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1.1
Mission impossible
On New Year’s Day of 1880, the young Fernanda Lesseps
stood on board of a steam launch in the mouth of the Rio
Grande, some 15 km east of the modern city of Colòn, on
the Carribean coast of the Isthmus of Panamà, then a
province of neighbouring Colombia. On that day, she
symbolically put a shovel full of sand into a box that had
been emptied of its champagne bottles, to mark the start
of the construction work for the Panama Canal. Fernanda
was performing this symbolic act on behalf of her father,
Count Ferdinand Lesseps. He was in his seventies and a
public hero because of his success as the architect of the
Suez Canal, which officially opened on 17 November
1869, and for which Guiseppe Verdi was commissioned
to write an opera. (In fact, Verdi did not complete the
piece in time, so his masterpiece Aida premiered in
Cairo on 24 December 1871, with pomp and glamour.)
Ferdinand Lesseps, therefore, had every reason to be
confident that he would also succeed in constructing the
long-desired maritime shortcut from the Atlantic to
the Pacific Ocean in due time. For this purpose, Count
Lesseps had just founded his new company ‘Compagnie
Universelle du Canal Interocéanique’ to finance the work.
Furthermore, in January 1881, around 200 engineers
from France and other European countries, together with
800 labourers, had arrived in Colòn to start the building
of the canal. How could Count Lesseps foresee that it
would take 34 years, from his daughter’s act on New
Year’s Day, and the involvement of American companies
and engineers to finish the project? Eventually, the canal
officially opened on 15 August 1914, by the passing of
the vessel SS Ancon. Over this time, an estimated 80,000
people worked on the canal and more than 30,000 lost
their lives in the effort. It was the parasites of the hot and
humid lowlands of Panama that proved the hardest problem to overcome. But let us see what happened.
Work on the canal began in 1882 along the route of
the Panama Railroad that was constructed in 1855.
Lesseps first started the task by erecting moorings, roads,
and barracks for the labour force. But the lowland tropics
were different from the Arabian deserts of the Suez Canal.
In fact, social insects proved to be the first problem and
an unexpected gateway to disaster. In particular, termites
were quick to destroy the wooden constructions that
had been erected. Furthermore, heavy trafficking by ants
inside the barracks proved to be a nuisance and a
challenge for maintaining hygiene. Lesseps, therefore,
decided to put housings and storage facilities on wooden
stilts. To prevent termites and ants gaining access to the
buildings above, and to deter them from attacking the
wooden structures, the stilts were placed in large, waterfilled drums. This counter-measure was a success and
termites were no longer a problem. However, the tropics
were far from defeated. These water drums soon attracted
hordes of mosquitoes that used the pools as their breeding grounds. Whereas this created additional nuisances
of more insect bites, the real threat emerged with the
arrival of yellow fever, for which mosquitoes act as a vector. By the end of 1881, already some 2000 men were at
work. In 1882, 400 deaths from yellow fever were
reported, and in 1883 a total of 1300 men had died from
1
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the disease. Probably as much as one-third of the labour
force became infected at any one time. By December
1888, the rampaging yellow fever, together with the everincreasing cost of the construction, led to the financial
collapse of Lesseps’ company, which was dissolved in
February 1889. The ambitious work was stopped by a
small, invisible parasite ( Wills 1996).
Yellow fever is caused by a single-strand RNA virus
belonging to the family of Flaviviridae (group B arboviruses), a family with several representatives causing severe
haemorrhagic fevers (like Ebola or Lassa). The virus affects
specialized surface cells, for example, in the liver, or the
heart. The first symptoms appear three to six days after
the infection with swellings and cell death. In the majority
of cases, the infection is short and intense, and the patients
fully recover; and recovered patients acquire a long-lasting immunity against the disease. In a minority of cases
(around 15% of patients), however, the infection develops
into a severe problem. Sudden high fever, yellow tint in
the eyes, jaundice, and bleeding that leads to ‘black vomit’
are the typical symptoms. In the process, the liver cells are
destroyed, which leads to acute liver failure (and so to
jaundice). Such infections, if untreated, are associated
with high case mortality of patients (40% of cases). The
blood remains infective and can be transmitted further by
mosquitoes during a period from the first to the third day
of fever (Cook and Zumla 2008).
