Ecology

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13
Parasitism
13 Parasitism
• Case Study: Enslaver Parasites
• Parasite Natural History
• Defense and Counterdefense
• Coevolution
• Ecological Effects of Parasites
• Dynamics and Spread of Diseases
• Case Study Revisited
• Connections in Nature: From Chemicals to
Evolution and Ecosystems
Case Study: Enslaver Parasites
Figure 13.1 Driven to Suicide
Some parasites can alter the behavior of
their host in order to complete their life
cycles.
Case Study: Enslaver Parasites
The hairworm life cycle begins when the
cricket drinks water that contains a
hairworm larva.
The larva enters the cricket’s body and
feeds on its tissues, growing into an
adult that fills the cricket’s body cavity.
The cricket then jumps into water and
drowns, the hairworm emerges and
mates, to start the life cycle again.
Case Study: Enslaver Parasites
Many other parasites “enslave” their
hosts.
Some fungi alter the perching behavior
of their fly hosts so that their spores
can be dispersed more easily.
Figure 13.2 Enslaved by a Fungus
Case Study: Enslaver Parasites
Rats infected with the protozoan
parasite Toxoplasma gondii do not
avoid cats, and in some cases are
actually attracted to cats.
This increases the chance that the
parasite will be transmitted to the next
host in its complex life cycle—a cat.
Case Study: Enslaver Parasites
The parasitoid wasp Hymenoepimecis
argyraphaga manipulates its host, the
orb-weaving spider Plesiometa argyra,
to spin a special “cocoon web.”
The wasp larva then kills the spider and
eats it, and spins a cocoon that is
suspended from the special web. This
arrangement keeps the cocoon from
being washed away by rains.
Introduction
Symbionts are organisms that live in or
on other organisms.
More than half of the millions of species
that live on Earth are symbionts.
Our own bodies can be a home to many
other species.
Figure 13.3 The Human Body as Habitat
Introduction
Some symbionts are mutualists, but the
majority are parasites.
A parasite consumes the tissues or body
fluids of the organism on which it lives,
its host.
Pathogens are parasites that cause
diseases.
Introduction
As a group, parasites typically harm, but
do not immediately kill, the organisms
they eat (unlike predators).
The degree of harm to the host varies
widely.
Compare: The fungus that causes
athlete’s foot, and Yersinia pestis, the
bacterium that causes the plague, which
can be lethal.
Parasite Natural History
Concept 13.1: Parasites, which constitute
roughly 50% of the species on Earth, typically
feed on only one or a few host species.
Macroparasites are large, such as
arthropods and worms.
Microparasites are microscopic, such as
bacteria.
Parasite Natural History
Most parasites feed on only one or a few
individual host organisms.
Defined broadly, parasites include
herbivores such as aphids or nematodes,
that feed on one or a few host plants.
Parasitoids, whose larvae feed on a
single host, almost always kill it.
Parasite Natural History
Most species are attacked by more than
one kind of parasite; even parasites
have parasites.
Many are closely adapted to particular
host species.
This specialization helps explain why
there are so many species of
parasites—many host species have at
least one parasite that eats only them.
Figure 13.4 Many Species Are Host to More Than One Parasite Species
Parasite Natural History
Ectoparasites live on the outer body
surface of the host.
They include plant parasites such as
dodder. Dodder obtains water and food
from the host plant via specialized roots
called haustoria.
Mistletoes are hemiparasitic—they get
water and nutrients from the host but
can also photosynthesize.
Figure 13.5 Ectoparasites
Parasite Natural History
Many fungal and animal parasites are
ectoparasites.
More than 5,000 species of fungi attack
important crop and horticultural plants.
Mildews, rusts, and smuts grow on the
surface of the host plant and extend
their hyphae (fungal filaments) into the
plant to extract nutrients from its tissues.
Parasite Natural History
Plants are also attacked by animals:
Aphids, whiteflies, scale insects,
nematodes, beetles, and juvenile
cicadas.
These animals can be thought of as both
herbivores and parasites (especially if
they remain on one plant their entire life).
Parasite Natural History
Animals also have many ectoparasites.
Examples: Athlete’s foot fungus, fleas,
mites, lice, and ticks.
Some of these parasites also transmit
disease organisms.
Parasite Natural History
Endoparasites live within the host, in the
alimentary canal, or within cells or
tissues.
