Purpose – To analyze the concept of emerging infectious diseases, departing from the accepted definitions adopted by the Centers for Disease Control and Prevention (CDC, USA) and the now classical definition suggested by Grmek (1993, 1995). The emphasis of this chapter is on the roles that socio-economic and cultural changes play on the emergence of diseases.
Grisotti, M. and Dias de Avila-Pires, F. (2010), "The concept of emerging infectious disease revisited", Mukherjea, A. (Ed.) Understanding Emerging Epidemics: Social and Political Approaches (Advances in Medical Sociology, Vol. 11), Emerald Group Publishing Limited, Bingley, pp. 61-75. https://doi.org/10.1108/S1057-6290(2010)0000011008Download as .RIS
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The decline in the incidence of certain diseases such as tuberculosis preceded the findings of Pasteur's microbiology, and was ascribed by historians of medicine to the improvement in the general conditions of housing, sanitation, and hygiene. The post-war belief that exogenous infections were on the wane proved to be premature. The expectations surrounding the conquest of infectious and parasitic diseases, with the advent of the theory of the microbial origin of infectious diseases followed by the production of serums and vaccines at the end of the 19th century and by the discovery of sulfa-based and other antibiotics in the 20th century, did not fulfill our optimistic expectations. The emergence of HIV/AIDS and of a number of zoonotic diseases at the end of the 20th century disproved the concept of an epidemiological transition where infectious and parasitic diseases would give way to endogenous, chronic, and degenerative conditions as the main causes of human morbidity and mortality.
Microorganisms are versatile, and display a wide array of adaptations to adverse environmental conditions both in the external world and in the internal milieu of their hosts. Advances in our understanding of their biological processes, in the production of new generations of antimicrobial drugs and vaccines, and in the improvement of effective barriers to their dispersal are actually slower than the possibilities of mutation, recombination, and dispersal shown by microorganisms (Ochman, Lawrence, & Groisman, 2000).
Furthermore, the supposedly chronic nature of several diseases is currently being questioned, since the description, in 1979, of Helicobacterium pylori, a bacterium that proved to be associated with gastric ulcers. Peptic ulcers, formerly thought to originate mainly from stress, may result from the colonization of the stomach and duodenum by H. pylori, which survives the extremely acidic environment of the stomach, being the only organism capable of doing so. Antibiotics are now used to treat ulcers (Relman, 1998; Ewald, 2002; O'Connor, Taylor, & Hughes, 2006).
This is the context in which the concept of emerging infectious disease arose. However, an analysis of the literature points to existing ambiguities in this concept, especially when viewed from a historical perspective. Different points of view lead to distinct meanings of this expression, resulting in confusion. What does a new disease mean? When can we recognize it as an emergent one? Is a given disease the same in distinct hosts, human and non-human, or even in different individuals (Sournia, 1984; Delaporte, 1998)?
Emerging diseases include both infectious and chronic/degenerative conditions. Our objective is to analyze the concept of emerging infectious diseases, departing from the accepted definitions adopted by the Centers for Disease Control and Prevention (CDC, USA) and the now classical definition suggested by Grmek (1993, 1995). The emphasis of this chapter is on the roles that socio-economic and cultural changes play on the emergence of diseases, with respect to changes in the factors that determine the natural history of disease.
In order to illustrate the concept of emergence, we present two case studies. The first describes the constitution of abdominal angiostrongyliasis in Costa Rica, where it is considered an endemic disease diagnosed as part of routine tests performed on patients with tumors and negative appendectomies. In Brazil, however, it is considered an emerging infectious disease, unknown to both medical doctors and the general public, and controversial as to its diagnosis and incidence. The second concerns an outbreak of Chagas disease that took place in 2005 in the state of Santa Catarina, Brazil, a disease that is endemic in most areas of Brazil and other countries in the American continent but ignored in this state.
How human infectious diseases emerge and spread
In order to understand the emergence of diseases we must learn something about the nature of diseases, the role of biological and sociocultural interventions and predisposing factors regarding incidence, the nature of parasitism, and the importance of the geographical distribution and dispersal of pathogenic organisms across the globe. To this end, we borrow some concepts from biogeography. A combination of biological and sociocultural factors is found at the root of all human infectious and parasitic diseases. As to their evolutionary origins, the great majority of such conditions were acquired from non-human reservoirs along our evolutionary history. Some became so well adapted to humans as to lose the ability to infect their former hosts (Sournia, 1984; Karlen, 2001). Among these we find measles, rubella, and falciparum malaria. A few others originated from a normal endogenous microbe, as Escherichia coli strayed from its normal microhabitat in the colon.
