understanding of disease, including dilemmas encountered in meeting Robert Koch’s criteria when attempting to determine the cause of an infectious disease.

• Understand the syndemic approach as one that supersedes two limitations of conventional biomedical approaches to disease—reductionism and mind-body dualism.

• Recognize the fundamental importance of biosocial interconnections and relationships in syndemics theory.

• Explain why syndemics were often not recognized in the past.

• Explain how the consideration of social factors, such as social disparity, differentiates syndemic processes from the biomedical conception of comorbidity and also differentiates syndemics among humans from synergistic disease inter-actions among animals.

ON NOT PLANTING CUT FLOWERS: THE WEIGHT OF HISTORY

It was just a few decades ago, in the 1970s, that medical anthropology, the source discipline for the syndemics concept, was a new field. George Foster and Barbara Anderson, in laying out an analytical approach to health-related issues for this new field, suggested a structural division of medical systems into two components: a disease theory system and a health care system, defining the first component as the “beliefs about the nature of health [and] the causes of illness” that prevail within a particular medical system (Foster & Anderson, 1978, p. 37). It is these beliefs that I am concerned with here.

The historical pathway leading to the contemporary biomedical and public health understanding of disease causation is both long and intricate (Richardson, 1991). On the one hand it is part of the larger historical course leading from prescientific to scientific modes of thought, and on the other hand it runs from simple to more complex scientific understandings of what disease is and how it develops within bodies, within populations, and within social and environmental contexts. The syndemic orientation, although recent in expression, is in fact an outgrowth of the new way of thinking about the causes of sickness that emerged and caught hold in the mid-1800s in a process commonly referred to as the rise of germ theory. This approach led first to the biomedical and public health conception of the nature of both contagious and noncontagious diseases (and more recently to reexamination of the assumed differences between these two broad categories of disease). This point then—the transition to a modern biological understanding of disease—is the starting place for examining the syndemic perspective, in that, as noted by historian Daniel Boorstin, trying to understand the present or plan for the future without a sense of the past is like trying to plant cut flowers (McCullogh, 2005).

GERM THEORY AND THE BIOMEDICAL CONCEPTION OF DISEASE

A critical moment in theevolution of biomedicine occurred during the mid-nineteenth century. During this epoch the healing system that was to evolve into modern biomedicine underwent a profound transformation, as detailed in the following sections.

Health as Balance

Prior to the mid-nineteenth century and dating back to the era of ancient Greece, physicians commonly understood health in terms of the balance among bodily fluids known as humors. Most prominent among ancient Greek physicians was Hippocrates (circa 460-370 B.C.), a man often credited in the West with being the father of medicine. Rejecting the notion of disease as a divine punishment for violations of spiritual laws—a disease theory that long predates ancient Greece yet lives on in the modern world (as seen, for example, in some religious interpretations of the HIV/AIDS epidemic as God’s punishment of a sinful world)—Hippocrates and his peers believed that certain human moods, emotions, and behaviors were directly under the influence of blood, yellow bile, black bile, and phlegm (and that these humors were, in turn, linked to the four elements of fire, air, water, and earth in the natural environment). When these four humors were not in balance (a state called dyscrasia, or “bad mixture”), a person fell ill and remained so unless balance was restored through medical intervention. As Erickson (2008) notes, Hippocrates rationalized disease, thereby laying the foundation for the “biomedical understanding that diseases—both individual . . . and epidemic . . . are natural processes not supernatural punishments” (p. 25).

The humoral notion of disease causation was elaborated further by another ancient physician, Galen (circa 131-200 A.D.), who stressed that understanding of disease must be based on experiential awareness of human anatomy and physiology. (Owing to a government ban on human dissection, Galen gathered his own knowledge of human anatomy, sometimes inaccurately, from examining the corpses of pigs, primates, and other animals.) Galen’s influence spread throughout the Western and Arab worlds and remained a factor in medical approaches to healing through the mid-1800s. As Hays (2000) observes, “Bleedings and purges . . . remained the order of the day for the early nineteenth century physician, however much he might have forsworn allegiance to Galenic humors” (p. 216).