Many disease organisms are
endoparasites.
The alimentary canal is excellent habitat
for many parasites. Many do not eat
host tissue, but rob the host of nutrients.
Figure 13.6 Endoparasites
Parasite Natural History
Tapeworms have a scolex, a structure
with suckers and hooks to attach to the
host’s intestinal wall.
Once it is attached, the tapeworm
absorbs food that the host has already
digested.
Human tapeworms can grow up to 10–20
m and block the intestines and cause
nutritional deficiencies.
Parasite Natural History
Plants also have endoparasites, including
pathogens.
Bacterial pathogens cause soft rot in
various plant parts; fungi can rot various
plant parts from the inside out.
Some bacteria invade vascular tissues,
disrupt the flow of water and nutrients,
causing wilting and often death.
Parasite Natural History
There are advantages and disadvantages
to both lifestyles.
Ectoparasites can disperse more easily.
Endoparasites have evolved various
mechanisms for dispersal, including
complex life cycles and enslaver
parasites.
Some parasites of the alimentary canal
are dispersed in feces.
Parasite Natural History
Ectoparasites can be exposed to
predators, parasites, and parasitoids.
Example: Aphids are eaten by many birds
and insects, and also attacked by
parasites and parasitoids.
Parasite Natural History
Endoparasites are relatively well
protected from the external environment,
and have relatively easy access to food.
But they can also be attacked by the
host’s immune system.
Defense and Counterdefense
Concept 13.2: Hosts have adaptations for
defending themselves against parasites, and
parasites have adaptations for overcoming
host defenses.
Host organisms have many kinds of
defense mechanisms.
Protective outer coverings include skin
and exoskeletons. Many parasites that
do gain entry are killed by the host’s
immune system.
Defense and Counterdefense
Vertebrate immune systems have
specialized “memory cells” that allow
hosts to recognize microparasites it has
been exposed to in the past.
Other immune system cells engulf and
destroy parasites or mark them with
chemicals that target them for later
destruction.
Defense and Counterdefense
Plants also have defense systems.
Plants have resistance genes, as well as
nonspecific immune responses.
Antimicrobial compounds attack the cell
walls of bacteria, other compounds are
toxic to fungi.
Figure 13.7 Nonspecific Plant Defenses
Defense and Counterdefense
Some plant cells produce chemical
signals that “warn” nearby cells of
imminent attack.
Still other chemicals stimulate the
deposition of lignin, a hard substance
that provides a barricade against the
invader’s spread.
Defense and Counterdefense
Hosts can also regulate biochemistry to
deter parasites.
Example: Bacterial and fungal
endoparasites require iron for growth.
Vertebrate hosts have a protein called
transferrin that removes iron from blood
serum and stores it in intracellular
compartments.
But some parasites can steal iron from the
transferrin.
Defense and Counterdefense
Plants have many chemical weapons
called secondary compounds.
Some animals eat specific plants to treat
or prevent parasite infections.
Example: Woolly bear caterpillars switch
from their usual food plants to poison
hemlock when parasitic flies lay eggs on
their bodies.
Defense and Counterdefense
Chimpanzees infected with nematodes
specifically seek out and eat a bitter
plant that contains compounds that kill
or paralyze the nematodes and can also
deter many other parasites (Huffman
1997).
Figure 13.8 Using Plants to Fight Parasites
Defense and Counterdefense
In some bird, mammal, and fish species,
females select mates based on traits
that indicate that a male has effective
defenses.
A group of proteins known as the major
histocompatibility complex (MHC) is a
key part of vertebrate immune systems.
The more MHC proteins, the better the
protection from a range of parasites.
Defense and Counterdefense
Female sticklebacks prefer to mate with
males that have many MHC proteins,
and are likely to have few parasites.
Other species may use other cues to
assess parasite loads.
Males of a cichlid fish court females by
constructing a sand bower. Females
prefer males that make large, smooth
bowers.
Defense and Counterdefense
Researchers have found that such males
have fewer tapeworm parasites than do
males that make smaller bowers.
Males with many tapeworms must spend
more of their time eating to compensate
for the nutrients they lose to the
parasites, and hence cannot build large
bowers.
Defense and Counterdefense
Parasites also have adaptations to
circumvent host defenses.