Yellow fever is not initially native to the Americas but
originated in West Africa. There, the virus has a reservoir
in wild animals, especially in monkeys. With the increasing trade connections between Africa and the Caribbean
in the sixteenth and seventeenth centuries, yellow fever
spread by trading ships to the New World. It was first
recorded in 1648 in the Yucatan peninsula and in the
Spanish settlement of Havana, Cuba (where it was eliminated in 1901 by destroying the breeding sites of mosquitoes). Twenty years later, in 1686, yellow fever had
reached Brazil and, in 1690, the island of Martinique.
Yellow fever (as well as other African-origin diseases) was
a prime factor in the depopulation of tropical America at
these times.
Following the trading routes, yellow fever subsequently
jumped back from the Americas to the European continent, where it caused an outbreak in Cadiz, Spain, in
1730. Later, such outbreaks were also observed in
Marseille, France, and in 1878 in England. After its first
introduction in Central America, yellow fever had established an animal reservoir too, mainly in howler monkeys. Epidemic outbreaks in howler monkeys had
repeatedly occurred, starting in Panama and spreading
along the east coast of Central America to Guatemala. In
1914, Sir Andrew Balfour (1873–1931), then the founder
of the Wellcome Museum of Medical Science and later
(1923) first director of the London School of Hygiene and
Tropical Medicine, noted that a yellow fever epidemic in
Trinidad lead to a ‘silent forest’, since all Howlers had died
from the infection (Balfour 1914; Cook and Zumla 2008).
In the meantime, epidemiologists have elaborated on
the forest cycle of yellow fever.
For people of modern western civilizations, the fear
induced by major diseases, such as yellow fever, is hard to
imagine. Yellow fever, in fact, was one of the most feared
diseases in the eighteenth and nineteenth centuries. Not
only at the Panama Canal construction site, but also elsewhere, the French paid a heavy toll to this disease. Around
1800, for example, the French controlled large territories
in the Caribbean, Central America, Mexico, Louisiana,
and Canada. In 1801 a rebellion under the black leader
Toussaint Louverture erupted in the French colony of
Haiti. Napoleon was forced to send his brother-in-law,
General Le Clerc, to subdue the rebellion, but over 27,000
troops, including Le Clerc himself, died from yellow fever
within months after their arrival in Santo Domingo. At the
same time, yellow fever had little effect on the black
African rebels whose ancestors came from West Africa—
the same region where yellow fever had been around for
a very long time and where people were less susceptible
to the infection. One consequence of the epidemic was
that the French withdrew from the Americas and sold
Louisiana to the United States (Oldstone 1998). But others
suffered, too. During an epidemic in Philadelphia in 1793,
the American capital at the time, the disease claimed over
10% of the population (around 40,000 people). Between
1793 and 1796, the British army in the Caribbean lost
about 80,000 men, over half of them to yellow fever. Even
in the peaceful period between 1817 and 1836, the annual
death rate of British soldiers in the West Indies was six to
ten times as high than at home, primarily due to diseases
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3
Figure 1.1 A fumigation car for the control of yellow fever in Panama City, 1905. Such controls measures were used in
preparation of the construction of the Panama Canal by American companies. Control of mosquito populations was first
introduced by the US Army medical scientist Walter Reed and his team in Havana, Cuba, after 1900.