Pollution Theory

Also important in historical thinking about disease causation, and reflective of the naturalistic and environmental understanding found in humoral theory, was the theory about the effects of miasma, or pollution theory. This understanding viewed toxic vapors given off by decomposing organic matter in the environment as the cause of many diseases. One such disease was malaria, believed to be caused by poisonous and foul-smelling environmental vapors arising from bodies of water found at low elevations and filled with particles of decomposed matter. This led European colonists in Africa, for example, to settle at high attitudes, a strategy that proved effective because it located the homes and offices of colonial administrators above the normal (temperature-sensitive) breeding elevation of mosquitoes, the real vectors of malarial infection. (Global warming and the resulting breeding of mosquitoes at ever higher elevations would make such a practice less effective today.)

Cholera in London From 1831 to 1833 and again from 1848 to 1849, London, then the most populous city in the world, experienced several epidemics of cholera. The name cholera is derived from the Greek term for bile and reflects that this water-borne disease was originally conceptualized as resulting from an imbalance of humors. However, in mid-nineteenth-century London, William Farr, a doctor who served as the assistant commissioner for the 1851 city census, asserted that cholera was transmitted by bad air and, in London, specifically by a noxious concentration of miasmata (a non-living entity of organic origin) found along the banks of the Thames (at that time a heavily polluted industrial river). During this era there was no understanding that a single disease could produce multiple symptoms, and thus the diarrhea caused by a cholera infection was seen as a totally different disease from the cholera itself (and not, as it was found to be many decades later, an adaptive strategy that creates an intestinal alkalinity favorable to Vibrio cholerae, the immediate causative agent of cholera). When a major cholera epidemic again broke out in London, in 1854, Farr was appointed by the General Board of Health to the Committee for Scientific Enquiries in Relation to the Cholera Epidemic. Although not as severe as the epidemic of 1849, the 1854 epidemic—during which about 11,000 Londoners succumbed (Winterton, 1980)—was especially devastating in the Broad Street area of the Soho district, where the death toll reached three times the rate in London as a whole.

Snow on Broad Street In addition to being the site of numerous cowsheds, animal slaughterhouses, grease-boiling pots, overcrowded working-class dwellings, and decaying sewers, Soho was home to the now infamous Broad Street pump. John Snow, a physician who had initially gained fame in 1846 by successfully administering the anesthesia chloroform to Queen Victoria during the births of Prince Leopold and Princess Beatrice, claimed that this public water station was the source of the local outbreak and that some kind of living entity in the water, an unseen germ of some sort spread by fecal contamination, was the cause. Snow was convinced the pump was a primary source of infection because the surrounding area was so hard hit during the outbreak. Between August 31 and September 10, over 500 people who lived on or near Broad Street (now renamed Broadwick Street) died of cholera (and ultimately 616 people in Soho were victims of the epidemic). People were fleeing the neighborhood in terror. Snow lived nearby, and he began interviewing the family members of those who had died, thereby inventing field epidemiology in the process. Using addresses that Farr had provided (despite his disagreement with Snow’s perspective on disease causation), it was not long before Snow realized that families who drew their water from the Broad Street pump were the hardest hit and that most of the deaths were among people who lived only a short distance from the pump. He also found that not one of the seventy workers at the nearby Broad Street brewery had gotten sick; these workers were given free beer everyday and consequently never drank water from the pump.