From a scientific evolutionary point of view, we may be interested in the investigation of a novel association between a pathogen and a host. Along the history of Homo sapiens and its ancestors, there were many occasions for the acquisition of new parasites, following with the changes in diet, level of activity, domestication of plants and animals, farming, and urbanization (Karlen, 2001); paleopathologists, paleoarcheologists, and paleoparasitologists are involved in this type of investigation. Besides, historians of medicine search for the routes of dispersal of diseases across the globe. The American continent, Australia, and the oceanic islands offer a good field for this type of investigation (Crosby, 1994) because many diseases emerged in these places that did not exist there prior to the arrival of European colonizers.
Regarding geographical origin, for instance, bubonic plague originated in Mongolia, with steppe marmot hunters, and followed the dispersion of the black rat, Rattus rattus, across Asia, Europe, Africa, and the Americas. Syphilis originated in Europe and not in Central America as was previously believed. The search for the geographical origin or source of the influenza pandemics that periodically occur points to southern China, where an ingenious system of rice cultivation leads to an epidemiological chain involving ducks and pigs, enabling non-human influenza strains to infect humans.
Before the advent of paleoparasitology, we were restricted to the often inaccurate or mythic description of symptoms by traveling medical doctors and naturalists. Recently, the search for parasites in coprolites became an important tool to pinpoint the advent of a given parasite to a given region as well as the parasite's provenance. In the case of old European colonies, paleoparasitology indicates if a parasite existed before the arrival of the colonizers.
Where emergence is concerned, it may be helpful to adopt the definitions used in the field of biogeography. Simpson (1953) defines an autochthonous organism as one that has evolved in the same place where it now exists. A native organism is one that exists naturally in a region, not having been introduced there by accident or purpose. Dubos, Shaedler, Costello, and Holt (1955) and Dubos (1965) adopted Simpson's definitions, and Hershkovitz (1958) equated native, autochthonous, and indigenous to be equivalent to Simpson's autochthonous. Simpson's, Dubos', and Hershkovitz’ suggestions as applied to animal evolution and geographical distribution are useful in our present context of emerging diseases.
Schistosomiasis mansoni (also known as bilharzia or snail fever), for instance, is autochthonous in Africa and is now native in Brazil, where it was first introduced with the slave traffic and found local viable intermediate snail hosts (Biomphalaria spp.) as well as alternative mammal reservoirs.
Changes in the physical environment or changes in social mores can also facilitate the emergence of infectious diseases. The expansion of schistosomiasis that resulted from the building of the Aswan reservoir has been widely reported. Scientists had predicted and expected an increase in the incidence of schistosome infection (snail fever) in consequence of the damming of the Nile River. Predictions were proved true when the annual floods became perennial. The Aswan High Dam and the Nile itself became a suitable habitat for year-round undisturbed populations of the snails that transmit the parasite to humans. Before the construction of the dam, irrigation canals dried up as there was an enforced period of 40 days of closure. During the ensuing flood of the river Nile, the silt with the snails and the weeds deposited on the dry beds were washed away. Population displacements and social disorganization resulting from revolutions or wars have given rise to well-publicized epidemics. Floods, earthquakes, and natural disasters always are followed by a rise in morbidity and mortality rates, and trade, travel, and deliberate or unexpected transportation and introduction of plants, animals, and microorganisms aid the worldwide dissemination of diseases.
Emerging infectious diseases, according to the CDC definition, are those infections that appeared recently in a population, or those that already existed but are spreading rapidly, in terms of both incidence and geographical distribution (Lederberg, Shope, & Oaks, 1992). Such spread may be due to the recent introduction of a new etiological agent or to a mutation arising in an existing agent, followed by its rapid dissemination in the population (Morse, 1995).
Throughout human history, many diseases have appeared and vanished, but it has not always been possible to ascertain if they were actually new or if they had been present but undetected. For this raison, Grmek (1993) substituted the idea of emergence for that of novelty and proposed five distinct historical instances for the recognition of emergence and novelty. In the first four, diseases may be considered emergent, and in the last one, as new.
It existed before being recognized, but escaped medical attention because it went unrecognized as a nosological entity of its own.
