Geography, ecology and emerging infectious diseases
Geography, ecology and emerging infectious diseases
Jonathan D. Mayer a,b
a Department of Geography, Box 353550, University of Washington, Seattle, WA 98195, USA
b Departments of Infectious Diseases, Family Medicine, and Health Services, Box 353550, University of Washington, Seattle, WA
98195, USA
Abstract
Emerging infectious diseases are the focus of increased attention and even alarm in the scholarly and popular
literature. The emergence of new diseases and the resurgence of older and previously recognized infectious diseases both in developing and developed country poses challenges for understanding the ecological web of causation, including social, economic, environmental and biological components. This paper is a synthesis of the major characteristics of emerging diseases, in an interdisciplinary context. Political ecology is one framework for analysis
that is promising in developing a modi®ed ecology of disease. # 2000 Elsevier Science Ltd. All rights reserved.
Keywords: Infectious diseases; Disease emergence; Disease ecology; Disease causation
Introduction
An important principle of disease ecology is that
population, society and both the physical and biologi-
cal environments are in dynamic equilibrium.
Signi®cant enough stress on this equilibrium can pro-
duce cascading e�ects on any of the aforementioned
components. The human-environment relationship, if
disturbed enough by major changes in land use, mi-
gration, population pressure, or other stressors can
show signi®cant maladaptation, as manifested by the
appearance or di�usion of new diseases. Much histori-
cal work has demonstrated the e�ects on both Europe
and the Americas of the early widespread contact of
the European explorers (e.g., Crosby, 1972, 1986;
McNeill, 1976; Whitmore, 1991; Denevan, 1992).
Other more contemporary manifestations of disequi-
librium include the tremendous increase in the inci-
dence of schistosomiasis following the construction of
the Aswan Dam, and the increase in schistosomiasis,
malaria and other infectious diseases following the
Volta River project in Africa. Examples from other
continents include increases in malaria following land
clearance for rubber plantations in Malaysia, increases
in vectored diseases with the construction of transpor-
tation routes in Brazil, and the appearance of Lyme
disease in the United States following the reforestation
of peri-urban areas in the northeast. The reforestation
occurred as previously agricultural areas were brought
into residential and even commercial usage, thus
increasing the proximity of humans and deer. Deer are
important in the transmission of Lyme disease, serving
as the main link between the rodent reservoirs of
Lyme disease and humans. The increased proximity
also increased the contact between people and deer
ticks. Since deer are edge dwellers, transmission of dis-
ease between the animal reservoir and humans via the
deer ticks increased by changes in land use patterns.
Despite the human toll taken by the AIDS pan-
demic, the major lesson to be learned from the pan-
demic is that the assumption that infectious diseases
Social Science & Medicine 50 (2000) 937±952
0277-9536/00/$ – see front matter # 2000 Elsevier Science Ltd. All rights reserved. PII: S0277-9536(99)00346-9
www.elsevier.com/locate/socscimed
E-mail address: jmayer@u.washington.edu (J.D. Mayer).
are a phenomenon of the past, largely restricted as major health threats to developing countries, and that
“international health” consists of the study of problem of developing countries, are all erroneous. HIV/AIDS is prototypical of emerging and resurgent infectious
diseases, which the medical and public health commu- nities now acknowledge to be a hitherto unappreciated reality and a severe threat to worldwide public health.
Many geographers have analyzed the spatial and eco- logical patterns and issues of HIV/AIDS (e.g., Shannon and Pyle, 1989; Shannon et al., 1990; Gould,
1993).
Human ecology and emerging infectious diseases
The social sciences consider scales from the individ-
ual to the global. Human ecology is the study of how individuals and groups interact with one another. This is best appreciated within the context of the natural en-
vironment as well. Disease ecology, so basic to medical geography and epidemiology, is also a powerful approach to understanding disease emergence and resurgence (May, 1958; Meade, 1976). Many changes
that are relevant to understanding emerging and resur- gent diseases are due to political and economic power at a variety of scales, ranging from the transnational
down to the household and individual levels. Some, or even much of this power is in¯uenced by which groups control decisions over land use. This, in turn, in¯u-
ences the relationships of people and the environment. This is a basic principle of political ecology which has received some attention in the geography of health and
disease (Mayer, 1996), and has been used increasingly in understanding the consequences of human±environ- ment interactions. The political ecologic approach is used at the end of this paper as an interpretative
framework for disease emergence. The emergence and resurgence of infectious diseases
is as much a matter of social, ecological and geo-
graphical change as it is of smaller scale molecular or microbiological phenomena. Indeed, the meaning of disease causation changes when considering it in social
and ecological contexts. The germ theory of disease and the doctrine of speci®c etiology concentrated much attention on the smaller scale, microscopic and submicroscopic scales of disease. Yet, causation can
also be expanded to larger scales, and though not refuting the germ theory, by so doing, it adds to our understanding of disease causation.
That there was complacency over the supposed con- quest of infectious diseases is, in part, understandable. Improvements in sanitation and nutrition in developed
countries in the nineteenth century, the development of antimicrobials and antibiotics by the mid-twentieth century, and the proliferation of vaccines by the mid
to late twentieth century led to a spirit of optimism.
This diverted funding and training to chronic, appar- ently non-infectious diseases in most developed countries. The World Health Organization embraced
the idea that there could be “Health for All by the Year 2000”. This assumed that most nations would already have undergone the “health transition”
whereby infectious diseases are displaced by non-infec- tious diseases as the major causes of mortality and
morbidity (Omran, 1971; Garrett, 1996). Moreover, the “Health for All” slogan presupposes that it is poss- ible to eliminate disease as part of the human experi-
ence. This is clearly impossible, and estimates are that the human life span is approximately 120 years maxi-
mum. Disease has always been present in society and it will remain part of all societies in the future. More salient issues are what types of diseases will be preva-
lent where, and for how long, and which social and economic groups will bear the burden of which types of disease. The statement in 1969 that it is “time to
close the book on infectious diseases, declare the war on pestilence won, and shift national resources to such
chronic problems and heart disease” came from none other than the Surgeon General of the United States. Yet, as Morse (1993a, p. 23) argues, “The lesson of
AIDS demonstrates that infectious diseases are not a vestige of our premodern past; instead, like disease in general, they are the price we pay for living in the or-
ganic world”. The general signi®cance of HIV/AIDS was not realized when it ®rst appeared in the Western
World. It is interesting in retrospect to note that one of the earliest reports of AIDS (Marx, 1983) termed it a new disease, but did not set it within any context of
a general context of “new infectious diseases”. This is certainly understandable, since only in retrospect can we realize that the appearance of HIV/AIDS would
presage other diseases to come. AIDS was seen in iso- lation, rather than as an early manifestation of the re-
appearance of then controlled infectious diseases, or the initial appearance of new infectious diseases. AIDS was the ®rst emerging disease of major threat to public
health that was recognized in contemporary history, and its initial emergence was not enough to establish
any concern over or identi®cation of a pattern. With the destruction of complacency comes uncer-
tainty, and it is this uncertainty that we now face as
our assumption of the conquest of major infectious diseases is negated. Originally termed “emerging infec-
tious diseases”, the new concentration on “emerging and resurgent infectious diseases” and their e�ects on society have been receiving increased attention world-
wide (Garrett, 1994). A clinical focus is important for treatment, and both surveillance and containment are crucial public health measures. However, the disease
ecological approach is essential for understanding the emergence of new diseases, the re-emergence of older
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952938
ones, and their mutual potential for rapid di�usion.
Emerging diseases have received only limited attention from geographers, yet they re¯ect the changing struc- ture of world society, including the globalization of so-
cieties, capital, and biotic entities (e.g., Cli� and Haggett, 1995).
