Basics of Ecology

Pathogen and Host Extinction

During the 14th century, Europe was ravaged by the bacterium yersinia pestis, also known as the
black plague. It killed as many as 30 to 80% of the people, depending on the geographic location. It
took more than 150 years, for most of the human population to recover in number. However, they
did eventually all recover and prosper.
Populations of other species have not been so lucky. During the last 150 years, several species of
Hawaiian honeyeater birds have died out altogether from avian malaria, following the introduction
of the parasite and its culex mosquito vector. Viruses, like canine distemper virus, were associated
with the recent near extinction of the Black-footed Ferret, and are a significant conservation threat
to many large African carnivores. Ebola is now the nail in the coffin, for some of the few remaining
wild populations of gorillas.
In the face of this, it's natural to ask, what type of pathogens might drive its host to the brink of
extinction and beyond? Surprisingly, it may not be the grizzly ones, of we most quickly think of.
When we think of pathogens with a major impact of human population, we might think of acute,
highly contagious pathogens that cause sudden and major epidemics, such as small pox or pandemic
flu. With high case fatality rates, such agents may reduce population size. However, they rarely drive
populations or species extinct. The reason is the inherently self-limiting nature of such pathogens. As
susceptible hosts are being depleted through the epidemic, transmission slows. And the chain of
transmission is almost always broken, while some fraction of susceptible individuals still remains
uninfected. The simple susceptible infected recovered model predicts an exponentially decaying
relationship between the pathogen basic reproductive number, and the fraction or hosts escaping
infection.
There's flu like pathogen with an R 0 of around 1.5, that's expected to leave around 20% of the
population unharmed, even if it killed all infected individuals. A lethal small pox like pathogen with
an R 0 as high as 5, would be absolutely devastating. But the epidemic would still be expected to
burn out with a percentage of the population remaining. Even in the absence of any control
measures, or behavioural changes in the host. Thus acute directly transmitted pathogens may bring
a population near the brink of extinction, but unlikely beyond. The inherent self-limitation of these
pathogens comes about because the force of infection acting on the susceptible population drops
quickly during the second half of the epidemic. Thus from the point of view of extinction, we are
concerned with characteristics that prevent this from happening.
Two key characteristics that reduce pathogen self-limitation and increase the chance of host
extinction are alternative hosts that can serve as a reservoir, and vector born transmission. Having
an alternate and resistant host, means that the pathogen can still circulate robustly, as the
susceptible population is depleted. This mechanism is an important driver in many Chytrid funguses
driven extinction of frogs throughout the Americas. Some species appear resistant, while in other
species, the disease is almost always fatal. Squirrel pox which is 100% lethal in some species, is
responsible for the disappearance of England's red squirrels. The North American Grey Squirrel,
which is resistant to this disease, was introduced to England and brought the virus with it. The red
squirrels has been wiped out, while they grey squirrels now has a thriving population that serves as a
robust reservoir for the virus. Having a blood feeding vector, can also secure robust circulation as the
hosts become rarer. The vector needs its blood meal, and will increase its focus on the remaining

Basics of Ecology
hosts. This is how flea born plague, recurrently kills entire prairie dog villages in the Midwestern US.
Once a flea is infected, the bacterium often even blocks it's digestive tract to increase its biting rate.
Thus the force of infection even increases, as the epidemic progresses. Jumping from host to host,
plague quickly spreads through prairie dog families and villages, leaving nothing but death in its
wake.
Native Hawaiian birds evolved in the absence of avian malaria, and many species are extremely
susceptible to the parasite. These birds, birds experienced a double whammy of getting infected by
highly virulent vector born parasite, and being surrounded by numerous introduced bird species that
could evolve with the parasite in their native range, and serve as a resistant reservoir. Avian malaria
has been implicated as a significant contributor to the extinction of least a dozen Hawaiian bird
species.