This sociogeographical patterning of disease cases, Snow concluded, could not be explained by miasma theory. To prove his case he even tried examining samples of water from the pump under a microscope, although not one powerful enough for him to see the microbes they contained. Nonetheless he was convinced by his other findings that the germs were there and the cause of the illness and death occurring around him. He consequently self-published a report for distribution to fellow physicians and friends, followed by an essay published in the London Medical Gazette (Summers, 1989). Meanwhile, William Budd, in Bristol, England, who would later gain medical fame by demonstrating that typhoid fever was a waterborne pathogenic disease, had reached a conclusion somewhat similar to Snow’s and published his view in a book a month after Snow’s essay appeared. The difference was that Budd thought the agent of cholera was a fungus, which he and a group of fellow physicians believed they had observed in the stools of cholera patients, a view that was soon discredited.

Contested Understandings The initial response of health officials to Snow’s assertion is reflected in the tone of the summary of it developed by John Simon, a physician who served as the head medical officer of London at the time: “This doctrine is, that cholera propagates itself by a ‘morbid matter’ which, passing from one patient in his evacuations, is accidentally swallowed by other persons as a pollution of food or water; that an increase of the swallowed germ of the disease takes place in the interior of the stomach and bowels, giving rise to the essential actions of cholera, as at first a local derangement; and that the morbid matter of cholera having the property of reproducing its own kind must necessarily have some sort of structure, most likely that of a cell” (quoted in Frerichs, 2001). Although Simon plainly understood Snow’s theory, lacking direct evidence of the cell in question he found the argument, so to speak, hard to swallow, and rejected the relevance of germ theory to the cholera epidemic.

Similarly, despite Snow’s national stature, the Committee for Scientific Enquiries, under Farr’s influence, eventually concluded that “[a]fter careful inquiry, we see no reason to adopt [the belief that the Broad Street pump was to blame for the outbreak]. We do not feel it established that the water was contaminated in the manner alleged [by Snow]; nor is there before us any sufficient evidence to show whether inhabitants of that district, drinking from that well, suffered in proportion more than other inhabitants of the district who drank from other sources” (Eyler, 1979, p. 118).

Instead, cleaving to miasma theory, the committee concluded that “on the whole evidence, it seems impossible to doubt that the influences, which determine in mass the geographical distribution of cholera in London, belong less to the water than to the air.” Indeed, the committee went so far as to scold those who followed Snow in accepting the germ theory of disease: “Many of the public believe that everything we eat and drink teems with life, and that even our bodies abound with minute living and parasitic productions. This is a vulgar error and the notion is as disgusting as it is erroneous” (quoted in Winterton, 1980, p. 17).

Another well-known proponent of the miasmatic theory at the time (although like others working in medicine she later embraced germ theory) was Florence Nightingale, who had gained an international reputation as a devoted nurse during the Crimean War (no mean accomplishment given the opposition to female nurses caring for wounded male soldiers). Because of her belief in miasma theory (and her statistical calculations showing that seven times as many British soldiers died from diseases contracted in the hospital as died from wounds received on the battlefield), she campaigned for the reform of hospitals, insisting that they be regularly cleaned and scoured until sanitary and fresh smelling. During the 1854 cholera epidemic, while serving as superintendent at the Institute for the Care of Sick Gentlewomen, in Upper Harley Street, London, Nightingale also volunteered at Middlesex Hospital, which received many of the victims of the epidemic. Of the 278 cases of cholera treated at the hospital, 123 died—a fatality rate of 53 percent—including one of the hospital’s nurses (Johnson, 2006). Yet to Nightingale’s mind’s eye what was occurring was not the transmission of living, disease-causing microorganisms but rather the emergence of impurities from foul environments. This view also led her to write about her experience with another disease (in a footnote in the pamphlet “Notes on Nursing for the Labouring Classes”), “I have seen with my eyes and smelt with my nose smallpox growing up in first specimens, whether in closed rooms, or in overcrowded wards, where it could not by any possibility have been ‘caught’ but must have begun” (quoted in Penner, 2004, p. 92).