The Institute of Medicine of the US National Academy of Sciences convened a meeting in 1992 to develop an understanding of the nature of emerging
diseases. The panel examined the causes of disease emergence, surveillance for their detection, and strat- egies for their containment (Lederberg and Oaks,
1992). It is ironic that the year after the Institute of Medicine released its report, three of the diseases that
were considered had signi®cant impact in the United States (Berkelman, 1994). These included an outbreak of Escherichia coli 0157:H7 that causes severe diarrhea,
and particularly in children, the severe renal compli- cation of hemolytic-uremic syndrome (HUS). This killed several children and was traced to contaminated
hamburgers served by one fast food outlet in the Paci®c northwest. A second disease was cryptospori-
diosis, which caused 420,000 cases of severe gastroen- teritis in the Milwaukee area and the hospitalization of 4400 people. It also caused over a dozen deaths,
almost all of which were in immunocompromised indi- viduals. The third disease was a new variant of a Hantaan virus, in the Four Corners area of New
Mexico, Colorado, Utah and Arizona. This species eventually became labeled the “sin nombre” (without a
name) virus. Several local physicians noted similar severe respiratory symptoms, leading to ARDS (acute respiratory distress syndrome) in several temporally
and spatially clustered Navajo patients, which alerted them to the possibility that a cluster of an unknown disease had emerged. Both the Epidemiology
Intelligence Service of the CDCP, and the State of Utah’s Health Department were mobilized for rapid
epidemiologic investigation. Tissue samples of the dead patients were used for molecular typing. In 1994, the Centers for Disease Control and
Prevention published a report which was a prevention strategy for infectious diseases for the United States (Centers for Disease Control, 1994), and this document
gave o�cial recognition to the necessity of acknowled- ging that infectious diseases are a major threat to pub-
lic health. Prevention must be of vital concern to public health agencies. An interagency conference on emerging and re-emerging infectious diseases was con-
cerned to a greater degree with international surveil- lance and prevention (Report of the NSTC Committee, 1994).
The de®nitions of “emerging and resurgent diseases” may, by now, be intuitively meaningful, yet many of
the formal de®nitions are ¯awed. For example, accord- ing to the Institute of Medicine’s report (Lederberg
and Oaks, 1992, p. 34) “Emerging infectious diseases are clinically distinct conditions whose incidence in
humans has increased”. This ®ts the criteria of any epi- demic. The basic de®nition of an epidemic is when the incidence of a disease, and particularly of an infectious
disease, is much greater than expected under usual conditions. Much more helpful is Morse’s (1993b) spe- ci®cation of emerging viruses, which can be expanded
to other pathogens: “We may use the term `emerging viruses’ to refer to viruses that either have newly appeared in the population or are rapidly expanding
their range, with a corresponding increase in cases of disease (p. 10)”. This echoes many other de®nitions, and leads to the generalization that major social and geographical trends, such as greater national and inter-
national connectivity, mobility, social interaction pat- terns, land use change, and changing cultural ecologies make it likely that new or previously unrecognized dis-
eases will be discovered. Older ones, once thought to be extinct, or not major public health problems, may reappear (Wilson, 1994). One of the major challenges
of research in emerging diseases is the meticulous documentation of empirical examples of human-biotic- interactions and their relationships to infectious dis-
eases. Another aspect in the de®nition of emergence is also
troublesome. What may be an emerging disease in one society may have been present, at low or high levels, in
other societies, for varying lengths in time. For example, the northward movement of dengue fever makes it a disease that is emerging in the United
States. However, it is hardly newly emerging in the tro- pical countries of Latin America and the Caribbean, where it has been endemic for decades. Conversely, the
appearance of chronic diseases such as ischemic heart disease and cancers in developing countries may re¯ect emergence to the populations of those countries, but these diseases have been highly endemic in developed
countries for centuries. Thus, there is a distinction between those diseases that are introduced into new areas through di�usion and those that arise de novo.
Microbial tra�c
There are several ways in which new pathogens can appear in a human population in a new region. Many
of these are encompassed in the concept of “viral traf- ®c”, as conceived by Morse (1993b). The concept is not applicable only to newly emerging diseases in the
contemporary era. It may be applied retrospectively to phenomena as diverse as the appearance of syphilis in new areas during the period of the conquistadors and
the transspecies transfer of viral and other pathogens, such as trypanosomiasis, yellow fever, and, as is very likely, AIDS.
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 939
Though originally developed in the context of viruses (Morse is a virologist), the term “tra�c” has
broader implications and is more appropriately labeled “microbial tra�c”, of which viruses are only one type of pathogen. The concept of “tra�c” inherently has
geographical implications, for it implies movement and interaction, and certainly should not be limited to viruses, though these pathogens pose the most daunt-
ing threats to human health. The appearance of new pathogens in populations
can therefore be due to the following factors:
1. Cross-species transfer. 2. Spatial di�usion. 3. Pathogenic evolution, or change in the structure and
immunogenicity of earlier pathogens. 4. The new description of a pathogen that had been
present in humans for years, but which is “newly recognized”.
5. Changes in the human±environment relationship. Morse did not mention this important component and it is inherently geographical.
Cross species transfer
Of these mechanisms, cross-species transfer and
spatial di�usion appear to be most important. The pathogens responsible for a multitude of infectious dis- eases can be transferred to and from humans and
other mammals. These include in¯uenza, which can be highly prevalent in swine and avian populations; yel- low fever, which is present in South American and
African monkeys, and, quite likely, HIV. There are two forms of HIV in Africa. HIV-1 is found mostly in East Africa, and is clinically more serious than its West African variant, HIV-2. RNA ®ngerprinting tech-
niques show remarkable homologies between HIV-2 and the simian immunode®ciency virus (SIV) in man- gabee monkeys. Considering this evidence, it is quite
reasonable to conclude that there has been a cross- species transfer of the pathogen, most likely from the mangabees to humans. The RNA techniques are so
speci®c that misidenti®cation of viral species is nearly impossible and SIV and HIV-2 di�er from one another only minutely in their nucleotide sequence. The mech- anisms of cross-species transfer are more a matter of
speculation than of concrete proof. Another example of cross-species transfer is that of
bovine spongiform encephalopathy (BSE) which is
caused by a prion, and the development of new variant Creutzfeldt±Jacob disease (nvCJD). Prions lack nucleic acids, and are essentially protein templates for their
own reproduction. In the popular press, this is known as “mad cow disease” and there is at least one popular book that gives a ®ne description of prions and the
logic in concluding that BSE caused nvCJD (Rhodes,
1997). BSE ®rst came to the attention of the popular
press in April 1996, when there was a statistically
meaningful temporal cluster of this very rare degenera-
tive neurological disease in the UK. There is a consen-
sus, but not a universal agreement among scientists,
that the appearance of nvCJD was due to the con-
sumption of infected beef. Most of the cases have been
in the UK, and banning British beef from the EU
countries became a major political issue.
In December, 1997, the US government banned the
import of British beef and sheep products. As of 1994,
no nvCJD cases had been detected in the United
States. However, because of the high mortality and dis-
ability associated with the disease, and the weight of
the evidence linking BSE with nvCJD, it seems reason-
able to have imposed an embargo on importation.
Recent concerns over some of the tropical hemor-
rhagic fevers serve to illustrate the potential import-
ance of cross-species transfer. For example, the recent
outbreak of Ebola hemorrhagic fever in May, 1995 in
Kikwit, Zaire (now named The Congo) posed a serious
question and remained a mystery: why did the disease,
which had been recognized and described two decades
earlier, make a sudden reappearance? This reappear-
ance was as deadly as its original appearance in the
same area of the world. The mode of transmission
seemed to be clear, since the highest risk groups for
transmission were either health care workers who had
had documented contact with the secretions of
patients, family members who had contact with infec-
tives either prior to the onset of symptoms, prior to
hospitalization, or family caretakers. There were and
are many mysteries that surround this disease. Why
did it make its appearance in Kikwit when it did?
What social and human±environment interactions pro-
vided the conditions that were appropriate for its
development and spread? It is equally mysterious that
there is no known natural reservoir for the Ebola
Virus. In the 1996 outbreak of Ebola-Zaire in Gabon,
almost all of the a�ected people shared the same dead
chimpanzee for food. Chimpanzees in this region are
predators of soota-mangabeys. This was the single epi-
demiological factor that united these cases. Research is
still ongoing and there is no de®nitive or singular ani-
mal reservoir that has been identi®ed for Ebola. Teams
of zoologists and entomologists were dispatched by nu-
merous agencies from several countries shortly after
the outbreak in Zaire waned to try to identify de®ni-
tive hosts, yet few de®nite conclusions have been
learned from this. The interesting footnote to this epi-
demic was described earlier, where the common risk
factor in the 1996 outbreak of Ebola in Gabon was
the consumption of meat from apparently infected
monkeys.