Ectoparasites face challenges similar to
those of herbivores and predators as
they cope with toxins and other
defenses of their food organisms.
Defense and Counterdefense
Endoparasites face different defense
mechanisms.
Some hosts can encapsulate parasites or
their eggs.
Some insects have lamellocytes—blood
cells that can form multicellular capsules
around large objects.
Defense and Counterdefense
The parasites are under strong selection
to develop a counterdefense.
Parasitoid wasps that attack fruit flies
avoid encapsulation in several different
ways.
When they lay eggs in the host fly, some
species also inject virus-like particles
that infect the lamellocytes and cause
them to self-destruct.
Defense and Counterdefense
Other parasitoid wasp species lay eggs
covered with filaments.
These filaments cause the eggs to stick
to and become embedded in fat cells
and other host cells, where they are not
detected by circulating lamellocytes.
Defense and Counterdefense
Some endoparasites have a complex set
of adaptations.
Plasmodium, the protozoan that causes
malaria, has a complex life cycle with
two hosts, mosquitoes and humans.
Figure 13.9 Life Cycle of the Malaria Parasite, Plasmodium
Defense and Counterdefense
Plasmodium faces two challenges in the
human host:
• Red blood cells do not divide or grow,
and thus can not import nutrients.
Plasmodium merozoites must have a
way to get nutrients.
• 24–48 hours after infection, Plasmodium
causes red blood cells to have an
abnormal shape that is detected by the
spleen, where they are destroyed.
Defense and Counterdefense
Plasmodium has hundreds of genes
whose function is to modify the red
blood cells.
Some genes cause transport proteins to
be placed on the red blood cell surface
so nutrients can be brought into the host
cell.
Defense and Counterdefense
Other genes direct production of special
knobs on the surface of the red blood
cells. The knobs cause red blood cells to
stick to other cells, preventing them from
reaching the spleen where they would
be destroyed.
The proteins on the knobs vary greatly
from one parasite to the next, making it
very difficult for the human immune
system to detect them.
Coevolution
Concept 13.3: Host and parasite populations
can evolve together, each in response to
selection imposed by the other.
When a parasite and its host each
possess specific adaptations, it
suggests that the strong selection
pressure hosts and parasites impose on
each other has caused both of their
populations to evolve.
Coevolution
This has been observed in Australia,
where European rabbits were introduced
in 1859.
The rabbit population exploded, and
consumed so much plant material that
cattle and sheep pastureland was
threatened.
Various control methods failed.
Coevolution
In 1950, the Myxoma virus was
introduced, which is transmitted by
mosquitoes.
In the beginning, 99.8% of infected
rabbits died. But over time, the rabbits
evolved resistance to the virus, and the
virus evolved to become less lethal.
Myxoma is still used, but it requires a
constant search for new strains of the
virus.
Figure 13.10 Coevolution of the European Rabbit and the Myxoma Virus (Part 1)
Figure 13.10 Coevolution of the European Rabbit and the Myxoma Virus (Part 2)
Coevolution
The rabbits and Myxoma virus illustrate
coevolution: When populations of two
interacting species evolve together,
each in response to selection imposed
by the other.
Gene-for-gene interactions—a specific
response that makes particular plant
genotypes resistant to particular parasite
genotypes.
Coevolution
Wheat has dozens of different genes for
resistance to fungi such as wheat rusts.
Different wheat rust genotypes can
overcome different wheat resistance
genes.
But periodically, mutations occur in wheat
rusts that produce new genotypes to
which wheat is not resistant.
Coevolution
The frequencies of wheat rust genotypes
vary considerably over time as farmers
use different resistant varieties of wheat.
Coevolution
Change in the frequencies of host and
parasite genotypes has also been
shown in a trematode worm and the
snail it parasitizes in New Zealand lakes.
The trematode causes sterility in the
snails.
The trematode parasite has a shorter
generation time than the snail.
Coevolution
When snails and parasites from three
different lakes were tested, parasites
infected snails from their home lake
more effectively than they infected snails
from the other two lakes (Lively 1989).
This suggested that parasite genotypes in
each lake had evolved rapidly enough to
overcome the defenses of the snail
genotypes found in that lake.
Figure 13.11 Adaptation by Parasites to Local Host Populations
Coevolution
The snails also evolved in response to
the parasites.
Abundance of different snail genotypes in
one lake was documented for 5 years
(Dybdahl and Lively 1998).