Photo supplied courtesy of Panama Canal Museum.
such as yellow fever. West Africa even became nicknamed
the ‘White Man’s Grave’, mostly because of the widespread
presence of yellow fever in this area; the associated mortality was thirty times as high as in the homeland (Crosby
1986). Ironically, African slaves were highly praised in the
New World precisely because black Africans showed
higher levels of resistance to the virus than did the native
Indians of the Americas. Up to the early years of the twentieth century, massive yellow fever epidemics repeatedly
swept through the Caribbean and up the North American
coasts regularly terrifying people. Yellow fever remains a
health problem in tropical America today. Local epidemics occurred as late as 1997–98 in Santa Cruz, Bolivia.
Transmission in the jungle forest cycle is documented for
the Amazon basin for the last decades and regular infections of humans occur in this area, usually with high case
mortality rates. In the Amazon basin, recurrent epidemics
are noticed every five to ten years, spreading along the
tributaries of the river Amazon in accordance with the reestablishment of susceptible monkey populations in the
gallery forests (Izurieta et al. 2009).
As early as 1881, an Havanna physician, Carlos Juan
Finlay, suggested that yellow fever was a mosquitoborne disease. In the Spanish–American War of 1898,
the United States backed the rebels in Cuba and Puerto
Rico. The presence of US military in these areas created
the health problems that so generated political pressure
to investigate the disease. With bold experiments in
research stations just outside Havana, where volunteers
were exposed to mosquitoes, the US Army medical scientist Walter Reed (1851–1902) and his team (‘The Reed
Commission’) finally proved, in 1900, that yellow fever
is indeed vectored by an insect (Aedes aegypti). This
insight led to successful campaigns against mosquito
breeding grounds. The control measures now made
possible allowed completion of the construction of the
Panama Canal during the years of 1906–1914 (Figure
1.1). By 1928 the South African virologist Max Theiler
(1899–1972) and his Harvard mentor Andrew Sellards
showed that the agent of yellow fever is a virus. In 1937,
Theiler, then working at the Rockefeller Institute, developed a safe and successful vaccine that is still in use
today, a discovery for which he was awarded the Nobel
Prize in 1951.
1.2 Some lessons provided by
yellow fever
This dramatic piece of history illustrates a number of
issues that will be covered in this book and we can list
them as follows.
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1.2.1 The parasite life-cycle can be complex
Yellow fever is a parasite that needs a vector—a more or
less passive transport vehicle—to get from one human
host to the next. Not all parasites are transmitted in this
way. Most can jump from one host to the next directly, for
example, via air in close contact (e.g. influenza virus), by
transfer of body fluids (e.g. HIV or Ebola virus), or by water
over larger distances (cholera, typhoid bacteria). Some
parasites have evolved to utilize an intermediate host.
For example, the causative agent of bilharzia, the digenean trematode, Schistosoma mansoni, uses the freshwater snail, Biomphalaria glabrata, as its intermediate host
from where it is transferred to the (final) human host, and
then back again to the snail. In the final host, Schistosoma
reproduces sexually and the eggs penetrate the host’s
veins, intestines, or bladder, where they cause harm. A few
parasites have incorporated more than two hosts in their
life-cycle, such as the lancet liver fluke (Dicrocoelium dendriticum) that passes through hosts of three phyla: snails
(mollusca), insects (arthropoda), and then to a vertebrate
(chordata). Finally, a large number of insect species have
evolved to become parasitoids. Parasitoid larval stages are
inside or on the surface of a host from which they extract
their resources. The adult insect is free-living, searches
for mates, and lays its eggs or larvae again into a host, on
its surface, or at least in its vicinity. These variations on
a theme have many consequences for the ecology and
evolution of host–parasite interactions.