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952940
Spatial di�usion
Spatial di�usion has, of course, been of tremendous interest to geographers and epidemiologists for centu- ries. Recent changes in travel patterns have altered the
human ecology of infectious disease. A well-known characteristic of contemporary society is the increasing speed with which individuals and transportation ve-
hicles traverse the earth. This is illustrated by the di�u- sion of new in¯uenza strains, as discussed previously. One estimate is that approximately 1 million people
travel internationally each day, and 1 million people travel from developed to developing countries (and vice versa) per week (Garrett, 1996). Thus, if some- body contracts a disease on one continent, it could be
transmitted to the population on another continent by the next day. The rates and patterns of di�usion depend on the
mode of transmission. With respiratory viruses, such as in¯uenza, where viral replication takes place on the epithelial cells of the respiratory tract, and then the
virus is transmitted via the airborne route, di�usion is rapid. The particular di�usion patterns are determined largely by understanding the origins and destinations
of human travellers. Where spatial interaction is more intense, the likelihood of spatial di�usion is greater. This is particularly signi®cant for rapidly di�using dis- eases with high attack rates such as in¯uenza. Travel
and migration have been established as the main reason for the di�usion of HIV/AIDS, but the spread of AIDS has been much slower than that of in¯uenza,
since transmission is more di�cult, and requires par- ticipation in speci®c behaviors (Quinn, 1995). Moreover, while in¯uenza, and most other respiratory
diseases have short latency periods that are frequently a matter of a few days, the latency period for AIDS can be over six months.
Pathogenic evolution
Pathogens can mutate easily to produce new strains, to which people lack immunity. The main reason for the ease of mutation is that these pathogens are small
and have relatively simple genetic (RNA and DNA) structures. Minor changes in the amino acid sequences of these nucleotides produce organisms that can cause severe disease in susceptible populations. Because of
the simplicity of their DNA or RNA sequences, viruses are particularly subject to mutation, with potentially major consequences for human health. Recently devel-
oped techniques in molecular biology allow the speci®c identi®cation of the DNA and RNA sequences. While much mutation may develop due to antimicrobial re-
sistance, as discussed subsequently, some mutations are purely random, yet they pose major threats to health. Minor changes in the structure of the genetic material
thwart speci®c immune responses. As with most
phenomena that are repetitive, minor “mistakes” may
have major rami®cations. Recurrent events occasion-
ally have random results, and pathogenic replications
are no exception. Viruses, and to a lesser extent, larger
organisms such as bacteria are particularly prone to
random mutations because of the sheer simplicity of
their genetic structures.
Genetic shift and genetic drift are responsible for the
regular and almost predictable emergence of new
strains of in¯uenza, thought by most infectious disease
experts to originate frequently in China because of the
chain of contagion from ducks to domesticated swine
(Kida et al., 1988; Betts, 1996). Genetic changes occur
within the swine population that are then communi-
cated both to the avian and human populations, result-
ing in new outbreaks of in¯uenza among susceptible,
non-immune humans. Since immunity is very speci®c
for a particular con®guration of the surface antigens
on the in¯uenza virus, anybody who has not been vac-
cinated against a particular strain, or who has not
gained immunity through actual exposure to the
speci®c viral strain, is highly susceptible to each new
variant of in¯uenza.
The geographical implications of genetic change are
important. If changes, however minor, in the genetic
structure of a microbe occur randomly, they also occur
in random places. However, these newly mutated
pathogens travel with the people who carry them.
Thus, the potential for spread of random occurrences
is great, particularly when transportation is readily
available and human spatial interaction is common.
The signi®cance of this will be further illustrated when
antimicrobial resistance is discussed subsequently.
This mechanism of transfer may either be due to
viral evolution, or to new interactions between human
activities and disease pathogens. The former is import-
ant, particularly in the case of viruses. In summary, as
Morse (1993a, p. 27) writes, “the seemingly insoluble
problem of viral origins thus reduced to a more man-
ageable. . . question of viral tra�c, and attacking the
problem includes better understanding and appreciat-
ing the viruses that already exist in nature, including
some viruses not yet discovered”.
How does a recently mutated virus or other patho-
gen become established in human populations? The
answer is based in the disease ecological principle that
for an infectious disease to occur, there must be coinci-
dence in time and space of agent and host. Thus,
humans must come into contact with infectious agents
that have either newly evolved, or have been intro-
duced to new areas. Either one of these should be con-
sidered to be an element of viral tra�c.
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 941
Newly recognized diseases
Newly recognized pathogens do not present a major conceptual problem. They are unrecognized for several reasons. This is either because the a�ected population
lacks the technological capacity to identify the patho- gen or the conceptual framework to correctly attribute a syndrome to a speci®c disease. One example of this
is Legionnaire’s disease (legionellosis) which was thought to have constituted a new form of pneumonia when it struck the American Legion convention in
Philadelphia in 1976. It was subsequently realized, however, based on serologic tests of previous blood samples from other outbreaks of mysterious pneumo- nias, that Legionnaire’s disease was not a new disease
at all, but was a newly recognized disease. One of the reasons for the new recognition of a dis-
ease stems from the di�erence between a syndrome
and a disease. A syndrome consists of a cluster of symptoms (and even the word “symptom” implies something subjective) without having any notion of the
underlying causal relationships. A disease is a more systematic biological concept of cause and e�ect: a set of symptoms that are subjective, signs that are objec-
tive, and an assumption of a unifactorial or multifac- torial cause or set of causes. Since syndromes and even diseases can resemble one another to the point of appearing, on the surface, as being identical, an appar-
ently emergent disease may simply be newly recog- nized. The di�erence between new recognition and actual emergence may even have implications for treat-
ment or therapy. Another reason that previously unrecognized dis-
eases become recognized for the ®rst time is that the
systems of disease surveillance and reporting in the United States and elsewhere are inadequate. It makes recognition and communication of that recognition all that much more di�cult (Lederberg and Oaks, 1992;
Centers for Disease Control and Prevention, 1994). Both the Institute of Medicine and the Centers for Disease Control and Prevention have emphasized the
need for increasing the resources, using existing and new technologies, to monitor the development of new diseases and to spread that information rapidly. While
surveillance systems are being developed for new dis- eases, their e�cacy in reporting and controlling new diseases is largely untested.
Changes in the human±environment relationship
A basic question in disease ecology is how changing human±environment relations and social activities can result in fundamental alterations in the interaction
between people, the biological environment, and the broader social and economic context. For example, a new dam built in a tropical area in which malaria and
other vectored diseases are present might be expected
to cause an increase in the prevalence of vectored dis- eases. If the a�ected upstream water is endemic for schistosomiasis, onchocerciasis and water-borne dis-
eases, the formation of a lake will similarly increase the prevalence of those diseases. This is particularly so in the absence of signi®cant changes in human beha-
vior toward the water and its immediate proximity. One of the most elegant schemata for understanding
the whole ecology of disease emergence is contained in the report by Lederberg and Oaks (1992). Economic and social causes of disease emergence Ð changes in
land use, human occupation and activity, urbanization Ð are integrated with biological factors in emergence
such as mutation, genetic factors, and changes in the zoonotic pool. These then a�ect both human and ani- mal hosts, as well as vectors. Knowledge of patterns of
human movement and transportation are essential in understanding patterns of emergence and all of these are integrated into the particular forms of social or-
ganization in society. The patterns are complex, and the ecology of the intersecting elements is di�cult to
understand or represent in any simple scheme. This is the case with Lyme disease, caused by the
spirochete, Borrelia burgdorferi. The story of this bac-
terial disease is familiar and has been described else- where on numerous occasions. When clusters of the disease were ®rst discovered in and around Old Lyme,
CT, and when the agent was identi®ed, some auth- orities suggested that it was a new disease. However, it
had been present for many years in Europe and Scandinavia, and was labeled as erythema chronicum migrans, because of its characteristic ringlike rash,
which expands radially. Lyme disease is the most prevalent vectored disease
in the United States. The chain of events that have led to the emergence and recognition of Lyme disease in New England is complex. To understand it, one must
understand the population, settlement, and transpor- tation geographies of these areas, both at present and historically; the political economy of land develop-
ment; the natural ecology of the areas, and their re- gional entomologies and zoogeographies. Following
European colonization, forests were cleared by the colonial settlers for agricultural land use in the 18th and 19th centuries. Cronon (1983) has demonstrated
that both the European colonials and the Amerindians both prior to and contemporaneous with the Europeans had left their imprint on the landscape, to
the point that it is meaningless to refer to the forest as “virgin”.
After the development of commercial agriculture in New England, the 19th century was a period of west- ward agricultural displacement because of the competi-
tive pressures for residential land use. Supply and demand increased land values, and agriculture simply
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952942
could not compete with other uses. In addition, with
the westward movement of population, and with the
development of commercial freight transportation,
there was more of a demand for agricultural land
farther to the west. Advances in transportation tech-
nology made the development of suburban commu-
nities possible at relatively great distances from
Central Business Districts. These communities were
principally commuter communities for central cities.
More recently, these communities have experienced
further population growth. Much of this growth has
been on the outskirts of the already developed suburbs,
and has required deforestation and land development
for tract housing. The forest surrounding the newer
suburban communities tends to be second growth for-
est This has created habitats that are conducive to
deer, and they abound in areas proximal to newer resi-
dential developments. This is signi®cant since the vec-
tors of East Coast Lyme disease are deer ticks which
are transported by white tailed deer as well as by cer-
tain avian species (Smith et al., 1996).