A seemingly new disease may have been confused with another disease for a long time or may simply not have been diagnosed and recognized by medical science. In this sense we agree with Latour and Woolgar (1979), accepting that social facts are socially constructed and, therefore, a disease is a social construct. We disagree with those authors in recognizing the objective reality of lesions, vectors, and parasites. They exist and have existed long before the appearance of humans, independent of the observer and of their official taxonomic, scientific, or popular recognition. Diseases, on the contrary, are collective descriptions of signals and symptoms as they affect different individuals mediated by culture (Avila-Pires, 2008). The highly subjective expressions “fever is high in most cases” and “many patients develop a rash, which may be absent in others” are clear evidence of the constructed character of diseases.
The case of Chagas disease is seminal. This disease actually emerged twice. The first time in 1909 when Carlos Chagas, a Brazilian medical researcher, described what he considered a new disease. Unfortunately, he gave a composite description of its symptoms and called it a “parasitic thyroiditis.” The second emergence occurred after bitter arguments among researchers and was due to the Argentinean researcher Romaña who showed that Chagas had combined the real American trypanosomiasis and goiter in a nosological chimera (Delaporte, 1999).
Ensuing epidemiological investigations revealed that Chagas disease was widespread on the American continent, affecting millions of people before it was recognized by scientists.
It existed, but was only detected after a qualitative and quantitative alteration of its characteristics made it noticeable.
Biological evolution is a law of life. Pathogens evolve as do their vectors, hosts, and reservoirs. Changes in microorganisms may be rapid, enabling the invasion and colonization of new hosts, or leading to an increase or reduction of virulence. Hosts and reservoirs of pathogens act as biological filters, selecting genomic lineages among the vast array of natural polymorphic variants, which are capable of surviving the host's body defenses. Avian influenza viruses, for instance, do not infect humans, but if they are passed on to pigs, they may acquire that ability. Before this can happen, pigs and birds must coexist, allowing viruses to adapt to mammalian hosts before they can mutate and pass on to humans. In this category, life style and social behavior and the organization of public health services are fundamental to the emergence of infectious diseases.
A good example is the widespread use of air conditioning in houses, hotels, and hospitals with poor maintenance, providing the necessary conditions for legionellosis (Legionnaire's disease) outbreaks to emerge. Another example, presented by Grmek (1993), is toxic shock syndrome. Although described in 1978 as a new disease, it is actually a particular expression of the pathogenic action of the old staphylococcus, which results from the increased use of high-capacity tampons by women, which allow for an increase in the bacteria's virulence.
Our present concern also lies with the forecasts based on the possible consequences of global warming. The rise in global average temperatures may affect the geographical distribution of existing vectors and reservoirs of infectious diseases, thus widening the prevalence of zoonotic diseases in humans.
It was introduced in a region where it did not occur previously.
Migrations, wars, and the movement of people are chief factors in the spread and emergence of diseases (Thomas, 1956), as Crosby (1986) illustrated with respect to the role of colonialism. European expansionism was responsible for the introduction of several infectious and parasitic diseases across the world. Migratory waves from Europe, and the introduction of slaves from the African continent into the Americas, accounted for the eruption of epidemics and for the subsequent endemization of Old World diseases in the New World. However, length of travel and distance prevented many diseases from spreading far. Either the sick or the non-human hosts, vectors, or microorganisms would die in route. Today, the speed of travel, tourism, and international trade contributes to the globalization of many infectious diseases.
The emergence of a disease acquired from a non-human reservoir.
The term zoonosis was incorrectly credited to the German pathologist Virchow. In 1951, a Joint Committee of Experts from the World Health Organization (WHO) and the Food and Agriculture Organization (FAO) of the United Nations adopted the current official definition: it applies to the transmissible diseases that naturally affect humans and other vertebrate animals.
Hemorrhagic fevers such as Ebola, Hanta, Nipah, Lassa, and Marburg, as well as severe acute respiratory syndrome (SARS) and bird flu, are good examples of viruses that caused epidemics in recent times. Not all epidemiological chains have so far been elucidated and, for some diseases, the original sources are not known. Outbreaks due to the importation of animals for laboratory research, surgical transplants or organs, and for the production of drugs occurred. Nipah virus passed from flying fox bats to pigs and to humans, in a chain of events propitiated by the special conditions where pigsties were located. Lassa and Hanta are passed from rodents to humans, and Ebola was transmitted from apes to humans.
A new disease, when the causal agent or the necessary environmental conditions for its occurrence did not exist before the first clinical observations identified its presence.