Ending the Epidemic Although the Committee for Scientific Enquiries was later to reach its conclusion that the cause of the cholera epidemic was bad air, when the members of the London Board of Governors heard Snow’s argument, they ordered the closing of the Broad Street pump, and the epidemic soon faded away. Consequently, although no one in London had seen the germ involved in the development of cholera, the 1854 epidemic ultimately gave considerable impetus to the rise to dominance of germ theory within biomedicine. Ironically, Italian biologist Filippo Pacini had already identified the cholera bacterium and had published a scientific paper on his discovery (“Microscopical Observations and Pathological Deductions on Cholera”) through the Paris Academy of Sciences. Using a microscope he had purchased with his limited savings while still a medical student, Pacini conducted histological examination of the intestinal tissues of individuals who had died of cholera in Florence and identified a comma-shaped bacillus that he named Vibrio. Unfortunately, as sometimes happens in science with findings that are ahead of their time, Pacini’s paper was ignored for thirty years, and it is unlikely that Snow had any awareness of it. (Pacini was finally credited with his discovery, eighty-two years after his death, when the International Committee on Nomenclature adopted Vibrio cholerae Pacini as the official name of the microorganism that is the proximal cause of cholera.)

The Rise of Germ Theory

Despite their considerable contributions, neither Snow nor Pacini was in fact the first to propose a germ theory of disease. Almost two thousand years earlier, Marcus Varro (116-127 B.C.), the architect whom Julius Caesar had assigned to the task of building a great public library in ancient Rome (a project that went unrealized because of Caesar’s assassination), had warned those looking to select hygienic locations for buildings to avoid areas near swamps, because “in swampy places minute creatures live that cannot be discerned with the eye and they enter the body through the mouth and nostrils and cause serious disease” (quoted in Amici, 2001, p. 4). How Varro, lacking the technology to identify them, came to believe in the existence of disease-causing microbes is not clear. The microscope was not invented until the late 1600s, although magnifying glasses and the use of emeralds for magnification purposes are mentioned in Naturalis Historia, written by Pliny the Elder, a Roman naturalist and philosopher who lived during the first century A.D. What is known is that Varro’s recognition had little impact on the medical perspective of his day or subsequently and is of interest today primarily as an intriguing footnote in the history of disease understanding.

During the sixteenth century, having observed epidemics of bubonic plague, typhus, and syphilis (and having written a 1,300-verse poem in Latin hexameters focused on a fictional shepherd named Syphilus, the source of the latter disease’s modern name), the Veronese physician Girolamo Fracastoro (circa 1478-1553) came to question miasma theory (as well as beliefs about divine retribution) as lacking in evidentiary support. In his major medical treatise, On Contagion and the Cure of Contagious Diseases, published in 1546 (and in which he dismisses his poem as a youthful endeavor), he asserted there was better support for the notion that diseases were spread by tiny living or at least lifelike seminaria (seeds) or germs (although his recommended treatment was bleeding the sufferer and administering mercury to return him or her to humoral balance). This view of disease causation has led some to nominate Fracastoro for the title “father of germ theory” (see, for example, Greenwood, 1953), although others question this titling (Magner, 2002) owing to ambiguities in Fracastoro’s sixteenth-century narrative and to his speculation that seminaria might arise from poisonous emanations born of planetary conjunctions (a factor in Stephen Jay Gould’s [2000] argument that the greatest “poetry” ever composed about syphilis was penned not by Fracastoro but by the scientists who methodically and meticulously developed the elegant map of the 1,041 genes that constitute the genome of the pathogenTreponema pallidum, now known to be responsible for the disease).

Less conflicted and ambiguous was the contribution of Jacob Henle (1809-1885), a prominent German pathologist after whom various structures within the human body, some of his own discovery, are named. Henle compared alternative explanations of disease in his 1840 book Misamata and Contagion. Although the book did not achieve instant recognition as a critical turning point in medical disease understanding, it “was retrospectively recognized as a landmark” (Magner, 2002, p. 256) with the subsequent confirmation of germ theory. This triumph was achieved when Louis Pasteur (1822-1895), demonstrated in the 1860s that specific microbes are responsible for specific fermentations and later linked microbes to disease (initially in silkworms), and when Henle’s student Robert Koch (1843-1910) isolated both the microbe causing cholera and the microbe causing tuberculosis.