There is a lively debate among entomologists over
whether there is any species di�erentiation between the
deer ticks in the northeastern and southeastern United
States. Rich et al. (1995) have used molecular sequen-
cing techniques and conclude that it is the di�usion of
what used to be called the “northern deer tick” (Ixodes
dammini ) rather than the “southern deer tick” (Ixodes
scapularis) which transmits Lyme disease in the South.
Indeed, they conclude that I. dammini have di�used to
the south and question the existence of I. scapularis.
The ecological conditions of suburbanization and
reforestation, with the concurrent existence of deer and
the deer ticks, are favorable for the transmission of
Lyme disease. Detailed epidemiologic studies estab-
lished the rapidity of Lyme disease’s becoming a highly
prevalent disease both on island o� the New England
coast and on the mainland (e.g., Lastavica et al., 1989;
Coyle, 1993; Ginsberg, 1993). Though Lyme disease is
fairly well understood by bacteriologists, entomologists
and zoogeographers, it has not been studied in depth
by social scientists or medical geographers, who can
synthesize both the biological and social causes and
e�ects of Lyme disease.
The real estate industry and land developers have
been inextricably involved in the complex nature of
land use change. An unintended consequence of real
estate development has been an increasing incidence
and prevalence of Lyme disease. Of course, the real
estate industry also acts in response to popular
demands for spacious housing on large lots. The real
estate industry, though deeply involved in the social
creation of Lyme disease, has not had any nefarious
intentions of propagating Lyme disease. Indeed, a tes-
table hypothesis is that people may take the prob-
ability of developing Lyme disease into consideration in their residential choices.
Consistent with the major lesson of disease ecology, wherein agent and host must come into contact at the same time, the incidence and prevalence of Lyme dis-
ease have increased. It would, however, be reduction- ism to identify only the pathogen, or the disease cycle, as the “cause” of Lyme disease, though this may be
the case in a purely biological sense. True understand- ing of this and other diseases, however, is rarely restricted to pure biology, and it is very obvious how
transportation, land development, land developers and population pressures are as much causes of Lyme dis- ease as are the spirochetes which cause Lyme disease in a more purely biological sense.
Antimicrobial resistance
The development of antimicrobial-resistant agents is
as serious a threat, and perhaps more of a threat, to the population in developed countries than are some of the more exotic agents mentioned above. Tuberculosis is the infectious disease that is responsible
for the greatest number of deaths worldwide, yet most of these deaths are in developing countries that lack the resources for adequate drug treatment. In the
United States and elsewhere, the development of multi- drug-resistant TB (MDRTB) threatens e�orts to mini- mize the impact of this disease. Though the prevalence
of TB has been declining in the United States in recent years, certain pockets of population are particularly susceptible to some very serious forms of the disease.
There are a limited number of antimicrobials available in the treatment of TB, yet the intersection of itinerant populations, homelessness, poverty and migration pro- vide a challenge for TB control. Drug protocols in
patents whose susceptibility to active TB requires the use of a minimum of two medications and up to four medications on a daily basis for at least six months
provides a formidable challenge. If they do not com- plete their medication regimens, the environment is creative for the selective breeding of drug resistant
organisms. Should the individual develop a form of TB that is then resistant to known drugs, this airborne disease may be easily communicated to others, and it is a sobering scenario that the medical community may
then lack the appropriate antimicrobials for treatment and prophylaxis of TB. The origins of the resistant forms of TB are social
and are not merely medical. In countries where poverty and homelessness do not present the severe problems that they do in the United States, drug resistant TB is
not a major concern. MDRTB is mostly a problem of the large Eastern and midwestern urban areas: areas where the social challenges of poverty are particularly
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 943
severe. It is quite reasonable to expect, though, that
MDRTB will not remain con®ned to the eastern US and will become a severe problem for the inner city urban populations of the whole country. Multiple drug
resistant TB, which is most prevalent in homeless and poor populations, is thus caused just as much by underlying social conditions as it is by the bacillus
itself. One recent study, for example, found that nearly 50% of those people enrolled in a tuberculosis treat-
ment program in New York City adhered to the pro- gram and many people dropped out and even disappeared into the vortex of impoverishment and
homelessness (Pablos-Mendez et al., 1997). In these same neighborhoods, conditions of powerlessness,
homelessness, social deprivation, and inadequate fund- ing of public health infrastructures also have a nega- tive impact on local health. This is as important in
understanding the emergence of MDRTB as is the comprehension of the smaller scale biological processes which are of great importance in the pathogenesis of
drug resistant TB. The social bases of MDRTB raise some vexing ethi-
cal issues, for there have been many examples of indi- viduals who have been detained against their wills to complete their TB treatments. Detention has been jus-
ti®ed by the argument that the interests of society in minimizing the spread of MDRTB are more important
than individual autonomy and freedom in extreme cir- cumstances. Patient autonomy, which has been taken as one of the presumptions of medical ethics in the
United States, is less important than collective well- being, when it is perceived that the interests of the public would be su�ciently threatened by adhering to
individual autonomy. The ease of transportation is as important in the
spread of resistant organisms as in the di�usion of new pathogens. If a resistant organism remains localized, then its e�ects will also remain localized. However,
transportation facilitates the movement of resistant organisms. This develops both from prescribing prac-
tices and biological processes such as mutation, but the di�usion itself is from personal travel. Two examples are helpful. Bifani et al. (1996) used DNA
sequencing techniques to trace the di�usion of a par- ticular genotype of Mycobacterium tuberculosis from New York City to several other states. The di�usion
was obviously the result of migration, transportation, or a combination of the two. The signi®cance of this
®nding was not lost on the authors: “The result of. . . molecular processes, coupled with dismantling of TB control programs and contemporary social trends [e.g.,
migration and transportation Ð added by author] has been dissemination of a cohort of bacteria throughout the most populous city in the United States”. The ®nd-
ings of this study also demonstrate that the spread was not limited to New York City alone.
Another example is that, for nearly a decade, the
¯uouroquinolones appeared to be e�ective treatments for gonorrhea (caused by Neisseria gonorrhea, or more popularly, by gonococci). In the 1990s, however, resist-
ance to the quinolones developed in Asia, principally in the Philippines, and subsequently appeared in Hawaii, Washington State and several other states in
the United States. This could only have occurred through travel and migration. The result is that more
complicated and more costly drug regimens are required to treat gonorrhea at present. Now, ¯uoroqui- nolone resistance has been reported in many other
countries (Knapp et al., 1997). Other organisms have developed degrees of resist-
ance to even newly developed drug protocols. Of great concern are hospital-acquired (nosocomial) infections. Methicillin resistant Staphylococcus aureus (MRSA)
has been of great concern in institutional settings, since the presence of this organism occurs periodically in epidemic proportions within hospitals. Moreover,
time±space clusters of MRSA are pronounced. There are few medications available to treat this frequently
lethal bacterium. It is transmitted principally via the nares of hospital workers and of patients and visitors. It tends to concentrate in larger hospitals and in inten-
sive care units, and the most e�ective strategy for deal- ing with an epidemic of MRSA is complete isolation of carriers. Vancomycin is usually the only e�ective
antimicrobials against MRSA, yet vancomycin-resist- ant staphylococci have recently appeared in Japanese
hospitals and these organisms may be expected to spread. Of even greater concern is the more recent develop-
ment of vancomycin-resistant enterococcus (VRE). For these bacteria (E. faecalis and E. faecium) vancomycin is the only available medication. When enterococci
become resistant, there is simply no available antimi- crobial treatment for patients, and supportive care is
the only alternative. It, too, occurs in clusters within hospitals and nursing homes and in clusters on a broader geographical scale. The case fatality rate is
high. Drug-resistant forms of communicable disease thus
constitute major threats in developed countries, and may ultimately prove to be more serious than the newly discovered more “exotic” diseases such as
Ebola, Marburg, and Lassa fever. Rapid surveillance and quick isolation of infected individuals is crucial in the case of MDRTB, MRSA, VRE and other drug-re-
sistant organisms. While the development of contem- porary molecular methods of microbial typing allow
the description and inference of probable patterns of di�usion, their relationship to the control of the di�u- sion is less obvious. The elegance of DNA and RNA
techniques can identify and specify the exact nature of pathogenic mutation, and geographical analysis can
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952944
then be joined with molecular biology in an overall project of delimiting the patterns and spread of resist-
ance (e.g., Bifani et al., 1996).