The most abundant genotype changed
from year to year.
Coevolution
One year after a genotype was most
abundant, that genotype had higher than
usual number of parasites.
These results suggest that parasite
populations evolve to exploit the snail
genotypes found in their local
environment.
Coevolution
Lab experiments showed that parasites
infect snails with a common genotype
more often than snails with a rare
genotype.
Snail genotype frequencies may change
from year to year because common
genotypes are attacked by many
parasites, placing them at a disadvantage
and driving down their numbers in future
years.
Figure 13.12 Parasites Infect Common Host Genotypes More Easily Than Rare Genotypes
Coevolution
Ever-escalating “arms races” rarely occur.
As with the snails and trematodes,
common host genotypes decrease in
frequency because they are attacked by
many; leading to increase in previously
rare genotypes.
Coevolution
An arms race may stop because a trait
that improves host defenses or parasite
counterdefenses reduces some other
aspect of the organism’s growth,
survival, or reproduction.
In the case of the fruit flies and their
parasitoids, there are costs for
encapsulation and avoiding
encapsulation.
Coevolution
Ability to encapsulate is associated with
lower larval survival rates.
Wasp eggs that avoid encapsulation by
embedding in host tissue take longer to
hatch than other eggs.
Coevolution
Studies of wild flax and a rust pathogen:
Some rust genotypes were more virulent
than others (they can overcome more
plant resistance genes).
Virulent rust genotypes were common
only in host populations dominated by
plants with many resistance genes.
Coevolution
A trade-off appears to be at work. Virulent
rust genotypes produce fewer spores
than other genotypes.
In flax populations with few resistance
genes, it is not an advantage to be
virulent. There are few resistance genes
to overcome, and fewer spores are
produced.
Figure 13.13 Virulent Rust Pathogens Reproduce Poorly
Ecological Effects of Parasites
Concept 13.4: Parasites can reduce the sizes
of host populations and alter the outcomes of
species interactions, thereby causing
communities to change.
Parasites can reduce survival or
reproduction of their host.
Experiments with a beetle and a sexually
transmitted mite showed a decrease in
egg production by infected females.
Figure 13.14 Parasites Can Reduce Host Reproduction (Part 1)
Figure 13.14 Parasites Can Reduce Host Reproduction (Part 2)
Ecological Effects of Parasites
At the population level, harm done by
parasites translates into reduction of
population growth rates.
Parasites can drive local host populations
extinct and reduce their geographic
ranges.
Ecological Effects of Parasites
An amphipod (Corophium) in North Atlantic
tidal mudflats can be extremely
abundant—up to 100,000 / m2.
A trematode parasite can reduce
amphipod populations dramatically.
In a 4-month period, attack by trematodes
caused extinction of a Corophium
population that initially had 18,000 / m2
(Mouritsen et al. 1998).
Ecological Effects of Parasites
The American chestnut (Castanea
dentata) once was a dominant tree in
eastern North America.
A fungal pathogen that causes chestnut
blight was introduced from Asia in 1904.
By mid-century, the fungus had wiped out
most chestnut populations and greatly
reduced the geographic range of this
species.
Figure 13.15 Parasites Can Reduce Their Host’s Geographic Range
Ecological Effects of Parasites
Population cycles may be influenced by
parasites.
Hudson et al. (1998) manipulated numbers
of parasites in red grouse populations,
which tend to crash every 4–8 years.
A parasitic trematode was known to
decrease survival and reproductive
success.
Ecological Effects of Parasites
When grouse populations were expected
to crash, two populations were treated
with a drug to kill the parasite.
Population sizes were estimated based
on numbers killed by hunters.
In control populations, numbers crashed
as predicted. Parasite removal did
reduce population fluctuations.
Figure 13.16 Parasite Removal Reduces Host Population Fluctuations
Ecological Effects of Parasites
By reducing host performance and growth
rates of host populations, parasites can
change the outcome of species
interactions, community composition,
and even the physical environment.
Ecological Effects of Parasites
Parasites can affect host performance,
and thus they can affect the outcome of
interactions with other species.
In a series of experiments, Park (1948)
looked at two species of flour beetles
(Tribolium castaneum and T. confusum)
and a protozoan parasite.
Ecological Effects of Parasites
When the parasite was absent, T.
castaneum usually outcompeted T.
confusum, driving it to extinction in most
cases.