There is also the possibility that as the result of laboratory manipulation of pathogenic organisms intended for research, biological warfare, or genetic engineering of agricultural products, a new disease emerges and spreads. In this fifth instance, Grmek recognizes the existence of a certain continuity with the past, as no organism may originate from spontaneous generation.
In addition to the categories proposed by the CDC and by Grmek we add the role of under-notification of those conditions presented by official lists of diseases subjected to compulsory notification, and also the failure to recognize and notify uncommon diseases.
Our knowledge about the incidence and prevalence of diseases depends on a reliable system of notification. There are lists of notifiable diseases at different levels of health administration and control: international, national, and regional (state, province, county, and municipality). International health regulations adopted by the WHO established smallpox, poliomyelitis due to wild-type poliovirus, human influenza caused by a new subtype, and SARS as notifiable diseases. They also include the following diseases because they have demonstrated the ability to cause serious public health impact and to spread rapidly and internationally: cholera, pneumonic plague, yellow fever, viral hemorrhagic fevers (Ebola, Lassa, and Marburg), and West Nile fever.
However, under-notification is at the basis of many emergent diseases. These cases occur and are diagnosed, but doctors and health authorities ignore or fail to report them. To justify this category we present two case studies illustrating the role under-notification plays in the characterization of emerging infectious diseases.
The case of angiostrongyliasis
From a medical point of view abdominal angiostrongyliasis is a disease in which the symptoms are vague, for which there is no cure, and which can usually only be diagnosed by viewing and isolating the parasite through biopsies or detecting it through serological tests, when the result indicates an infection. There may be crossed reactions with other simultaneous or past parasitic infections and the treatment with anti-helminthics; drugs that kill pathogenic worms may result in the parasite migrating to other organs. The clinical manifestations occur in sites where such symptoms as severe abdominal pain, vomiting, and general weakness progressing to fever may be erroneously diagnosed as those of other diseases such as appendicitis or abdominal tumors.
In 1967, in Costa Rica, Céspedes et al. described a clinical case of a new disease for the medical science. In the same year Morera (1967) recognized its parasitic nature. In 1970 the intermediate (slugs) and definitive hosts (rodents) of the parasite were identified, and in 1971 Morera and Céspedes (1971), Morera (1971), and Morera and Ash (1971) described in greater detail the etiology, biological cycle, pathology, and the clinical characteristics of the disease.
In Brazil, a medical pathologist (Agostini, Marcolan, Lisot, & Lisot, 1984) described the first findings of the parasite and identified the characteristic intestinal lesions and was instrumental in expanding the study of this disease in the country. His former student and collaborator, Graeff-Teixeira became one of the foremost experts of angiostrongyliasis. In his doctoral thesis Graeff-Teixeira (1991) considered whether it was a new human parasitic disease or one that had been under-diagnosed, deciding in favor of the latter alternative. His own field research showed that the disease is commonly asymptomatic. His findings differ from those published in Costa Rica, where the disease seemed to be endemic. For Morera, the lack of medical knowledge was the main obstacle to showing the high prevalence of the disease, but for Graeff-Teixeira, the apparent rarity of this parasitosis in Brazil was due to the fact that, despite impressions that the disease occurs frequently, it is actually rare and, in most cases, asymptomatic. These differing conclusions derived from the different approaches taken by the researchers. Morera concentrated on individual case studies and anatomopathological (physically evident morbidity) results of tests, while Graeff-Teixeira (1991) relied on seroepidemiological (population-level clinical study) investigations in populations exposed to contamination, in areas where intermediate hosts were present using a test he developed.
Several articles reported the occurrence and distribution of cases in Brazil, although the disease went unreported in many states. In spite of the Graeff-Teixeira's conclusions regarding the possibility of under-diagnosis, we can neither rely on the prevalence of angiostrongyliasis nor dismiss the possibility of its wide presence, undetected, because of the lack of investigation.
Graeff-Teixeira's research indicated the need to revise the accepted diagnosis of the disease as described by Morera and the accompanying prophylactic procedures. Despite their differing conclusions, both Graeff-Teixeira and Morera agree that angiostrogyliasis is not a new disease but is under-diagnosed. From these facts, we conclude that this disease is endemic in Costa Rica and emergent in Brazil.
To be able to characterize a disease as emergent in a certain place and time, we depend on the following criteria: the ability to diagnose, and the medical outlook in a given place, at a given time; the state of the art concerning research in the relevant field and the available techniques at the disposal of medical doctors and scientists; and the priorities established by health authorities.
