Today, there is widespread recognition that our most powerful enemy may not be the
next world war, a nuclear bomb, or even acts of terrorism, but rather Mother Nature.
A new disease with high transmissibility and mortality could emerge from an unnoticed
quarter and drastically reduce the human population before sufficient resources and
expertise could be marshaled. It is likely that such a new and deadly disease would
have its origin in the animal world. In fact, a full 75% of emerging diseases of humans
come from animals. As the human population expands, and we hop from continent to continent;
as we mix various species together for trade, personal satisfaction, or to advance
our technology, we are certain to move more microorganisms into novel niches, with
Many outbreaks of emerging disease in humans are preceded by a similar emergence in
an animal population. In general, emerging disease agents can be broadly defined to
include three groups: known agents appearing in a new geographic area, known agents
or their close relatives occurring in a hitherto unsusceptible species, and previously
unknown agents detected for the first time. This review seeks to describe some of
the emerging diseases of animals and their relations to the corresponding and subsequently
emerging diseases in the human population. As a framework, diseases will be clustered
into one of the three groups listed above: agent in a new geographic area, agent in
a new species, and previously unknown agent detected for the first time.
Emerging zoonotic disease—occurrence in a new area
Some of the most worrisome infectious diseases are those that are already recognized
as endemic in one area, so that current control practices keep these diseases in check
and off the international public health radar screen. With globalization, pathogen
distribution patterns become redrawn in haphazard and unpredictable ways. Almost invariably,
the new host region is taken by surprise. Two examples are Rift Valley fever, an African
disease that recently emerged with ferocity for the first time outside Africa, and
alveolar echinococcosis, a smoldering and highly fatal parasitic infection that is
making insidious moves from its historic home in the Arctic to many new and more southerly
Rift Valley fever
Rift Valley fever (RVF) is a mosquito-borne viral disease that causes mass mortality
among newborn ruminants, especially sheep, and a flu-like illness in humans. The disease
had always been confined to the African continent. Then, in 2000, a severe epidemic
occurred in the Arabian peninsula. In this outbreak, the unusual presentation of disease,
the high human case-fatality rate, and the presence of multiple potential mosquito
vectors made the disease a serious cause for concern.
RVF virus was first isolated in 1930 in an epizootic situation among sheep on a farm
near Lake Naivasha in Kenya's Rift Valley . A characteristic feature of the disease
is hepatic damage, as described in the original report, “Enzootic hepatitis or Rift
RVF virus can infect a very wide host range; severe, often fatal disease has been
documented in lambs, calves, goat kids, puppies, kittens, mice, and hamsters. Moderate
disease has been seen in many other species . The incubation period is 2 to 6 days.
The virus replicates primarily in hepatocytes. Clinical signs in ruminants include
weakness, anorexia, jaundice, and death. Pregnant animals will abort or give birth
to malformed young. The disease is usually more severe in sheep than in cattle. Most
infections in humans are asymptomatic. Those who become clinically ill most commonly
experience a flu-like illness. Photophobia and symptoms of hepatic impairment may
be evident. Approximately 5% of clinically ill people will develop complications,
which are often grave. These include encephalitis, retinopathy, hepatorenal failure,
and disseminated intravascular coagulation leading to massive hemorrhage. Disease
in humans is almost invariably noted after mass mortality among animal species.
RVF is transmitted by mosquitoes. At least 30 species of mosquitoes in eight genera
can effectively carry the virus from one mammalian species to another. This lack of
“monogamy” with respect to vector competence ensures that RVF could easily become
established in a number of areas outside its historic range. Transovarial transmission
occurs, and the virus can remain in dormant eggs oviposited in dry areas. With rainfall,
eggs hatch, and the resulting mosquitoes can transmit the disease. Outbreaks usually
occur subsequent to climatic conditions that favor an increase in the vector population.
Ruminants are considered to be amplifier hosts and can experience a significant viremia.
This animal infection results in expansion of the infected vector populations, with
the disease spreading to the human population.