1.2.2 Not all host and parasite strains are the same
Not all people infected by yellow fever progress to the
second, more dangerous stage of the disease. Similarly,
West Africans proved more resistant to yellow fever than
French or British soldiers. In other words, hosts within
or among populations vary in their susceptibility to a
given parasite. On the other hand, not all yellow fever
strains are the same either. Today, epidemiologists distinguish between urban yellow fever that is transmitted by
the mosquito, Aedes aegypti, and which is prevalent in
tropical urban areas. Sylvatic or jungle yellow fever is the
same parasite but a variant that primarily causes a disease of monkeys in the tropical forests of South America
and Africa. Humans only occasionally become hosts. It is
transmitted by various species of mosquitoes. In addition,
the infection is transmitted to offspring of an infected
female mosquito from where it can again infect a monkey or a human. Differences not only exist between urban
and jungle forms of yellow fever, there are also more or
less virulent strains in general. For example, the standard
yellow fever vaccine (YF-VAX) is based on strain 17D that
was originally isolated from a patient named Asibi. The
properties of this strain allowed Max Theiler to maintain
it in cell culture, where it could be attenuated to become
a safe, live vaccine. Hence, variants of the parasite play
an obviously important role. Against the background of
various flu epidemics caused by different strains (such as
influenza type H1N1 ‘swine flu’, H5N1 ‘bird flu’, etc.), this
has become an issue in our days again.
1.2.3 Complex physiological and molecular
mechanisms underlie the infection
The yellow fever virus has to reach a new host through
the bite of an infected mosquito. Once inside the bloodstream of the human host, it must enter a target cell and
multiply. These processes unfold at the physiological and
molecular level, where a range of different proteins and
biochemical mechanisms are involved. For example,
the virus gains entry by a process of receptor-mediated
endocytosis, i.e. it is ingested by the host cell. The synthesis of new viral RNA occurs in the cell cytoplasm. At the
same time, the synthesis of viral proteins happens in the
endoplasmic reticulum of the host cell. Then, new viruses
(the virions) are assembled and can infect the next cells.
Many of the proteins responsible for these processes
have been identified. For example, structure protein C
binds RNA to the viral nucleocapsid and thus ensures
proper packaging of the genetic information (on RNA)
into a (protein) capsule. The protein NS1 is involved in
viral assembly and affects the release from the host cells.
Viral structural protein E is an envelope protein crucially
important for the attachment of virions to host cells, but
also for haemaggluttination (clotting of red blood cells)
and virus neutralization by the host. Changes in this
protein are associated with a change of virulence and
attenuation of virus strains. The host’s immune system
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responds to infection by activating a number of signalling cascades and expressing the genes responsible for
anti-viral defence; this includes the recruitment of lymphocytes that are able to recognize virus-infected cells
and destroying them. This machinery is exceedingly
complex and will be treated in more detail in Chapter 4.
Note that parasites like yellow fever requiring a vector for
transmission not only have to outwit the human (vertebrate) immune system, but also, for instance, that of the
mosquito (an insect).
These physiological and molecular mechanisms produce macroscopic phenomena that we know as parasite
virulence and host resistance. Furthermore, these mechanisms are based on genes that become differentially
expressed at various stages of infection, replication, and
transmission. There is, therefore, a distinction between
the mechanisms that lead to a certain outcome of the
infection, the underlying genetic basis for these mechanisms, and the function of parasite virulence and host
resistance, that is, their value for survival and reproduction (the fitness) of host and parasite. Indeed, there is
overwhelming evidence that virulence and resistance are
traits that show phenotypic and genotypic variation
within populations and are able to evolve. We must,
therefore, expect that these traits have been shaped by
natural selection to increase the fitness of the carriers.
Although it is necessary to consider the underlying physiological and molecular mechanisms, the mechanisms
cannot answer questions about adaptive value and fitness, and vice versa.