Trade and transportation
As we have already seen, trade and transportation constitute potential bases for the introduction of new
diseases into new areas. As such, it is a factor in dis- ease emergence. One estimate is that 1 million people traverse national boundaries each day, and every week, 1 million people travel between developed and develop-
ing countries (Garrett, 1996). The various regions of the world are increasingly interdependent. Development theory considers interdependency,
regardless of the theoretical framework that is espoused. Interdependency can introduce diseases in several speci®c ways, all related to di�usion. First,
humans may serve as vectors themselves. People travel- ling from one region to another who may be carrying a communicable disease can introduce that disease into a new region with relative ease. This is particularly so
for airborne diseases that are readily transmitted, but also holds, though less dramatically, for vectored dis- eases, sexually transmitted diseases and nonvectored
bloodborne diseases. Second, transportation vehicles can, themselves,
serve as mechanical vectors for the di�usion of diseases
or disease vectors. It is well known that one of the vec- tors of dengue fever, Aedes albopictus, was introduced into the United States from Asia via automobile tires
on ships coming from Asia. The tires were damp or actually contained pools of water, which provided the vectors with ideal conditions for survival and replica- tion. This has potentially serious consequences for the
United States, since the possibility exists that dengue will be introduced into even temperate areas of the country once the vector is present.
Other examples abound wherein the transportation vehicle itself serves as a vector for transmission. The introduction of cholera into the Americas in the most
recent outbreak was due to a ship from Asia dumping its bilgewater into the ocean o� the coast of Peru. The cholera epidemic in the Americas has been spreading rapidly as a result of this. Thus, over 1.4 million cases
of cholera have been reported in the Americas, mostly south of Mexico, and at least 10,000 deaths have been recorded. Commercial transportation was therefore re-
sponsible for the reintroduction of cholera, but passen- ger transportation is now implicated in the further di�usion of the disease in the Americas. Sanchez and
Taylor (1997) discuss the example of 75 passengers on a ¯ight of 336 passengers developing cholera after ¯y- ing from Argentina to Los Angeles. This was because
contaminated seafood salad was loaded onto the airli-
ner for a meal during a stop in Lima, Peru. The proliferation of trade and transportation is the
result of economics and political factors, and a�ects re-
gional development, individual ®rms and corporations, local economies and the broader society. In a general
sense, the “cause” of the diseases that are conveyed via transportation modes is not just biological. The conti- nuing drive for local and regional development is one
of the anthropogenic causes of disease, particularly in developing countries, where regional and economic growth can be important determinants of human wel-
fare. The movement of raw materials, commodities, may be motive forces behind regional development,
but they can also be responsible for the di�usion of emerging diseases. At all scales, regional interconnectivity is increasing
in much of the world. The causes for this interconnec- tion are complex, and are embedded in the contexts of the various societies that are increasingly intermingled.
It is exactly this interconnection, the development of a world tied together through transportation and move-
ment of goods and people, which is responsible for the sometimes apocalyptic visions of global epidemics due to emerging diseases. What these visions do underscore
is that it is conceivable for new agents to move rapidly across space and it is equally conceivable for emerging agents to have very high prevalence and case-fatality
rates. After all, this is a phenomenon that is not new in history. The European “conquest” of the Americas
carried with it great mortality, as documented by geo- graphers, historians, and anthropologists. The in¯u- enza pandemic of 1918±1919 killed between 20 and 50
million individuals. The numbers are impossible to con®rm because of the lack of the technology or infra- structure for surveillance at that time. It is also im-
possible to con®rm virologically exactly what happened in that pandemic, but it was almost certainly
due to antigenic shift and genetic mutation of the in¯u- enza virus. This is presently being tested in an ex- pedition, led by a medical geographer, to exhume a
number of bodies from a cemetery in northern Norway. The site is ideal since the bodies are well pre- served. The molecular biologists on the team will be
able to use their techniques to specify which strain of in¯uenza resulted in these deaths. The strain of in¯u-
enza that caused morbidity and mortality in the com- munity can be inferred from this information. Major genetic shifts have been documented in the
latter half of the twentieth century. That there was a major pandemic of in¯uenza in 1918±1919 is itself tes-
timony to the fact that transportation systems and mobility were already well established, for the virus cannot live, much less travel, outside of living cells Ð
principally, of humans. Interaction between the United States and Europe during World War I provided the
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 945
mobility for the easy transportation of a genetically shifted in¯uenza virus. Close personal contacts in small
spaces that troops faced provided the basis for an even more rapid spread of in¯uenza than would have been the case in other settings.
Food and waterborne diseases
One area of great concern is the internationalization and globalization of the food supply. The UN Food
and Agricultural Organization estimates that the net value of the global trade of food is about US$270 bil- lion per year. For the purposes of this discussion, foodborne and waterborne diseases will be grouped
together, since people consume them both. Both E. coli 0157:H7 and cryptosporidiosis occurred because of breakdowns in the local infrastructure for producing
and monitoring food and water. In the former case, the outbreak was due to abattoir practices that led to the contamination of the hamburger meat and totally
inadequate meat inspection policies. Microbiologic techniques were not used because of the cost, and meat was inspected only on the basis of its overall appearance. Multiple outbreaks of foodborne diseases
in the past few years have emphasized the inadequacies of the capabilities to regulate and inspect food quality in the United States. In late 1997, the US Food and
Drug Administration approved the irradiation of meat supplies, which should virtually eliminate the threat of E. coli 0157:H7, as long as funding is provided, and
the infrastructure is appropriately supported and devel- oped. In the case of cryptosporidiosis in Milwaukee, the
metropolitan water ®ltration was inadequate to protect the population from the protozoan causing cryptospor- idiosis (Cryptosporidium parvum). In retrospect, cattle were allowed to excrete upstream of one of the major
sources of the metropolitan water supply, and con- taminated the supply. Neither of these diseases, how- ever, were totally new to the United States, because
there had been lower level epidemics of these diseases for years. Unfortunately, the public infrastructure could not detect or contain either of these epidemics.
Because of this, C. parvum and related pathogens have been designated as “new” (Ortega et al., 1993). The epidemiology and microbiology of cryptosporidiosis and its pathogen have been reviewed in detail recently
(Goodgame, 1996; Meinhardt et al. 1996). C. parvum is normally found in the gastrointestinal systems of many animals. It is also di�cult to ®lter and is una�ected by
chlorination of the water supply. Another example of the inadequacy of the public
health infrastructure to detect and regulate the quality
of imported food was the widespread outbreak of gas- troenteritis in the United States, which was due to the importation of raspberries from Guatemala. These ber-
ries were contaminated with another rare and emerging
pathogen, Cyclospora cayatensis (Herwaldt and Ackers, 1997). Like cryptosporidia, cyclospora have only recently been recognized to be potentially major
causes of contamination (Huang et al., 1993; Ortega et al., 1993). The raspberries which were implicated after painstaking epidemiologic ®eld research were ®rst
introduced into the United States from Guatemala in 1988, following their introduction into Guatemala in
1987 for domestic production and international ship- ment (Herwaldt and Ackers, 1997). On December 22, 1997, the United States instituted a ban on raspberries
imported from Guatemala. The outbreak associated with Guatemalan raspber-
ries illustrates a broader concern with the potential mi- crobial contamination of imported food (Hedberg et al., 1994). The reasons for the internationalization of
foodstu�s are complex, and are one example of the broader, yet sometimes ill de®ned, “global change” in the world. Certainly, the availability of inexpensive
labor, and the year-round availability of arable land are factors in the internationalization of food that is
imported to the United States and other nations in temperate climates. Food, though, is, of course, needed for human survi-
val, and the degree to which the American food supply is international is surprising to some. Most American travellers take precautions to avoid contaminated food
and whatever when they travel to Latin America and other developing areas. However, much of the produce
which is consumed in the United States, depending on the season and the location, is actually produced abroad, and can cause diarrheal disease as easily as
foreign travel in relatively unsanitary areas. The Institute of Medicine devoted a large section of
their report on emerging diseases (Lederberg and Oaks, 1992) to the internationalization of the food supply and argued that earlier in the century, produce
was grown for the local market and could only remain fresh for a few weeks, but that the introduction of re- frigerated overseas transportation carriers made it
possible to ship food from distant locations. The report noted emphatically that the existing infrastruc-
ture for testing the safety of foods is insu�cient to detect many foodborne pathogens. The authors further suggested that the North American Free Trade
Agreement might even exacerbate the problem of pro- duce contaminated with bacteria and other pathogens, since the free ¯ow of food from Mexico to the United
States and Canada would be greatly facilitated. Mexico is considered to be a high-risk country for
diarrheal diseases by travel medicine experts, the World Health Organization, and the Centers for Disease Control and Prevention. Food which Mexico
and other countries export does not receive any special sanitary sampling or treatment, and by the time it
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952946
reaches the consumer, the food may be laden with pathogens, as occurred with raspberries and cyclos-
pora. The regulation and control of emerging infectious
diseases due to the contamination of imported food
must be a priority for international policy. The legal infrastructures are highly fragmented. Plotkin and Kimball (1997) provide an excellent overview of exist-
ing regulations but conclude that these must be devel- oped further before they are e�ective. The major need is that regulations must not be fragmented across
di�erent agencies in an uncoordinated manner, as they are now. A waterborne disease that is of great danger to the
United States is the new strain of El Tor cholera that
was introduced in Peru. It has been di�using north- wards, into the northern parts of Mexico. The disease is caused by a particular vibrio, and noncholera vibria
have been observed in the Paci®c Ocean as far north as the State of Washington and the Province of British Columbia. The sanitary systems in the United States
and Canada are certainly more e�ective than those found in Latin America, yet it would be unwise to be complacent about the possibility that the current cho-
lera pandemic might spread into the United States and Canada. Cholera has been enormously costly in Latin America, not only in its human toll, but also in the direct costs of controlling cholera and treating patients.