Before 1977, RVF was confined to Africa south of the Sahara; however, the construction
of the Aswan Dam and the subsequent development of flood plains for agriculture resulted
in a large outbreak in Egypt in the late 1970s. Likewise, construction of the Diama
Dam on the Senegal River precipitated an outbreak in Mauritania in 1987. Excessive
rainfall, largely brought about by the El Niño Southern Oscillation Effect, created
moist, mosquito-enhancing conditions that contributed to an outbreak in Kenya and
Somalia in 1997 to 1998 . In each of these instances, mass mortality in animals
preceded human infections. Then, in September of 2000, the Ministries of Health in
both Yemen and the Kingdom of Saudi Arabia received reports about acute disease in
humans that was compatible with RVF. The focus of disease was the northwestern region
of Yemen and the southwestern corner of Saudi Arabia. Just before reports of human
disease, there were records of extensive morbidity and mortality among livestock,
In Saudi Arabia, there were a total of 886 suspected cases during the outbreak. Laboratory
confirmation was attempted on 834 of the patients; positive results were obtained
on 683 (81.9%). The male-to-female ratio was 4:1. Of these 683 laboratory confirmed
cases, 95 died, for a case-fatality rate of 13.9%. Seventy-seven of the 683 cases
were Yemenis living and working in Saudi Arabia; the case-fatality rate for these
patients was 26%. The higher case-fatality rate for Yemenis may be related to the
lack of affordable access to health care and thus to late presentation . Also,
most of the Yemenis living in Saudi Arabia were male rural workers, who proved to
be the highest risk group.
Clinical and epidemiologic data from Yemen are not as readily available. According
to Centers for Disease Control and Prevention records, between August and November
2000 there were 1087 suspected cases, including 121 deaths . Three quarters of
the patients reported exposure to sick animals, handling an aborted fetus, or participating
in slaughter of animals.
The key presenting complaints in the outbreak in Saudi Arabia were nausea, vomiting,
abdominal pain, and diarrhea, all related to the acute hepatitis developing. In addition,
renal failure was a common complication, occurring in one fourth of the patients.
That factor makes this outbreak quite different from what has been seen in past outbreaks
in Africa, where the majority of cases were reported as flu-like illness. The case/fatality
rate also was much higher than that reported in previous outbreaks . The reasons
for the higher death rate may be related to underreporting of mild or asymptomatic
cases, or to pre-existing subclinical liver disease caused by the schistosomiasis
and viral hepatitis that are known to exist in this part of Saudi Arabia .
The genetic sequence of the virus obtained from this outbreak is closely related to
that of the virus that was circulating and causing disease in Kenya and Somalia in
1997 to 1998, a fact suggesting that it was introduced into the Arabian peninsula
from eastern Africa . The lack of variation among isolates from this outbreak indicates
that the agent had only recently been introduced to the area. The suspected route
of introduction is in infected livestock. Rainfall had been heavy the previous year,
as aerial surveys and satellite images revealed an increased vegetations index .
This outbreak of RVF in the Arabian peninsula underscores the interconnectedness of
human and animal populations. The blurring interface created by trade, combined with
favorable climatic factors, made possible a portal of entry and subsequent amplification,
creating first an emerging disease in livestock, then a significant public health
crisis for the region.
Alveolar echinococcosis is a chronic disease caused by infection with the intermediate
form of the tapeworm Echinococcus multilocularis. This parasite is geographically
distributed in the northernmost part of the northern hemisphere, including areas of
western Europe, Asia, China, northern Japan, Alaska, Canada, and the north central
region of the United States . In these areas, E multilocularis is maintained in
a sylvatic cycle that involves foxes and small rodents as the definitive and intermediate
hosts, respectively. While other wild canids and domestic dogs and cats can serve
as alternate definitive hosts, infected humans are an aberrant or intermediate host
. Once ingested by humans, the egg releases an oncosphere that finds its way from
the duodenum to visceral tissues, usually the liver, where the metacestode stage develops
as multiple infiltrating hydatid cysts of slow but constant growth and expansion .
The infection is so aggressive that the lesion was initially thought to be a neoplasm.
It was Rudolf Virchow, the father of modern pathology and also the first person to
use the term “zoonosis,” who correctly identified the disorder as an infectious process.
Because clinical signs usually develop 5 to 15 years post–initial infection when tissue
invasion is extensive, often the only treatment possible is radical surgery with concurrent
long-term antiparasitic treatment . In many instances more drastic measures, such
as liver transplantation, are the only alternatives. These treatments represent a
considerable cost burden to patients and countries where the disease is endemic.