When the parasite was present, the
opposite occurred.
The outcome was reversed because the
parasite had a large negative effect on T.
castaneum, but virtually no effect on T.
confusum.
Figure 13.17 Parasites Can Alter the Outcome of Competition
Ecological Effects of Parasites
In the field, the malaria parasite
Plasmodium azurophilum reduced the
competitive superiority of the lizard
Anolis gingivinus over its smaller
counterpart, A. wattsi (Schall 1992).
Ecological Effects of Parasites
Parasites can alter the outcome of
predator–prey interactions by
decreasing the physical condition of
infected individuals.
Predators may be less able to catch their
prey, or prey less able to escape
predation.
Ecological Effects of Parasites
Parasites can also alter behavior of their
host, such as the protozoan that makes
rats less wary of cats.
Some worm parasites cause amphipods
to move from sheltered areas to areas of
bright light, where they are more likely to
be seen and eaten by fish or bird
predators.
Ecological Effects of Parasites
In both cases, the parasite induces a
change in host behavior that makes the
host more likely to be eaten by a
species (the cat, fish, or bird) that the
parasite requires to complete its life
cycle.
Ecological Effects of Parasites
A parasite that attacks a dominant
competitor can suppress that species,
causing other species to increase (just
as a predator or herbivore can do).
This was documented in studies of
stream communities by Kohler and
Wiley (1997).
Ecological Effects of Parasites
A caddisfly Glossosoma nigrior was the
dominant herbivore before outbreaks of
a fungal pathogen.
The fungus reduced Glossosoma
population densities by 25-fold.
This allowed many other species to
increase, including algae, other grazing
insects, and filter feeders. Many species
were previously rare.
Ecological Effects of Parasites
The physical environment can be
changed when a parasite attacks a
species that is an ecosystem engineer—
a species whose actions change the
physical character of its environment, as
when a beaver builds a dam.
Ecological Effects of Parasites
The amphipod
Corophium is an
ecosystem engineer
in the tidal mudflats.
The burrows it builds
hold the mud
together, preventing
erosion and forming
“mud islands” at low
tide.
Figure 13.18 C
Ecological Effects of Parasites
When the
trematode parasite
drives the
amphipod
populations to
extinction, erosion
increases, silt
content increases,
and the islands
disappear.
Figure 13.18 D
Figure 13.18 A, B Parasites Can Alter the Physical Environment
Dynamics and Spread of Diseases
Concept 13.5: Simple models of host–
pathogen dynamics suggest ways to control
the establishment and spread of diseases.
Pathogens have had a major effect on
human populations—they are thought to
have played a major role in the rise and
fall of civilizations throughout history.
Despite medical advances, millions still
die of diseases such as malaria.
Dynamics and Spread of Diseases
Mathematical models of host–pathogen
population dynamics differ from models
discussed previously:
• Host population is divided into susceptible
individuals (S), infected individuals (I), and
recovered and immune individuals (R).
• It is often necessary to keep track of both
host and pathogen genotypes.
Dynamics and Spread of Diseases
• Other factors can influence spread of the
disease, such as:
1) Different chances that hosts of different
ages will become infected.
2) A latent period in which an individual is
infected but can not spread the disease.
3) Vertical transmission—spread of the
disease from mother to newborn, as can
occur in AIDS.
Dynamics and Spread of Diseases
These models can become quite complex.
Consider a simple model that looks only
at host population density:
A disease will spread only if the density of
susceptible hosts exceeds a critical,
threshold density.
Dynamics and Spread of Diseases
Density of susceptible individuals = S,
density of infected individuals = I.
For a disease to spread, infected
individuals must encounter susceptible
individuals. The probability of this is
proportional to the densities of each (SI).
A transmission coefficient (β) indicates
how effectively the disease spreads; the
term is now βSI.
Dynamics and Spread of Diseases
Density of infected individuals increases
when the disease is transmitted
successfully and decreases when
infected individuals die or recover.
Death and recovery rate = d.
dI
 SI  dI
dt
Dynamics and Spread of Diseases
A disease will spread when dI/dt > 0
This occurs when βSI – dI > 0
or S > d/β.
A disease will establish and spread when
the number of susceptible individuals
exceeds the threshold density, ST = d/β.