A localized outbreak of possibly emerging Chagas disease
In 2005 an unknown disease struck the members of a family from the municipality of Penha, northern Santa Catarina state, Brazil. It was eventually identified as Chagas disease. Early symptoms may not be easily recognized and include fever, anemia, swelling of lymphatic glands, and headaches, evolving to a pathological enlargement of certain organs as the esophagus, colon, and heart. A characteristic swelling of the site of the insect-vector bite is present. This disease has been considered, at different times, to be emergent, endemic, and under-notified, in view of the absence of official records of previous such cases in Santa Catarina.
A literature search showed that, since 1959, reports of the presence of the insect vectors of the disease have been on file in the official state health institute. In 1961, a scientific paper divulged the results of field investigations showing that in the state capital, Florianópolis, 40% of the insect vector Panstrongylus megistus and 70% of Rhodnius domesticus from natural environments, including nests of rodents and marsupials, were infected with a Trypanosoma cruzi-like protozoan. P. megistus is the most common species of the Chagas bug in Santa Catarina and is found living around houses and in chicken pens and other outbuildings in urban areas (Galvão, Mello, Ferreira Neto, & Leal, 1961).
By 1971, experts recognized that the situation of autochthonous Chagas disease was little known in Florianopolis and in the state of Santa Catarina. In 1985, a new study showed that 23.5% of all captured opossums and 5.2% of rodents found near human habitations were infected and reported two new cases of Chagas disease from Santa Catarina, one probably from Florianopolis. Although several papers reported new findings, no action was taken in order to investigate the occurrence of the disease in humans in the state (Schlemper et al., 1985).
In 2002, a doctoral dissertation (Silva, 2002) used the records at the Blood Bank (HEMOSC) of Florianopolis to show that there were prospective blood donors in the state of Santa Catarina, who were – or had been – infected with T. cruzi.
Current maps of the occurrence and geographical distribution of Chagas disease in Brazil show the state of Santa Catarina as free of this disease, in spite of the confirmed presence of infected animal reservoirs and vectors within its political borders. In consequence, there is no system of health surveillance for Chagas disease. The distribution of a disease can only be understood in terms of the ecology and environmental requirements of animal reservoirs, vectors, and parasites, which seldom coincides with political borders, as national, state, or municipal limits.
Chagas disease may also be present in large numbers of individual carriers that show no symptom of the infection. They are infected but not sick, or clinically ill. That was the situation in March 2005, when three deaths in the same family were officially recorded, soon to be followed by further cases in the area. At that time, a meeting on tropical medicine was taking place at Florianopolis, in which a paper on the possibility of oral transmission of Chagas disease in northeastern Brazil was read (Shikanai-Yasuda et al., 1991). The members of the affected family blamed sugar cane juice they had consumed at a roadside establishment. As the first tentative diagnosis of that unknown condition had been of leptospirosis, a water-borne infection, discarded when no contaminated source was found and laboratory tests showed presence of the parasite of Chagas disease in the blood of patients, the investigators assumed that the origin of the epidemic was the sugar cane juice.
Anyway, if the patients were contaminated orally or through the conventional pathway (an insect vector), the disease would be classified as emergent in Santa Catarina on the account of under-notification of this disease in this state.
It is time for us to reconsider the possibility of adopting a single, all-embracing definition of emergent diseases for the following reasons.
From a philosophical point of view, the alternative conceptions of infectious diseases as independent entities or as physiological alterations of subjects are of fundamental importance. Also of significance is the argument raised by Delaporte concerning the identity of diseases as they affect human or non-human hosts: what passes from a non-human host to the human species is a pathogen or parasite, not a disease. For that reason, Delaporte (1998) discounts Grmek's fourth category, the passage of a pathogen from a non-human reservoir to a human one as an emergent disease. Can we say, for example, that Chagas disease in an armadillo is the same as in humans? For that matter, what about different persons with the same disease but showing different symptoms? We are aware that the movement of a pathogen along a biological/epidemiological chain produces organic modifications. The introduction of organisms into a new environment may change the genetic composition of its populations. Dobzhansky (1941) described this phenomenon as a balanced polymorphism, as he observed the variation in the genetic composition of a population of Drosophila flies in the Amazons, and verified that certain genes were dominant at certain times of the year, according to changes in microclimatic conditions.