The range of E multilocularis is currently expanding to areas where it was not previously
reported, and this expansion is apparently due to the translocation of the definitive
host. In Europe, the increasing fox population, in part the result of successful rabies
control programs, has resulted in animals invading urban centers. These urban centers
provide not only abundant small rodent intermediate hosts, but also alternative definitive
hosts such as the domestic dog and cat.
As the range of E multilocularis increases, incidence of human disease is carefully
monitored. In Alaska, there is considerable evidence of the disease among Eskimos.
Children are most likely to be infected, presumably because of play habits and increased
oral exposure, with the disease appearing as they become young adults , .
In some areas, seroprevalence among the human population is increasing, although a
specific rise in clinical cases has not yet been seen. It is unknown whether this
seroprevalence is due to immunity or to an early stage of infection, before cyst development
, . More extensive epidemiologic investigations are warranted.
Control of alveolar hydatid disease is problematic. Focal geographic eradication of
the cestode has been reported on the small Japanese island of Rebun by eliminating
dogs and foxes on the entire island. This method is impractical in larger geographic
areas because of ecological, ethical, and humane considerations . It has been
proposed that control of E multilocularis could be better achieved by broad ecological
study of the region in question and implementation of education programs. These educational
programs can focus on the modification of specific high-risk behaviors, the periodic
administration of anthelmintics to companion pets, and baiting methods with anthelmintics
for the wild reservoir . Education appears to be an economically feasible control
measure in small urban areas, where it has shown promising results in decreasing E
multilocularis environmental contamination .
Over 100 years have passed since Rudolf Virchow cast a spotlight on alveolar echinococcosis
by clarifying the infectious nature of the process. The lethality of the disease,
the economics of treatment options, and the spread into nonendemic and often urban
areas are all considerable causes for modern concern.
Emerging zoonotic disease—occurrence in a new species
It is well known that 75% of all emerging infectious diseases of humans occur as a
result of an animal pathogen's moving into a human host. A less-recognized possibility
is that of an infectious agent in one animal species moving into a second animal species
to create an emerging disease of animals. What is the total number of potential pathogens
currently present in animals? How many are capable of moving from animals to humans,
or from one animal species to another?
A recent paper by Dr. Sarah Cleaveland et al  catalogs and categorizes all known
pathogens of humans, domestic livestock, and domestic carnivores based on their ability
to move from one species to another. Surprisingly, of the 1415 known pathogens of
humans, 61.6% have an animal origin. A total of 616 pathogens were documented for
domestic livestock, with 77.3% considered “multiple species” (ie, capable of infecting
more than one type of animal). For domestic carnivores the total was 374 pathogens,
with 90% classified as “multiple species.” So it is apparent that there is considerable
promiscuity among animal pathogens. As unusual species are grouped together, swapping
of flora can easily occur.
Cleaveland makes no efforts to catalog the number of agents found in wildlife—understandably
so. The list would be not only enormous but also notably incomplete, because we lack
detailed knowledge about existing diseases of so many wild species of animals. In
this light, it is notable that many of the emerging human and animal diseases we have
dealt with in recent years have come from wildlife. This is a largely unexplored arena,
with many more pathogens yet to emerge. The following two examples demonstrate how
a pathogen moving from one animal species to another can have a very significant subsequent
impact on public health.
Monkeypox made headlines in the spring of 2003 as an African disease that sneaked
into the Midwestern United States through the exotic pet trade and generated dozens
of human infections in four different states. Contrary to popular belief, this was
not the first incursion of the virus into the United States. During the late 1950s
and 1960s, six outbreaks of monkeypox were reported among captive nonhuman primates
in research facilities throughout the United States , . In four of these cases,
the origin of the incriminated monkeys was not Africa but India and Southeast Asia.
However, subsequent serologic surveys in wild populations in South Asia failed to
identify this area as a possible niche of the virus. It is probable that these animals
were exposed at some point during their transportation or quarantine process. Traceback
investigations on the remaining two outbreaks were not reported, and human infections
did not occur on any occasion—perhaps because vaccinia immunization provides good
cross-protection against monkeypox, and smallpox vaccination was very active during
The monkeypox virus belongs to the Orthopox genus in the family Poxviridae and was
originally isolated in 1958 from a sick cynomolgus monkey at the Statens Seruminstitut
in Copenhagen, Denmark. The term monkeypox may be something of a misnomer, because
this virus is more frequently associated with small rodents than with primates .