Basics of Ecology
Forces of Infection
In an epidemic, there is often great concern about the degree to which an infected individual can
spread infection to the susceptible individuals in a population. We already know that one way of
measuring this is with R-naught, but we can consider using another concept known as the force of
infection. We can formally define this as the per capita rate at which susceptible individuals contract
infection. Intuitively, the force of infection should increase with the transmissibility of the pathogen
and the prevalence of infection in the population.
The transmissibility of the pathogen will depend on both characteristics of the pathogen, what is the
mechanism of transmission, how prolific is the pathogen within each host, and the characteristics of
the population. How many potentially infectious contacts does each individual make in a day? The
prevalence of infection, defined as the proportion of the population that is infectious at any given
time, gives a measure of the likelihood that any potentially infectious contact is with an infectious
individual.
Thinking about the force of an infection from the perspective of each susceptible individual offers
some new insights into the patterns we expect to see at the scale of the population. In particular, if
the force of infection is high then the rate at which individuals come in contact with infection is high
and on average, we would expect the interval between infectious contacts to be short. For an
immunizing infection, one where getting infected once protects you forever, this would mean that if
the force of infection is high we would expect to see infection in younger individuals. On the other
hand, if the force of infection is low, either because we're talking about a pathogen with lower
inherent transmissibility or a population with a lower rate of contact, then we would expect
individuals to be older on average by the time they are first exposed to an infection. Given the
intuitive relationship between the force of infection and the basic reproductive number from earlier,
we would then expect that the higher the basic reproductive number, the earlier on average that
individuals would become infected.
In fact, one can derive an approximate relationship between the mean age of infection in the
population and the basic reproductive number. R-naught equals 1 plus L divided by A where A is the
mean age of infection and L is the average life expectancy. This provides a way of estimating the
transmissibility of a pathogen, a hard thing to observe directly, from a pattern, the age of first
infection that is relatively easy to observe. Here is a survey of the mean age of infection for a variety
of pathogens in different places as presented by Andersen and May in 1991. And from this
relationship, we can make an approximate estimate of R-naught for each, which indicates
differences in R-naught for each pathogen, but also differences for the same pathogen in different
places. Of course this simple view has presumed that the force of infection is a constant value for
everyone in the population. And intuitively, we may think that not everyone will encounter infection
at the same rate.
The force of infection is often presumed to be different for individuals of different ages. For example,
school children often have very high contact rates within schools compared to adults. Thus we might
expect the force of infection to be higher at younger ages. From the patterns we've discussed, we
would still expect that the older you are the more likely that it is that you've been infected sometime
in the past. But rather than being a function of age alone, this pattern is now expected to be a
function of the cumulative force of infection up to your current age. And we can directly measure

Basics of Ecology
whether someone has ever been infected by looking for the presence of antibodies to that specific
pathogen.
Again, while this age specific force of infection might be very difficult to observe directly, the
resulting pattern of the proportion of individuals at each age that have antibodies indicating prior
exposure is something that can be measured relatively simply by conducting a serological survey.
Using calculus, we can back calculate the age specific force of infection from this observed pattern of
the proportion of individuals at each age with antibodies indicating prior exposure. These types of
observations have been used in the past to highlight which classes of individuals are at the highest
risk for infection based on the existing pattern of infection across all individuals.
Ultimately, the force of infection provides a way of translating the individual base process of
transmission into a population scale pattern of infection that can allow us to quantify properties of
pathogens spread in real populations that are otherwise very difficult to see.

Basics of Ecology
Cycles
Infectious diseases exhibit different dynamic patterns. A pattern of relatively stable incidence of
infection or disease over time is called stable endemicity. Some sexually transmitted infections, like
HIV in the USA, show this type of behaviour. There are roughly 50,000 new cases a year, and this
number has remained fairly constant during the last decade. Many waterborne and respiratory
infections exhibit seasonal endemicity because transmission rates vary with environmental
conditions.
For these, incidents may vary a lot within a year, but less between years. Cholera and seasonal
influenza are example of such diseases. Stable and seasonal endemicity are normally associated with
diseases against which acquired immunity is ineffective in either clearing the infection or preventing
reinfection. Immunizing infection with relatively short infectious periods in contrast often exhibit
epidemic cycles with recurrent outbreaks spaced out by predictable inter-epidemic periods. Many of
the vaccine preventable childhood infections show this type of dynamics. Measles, for example,
historically have major outbreaks every few years, in most Western countries. Whooping cough
incidents typically peaked every three to four years. The susceptible, infectious, removed model
revealed that the epidemic cycles are due to what ecologists call consumer-resource interactions.
For an infectious agent, susceptible individuals represent the resource that can sustain the chain of
transmission. Transmission from an infected individual (the consumer) to a susceptible individual,
the resource will result in a new infection. The infection thus converts the resource into more
consumers, much like a predator converts prey into more predators when it feed its young.
Consumer resource interaction generally has a propensity to cause population cycles. And we see
this born out in many diseases. Key characteristics resulting in population cycles are high
transmissibility, short infectious period, and transmission-blocking immunity upon recovery. The
reason is that when such pathogens enter a susceptible population, they spread very rapidly,
converting more and more susceptible individuals into infectious individuals in an epidemic of
growing momentum.
However the short duration of the infection means that the infectious individuals rapidly become
immune. After a while the epidemic begins to recede because of the resource depletion. Much like a
forest fire ebbs as it is burning out of fuel. The next epidemic cannot take off until a critical number
of new susceptible individuals have been born. The inter-epidemic period, which is often very
predictable in large cities, is determined by the birth rate of the host, and the transmission rate of
the pathogen. Increasing either of these kinds of characteristics, leads to faster cycles. For measles,
we saw a mat, manifestation of this in many European countries after the Second World War. During
the baby boom, birth rates increased by as much as 30%. There followed a decade of annual
epidemics before the birth rate returned to the normal of about twenty births per thousand
individuals per year. And the intra-epidemic interval reverted to major outbreaks every two years.
Vaccination effectively reduces the number of susceptible individuals born into the population
because of the immunized children directly entering the removed clause. Mass vaccination therefore
often increases the inter-epidemic period.
Measles for example used to cause annual outbreaks in Kenya before the implementation of routine
and supplemental vaccine activities. During the last decade measles is largely absent but have
caused a major outbreaks every five years or so. Theoretical models have shown that some level of