Dynamics and Spread of Diseases
There are several ways of keeping the
number of susceptible individuals below
the threshold.
Susceptible domestic animals are
sometimes slaughtered to reduce
density, especially if the disease can
also affect humans, such as bird flu.
Dynamics and Spread of Diseases
For human populations, mass vaccination
programs can reduce density of
susceptible individuals.
These programs have been successful
for several diseases, including small pox
and measles.
Figure 13.19 Vaccination Reduces the Incidence of Disease
Dynamics and Spread of Diseases
Public health measures can raise ST:
Increase recovery rate of infected
individuals who then have immunity, by
early detection and improved treatment.
Decrease β by quarantining infected
individuals or by convincing people to
engage in behaviors that make it more
difficult for the disease to be transmitted.
Dynamics and Spread of Diseases
Threshold densities were determined for
wild populations of bison susceptible to
the bacterial disease brucellosis.
Dobson and Meagher (1996) used
National Park data on previous
exposure among bison herds and found
ST to be 200–300 per herd.
ST calculated by a model was 240.
Figure 13.20 Determining Threshold Population Densities
Dynamics and Spread of Diseases
Herd sizes in the parks were 1000 to
3000 individuals.
Neither option for reducing ST was
feasible:
A vaccine was not available; killing large
numbers of bison was not acceptable,
politically or ecologically (small herds
have higher risk of extinction).
Case Study Revisited: Enslaver Parasites
Parasitoid wasp Hymenoepimecis larvae
attach to the exterior of a host spider’s
abdomen and suck the body fluids.
When a larva is fully grown, it induces the
spider to build a cocoon web, then the
larva kills the spider and eats it.
The larva spins a cocoon and attaches it
to the cocoon web.
Figure 13.21 Parasites Can Alter Host Behavior
Case Study Revisited: Enslaver Parasites
If wasp larvae were removed from the
host spiders just before a cocoon web
would be made, the spiders constructed
webs that were different from both
normal webs and cocoon webs.
Some spiders recovered normal webmaking ability after several days.
Case Study Revisited: Enslaver Parasites
This suggests that the larva injects a fastacting chemical into the spider to alter
behavior.
The chemical appears to be dosedependent, as evidenced by the
intermediate web type. Otherwise, any
exposure to the chemical would result in
cocoon webs.
Case Study Revisited: Enslaver Parasites
Spiders build cocoon webs by repeating
the early steps of their normal webbuilding sequence; thus, the chemical
appears to act by interrupting the
spiders’ usual sequence of web-building
behaviors.
Case Study Revisited: Enslaver Parasites
Other enslaver parasites appear to
manipulate the host’s biochemistry.
Hairworms alter concentrations of three
amino acids in the brains of the cricket
hosts.
The amino acid taurine is an important
neurotransmitter in insects, and also
regulates the sense of thirst.
Case Study Revisited: Enslaver Parasites
The hairworm may induce the cricket to
commit suicide by altering its perception
of thirst.
Not all enslaver parasites appear to act
by manipulating the host’s chemistry,
but the mechanisms are still unknown.
Case Study Revisited: Enslaver Parasites
Isopods parasitized by a worm spent little
time under cover, where they were
protected from predation by the creek
chub, the next host in the parasite’s life
cycle (Hechtel et al. 1993).
In a choice experiment, unparasitized
isopods would avoid chubs, but
parasitized isopods were drawn to the
chubs; a benefit for the parasite but
disaster for the isopod.
Figure 13.22 Making the Host Vulnerable to Predation
Connections in Nature: From Chemicals to Evolution and
Ecosystems
Interactions between enslaver parasites
and their hosts provide evidence of
previous evolutionary change.
An enslaver parasite has many
adaptations that allow it to cope with
host defenses.
A parasite that uses a chemical is well
adapted to take advantage of the body
chemistry of its host.
Connections in Nature: From Chemicals to Evolution and
Ecosystems
It can be difficult to separate host–
parasite ecological interactions from
host–parasite evolutionary interactions.
As evolutionary change tips the balance
back and forth, first in favor of the host,
then in favor of the parasite, we can
expect concomitant changes in the
dynamics of other species.
Connections in Nature: From Chemicals to Evolution and
Ecosystems
Communities and ecosystems are highly
dynamic, always shifting in response to
the ongoing ecological and evolutionary
changes that occur within them.
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