Since the first human report in 1970, in what is today the Democratic Republic of
Congo (DRC), numerous reintroductions to the human population have occurred, mostly
in central and western Africa, including a large outbreak from 1996 to 1997 in the
DRC involving more than 400 individuals , .
A unifying factor in all human monkeypox clusters is the close interaction of humans
with wildlife. During African outbreaks, humans were exposed either during seasonal
hunting activities or when they were forced to retreat deeper into the rain forest
during civil turmoil , . Index cases in these outbreaks are usually associated
with exposure to rodents rather than monkeys. Close and continuous human/wildlife
interaction is needed to maintain monkeypox in a human population; human-to-human
transmission alone will not sustain the virus among humans. Nevertheless, if the herd
immunity of a population is low, person-to-person transmission and repeated introductions
of the virus from the wild reservoir can lead to more and larger clusters of human
monkeypox. Several serologic and epidemiologic studies implicate squirrels and the
Gambian giant rat as the key players in the circulation of the virus in nature ,
The introduction of monkeypox to humans in the central United States during the 2003
outbreak provides a good example of cross-species and cross-continental trafficking
of infectious agents. The monkeypox virus, a specifically African entity, was quiescently
exported from its home continent in one of its customary hosts, a Gambian giant rat,
and jumped ship, as it were, into a previously unexplored and proximate microbial
niche, prairie dogs that had been housed with the exported Gambian rats. The virus
flourished in this new and foreign microbial habitat, creating an acute and emerging
disease problem for this North American species of rodent. It was not long before
an emerging disease of prairie dogs became a significant public health crisis.
In the spring and early summer of 2003, there were 35 confirmed human cases of monkeypox,
scattered across four Midwestern states. All of these individuals were infected by
direct or indirect contact with infected prairie dogs , . An unexpected finding
was the relatively mild clinical presentation of the disease when compared with outbreaks
Traceback investigation revealed that prairie dogs, source of the human infection,
became infected at an animal distributor facility in Illinois when they were housed
together with infected Gambian giant rats and dormice imported from Accra, Ghana .
Out of 200 prairie dogs that were estimated to have been exposed to the infected African
animals in this facility, 93 were traced forward. The remaining 107 animals either
died or were sold in informal transactions without sufficient record-keeping to allow
With no knowledge of the fate of more than 100 potentially exposed prairie dogs, not
to mention the unknown number of African rodents in various collections throughout
the United States, we cannot predict the future of monkeypox in the Western Hemisphere.
Its impact on native wildlife populations of rodents and its potential establishment
as an enzootic disease in the United States are worrisome.
Since its emergence in 1976, the Ebola virus has become a “sleeping giant” in western
and central Africa. Following its first documented emergence, Ebola has re-emerged
to be recognized on at least 18 more occasions, mostly in the African continent. Each
new outbreak tends to generate screaming media attention, perhaps because of the gruesome
and rapid clinical course of the disease or, more likely, because of previous highlighting
of the disease in best selling books and motion pictures. In fact, Ebola has become
a kind of poster child for the whole field of emerging disease. In terms of human
morbidity and mortality, Ebola is a bit actor in the overall drama of emerging diseases,
but its occurrence and documented recurrences have generated considerable public consciousness-raising
and have increased funding levels for infectious diseases overall and emerging diseases
Studies in Africa have determined that monkeys and apes are important players in the
transmission of the virus to humans . In fact, most outbreaks in humans have been
preceded by primate die-offs or traced back to contact with dead primate carcasses.
Close exposure to these ape carcasses and consumption of bushmeat from these primates
are targeted as possible conduits of infection to the human population. In addition,
carcasses of duikers found near dead apes were also positive for Ebola virus, indicating
not only a broader host range but also the possibility of additional sources of bushmeat
for human infection. However, neither primates nor duikers are considered the natural
host, because the virus is highly lethal in these animals , .
The reservoir of Ebola remains anonymous. Many sampling surveys have been performed
but provide only limited information regarding the wild reservoir , . More
encouraging information has been obtained from experimental infections of possible
wild candidates, such as the fruit bat. In these experiments, bats were capable of
sustaining and allowing viral replication with negligible clinical signs . Recently,
an ecologic niche modeling study has suggested several characteristic features of
this unknown reservoir. The study establishes the reservoir distribution in the evergreen
broadleaf forest, mainly in the Congo Basin . In addition, climate variability
may play a role in filovirus transmission and might be useful as a predicting factor,
as rainfall has proved to be a factor in “triggering” the emergence of Ebola hemorrhagic
It is clear that an ecological approach to pathogen transmission can benefit our understanding
of emerging diseases, and Ebola hemorrhagic fever exemplifies this principle. The
limited genetic variation between isolates of Ebola subtype Zaire isolated 20 years
apart suggests that ecological rather than genetic factors play a central role in
the initiation of outbreaks .