1.2.4 Parasites and hosts are populations
Parasites and hosts consist of individuals that form interacting populations. On the ecological scale, a population
dynamic process unfolds from this interaction. Throughout
history, yellow fever has caused many epidemics in different parts of the world. An epidemic emerges from
the processes of infection, replication, and transmission
of the parasite to the next host. This in turn depends on
susceptibility, resistance, and clearing of infections by the
hosts. But an epidemic is also an ecological process in
which two species (host and parasite) interact with each
other; their relative numbers, densities, and population
5
dynamics produce the changes in the level of infection
over time. An epidemic is, therefore, as much governed
by the laws of ecology and population dynamics as it
depends on molecular mechanisms. At the same time,
the interaction of the two populations generates selection for host and parasite. Therefore, hosts and parasites
also change by the process of evolution as an epidemic
unfolds. Hosts might not only become protected individually by their immune memory, but the host population as a whole adapts to the parasite through selective
deaths. Descendants inherit the selected favourable
resistance traits and will be protected for some time until
a new epidemic starts with a different parasite or a sufficiently different variant of the same. Epidemics strongly
remind us that host–parasite interactions are also a piece
of evolution and ecology, not just of molecular biology.
1.2.5 Parasites can be controlled when
we understand them
The control of yellow fever is achieved by the control of
mosquito breeding grounds as initially suggested and
carried out in Havana by Walter Reed and his team. In
addition, the host population can be protected by mosquito nets and by vaccination. The yellow fever vaccine is
one of the safest known and it provides protection for at
least ten years. Vaccination is possible because the vertebrate immune system contains memory cells that allow a
faster and more efficient response to a second challenge
of the same kind. Such highly specific memory is particular to the higher vertebrates but may exist in similar
form in invertebrates too (Kurtz 2004). Not all vaccines
and parasites allow for such a safe and durable protection, however. How protective memory forms is a question of immunology. However, ecology and evolutionary
biology tell us that the consequences of vaccination are
not only restricted to the individual host that gains protection, rather, vaccination alters the selection regime for
the parasite population as a whole. Successful vaccination
protects one part of the host population from infection
and thus decreases the number of available hosts for the
parasite. If enough hosts are so protected, the parasite
may find itself unable to find a new host and becomes
eliminated. On the other hand, the vaccine-associated
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PARASITES AND HUMANS
selection pressure on the parasite leads to adaptations
that might counteract the effect of the vaccine in the long
term, especially when vaccination is not perfect. Again,
we are reminded that the study of host–parasite interactions is not possible without an integrated approach that
spans all levels from molecules to ecology and evolution.
This approach touches on the traditional fields of population biology, behavioural studies, genetics, immunology, parasitology, physiology, biochemistry, or molecular
biology to mention some. Furthermore, it requires the
tools used in ecological and behavioural field studies,
laboratory experiments, molecular techniques, mathematical modelling, computing, and a good nose for what
might be going on between hosts and parasites. In fact,
studying parasites and their ways has often be equated
with the work of a detective (De Kruif 1926) and much
of the fascination of the subject comes from the vast and
yet unexplored terrain on which hosts and parasites—to
paraphrase George E. Hutchinson (1903–91)—act out
their evolutionary play in the ecological theatre.
1.3
Parasites in our times
Is the worry about parasites and epidemics a thing of the
past? Not really. Whereas we have vastly better means to
deal with novel pathogens, parasites are not only present in less-developed countries, but are also a source of
disquiet for the industrialized countries with high living
standards (Barrett et al. 1998). Even conservative estimates
suggest that hundreds of millions of people are infected by
parasites worldwide and many thousands die because of
infections every year. Influenza is an example well-known
to the industrialized countries. It has a very long history
in human populations, dating back to antiquity. A major
pandemic (an epidemic spanning large parts of the world)
was already recorded in the late-sixteenth century. Today,
three types of influenza viruses (types A, B, and C) circulate, with types A and B the most prevalent and dangerous
ones. Influenza virus has only eleven genes (!)—apparently
enough to cause a lot of trouble. Type A viruses especially
have caused major epidemics in recent history.