Aftermath of the Epidemic Living on the cusp of the great transition from the miasmatic to the germ theory of disease causation, William Farr eventually came to embrace Snow’s (and Pacini’s) understanding of cholera and of infectious disease generally, as did most of his fellow biomedical physicians. His conversion to the new paradigm marked both the broader transformation going on in medicine—namely its emergence as a bioscience—and the celebration of Snow’s role in that process. Indeed, in a March 2003 survey that Hospital Doctor magazine conducted of its readers, John Snow was voted the “greatest doctor” of all time, with Hippocrates coming in second (Oleckno, 2008). Although it has been suggested that Farr did not initially accept Snow’s ideas about germ theory because, unlike Snow, he was not open to new perspectives, Eyler (2001) stresses that the reverse may have been the case: “Judged by the standards of his time Snow was the dogmatic contagionist and premature reductionist. Farr was the more cautious in weighing all evidence” (p. 230). As a result of Snow’s and others’ dogged commitment to an idea (and to seeking out the evidence to support it), germ theory evolved from a controversial notion into the cornerstone of biomedical disease theory. In the process, biomedicine came to privilege understanding cell biology over understanding the social origins of disease and other disorders, an emphasis that has hindered a broad ecological conception of human illness (Singer, 1986).

Separation of the Part from the Whole The scientific discoveries that propelled the acceptance of germ theory not only undercut older views of disease causation but have also contributed to the development of an understanding that differentiates biomedicine from other ethnomedical systems around the world. Davis-Floyd and St. John (1998) have called this understanding “the principle of separation,” and see it as a product of “an overwhelmingly linear mode of thinking” (p. 17). This principle stipulates that each of the world’s various entities is best understood when considered independently of the other entities of its natural environment. Davis-Floyd (1994) observes that “the essence of [biomedical] research and description is separation—of elements from the whole they compose, of humans from nature, of mind from body, of mother from child” (p. 1127). Similarly, George Engel (1977), an anthropologically informed physician who during his life specialized in the psychophysiological aspects of human health and illness, argued that the distinctive feature of biomedicine is its embrace of “both reductionism, the philosophic view that complex phenomena are ultimately derived from a single primary principle [in this case, that everything can be explained in terms of chemistry and physics], and mind-body dualism, the doctrine that separates the mental from the somatic” (p. 130).

Reflective of this atomistic approach to knowledge, biomedicine separates the person with an illness from his or her immediate social context and community, diseased organ systems from the whole body, and one disease from another. Further, it breaks every disease into its constituent parts and manages disease treatment through a complex and atomistic array of medical specialties. As Davis-Floyd and St. John (1998) stress, a “drive toward separation” if carried to its logical extreme, as has more or less occurred in biomedicine, can “obscure the many meanings in the non-linear” and “the interconnections and relationships between entities” (p. 17). In his widely cited article quoted earlier, George Engel (1977) maintained that biomedicine’s adherence to “a model of disease [that is] no longer adequate for the scientific tasks and social responsibilities” of the discipline has led to a crisis in biomedicine. Herein lies the value of a syndemic perspective, which seeks to clarify the impact of biosocial interconnections and relationships (p. 129).

REVOLUTIONS IN BIOMEDICAL REALITIES

Although biomedicine “purports to be belief- and value free” (Gaines & Davis-Floyd, 2004, p. 100), its understanding of reality—its ontological conception of the nature of nature and of basic life processes—is rooted in a particular construction of the world, an ideology that has both driven and reflected the encompassing Western cultural worldview. Germ theory, and biomedical understanding generally, initially assumed that like cholera each infectious disease is caused by a specific, identifiable pathogen.