Estimates are that by the end of 1993, nearly 1 million people had contracted cholera in Latin America and that it was responsible for at least 8000 deaths.
Moreover, the Pan American Health Organization (PAHO), which is one of the regional divisions of the World Health Organization, estimated that the cost
would exceed US$200 billion to control cholera in Latin America (CDC, 1994, p. 11.)
Migration, mobility, and disease emergence
Many statements have been made to the fact that society is becoming more mobile, yet this is not entirely valid. True, when considering a�uent, devel-
oped nations, and the subpopulations in those societies who travel for business and pleasure, there is a great deal of domestic and international movement. However, among the poor, and in less a�uent so-
cieties, mobility on the scale typi®ed by the generaliz- ation that “society” is becoming more mobile, a major question is “which societies and which populations?”
Moreover, the underlying reasons for mobility must be considered to understand the e�ects of mobility on dis- ease emergence and di�usion.
The world should be considered as a continuum of mobility. In traditional societies, mobility is limited. In hunting and gathering groups, mobility is dictated by
the seasons, by natural hazards such as drought, and
by the periodic movement of the animals to be hunted. The hierarchy of mobility ranges from some popu- lations that are not mobile at all, to members of other
a�uent societies where intercontinental business and pleasure trips are the norm. Lack of mobility Ð a kind of permanence in space Ð tends to favor stability
in the spatial distribution of infectious diseases, while highly mobile individuals and the availability of speedy
overseas transportation favors the possibility of very rapid international di�usion of new diseases. Similarly, immobile societies may even be protected from disease
di�usion due to lack or minimization of contact with other geographically remote social groups. It is an
overgeneralization to argue that the world is uniformly facing increasing mobility, which predisposes most populations to the rapid in¯ux of new disease agents.
It is also crucial to consider the reasons for mobility, and the political, social, and settlement characteristics at the origin and destination of migrants. Migration
implies a more permanent movement than does travel, though population geographers and demographers
classify migration into a typology which includes forced vs. voluntary migration, periodic vs. permanent or semipermanent migration, and other typologies of
migration. Forced migration due to political or reli- gious persecution, natural hazards such as drought, or
war, in which many refugees end up in densely settled and unhygienic refugee settlements, clearly favors the di�usion of many infectious. Voluntary migration
more typical of a�uent societies entails little change in disease risk and disease di�usion. Thus, it is very im- portant to be speci®c about the type of mobility that is
considered. Of less signi®cance in terms of pure numbers of
a�ected individuals, but of great conceptual import- ance has been the phenomenon of “airport malaria”. In this apparent anomaly, some who live within several
kilometers of international airports have contracted malaria. These individuals have not been in areas
where malaria is endemic, and may have even not left their home countries for any travel. Such outbreaks have happened in the past few years around the
Geneva airport in Switzerland, Newark Airport, Heathrow and Detroit Metropolitan Airport. Experimental data indicate that anophelines may sur-
vive a ¯ight from a tropical country in the wheel wells of aircraft, and then ¯y into the areas surrounding the
airports. This is the only way that those a�ected by “airport malaria” could possibly have contracted the disease. Should this occur in areas where anopheline
replication is easy due to climatic and ecological fac- tors, the potential exists to introduce malaria into pre- viously non-endemic areas. A recent report on the
Internet-based ProMED, which is an e�ort ®nanced by the Federation of American Scientists, to serve as a
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 947
forum for the rapid reporting of disease outbreaks, documents a case of malaria acquired indigenously in
the Toronto area. The patient had not been out of the country, nor had she been near a major international airport, as had “airport malaria” patients. The only
putative source of contagion was that an anopheline in the Toronto area had taken a blood meal from an infected individual and had transmitted the disease in
the usual manner. This kind of phenomenon indicates that vectored
transmission can be a potential threat even in areas
that are free of a particular disease. This is particularly the case with tropical countries where climatic con- ditions are conducive to vector survival and multipli- cation. One fascinating example is that yellow fever is
con®ned to tropical Africa and Latin America, yet it has apparently never been present in Asia, which has the correct habitats for vector survival, and potentially
a highly susceptible population, lacking any immunity due to no previous exposure. Why has yellow fever not di�used to Asia? This remains an unanswered ques-
tion. Two examples, however, do indicate the possibility
of vector transportation with major public health con-
sequences. Dengue was probably introduced to the Americas from Africa because of the slave trade. It had been endemic in Africa (Morse, 1995). It has since become a major problem and is epidemic in Latin
America and the Caribbean. It is almost certain that the movement took place because of worldwide ship- ping patterns.
Global climate change and infectious diseases
Obviously, much attention in the scienti®c and pol- icy communities has been devoted to the dual pro-
blems of global warming and ozone depletion. Global warming will undoubtedly a�ect human health by increasing the latitudes at which the vectors for ma-
laria, dengue fever and vectored encephalitides can sur- vive. Thus, a reasonable prediction is that these diseases will be seen in more temperate areas than they
are currently endemic. Indeed, dengue has been mov- ing northwards in the Caribbean and has reached epi- demic proportions in the Caribbean islands. Parts of Mexico in which dengue was not seen are now experi-
encing outbreaks of dengue, and in 1996, several cases of locally acquired dengue occurred for the ®rst time in many years in the United States. Dengue serves to
illustrate the generalization that there will be latitudi- nal movement of vectors for a number of infectious diseases, as suggested by the Intergovernmental Panel
on Climate Change (1995). Many vectored diseases were identi®ed as having signi®cant potential for di�u- sion, but none is more notable than malaria. This dis-
ease, which was nearly eradicated in the 1960s, now results in 300±400 million new infections per year and
the World Health Organization (1995) estimates that the population at risk of developing malaria will increase to 2.5 billion people with scenarios of moder-
ate temperature change. An indirect e�ect of climate change is on the human
immune system itself. Ozone depletion, which, fortu-
nately, is greatest over Antarctica, results in the absorption of ultraviolet radiation, and, of particular interest, of ultraviolet B radiation. Halocarbons and
other greenhouse gasses contribute to this depletion. There is great consensus that human absorption of UV-B radiation a�ects our immune response by alter- ing the e�ects of the skin’s Langerhans cells, and there-
fore compromises our cell-mediated immunity, and particularly, our suppressor T-cells (Bentham, 1994; Intergovernmental Panel on Climate Change, 1995).
The relationship between ultraviolet radiation and immunity is an area of active research. The e�ects of ultraviolet B radiation on the immune system is with-
out controversy, though the dose-response relation- ships, particularly with very low levels of exposure, is not ®rmly established. In summary, ozone depletion,
leading to immunosuppression, will surely compromise our immune systems’ abilities to respond to pathogenic challenge, and, as Bentham (1994) notes, it is fortunate that the greatest ozone depletion, until now, has been
in relatively unpopulated areas such as Antarctica. There is no assurance that this will be the case in the future.