Undoubtedly, the most famous pandemic is the one
caused by H1N1-type (strains are labelled by the type of
haemagglutinin, H, and neuraminidase, N) from spring to
winter 1918 (the ‘Spanish flu’). It had a much higher casemortality rate than any recorded strain before and killed
somewhere between 20 and 40 million people—equivalent to the number of casualties during World War I. The
relationship of Spanish flu to swine and avian reservoirs is
unclear. It is possible that swine served as host where
influenza virus evolved before breaking out into the
human population (Bush 2007). Influenza caused another
major epidemic in 1957 (types H2N2 ‘Asian flu’ and H3N2
‘Hong Kong flu’), starting from China and spreading
worldwide. This pandemic strain emerged from a recombination of the still circulating H1N1- strain and elements
of avian flu. The new strain displaced the old H1N1 in the
process. In 1968, a human H2N2-strain again re-assorted
with avian influenza virus to produce the pandemic
H3N2 ‘Hong Kong flu’. And yet again, the previously circulating strains were displaced. Such serial replacement
was undercut with the re-appearance of H1N1 in 1977 in
China but which now caused only mild symptoms. H1N1
and H3N2 have now been circulating in humans for several decades.
Seasonal influenza is a common occurrence and no
real cause for major worries. As the historical record and
the analysis of viral serotypes and genotypes show, this
normal pattern is interrupted by major pandemic strains
at intervals of some ten to twenty years. Such strains often
emerge by recombination of human-adapted virus with
elements of others, notably bird- or swine-adapted influenza. Against this background, the outbreak of bird flu hit
the news in 2004. But avian influenza was no newcomer
but had already been noticed in 1959; worldwide (up to
2006) it had caused 24 highly pathogenic outbreaks in
birds (poultry), although each within a limited geographic
area. Avian influenza is caused by several type A strains, of
which four (H5N1, H7N3, H7N7, H9N2) have infected
humans. Of those, strain H5N1 proved to cause the major
worries as it seemed to readily cross the species’ barrier
and jump from birds to humans. The case of 2004 was not
the first appearance of H5N1. The strain had already been
isolated from a goose in China in 1996. It was then seen in
1997 in Hong Kong, where it infected chicken and was
transmitted to humans (18 cases, six deaths) and again in
Hong Kong in February 2003 (two cases, one death). In
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1997, around 1.5 million chickens were culled to contain
the disease. In late 2003, a highly pathogenic flu virus hit
farms in Vietnam, confirmed as type H5N1 in January
2004; thousands of birds were culled but soon a few
humans were hospitalized with severe respiratory illness
that turned out to be H5N1 infections. During 2004, H5N1
continued to spread among birds in Japan, Hong Kong,
Thailand, Cambodia, Laos, China, Indonesia, and Malaysia.
At the same time, cases of human infections and fatalities
accumulated in Vietnam and Thailand.
The situation was very similar in 2005 when the virus
spread further to Russia and central Asia. H5N1-viruses
reached poultry in Turkey, wild birds in Croatia, and was
found in an imported parrot in the UK in October 2005.
By early 2006, the flu had spread further in wild bird populations, primarily waterfowl (swans), that were embarking on their spring migration. The study of bird migration,
so far considered an enjoyable hobby of bird lovers and
conservationists, suddenly looked like an important topic
for human health. Also, human flu infections continued to
occur. The symptoms were variable but nevertheless
caused fatalities in many cases. Not surprisingly then, the
scare in Europe and North America reached new heights.
With few exceptions, it still seemed that bird-to-human
transmission was the relevant route of infection. One
reason seems to be that avian virus infects the lower respiratory tract (lungs), allowing for rapid progression to
pneumonia, but from where it is not so readily transmitted, compared to human influenza viruses that primarily
reside in the nose and throat. But analyses of viruses circulating in Asia during 2005 had shown that several amino
acids near a receptor-binding site (affecting transmissibility) were changing. The virus was thus evolving and perhaps capable of direct human-to-human transmission. As
the autumn of 2006 approached, more humans became
infected, mainly in Asia and the Near East, and some viral
isolates now carried mutations that made them resistant
to some anti-viral drugs. Trade restrictions were put in
place by many countries. In Germany, army contingents
were deployed to control access to outbreak areas; people had to leave and enter through locks with disinfectants. Some panic buying of food items set in. Worries that
there might not be enough medication or facemasks
for everybody became prominent. Inevitably, religious
7
fanatics claimed the epidemic to be a fulfilment of divine
prophecies. But then, in the winter of 2006–07, the major
thrust of the epidemic in humans seemed to subside.