Although this view opened the world up to new insights (including the discovery of a wide array of pathogens), it has also carried conceptual restrictions. As Francois Jacob (1988), winner of the 1965 Nobel Prize in medicine, notes: “In analyzing a problem, the biologist is constrained to focus on a fragment of reality, on a piece of the universe which he arbitrarily isolates to define certain of its parameters. In biology [including medicine] any study begins with a ‘system.’ On this choice depend the experimenter’s freedom to maneuver, the nature of the questions he is free to ask, and even the type of answer he can obtain” (p. 16).

When constraint is imposed on biomedical thinking, it limits not only, as Jacob suggests, the nature of the questions that are asked but also the answers that are meaningful, acceptable, even thinkable. As historian of science Thomas Kuhn noted in The Structure of Scientific Revolutions, a seminal book on the scientific process, this is the everyday or normal way scientific understanding operates. In any specialized subfield (including biomedicine), science tends to be guided by a reigning paradigm, that is, by “an entire constellation of beliefs, values and techniques, and so on, shared by the members of a given community” (Kuhn, 1970, p. xii). In common contemporary parlance, scientific thinking normally takes place “within the box,” because unless doubts and uncertainties about basic assumptions have arisen to rattle confidence in that box (for example, through research findings that cannot be explained because they appear to fall “outside the box”), the box defines reality. Thus once germ theory and its “to each disease its own unique pathogenic cause” perspective gained dominance in biomedicine, a paradigm effect occurred, canalizing thinking and hindering attention to other ways of seeing the available evidence.

PROBLEMS WITH THE POSTULATES

Despite the compelling force of reigning paradigms, as Kuhn emphasized, science is not stagnant (by design!) and revolutions in scientific thinking are, one might argue, equally a normal part of science. Consequently, since the adoption of germ theory, scientific understanding about the causes of disease has continued, in stages, to evolve. These changes can be seen as stemming in part from problems encountered in implementing a set of postulates developed by Koch (and broadly accepted in the field as the gold standard) for determining whether a particular microbe is the cause of a specific disease. For medical science to affirm that a particular organism causes a disease, Koch (1890/1987) argued:

1. The organism must be present in every case of the disease but not in healthy individuals.

2. The organism must be capable of being isolated from the sufferer and grown in pure culture.

3. The specific disease must be reproduced when a pure culture of the organism is inoculated into a healthy, susceptible host.

4. The organism must be recoverable from the experimentally infected host.

The problems began during the period just after the achievements of Snow, Pasteur, and Koch became generally known, an epoch often thought of as the golden age of breakthroughs in medicine and infectious disease research. For Theobald Smith, a physician turned pathology researcher who was to become a preeminent pioneer in American microbiology, it was an exciting time of regular discoveries of pathogens, vectors, and disease causation. It was also a time during which diseases like hog cholera (now called classical swine fever) “swept through the countryside, causing devastating losses. During the fall months, looking across the prairies of the Middle West, one could often see smoke ascending from perhaps a half-dozen farms where pigs dead of cholera were being burned” (McBryde, quoted in U.S. Department of Agriculture and Agricultural Research Service, 2006). In 1884, as a lowly lab technician in the newly created U.S. Department of Agriculture’s Bureau of Animal Industry (BAI), a center established by Congress to respond to costly waves of livestock epidemics, Smith set out to discover the cause of hog cholera, one of the most economically damaging pandemic diseases of pigs in the world.