A political ecologic interpretation of emerging infectious diseases
The political ecology of disease is a promising if as
yet underdeveloped approach to understanding disease dynamics and it is potentially useful in a social in- terpretation of emerging and resurgent diseases. It
combines the elements of traditional disease ecology with the concepts of political economy that have been very productive in explaining a whole variety of
human projects (Mayer, 1996). Political ecology emphasizes the unintended human and natural conse- quences of individual, corporate and governmental projects, and demonstrates aptly that disease has its
“human-made” components as well as its natural com- ponents. Bryant (1992, p. 13) succinctly summarizes political ecology: “broadly. . . political ecology may be
de®ned as the attempt to understand the political sources, conditions and rami®cations of environmental change”. Political ecology has been most widely
applied to land development and management and combines elements of cultural ecology with political economy (Blaikie and Brook®eld, 1987). In the future,
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952948
applying its underlying concepts to speci®c diseases
and populations may test its potential. At its deepest, political ecology can alter the concepts of the causality of disease from a purely biomedical concept to one
that also incorporates the unintended aspects of human action. Unfortunately, however, the most recent work on political ecology (a whole book),
argues that there are two issues on which political ecol- ogists appear to agree. As the authors write: “the en-
vironmental problems facing the Third World are not simply a re¯ection of policy or market failures. . . but rather are a manifestation of broader political and
economic forces. Those forces are associated with the worldwide spread of capitalism (Bryant and Bailey, 1997, p. 3)”. The authors continue that the second
area of agreement “is the need for far-reaching changes to local, regional and global political-economic pro-
cesses (Bryant and Bailey, 1997, p. 3)”. Essentially the authors argue that political ecologists agree that there is a need for fundamental changes to the structures of
society. This is overly restrictive, since those who have dominated political ecology only in the context of social change have cast a useful framework for in-
terpretation, and the utility of this approach has been therefore narrowed.
A third area of implicit agreement is that political ecology considers only the Third World. However, pol- itical ecology can be a useful and a powerful method
of explanation in countries like the United States, and in the absence of any implicit need to promote funda-
mental changes in social and economic structure. Thus, my enthusiasm over political ecology is that it can explain relationships of phenomena, and that such ex-
planation need not occur in a Third World setting. Political ecology can help to clarify the dynamics of Lyme disease in New England just as well as it can be
used as a tool of change in Nigeria. As discussed previously, it is strongly in¯uenced by
land developers who, in pursuit of pro®t, obviously respond favorably to individual desires for large pri- vate homes with private lots, facilitated by the avail-
ability of transportation for access to employment centers and other amenities. Political ecology therefore has possibilities Ð but a largely untested promise Ð
for facilitating a deeper understanding of the inter- action between population, environment, power, and
disease (Mayer, 1996). Most political ecology has involved critical and
usually Marxist concepts of political economy, yet, as
Staniland (1985) has established, political economy is itself a loosely de®ned term. Peet and Thrift (1989)
a�rm the diversity of de®nitions of political economy and then argue in favor of using the term in the con- text of critical social science. The only commonality
between neoclassical political economy and Marxist or post-Marxist political economy is that political econ-
omy emphasizes the relations between politics and
power on the one hand and on pro®t and revenues on
the other hand. The approaches are so disparate that it
is di�cult to develop a de®nition beyond that. As sta-
ted in The Dictionary of Human Geography (Johnston
et al., 1994), two concepts of political economy have
remained pivotal since the initial use of the terms by
Ricardo and others (p. 446):
®rst, production and accumulation; and second, dis-
tribution of the `surplus’ so produced. It is the
focus on distribution that really accounts for the
political part of political economy; for questions of
apportioning the surplus among the classes of so-
ciety necessarily pushes inquiry beyond the purely
economic, and into the spheres of the social and
political.
Echoing the argument that it is di�cult to ®nd a uni-
versally accepted de®nition of political economy that,
nonetheless, is a term used so widely that Milton
Friedman and the free market economists at The
University of Chicago used it in the 1960s, The
Dictionary of Human Geography continues (p. 447):
Admittedly, it is di�cult to ®nd a common thread
among the many uses of political economy within
geography but if it exists it is that in all practices
the political and the economic are irrevocably
linked; a sentiment not that distant from that pro-
posed by the originators of the term.
This is not the place for an extensive review and cri-
tique of either political economy in general or of politi-
cal economy and health. An excellent review of the
diversity of concepts of the former is provided by
Staniland (1985) Two reviews of the latter are by
Brenner (1995) and Reich (1994).
As mentioned previously, Bryant (1992) provides a
convenient summary of most of the major concepts of
political ecology, while Peet and Watts (1996) develop
a basis for a “poststructuralist” political ecology,
which they label “liberation ecologies,” which has an
unabashed political agenda. Rochelau et al. (1996)
apply feminist perspectives to political ecology, and
vice versa. In none of these works are health and dis-
ease even mentioned. Using an interpretive framework
developed in the context of advocating social change
provides a challenge for the sociomedical interpretation
of disease.
If new understanding is to come, it will arise from
the fact that many diseases, and their emergence, result
directly from the unintentional consequences of human
action. For example, if ebola hemorrhagic fever may
be taken as one prototype of an emerging disease,
there are only two things that are clear about the dis-
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 949
ease. One is that it is poorly understood, and the other is that it has a very high case fatality rate. While the
viral basis of the disease has been identi®ed, its human and political ecologies are enigmatic and remain mys- teries despite intense attempts at identifying how the
virus moves from an enzootic into one that a�ects. Sometimes groups with limited contact with the rest of the world populate an area such as an isolated valley,
and a disease may therefore remain restricted to that valley. Kuru, for example, is a degenerative neurologi- cal disease that was restricted to one valley in New
Guinea. An ethnic group called the Fore populates this valley. Gajdusek and colleagues described this dis- ease (Gajdusek and Zigas, 1957; Zigas and Gajdusek, 1957), A prion was eventually suggested to be the cau-
sal agent. Prusiner won the Nobel Prize for Medicine and Physiology in 1997 because of his work on prions that began with his research on kuru (e.g., Prusiner,
1987). Ritual cannibalism was thought to be the mech- anism of contagion, which explains the puzzling obser- vation that morbidity and mortality were restricted
almost entirely to women. Since cannibalism has ended in the area, no new cases of kuru have been described. When it was ®rst discovered, kuru was a disease that
should be regarded as “emerging” in the sense that it had not yet been identi®ed or even recognized by those other than the Fore, yet the proviso must be added again, “recognized by whom?” Kuru was not emerging
for the Fore; the evidence was clear through oral his- tories that it had been present for generations. Kuru was thus the result not only of isolation, but also of
cultural practices. In other cases, as human activities expand the range
of human action to include new portions of tropical
rainforest, the potential for diseases hitherto unknown or very rare in the human population to appear in the population is high. Species jumps are common, and are not particularly exotic. In¯uenza is present in
avian populations; psittacosis is primarily a disease of psittacine birds that have become fond pets in the wes- tern world, and hantavirus pulmonary syndrome has
its reservoir in rodent populations.
Conclusion
The world is undergoing rapid change as human±en-
vironment relations evolve, global interdependency increases, and previously stable equilibria are dis- rupted. One of the consequences of these global
changes is that infectious diseases, once thought to be on the wane, are still very much a factor both within developed and developing countries. The complacency
with which much of the medical community viewed infectious diseases until the 1980s is understandable, for smallpox had been eliminated, tuberculosis was
well on the way to being a minor problem in the United States, and many infectious diseases in the tro-
pics appeared to be on the wane. However, infectious diseases are a cause for concern in some places, and for alarm in other places. HIV has devastated much of
sub-Saharan Africa; drug-resistant tuberculosis con- tinues to increase in the United States, particularly among the urban poor and homeless, and hospital
acquired infections are increasing. Several of these have extremely high case-fatality rates, since they are responsive to no known antibiotics. Over the long
term, disruption of the ecosystem, and its fragile equili- brium with humans, continues to take its toll.
References
Bentham, G., 1994. Global environmental change and health.
In: Phillips, D.R., Verhasselt, Y. (Eds.), Health and
Development. Routledge, London, pp. 33±49.
Betts, R.F., 1996. In¯uenza virus. In: Mandell, G.L., Bennett,
J.F., Dolin, R. (Eds.), Mandell’s, Douglas and Bennetts
Principles and Practice of Infectious Disease. Churchill
Livingston, New York, pp. 1546±1567.
Blaikie, P., Brook®eld, H., 1987. Land Degradation and
Society. Methuen, London.
Berkelman, R.L., 1994. Emerging infectious diseases in the
United States, 1993. The Journal of Infectious Diseases
170, 272±277.
Bifani, P.J., et al., 1996. Origin and interstate spread of a
New York City multi-drug resistant Mycobacterium tuber-
culosis clone family. JAMA 275, 452±457.
Brenner, M.H., 1995. Political economy and health. In:
Amick, B.C., Levine, S., Taylor, A.R., Walsh, D. (Eds.),
Society and Health. Oxford University Press, Oxford, pp.
211±246.
Bryant, R.L., 1992. Political ecology: an emerging research
agenda in third world studies. Political Geography 11, 12±
36.
Bryant, R.L., Bailey, S., 1997. Third World Political Ecology.