Basics of Ecology
seasonality in transmission rates is necessary to sustain population cycles indefinitely. The epidemic
cycles of childhood infections are generally sustained by the seasonality in contact rates caused by
aggregation of the children during the school term. Historical records from Britain show that measles
transmission was about three times faster during term-time than holiday time.
Predictable population cycles occurred for at least two centuries and probably for as long as it has
been around, ending only when vaccination became so prevalent that the susceptible pool very
nearly dried out.

Basics of Ecology
Seasonality
In the Northern hemisphere, the flu season typically runs from early December through March. The
Southern hemisphere is the mirror image of this pattern. The flu season there runs from May
through October. 80 years ago, whooping cough was a summer epidemic of children in the Northern
hemisphere. Today most children receive the three dose DPT. Diphtheria- Pertussis-Tetanus vaccine
which protects against infection for several years and whooping cough is now a full epidemic in
teenagers.
Seasonality seems to be the norm rather than exception for diseases with relatively short infectious
periods. The course of the seasonality is relatively obvious in many cases. Vector-born infections for
example circulate most widely when vectors are most abundant. Since many vector populations are
influenced by temperature. Transmission often peaks during the summer in temperate regions.
Water-born infections are also often driven by environmental conditions. Cholera in Bangladesh for
example, shows two peaks per year, a smaller epidemic in the spring just before the monsoon
followed by larger epidemic in the fall towards the end of the monsoon. The thought is that these
are associated with periods when the environment is most favourable for the Vibrio bacterium
responsible for the disease.
Environmental factors are also likely to be associated with the winter peak in influenza and the
historical summer peak of whooping cough. Influenza viral particles survive longest when the
absolute humidity is lowest. As it is during the winter in temperate regions thus transmission is most
robust during this period. The bacteria that cause whooping cough in contrast prefer warm periods
with high relative humidity during the summer time. When seasonality is determined by
environmental factors we call it environmentally-forced disease dynamics. Surprisingly the current
fall peak in whooping cough is not associated with the environmentally most favourable season for
the pathogen. It does, however, coincide with peaks of several other respiratory pathogens. Instead
of being driven by the environment, this seasonality reflects seasonal changes in contacts among
hosts. Contact rates among school age children are usually many times greater during the school
term than during vacation time.
In addition, new culture of children, many who are susceptible enter into schools each fall. As a
consequence we get seasonal outbreaks fuelled by a lot of mixing of susceptible uninfected
individuals in a close contact environment. We call this type of seasonality term-time forcing
because of its association with opening and closing of schools. We see similar behaviourally
associated seasonality in Measles outbreak in West Africa. There however, contact rates are not
moulded by schools so much as by the urban-rural seasonal migration associated with subsistence
agriculture. During the wet season, contact rates are low because people are spaced out in rural
communities. During the dry season, contact rates are high and transmission is robust because many
families congregate for work in peri-urban settings. Seasonality in most infectious diseases reflects a
combination of environmental and behavioural forces.