When Smith came to this line of work, he had two years of medical training and had read, on his own, the papers of Pasteur. At the BAI he was supervised by veterinary pathologist and BAI chief Daniel Salmon (for whom Salmonella, the enterobacterium that causes diseases like typhoid fever, paratyphoid fever, and food poisoning, is named, even though it was actually discovered by Smith, a point of enduring tension between the two scientists; Dolmon, 1969). Having confirmed that a microbe, Salmonella choleraesuis (now called Salmonella enterica), was found consistently in pigs suffering the symptoms of hog cholera and could be isolated and grown in pure culture, having seen the disease after healthy hogs were infected with the microbe, and having recovered the bacterium from animals that had been infected in this way, Smith (although Salmon insisted on first authorship of the published findings) concluded that Koch’s postulates had been met, and declared that the cause of hog cholera had been discovered. Notably, both Pasteur and Koch accepted this conclusion and assumed that the problem of hog cholera was well on its way to resolution (Zinsser, 1936). This proved not to be the case, as Marion Dorset, another BAI scientist, had no success with a serum made from the Salmonella choleraesuis bacterium during an 1897 outbreak of the disease in Iowa. Six years later, Dorset was able to show that the actual cause of hog cholera was not a bacterium at all but a virus (genetically a much simpler entity), a discovery leading to the eradication of the disease in the United States.

Why had Smith, known to be a cautious worker, gone wrong? As it turned out, swine infection with S. enterica, which causes its own health problems (salmonellosis and typhoid fever), was secondary to the viral infection. Smith, in other words, had unknowingly stumbled on a synergistic interaction among animal pathogens in which one (a virus) facilitated infection by another (a bacterium) producing frequent coinfection, and he had identified the wrong pathogen as the cause of hog cholera. Because of his many subsequent discoveries (such as the role of a protozoan parasite, babesia, in the development of Texas fever among cattle and the activity of ticks in its transmission), this mistake did not hurt Smith’s career, but its occurrence is instructive about the potential consequences of assuming one has successfully isolated a pathogen.

Disease Carriers Over time other problems with Koch’s postulates also emerged. First, the discovery of asymptomatic disease carriers threw into doubt the idea that a known pathogen could not be found in healthy individuals. Mary Mallon, an early twentieth century cook for several New York families, for example, was found to be a carrier for typhoid fever (caused by S. enterica). Although she had no disease symptoms, she did pass on the bacterium to twenty-two members of the families she worked for and who did become sick, earning her infamy as Typhoid Mary. As a public health measure, she was forcibly quarantined in an institution on an island in the East River for much of the rest of her life. Mary Mallon was not unique; asymptomatic carriers (sometimes called well carriers) are now known to be a common feature in the spread of many infectious diseases, including polio, herpes simplex, and hepatitis. When Koch discovered that there were asymptomatic carriers of disease, he dropped the second half of his first postulate.

Uncultivable Microbes It has also turned out that some microbes cannot be successfully grown in pure culture. For example, bacteria in the rickettsia family (responsible for an array of diseases, such as Rocky Mountain spotted fever) cannot live in artificial nutrient environments. Similarly, Mycobacterium leprae, the bacillus that causes leprosy, has never been cultivated in vitro in its classic rod-shaped form, because it appears to lack the genetic capacity to grow outside the human body. Further, although a significant number of bacteria have been isolated in the human mouth, it is estimated that only about half the species that dwell in the oral cavity can be cultured (Rolph et al., 2001).

Over time other strategies, such as molecular techniques, have been adopted to identify bacteria species that have never been cultivated. It was only with the introduction of molecular genetic strategies, for example, that the uncultivable bacterium Tropheryma whippelii was identified as the cause of Whipple’s disease, a chronic, systemic infectious disease, most common in middle-aged men, that typically causes malabsorption in the small intestine and a wide range of other clinical manifestations including arthritis. Additionally, new culture methodologies have been invented in recent years, such as chicken tissue and embryo cultures (which can be used to grow rickettsia bacteria). Still, it is assumed by most microbiologists and pathologists that there are many pathogenic microorganisms at play in human health that have yet to be identified because of the limitations of existing technologies. Only in very recent years, as discussed in Chapter Five, have researchers discovered the viral origins of some chronic diseases previously believed not to be contagious (such as peptic ulcer disease, in which Helicobacter pylori plays a role, and cervical cancer, which involves several human papillomaviruses).