Routledge, New York.
Centers for Disease Control and Prevention, 1994. Addressing
Emerging Infectious Disease Threats: A Prevention
Strategy for the United States. US Public Health Service,
Washington.
Cli�, A., Haggett, P., 1995. Disease implications of global
change. In: Johnston, R.J., Taylor, P.J., Watts, M.J.
(Eds.), Geographies of Global Change: Remapping the
World in the Late Twentieth Century. Blackwell
Publishers, Inc., Oxford, pp. 206±223.
Coyle, P.K., 1993. Lyme Disease. Mosby, St. Louis.
Cronon, W., 1983. Changes in the Land: Indians, Colonists
and the Ecology of New England. Hill and Wang, New
York.
Crosby Jr., A.W., 1972. The Columbian Exchange: Biological
and Cultural Consequences of 1492. Greenwood Press,
Westport, CT.
Crosby Jr., A.W., 1986. Ecological Imperialism and the
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952950
Biological Expansion of Europe, 900±1900. Cambridge
University Press, Cambridge.
Denevan, W. (Ed.), 1992. The Native Population of the
Americas in 1492. University of Wisconsin Press,
Madison.
Gajdusek, D.C., Zigas, V., 1957. Degenerative disease of the
central nervous system in New Guinea. The endemic
occurrence of `kuru’ in the native population. New
England Journal of Medicine 257, 974±978.
Garrett, L., 1994. The Coming Plague: Newly Emerging
Diseases in a World out of Balance. Farrar, Strauss and
Giroux, New York.
Garrett, L., 1996. The return of infectious disease. Foreign
A�airs 75, 66±79.
Ginsberg, H.S. (Ed.), 1993. Ecology and Environmental
Management of Lyme Disease. Rutgers University Press,
New Brunswick.
Goodgame, R.W., 1996. Understanding intestinal spore-form-
ing protozoa: cryptosporidia, microsporidia, isospora and
cyclospora. Annals of Internal Medicine 124, 429±441.
Gould, P., 1993. The Slow Plague: A Geography of the AIDS
Pandemic. Blackwell, Oxford.
Hedberg, C.W., et al., 1994. Changing epidemiology of food-
borne disease: a Minnesota perspective. Clinical Infectious
Diseases 18, 621±682.
Herwaldt, B.L., Ackers, M.L., 1997. An outbreak in 1996 of
cyclosporiasis associated with imported raspberries. New
England Journal of Medicine 336, 1548±1556.
Intergovernmental Panel on Climate Change, 1995. Climate
change 1995: impacts, adaptations and mitigation of cli-
mate change: scienti®c±technical analyses. Contribution of
Working Group II to the Second Assessment Report of
the Intergovernmental Panel on Climate Change.
Cambridge University Press Cambridge.
Johnston, R.J., et al. (Eds.), 1994. The Dictionary of Human
Geography, 3rd. ed. Basil Blackwell, London.
Kida, H., et al., 1988. Origin of the hemagluttinin gene of
H3N2 in¯uenza viruses from pigs in China. Virology 179,
759±767.
Knapp, J.S., et al., 1997. Fluoroguinolone resistance in
Neisseria gonorrheae. Emerging Infectious Diseases 3, 33±
39.
Lastavicam, C.C., et al., 1989. Rapid emergence of a focal
epidemic of Lyme disease in coastal Massachusetts. New
England Journal of Medicine 320, 133±137.
Lederberg, J., Oaks, S.C., 1992. Emerging Infections:
Microbial Threats to Health in the United States.
National Academy of Sciences, Washington.
Marx, J.L., 1983. Acquired Immune De®ciency Syndrome
abroad. Science 222, 998±999.
May, J.M., 1958. The Ecology of Human Disease. M.D.
Publications, New York.
Mayer, J.D., 1996. The political ecology of disease as one
new focus for medical geography. Progress in Human
Geography 20, 441±456.
Meade, M.S., 1976. Land Development and Human Health in
West Malaysia. Annals of the Association of American
Geographers 66, 428±439.
Meinhardt, P.L., et al., 1996. Epidemiologic aspects of human
cryptosporidiosis and the role of waterborne transmission.
Epidemiologic Reviews 18, 118±136.
McNeill, W., 1976. Plagues and Peoples. Anchor Books,
Garden City.
Morse, S.S., 1993a. AIDS and beyond: de®ning the rules for
viral tra�c. In: Fee, E., Fox, D.M. (Eds.), AIDS: The
Making of a Chronic Disease. University of California
Press, Berkeley, pp. 23±48.
Morse, S.S., 1993b. Examining the origins of emerging
viruses. In: Morse, S.S. (Ed.), Emerging Viruses. Oxford
University Press, New York, pp. 10±28.
Morse, S.S., 1995. Factors in the emergence of infectious dis-
eases. Emerging Infectious Diseases 1, 7±15.
Omran, C., 1971. The epidemiologic transition. Milbank
Memorial Fund Quarterly 49, 508±539.
Ortega, Y.R., et al., 1993. Cyclospora species-a new pathogen
of humans. New England Journal of Medicine 328, 1308±
1312.
Pablos-Mendez, A., Knirsch, C.A., Barr, R.G., Lerner, B.H.,
Frieden, T.R., 1997. Nonadherence in tuberculosis treat-
ment: predictors and consequences in New York City.
American Journal of Medicine 102, 164±170.
Peet, R., Thrift, N., 1989. Political economy and human ge-
ography. In: Peet, R., Thrift, N. (Eds.), New Models in
Geography. Unwin Hyman, London, pp. 3±29.
Peet, R., Watts, M. (Eds.), 1996. Liberation Ecologies.
Routledge, London.
Plotkin, B.J., Kimball, A.M., 1997. Designing an international
policy and legal framework for the control of emerging
infectious diseases: ®rst step. Emerging Infectious Diseases
3, 1±9.
Prusiner, S.B., 1987. Prions causing degenerative neurological
disorders. Annual Review of Medicine 38, 381±398.
Quinn, T.C., 1995. Population migration and the spread of
types 1 and 2 Human Immunode®ciency Virus. In:
Roizman, B. (Ed.), Infectious Diseases in an Age of
Change. National Academy Press, Washington, pp. 77±98.
Reich, M., 1994. The political economy of health transitions
in the third world. In: Chen, L.C., et al. (Eds.), Health
and Social Change in International Perspective. Harvard
School of Public Health and Harvard University Press,
Boston, pp. 413±452.
Report of the NSTC Committee on International Science,
Engineering, and Technology (CISET) Working Group on
Emerging and Re-emerging Infectious Diseases, 1994.
Global Microbial Threats in the 1990’s. Washington:
National Science and Technology Council, O�ce of the
President of the United States.
Rhodes, R., 1997. Deadly Feasts: Tracking the Secrets
of a Terrifying New Plague. Simon and Schuster, New
York.
Rich, S.M., et al., 1995. Distribution of Ixodes ricinus-like
ticks of eastern North America. Proceedings of the
National Academy of Science 92, 6284±6288.
Rochelau, D., et al. (Eds.), 1996. Feminist Political Ecology.
Routledge, London.
Sanchez, J.L., Taylor, D.N., 1997. Cholera. The Lancet 349,
1825±1830.
Shannon, G.S., Pyle, G.F., 1989. The origin and di�usion of
AIDS: a view from medical geography. Annals of the
Association of American Geographers 79, 1±24.
Shannon, G.S., et al., 1990. The Geography of AIDS.
Guilford Press.
J.D. Mayer / Social Science & Medicine 50 (2000) 937±952 951
Smith Jr., R.B., et al., 1996. Role of bird migration in the
long distance dispersal of Ixodes dammini, the vector of
Lyme disease. The Journal of Infectious Diseases 174,
221±224.
Staniland, M., 1985. What is Political Economy? A Study of
Social Theory and Underdevelopment. Yale University
Press, New Haven.
Whitmore, T.W., 1991. A simulation of the sixteenth-century
population collapse of the Basin of Mexico. Annals of the
Association of American Geographers 81, 467±487.
World Health Organization, 1995. Action Plan for Malaria
Control, 1995±2000. Unpublished in-house policy docu-
ment.
Wilson, M.E., 1994. Disease in evolution. In: Wilson, M.E.,
Levins, R., Spielman, A. (Eds.), Disease in Evolution:
Global Changes and Emergence of Infectious Diseases.
New York Academy of Sciences, New York.
Zigas, V., Gajdusek, D.C., 1957. Kuru: clinical study of a
new syndrome resembling paralysis agitans in natives of
the Eastern Highlands of Australian New Guinea. Medical




Leave a Reply
Want to join the discussion?Feel free to contribute!