Basics of Ecology
Flu 1918
The 1918 influenza pandemic affected almost 30% of the global population and killed over 50 million
people. There are still many unanswered questions about the 1918 flu pandemic, but investigations
on the history of this pandemic have provided a framework for early detection of contemporary flu
pandemics.
Let's consider some of the properties that distinguish the 1918 flu pandemic from seasonal flu
outbreaks and why they can alert us of flu pandemics today. Well, what was unusual about influenza
in 1918? I don't need to remind you that flu occurs every year. This is typically just one flu season a
year - that in North America peaks in the winter months of December, January and February- and
then tapers off by the end of March. One of the first clues that something was amiss with influenza
in 1918, 1919, was the timing of the flu outbreak. The 1918 flu had three peaks of flu-related
mortality in a 12-month period: an early summer, fall, and late winter. A harbinger of a flu pandemic
is a change in the seasonal pattern of disease. In fact, it was a change in the predictable pattern of
flu-like illness that alerted public health officials to the 2009 H1N1 flu pandemic. A second unusual
feature of the 1918 flu outbreak was the number of infected persons who died. Influenza certainly
causes its share of deaths on an annual basis, but the death rate during the 1918 flu, was over
tenfold higher than expected for flu. Influenza viruses typically replicate in the upper respiratory
tract. And causes signs everyone is familiar with, a runny nose, a sore throat sometimes a cough,
generalized fatigue and muscle ache.
The 1918 influenza virus caused pneumonia, a disease of the lungs. Differences in clinical disease can
be due to changes in the genetic makeup of the virus, which allow it to infect a different type of cell.
The incidents of very serious disease and the high mortality rates observed during the 1918 flu
pandemic, suggested that something had changed in the influenza virus itself. So was the influenza
virus that caused the 1918 flu pandemic different? We determine how similar viruses are by
comparing their genomes. Influenza viruses encode the genes that they need to reproduce on
individual short pieces of RNA. There is tremendous diversity of influenza viruses in wild bird
populations. A few strains of influenza virus are also resident in pigs and humans. Occasionally, an
influenza virus from a bird infects a pig or a human. The avian flu virus can exchange whole genes, a
process called reassortment, with influenza viruses already present in the pig or human. This
provides a ready-made way to produce a virus with a completely different set of proteins which is a
much faster way for a virus to evolve than relying on the slower processes of accumulating
mutations in a gene.
Our ability to resist infection with the influenza virus requires that our immune systems recognize
specific sequences in virus proteins. If these virus proteins change, the virus can escape immune
detection. Influenza viruses do evolve by mutation, which is one of the reasons you need a flu shot
every year when a whole new protein appears because the flu virus has acquired the gene that
encodes it from another flu virus. Remember, this is called reassortment. Vaccines in our immune
defenses don't work. The 1918 flu virus was apparently new in the human population although there
are no convincing data on its animal origin. This means that the global human population was
subjected to an influence of virus for which there was no immunological defense. Everyone was
susceptible. And the virus also had properties that enabled a more severe disease than the seasonal
flu. The lessons learned from the 1918 flu pandemic are that a change in the seasonal occurrence of

Basics of Ecology
flu is an indicator of a potential pandemic. This is why public health officials pay close attention to
reports of flu cases each year.
Additionally, it is important to sample the influenza viruses in animal populations to look for
evidence of changes in virus genetic makeup which could allow a new flu virus to infect humans.
Surveillance of annual flu cases and virus genetics in animals needs to be conducted globally and all
information must be shared, because influenza pandemics are global health concerns.

