Invasion Theory
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In the immediate area surrounding our homes and offices,
we are experiencing an outbreak by a highly destructive species – the emerald
ash borer. This beetle invaded the
Windsor-Detroit area and is spreading via both diffusive population growth, and
jump (or long-distance) dispersal. This
beetle kills native ash trees and has the potential to become as great (or
greater) a problem as Dutch elm disease (e.g. 1,000,000,000 and 900,000,000 ash
trees are at risk in Ontario and Michigan, respectively). We are interested in a number of questions
regarding this beetle including:
1) How
was it vectored to North America (from China)?
2)
How quickly is the species spreading, and by what mechanisms?
3) Can
we reduce or stop its outward spread, and if so, by what means?
To answer these questions, as well as those pertinent to
other recent outbreaks by pathogenic diseases (west Nile, SARS, Monkey Pox, Mad Cow), we think it necessary to proactively target
vectors that transfer these species from their native areas to North
America. By focusing on vector biology,
we may help address issues of human disease, and plant and animal disease or
pest transmission.
Invasion biology really took off after publication of
Charles Elton’s excellent volume in the 1950s.
This book focused ecologists’ attention on the importance of issues
including habitat disturbance, insularity (continents vs. islands) and native
species diversity in affecting invasion success. While papers continue to be published on
these topics, often supporting tenets of Elton’s work, many other studies have
revealed that invasion success is a very complex area of study. For example, we
contend that invasion hypotheses ought to be tested in a logical sequence, beginning with the question of propagule pressure
(no invasion is possible unless propagules are transferred to the new
ecosystem. If we can satisfy ourselves that sufficient propagule pressure
exists (appropriate ratio and number of reproductive males and females, for
example), then we can ask questions regarding the physical and chemical nature
of the habitat. Some species may fail to
succeed despite sufficient propagule pressure because they are physiologically
intolerant of conditions in the habitats (UV light and acidity, for example
affect zooplankton species, soil nutrients/toxins affect plants). If the propagule supply is not limiting, and
the species appears capable of surviving ambient conditions, then we can ask
questions regarding species interactions.
Predators, competitors, or pathogens in the new habitat, all of which
may reduce invasion success, may affect invading species. So by asking the appropriate questions, at
the appropriate times, we may help determine the factors that affect invasion
success.
We are also interested in the growing popularity of the Enemy
Release Hypothesis. This
hypothesis suggests that invaders perform better in their introduced range than
their native range because they lose their enemies (often but not always
parasites) during the colonization process.
Essentially, the colonizing population carries only a subset of the
complement of natural enemies from the home range because only a small (usually)
number of colonists manage to invade the new
habitat. This causes a founder effect
for both the colonizing species and its enemies. We think this hypothesis
should be subjected to critical examination because alternative hypotheses may
account for the loss of enemies and because, paradoxically, the colonizing
population may not want to lose its associated flora/fauna. Imagine an invader carrying a pathogen that
reduces its viability or reproductive output.
Loss of this species during colonization would ordinarily be viewed as a
positive event (for the colonist), but what happens if the pathogen also has
the potential to affect the viability of species in the introduced range with
which the colonizing species will compete for resources? North American squirrels that invaded Great
Britain provide a good example of this.
These squirrels carried a virus that affected them adversely; however,
when the North American squirrel came into contact with the native British squirrel,
they transmitted the virus to the native, causing massive losses to the native
population. Thus,
carrying the pathogen – even though harmful to itself - ultimately proved
beneficial to the invader because competition with native squirrels was
dramatically reduced. Moreover,
if an invader can lose it enemies during colonization, it could also lose its
facilitators. Losing symbiotic fungi
could adversely affect colonizing plants, so loss of associated species does
not always translate into a benefit for the colonizing species. We are interested in looking at all of the
possible permutations of the Enemy Release Hypothesis to determine when the
loss of beneficial versus when it is harmful.
Another popular hypothesis that may suffer from confounding is the Invasional
Meltdown Hypothesis.
Most of the work in our lab focuses on invasion vectors
into the Great Lakes and Chesapeake Bay. Once species establish in the Great
Lakes via long-distance movement by, for example, commercial ships, then other
human-mediated vectors may allow them to spread to inland lakes. These vectors, including contaminated fishing
lines and live-well water in pleasure boats, cannot spread the species from the
native region to North America, but they may effectively disperse the species
once it is already here. By measuring
the human vectors, we are developing model to predict where aquatic invaders
will spread.