One consequence of encountering an uncultivable microbe is evident in the case of Lyme disease, which is caused by several species of the hard-to-culture spirochetal Borrelia bacterium. Although Lyme disease is recognized as the most common tick-borne disease in North America and Europe, as well as one of the fastest-growing infectious diseases in the United States (with over 20,000 cases a year nationally since the turn of the twenty-first century and over 30 cases per 100,000 persons in the ten most heavily infested states), inability to culture its causative agent has led to considerable professional disagreement and intense acrimony over the guidelines to be used in diagnosis. The Centers for Disease Control and Prevention (CDC) has been forced to rely on such potentially ambiguous criteria as presentation of symptoms (which can vary considerably across infected individuals), physical findings (such as a bull’s-eye rash, which does not appear in many cases), and the possibility of exposure to infected ticks (such as the black-legged tick in North America and several other tick species in Europe) based on place of residence or visitation (CDC, 2006b).

Masked Infections Problems with Koch’s third postulate began with the fact that some pathogens cannot be cultured, but other difficulties have arisen as well. For various reasons (such as acquired immunity from prior exposure to a pathogen, as occurs with influenza, and genetic immunity, as seen for example in individuals who acquire a sickle cell allele from at least one parent), exposure to a pathogen does not necessarily lead to detectable infection. Of even greater importance for the issues under consideration is the fact that the presence of a second pathogen (for example, one that weakens the immune response to the presence of foreign organisms generally) can increase the likelihood that infection will develop in exposed individuals. In other words, in many instances, without the bodily effects of synergistic interaction among diseases, mere exposure to a single pathogen (including intentional inoculation) does not produce disease. At the same time, if the disease of concern is in fact the consequence of interaction among pathogens or other disease causes, it will not develop (or have the same expression) unless the new host is exposed to all those pathogens or causes.

Immune Response and the Reisolation of Pathogens In addition to the challenges to Koch’s postulates already discussed, there can be difficulties with the reisolation of a pathogen from an inoculated individual because that requires the capacity to segregate and culture the pathogen. This capacity does not exist for some microorganisms (including those that infect only humans and hence, for ethical reasons, can never be tested using Koch’s postulates), and it does not exist in cases of a healthy immune system because the body has eliminated the pathogenic agent (although it may exist in cases of coinfection owing to degradation of immune system capacity). Additionally, the modus operandi of some pathogens, as found for example in rheumatic heart disease (which begins with a streptococcal throat infection), involves what might be called a hit-and-run pattern, in which the organism is no longer in the host by the time the disease is evident.

Complexities of Disease Understanding Multiplying the difficulties encountered in using the postulates was the realization that a single disease might have multiple causes (a situation known as multifactorial disease) and that a single pathogen might produce more than one disease. These issues extend beyond infectious disease to disease with an environmental or genetic origin. For example, with regard to the first point, it is recognized that the chronic eye infection known as trachoma is a common source of blindness in developing countries. This disease has been linked to sexually transmitted infection with the pathogen Chlamydia trachomatis. Research by Dean, Kandel, Adhikari, and Hessel (2008), however, has found that trachoma can also be caused by Chlamydophila psittaci and Chlamydophila pneumoniae. Consequently, these researchers conclude that the existence of multiple agents causing trachoma helps to “explain the failure to detect chlamydiae among active trachoma cases, when only C. trachomatis is assayed,” “the failure of active trachoma cases to resolve their clinical disease following effective C. trachomatis treatment, and the limited effectiveness of the WHO strategy to control trachoma” (p. e14). Also of note in this regard is the potential effect of interaction among copresent trachoma-causing pathogens. Similarly, coinfection with multiple strains of the microbe that causes dengue can significantly change the clinical picture and severity of that disease (a topic to be discussed in Chapter Six).