Basics of Ecology
Host Diversity Host Range
Like many consumers in the natural world, parasites can be either specialists or generalists. One
parasite may simply focus all their attention on one host species, or alternatively exploit a wide
range of host species.
Specialized viruses have the opportunity to really evolve closely with their host, and a good example
would be the human chicken pox virus. This is an intriguing virus in the while this is really an
airborne childhood disease transmitted by coughing, can also be transmitted through contact with a
rash. It has evolved a persistence mechanism, which has allows it to become dormant in the body's
nervous tissue, but then will re-emerge when the host is much older and the immunity has waned at
which point it causes the painful disease shingles in adults. Epidemiologically this is a clever strategy
since all the children in an area recover from the infection and so carry antibodies preventing
subsequent infection, the virus can still persist, and emerge later when these children become adults
and they can, the adults can then initiate a new epidemic in children.
Another infection of the nervous system that in contrast to chicken pox will infect does not infect a
single host species but a wide range of host species is the rabies virus. And this will infect raccoons,
skunks, foxes, coyotes, ferrets, bats, domestic cats, dogs, humans, and many, many other animals.
The infection process at the cellular level for the rabies virus is similar, similar to many other species,
and starts with the G-protein projections on the virus interact to the receptors on the host cell
surface. The interesting feature about rabies is the viruss high affinity for nervous tissue, in
particular that it binds to the acetylcholine receptors, which are not only expressed in high levels of
nerve cells but are also highly consistent between many, many species so the way these virus can
infect the nervous system of many different animal species. On the one hand this provides flexibility,
so the virus has more opportunities to infect different host species. But alternatively it does not have
a within host presistent mechanism that we just heard about in chicken pox. So it's the fact that it
infects multiple species, allows it to persist. Instead, it must invade many more species in the
ecosystem, and in so doing attempt to persist over time. When parasites are driven from a tolerant
host species to a vulnerable host species, then the more vulnerable host species can actually be
eliminated through parasite mediated, or apparent competition.
A nice example of this is in the United Kingdom, where American Grey Squir, Squirrels were brought
over and released into the English countryside, and they have wiped out the resident red squirrels.
The reason they've done this is because they both share a pox virus, but the greys are more tolerant
of the pox virus infection than the reds. So the outcome is that the greys continue to spread the
virus to the reds, and the reds die out, and they've been effectively been wiped out from most of
their distribution quite simply through the effects of the virus as an infective competitive weapon.
This doesn't happen in specialist infections because this is similar to what has happened in the
tolerant species. Here transmission is dependent on the density of the host population, and so more
hosts get infected when density's high but less when density's low, such that below the threshold
host density the disease effectively fades out.

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Basics of Ecology
Critical Community Size
Even if transmission is likely on average, there is always a chance that an infectious individual will
not manage to transmit. You can think of this like a coin flip. Even if the probability of getting ahead
when you flip a coin is high, say 90%, there is a real chance that any given flip will come up as a tail.
Of course, if you flip lots of coins, you're pretty likely that about 90% of them are going to come up
heads. Even if you can't tell which ones exactly will do so. This is relevant to the establishment and
persistence of transmission in populations, because each contact between an infectious and
susceptible individual can either result in transmission, or not.
Just like a coin can only come up heads or tails, for an infection to spread in a population, it is not
necessary for all infected individuals to successfully transmit so long as, on average, the number of
new infections is greater than or equal to the number of old infections. For an infection to persist in
a population, it is necessary for at least one infected individual to pass that onward. And if all the
infected individuals in a population fail to transmit, then the infection will go locally extinct, or
fadeout, in that population. Again retuning to the coin flipping analogy, fadeout occurs when all the
coins come up tails. And intuitively, this more likely to happen if your only flipping a few coins, and if
the chance of getting a head on each coin is low.
From the standpoint of disease transmission, the number of possible coins that can be flipped is the
number of contacts between infectious and susceptible individuals. And the chance of that contact
resulting in transmission is dependent on the transmissibility of the pathogen itself. Following this
line of reasoning, we might intuit that the number of infectious and susceptible individuals will scale
with the population size so larger populations will have more opportunities for transmission. That is,
more coins to flip. Then, for any given pathogen, the probability of continuing to get at least one
transmission event at any point in time should scale with the population size. And at some point, the
population size should be large enough that transmission at any given time point is a virtual certainty.
We refer to this population size as the critical community size. Formally, we can define the critical
community size as the smallest population size for which any given infection does not go extinct.
One of the most classic exhibitions of the critical community size has been the observation that
measles infection in the era preceding the development of measles vaccines. It was always present
in cities of greater than 300,000 to 500,000 but was frequently absent in smaller towns, and more
frequently absent the smaller the town. Practically, this has important consequences for control.
Effectively, in communities below the critical community size infection would be expected to go
extinct naturally due to the stochastic failure of chains of transmission. If infection persists in large
communities, however, there is always the possibility of reintroduction. This pattern, large cities
with persistent infection continually re-infecting small towns that experience local fade out, was
readily apparent in the pattern of measles epidemics in\ England and Wales prior to the
development of the vaccine for measles. This led to a dramatic pattern of directional waves of
infection spreading outward from large cities, like London and Manchester, which were above the
critical community size, to smaller towns in the countryside.
Vaccination, by reducing the number of susceptible, can reduce the effective community size in large
cities, making local fade out more likely and breaking the cycle of reintroduction to smaller towns.
Now, the value of the critical community size will depend on both the characteristics of the
population and the characteristics of the pathogen for immunizing infections. Once infection has