Elucidation of the ecology of Ebola virus and definitive identification of its natural
reservoir are pivotal for the development of prevention programs. Such prevention
programs will benefit not only the human population but also the declining endangered
monkey and ape population in the region , . In the meantime, human disturbances
of pristine ecosystems along with the unsafe practices of the bushmeat trade will
provide ideal settings for Ebola re-emergence.
Emerging zoonotic disease—brand new agent
Perhaps the most frightening and unpredictable category of emerging disease is that
of those that are caused by a previously unknown virus or bacterium. Of course, the
agents are not really brand new, only new to our knowledge. Recent years have seen
such agents emerge in disastrous ways to affect human populations. Although the new
disease usually makes screaming headlines at the moment when large numbers of humans
become infected, in fact, in many instances the “new” agent has surfaced just previously
as an emerging disease in an animal population. It is this proximate source that extends
to infect humans.
Nipah virus is a recently discovered member of the Paramyxovirus family that was quiescent
in its ecologic niche for countless years until anthropogenic factors allowed it to
replicate in an environment that engendered extensive human exposure. An outbreak
of disease in pigs preceded the human clinical disease. The illness in swine was originally
attributed to classical swine fever infection, but it soon became apparent that a
novel infectious agent was responsible. Extensive replication in bronchiolar epithelium
coupled with an exertional cough ensured that the infected pigs were spewing prolific
amounts of virus into the environment. In humans, Nipah virus infection presents clinically
as an acute febrile encephalitis. Nipah virus was first isolated from the cerebrospinal
fluid of a patient from the Sungai Nipah village in Malaysia , 6 months after
its emergence in late September 1998. Close similarities of the new virus to another
recently discovered paramyxovirus, Hendra virus, prompted virologists to create a
new genus, Henipavirus, to include both entities. In Malaysia, the Nipah virus outbreak
came to an end after the establishment of strict control measures and the culling
of over a million pigs . The outbreak extended to Singapore, where it was halted
by ceasing the importation of pigs from Malaysia. At the end of this episode, a total
of 283 human cases of viral encephalitis with 109 deaths were reported, for a fatality
rate close to 40% .
Because fruit bats had been identified as the natural reservoir for Hendra virus,
several ecological surveys were undertaken to investigate the possibility that Nipah
virus also had originated from fruit bats. Early studies were able to detect antibody
titers against Nipah virus in five species of fruit bats , and eventually the
virus was isolated from the urine of an Island flying fox and from a partially eaten
fruit regurgitated from one of these bats . These findings implicated bats of
the Pteropus species as the natural reservoir for Nipah virus. The critical link with
the human population was made when the virus moved from fruit bats to swine. The susceptibility
of swine and the marked respiratory involvement created an outbreak situation, with
resulting spread to humans and a major public health crisis. The proposed chain of
events that enabled this interaction began around 1997 when extensive slash-and-burn
deforestation produced a haze that extended all over Southeast Asia . This deforestation
and haze, aggravated by an El Niño Southern Oscillation drought, decreased the already
scarce quantities of fruiting forest in the region. Impelled by these anthropogenic
factors, Pteropus bats invaded areas of fruit cultivation, like the index farms, that
were also used as piggeries.