This issue involves the definition of disease and the conception of diseases as constructs, which also depends on the sociocultural context in which the researcher works (Avila-Pires, 2008). If we follow the CDC definition of emerging infectious diseases as infections that appeared recently in a population, or those that already existed but are spreading rapidly, we adopt a pragmatic point of view. It may be useful in the realm of public health administration, where actions do not always depend on the investigation of the origins and evolution of diseases. Controlling measures are often a generic nature, regardless of the specific identity of the pathogen, and are directed toward the manipulation of environmental factors and conditions, and to the adoption of sanitary measures concerning the quality of air, soil, water, wastes, vectors, and reservoirs. Those measures are intended to block the roads of disease transmission. Manson (1900) showed that it was possible to control a disease – malaria – without attacking the disease directly, or treating patients, but by using a model to estimate risk, and controlling the populations of mosquito vectors. Strategies are the same for groups of diseases, according to their ecology and means of dissemination, and are seldom – if ever – specific.
For a practicing physician who is required to arrive at a precise diagnosis and prescribe a proper treatment, these philosophical issues are both academic and immaterial. For historians and epidemiologists, however, the search for the index case in an epidemic is a valid endeavor, as it is also the search for the original non-human reservoirs and vectors of new human pathogens. For recent examples, see the searches for the non-human sources of hemorrhagic fevers and HIV.
On the other hand, if we adopt Grmek's proposal, we end by considering almost every infectious disease to be emergent. For instance, seasonal common influenza emerges every year. Diseases that are endemic within the confines of a given geographical region would be considered emergent when introduced elsewhere, which happens all the time. Children's diseases, such as measles and mumps, reemerge every seven or eight years in places where vaccination is not the rule, as a new generation reaches school age.
Another source of confusion when we try to adopt a single definition arises from the fact that different researchers may define and classify diseases in different ways or even use the term “disease” ambiguously. For example, the history of medicine records three major pandemics of plague: the first began during the 14th century, the second in the 17th century, and the third in the 19th century. The pathogen was Yersinia pestis in all cases, but, with respect to clinical symptoms, they were distinct diseases. The first epidemic was bubonic plague, which is not airborne and requires a flea vector to be transmitted from one human to another. The 17th-century epidemic, which became known as the Black Death, was pneumonic plague, which is one of the most contagious airborne diseases known and necessitates the isolation of patients and the institution of quarantine. For a bacteriologist they are the same disease, but for the practicing medical doctor they require different approaches and treatments, while for the public health official they demand different responses and controlling measures. Another disease that provokes distinct symptoms in its hosts is rabies. Rabies is a viral zoonotic neuroinvasive disease that causes acute encephalitis and has a lethality of 100% in humans. It affects several species of mammals and the infected saliva of a diseased animal transmits it through a deep bite. In carnivores and in humans, an incontrollable excitation is characteristic, while in ruminants it causes paralysis. Bats may become infected without any apparent symptoms or they may suffer an acute infection, followed by unusual behavior when insectivorous and herbivorous species attack mammals.
Such considerations demonstrate the conflation of situations which are clearly distinct under a single definition without making a distinction between diseases and their pathogens. We may continue to do so, for logistical reasons, but it is crucial that we consider, as social scientists, policy makers, and medical practitioners, what the political and practical implications of such conflation might be.
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- Policy, polity, and the HIV crisis in emerging economies: India and Russia compared
- The concept of emerging infectious disease revisited
- Sounding a public health alarm: producing West Nile virus as a newly emerging infectious disease epidemic
- Emerging and concentrated HIV/AIDS epidemics and windows of opportunity: prevention and policy pitfalls
- The social politics of pandemic influenzas: the question of (permeable) international, inter-species, and interpersonal boundaries
- The poetics of American circumcision on the margins of medical necessity
- Of rebels, conformists, and innovators: applying Merton's typology to explore an effective home care policy for the emerging Alzheimer's epidemic
- ‘Promoted by Hong Tao, the Chlamydia Hypothesis Had Become Well Established...': Understanding the 2003 Severe Acute Respiratory Syndrome (SARS) Epedemic - But Which One?
- The rhetoric of science and statistics in claims of an autism epidemic
- Bipolar disorder and the medicalization of mood: an epidemics of diagnosis?
- What epidemic? The social construction of bipolar epidemics
- The depression epidemic: how shifting definitions and industry practices shape perceptions of depression prevalence in the United States
- Biomedicalizing mental illness: The case of attention deficit disorder
- Contagious youth: deviance and the management of youth sociality
- A social change model of the obesity epidemic
- Who says obesity is an epidemic? How excess weight became an American health crisis
- “Who are you calling ‘fat’?”: the social construction of the obesity epidemic