Soon, H5N1 dropped out of the news and got forgotten.
But H5N1 continues to infect birds (cases in Asia, Russia,
Egypt, and Europe during 2009) and humans (cases in
Egypt still reported in summer 2009).
With rapidly-changing parasites, forgetting is not a
good defence strategy. H5N1 is still among us. And an old
foe, H1N1, came back as swine flu and was first noticed
in spring 2009 in Mexico, although its actual origin is still
controversial. Similar to the history of bird flu, a swine flu
outbreak already had hit the US in 1976. This virus
seemed to be related to H1N1 of the Spanish Flu. Hence,
major concerns were issued and a nationwide vaccination campaign launched. Yet, the viruses never went far
from the original area around Fort Dix, New Jersey. The
H1N1 of 2009 was not really the same virus as before,
however. The new swine flu virus transmitted easily from
person-to-person causing flu-like symptoms but with
generally mild effects similar to seasonal influenza. The
virus spread like a bushfire, mainly among younger people. As of summer 2009, 168 countries or territories have
reported the presence of H1N1. On 11 June 2009, the
WHO declared the first flu pandemic since 1968.
Fortunately, in hindsight, the effects were severe only in
vanishingly few cases and the epidemic remained without much negative effect.
The story of influenza viruses is in many ways similar to
yellow fever, but influenza shows high rates of evolutionary change and can cause widespread epidemics much
more easily. Clearly, direct transmission is a much better
way to generate a pandemic than vector transmission, on
which yellow fever depends. Because influenza is so
changeable, it has been scrutinized as a case where the
holy grail of evolutionary biology might be unlocked—
the prediction of future evolution. The need is obvious:
because it takes several months to produce a vaccine in
large quantities, it would be an enormous advantage to
be able to predict which viral strain is likely to cause the
next seasonal influenza or even the next major pandemic.
This attempt has so far met with limited success (Bush
et al. 1999). Even for a simple organism like influenza
A virus, it seems difficult to predict the course of future
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PARASITES AND HUMANS
evolution. There is no simple relationship between
genetic sequence (which is what can be screened at large
scales in a population) and the phenotype that determines the antigenic properties of the virus and thus the
likelihood that it might successfully infect a host (Bush
2007). Nevertheless, progress is made and such predictions will certainly become more accurate in the not too
distant future.
These dramatic examples thus illustrate a number of
issues that will be covered in this book and suggest that
we humans should pay attention to our parasites. In fact,
much of the progress in human medicine and welfare is
due to improving public health by sanitation and hygiene,
alongside the discovery of new medication. Progress can,
therefore, not be confined to understand the physiological, biochemical, and molecular basis of how parasites
and their hosts interact. Rather, the interaction is among
living organisms that are subject to evolution by natural
selection in a given ecological context. The traditional
boundaries between fields are not helpful for this necessarily integrating approach and must be put aside. The
terms ‘host’ and ‘parasite’ are probably the most universal
ones throughout this book and they so capture the notion
that the ultimate job is to understand how and why they
interact in the way we see it, regardless from which field
our wisdom comes from, and regardless of whether we
take ‘parasite’ to mean a virus, nematode, or a parasitic
insect. This is the idea this book will focus on.
SUMMARY
• Parasites have played an important but often underestimated role in human history. A virus (yellow
fever) is one example of a deadly infection that
changed the history of the Americas.
• Major epidemics are still happening today. Influenza
is a prominent case where recent outbreaks generated well-founded fears.
• Human parasitic diseases illustrate the general principles. Only a combination of molecular understanding and insights from ecology and evolution
will eventually be fruitful.