Nipah virus elicits major public health concerns because of its high mortality rate,
ability to infect a wide range of hosts, and broad geographic distribution of the
reservoir host. This concern is accentuated by its negative economic impact and its
official listing as a critical biologic agent for public health preparedness. During
the 1998 outbreak, it was demonstrated that in addition to pigs various domestic animals
could serve as hosts, namely dogs, cats, and horses . Also, rodents have recently
been experimentally and productively infected . This wide availability of potential
hosts, along with the globally limited but regionally widely distributed reservoir,
represents a potential threat of emergence beyond Southeast Asian boundaries. Approximately
60 species of Pteropus bats have been identified, and all are distributed in a range
that extends from the islands of Mauritius, Madagascar, Pemba, and Comoro, along the
sub-Himalayan region of Pakistan and India, through Southeast Asia, the Philippines,
Indonesia, New Guinea, and the southwest Pacific islands as far east as the Cook Islands
and Australia. Although the distance these animals will travel, and thus their disease-carrying
capacity, is debatable, it is recognized that the overlapping distribution of three
species of flying foxes is all that is required to form a continuous link between
the east coast of Australia and Pakistan . This important ecological aspect must
be taken into consideration during epidemiologic investigations of future emergences
outside Malaysia, such as the outbreak recently (February 26, 2004) reported in Bangladesh
Severe acute respiratory syndrome
Two years after welcoming a new millennium, humanity experienced severe acute respiratory
syndrome (SARS), the first pandemic of the twenty-first century. This event catalyzed
global public health emergency responses in a way no previous disease had. The outbreak
in humans began in November 2002, as atypical pneumonia appeared first in the southern
Chinese province of Guangdong and subsequently spread to nine countries, including
the United States . All told, there were approximately 8435 human cases and 789
deaths in 33 countries around the world . A novel coronavirus (SARS-CoV) was eventually
identified as the culprit in SARS .
Despite extremely rapid and sophisticated molecular characterizations, the source
of the SARS virus remains speculative. The SARS-CoV proteins share little similarity
with the proteins of any of the three major existing serogroups of coronaviruses.
Various coronaviruses are well recognized for causing disease in animals—specifically,
infectious bronchitis in chickens, infectious peritonitis in cats, and diarrhea in
piglets and calves. However, the SARS-CoV had very little in common with any of these
well-studied pathogens. There is, however, mounting evidence to suggest that SARS-CoV
has a zoonotic origin. A promising lead arose when a SARS-CoV–like virus was isolated
from Himalayan palm civets found in the Guangdong live-animal market, and a subsequent
serosurvey study demonstrated viral titers among asymptomatic animal traders in Guangdong,
suggesting previous infection with a SARS-CoV–like virus , .
Speculation about a genetic reassortment of an animal coronavirus with further adaptation
to the human host is presently being evaluated. Certainly, a wild animal market could
provide the ideal setting for such reshuffling of genes among different wild animals
and eventually humans.
Evidence indicates that the introduction of SARS-CoV to humans was a fairly recent
event . Epidemiologic studies have shown that at least 2 months before the outbreak
the virus was circulating in the capital of Guangdong, Guangzhou, a city noted for
its “wet markets” where wild game trade for human consumption is very popular. Food
handlers made up more than one third of the initial cases. Only half of the cases
could be attributed to contact with SARS patients, suggesting transmission from an
unknown reservoir .
The SARS pandemic catalyzed public health systems worldwide, and the economic costs
were staggering. Despite the most intensive epidemiologic investigations and emergency
response ever mounted against an infectious disease, the source of the agent remains
elusive, making it extremely difficult to predict when and where the next resurgence
Wild game meat, livestock trading, pocket pets, and Arctic tapeworms—decades ago,
who would have envisioned that these disparate entities would be threaded together
in a great haiku of public health problems? Emerging diseases have created a new kaleidoscopic
lens through which we view the world. These emerging diseases will not only continue
to emerge but will probably do so at an ever-increasing rate. As was articulated in
a recent National Academies of Science report, myriad factors in our interconnected
global village are creating the microbial equivalent of a “perfect storm” . However,
unlike a major climatic event, where various meteorologic forces converge to produce
a tempest, this microbial perfect storm will not subside. There will be no calm after
the epidemic; rather, the forces combining to create the perfect storm will continue
to collide, and the storm itself will be a recurring event.
Watching the steady stream of new and emerging diseases, one is reminded of the carnival
game “Whack-a-mole.” In this game, the participant is given a rubber mallet and tasked
with defeating each mole that pops out of a series of holes. The satisfaction derived
from neutralizing one mole is immediately replaced with the drive to beat back the
next. The operator must act quickly to eradicate each new surfacing mole. Perhaps
today we need an entirely different strategy. Rather than responding to each new crisis
as it arises (ie, each new mole that emerges), we need to address the underlying factors
in disease emergence seriously and expeditiously. Instead of focusing on the next
big health crisis, we need to conduct thoughtful and thorough studies of the ecology
and overall species susceptibility of disease.