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Basics of Ecology
spread through a population, a large proportion of the population may be immune due to prior
exposure. And the more transmissible the infection, the higher they are not, the larger will be the
proportion of the population that is immune. And the fewer infectious and susceptible individuals
will be around. Thus, more transmissible infections are more likely to burn themselves out in all but
the largest populations.
Pathogens that induce a long infectious period are less likely to fade out as each infectious
individual has more time to encounter a susceptible individual and successfully transmit infection.
Many pathogens exhibit seasonally varying transmission rates which are famously shown by the
increase in childhood infection rates during school terms and the corresponding decrease during
school holidays. For such infections, it is not the average number of infections that is critical to the
probability of local extinction, but the depths of the troughs between epidemic peaks. It is at these
points when the number of infectious individuals is at its lowest and thus the probability that all of
them will fail to transmit infection is at its highest. As an example of this, the critical community size
for measles in Niger was estimated to be about three times higher, nearly 1.5 million people, than
was classically observed in Europe. This was shown to occur because seasonal changes in urban
population density, due to agricultural practices resulting in very low incidence of infection, and very
low transmission rates during the rainy season when many people are widely distributed on their
individual farms. As a consequence, even in the largest cities in Niger, measles would frequently go
locally extinct following outbreaks.
This erratic pattern of outbreaks and local extinction is exacerbated by the high birth rate in Niger.
Following local extinction, all the children born are not exposed to measles infection until the next
outbreak. And given that some children won't be vaccinated, the population of susceptible builds up
over time. This build-up of susceptible sets the stage for an increasingly big outbreak once measles is
re-introduced from elsewhere. A big outbreak spreads fast, rapidly depleting the susceptible
population, leading to a high likelihood of local extinction, thus continuing the boom and bust
dynamics. These dynamics of local fadeout and transmission may also play a role in the
establishment of an outbreak.
Consider the first infectious individual in a susceptible population and let P be the probability that
infection goes extinct before it causes a major epidemic. That first individual can either recover from
infection at a rate gamma or can transmit infection at a rate beta. If transmission occurs, then there
are two infected individuals who must fail to transmit if the infection is to go extinct. Thus the
probability of extinction P can be expressed as P equals the probability of the first individual
recovering before transmission plus the probability that the first individual transmits before
recovering, times the probability that both infected individuals fail to transmit. With some algebra,
we can then show that this can be expressed as the probability of extinction before a major
epidemic, is equal to the rate of recovery divided by the transmission rate or, 1 over or not. Thus,
not only do pathogens with high R not spread fast in populations. If they arrive, they are highly likely
to result in an outbreak in the first place.

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Basics of Ecology
Pathogen Microbiome Interaction
We are covered in microbes. So many of them that each of us can be considered to have our own
ecosystem, or microbiome. Many of these microbes are beneficial, or neutral. When we're healthy
the microbes we host are mostly confined to the outside of our bodies. And that means everywhere
that they can get to without crossing an epithelial layer, all our skin surfaces, as well as the long dark
passage from our mouth to our anus. It's not surprising that the largest numbers of microbes lives
along those paths, since we feed them each time we eat, several times a day. But there are plenty of
nutrients and relatively mild conditions for bacteria on all of our surfaces. So lots of them cover us
from the moment we're born.
Just as bacteria that have evolved exceptional mechanisms to allow them to grow in the Arctic
tundra, the desert, or deep-sea hydrothermal vents. Bacteria will similarly adapt and evolve to face
the specific challenges of each of our body surfaces. These adaptations to specific regions of our
body result in particular bacteria being commonly found in particular sites for example on our skin
and not our mouths or vice versa. The recent use of high through put sequencing has revealed just
how many organisms are present in a healthy microbiome and how each site in our body has its own
complex ecology of interacting microorganisms. These organisms generally live as dense
communities called biofilms, within which there is intense competition. Because only the fittest
survive, propagate, and spread from us to the others around us. Many of the microorganisms that
live on our skin need the components of our skin cells. Or the various molecules we secrete via
glands such as our sweat or sebaceous glands. Others live primarily on the molecules secreted by
other microorganisms. Still, others have evolved to kill and eat the bacteria around them given the
intense competition in these biofilms. It's not surprising that bacteria have mechanisms to parasitize
or kill other bacteria.
What has been surprising is the sophistication, the complexity of some of these mechanisms.
Bacteria can make toxins or directly attack and poke holes in the membranes of their neighbours.
But they also have complex molecular machines, like the type six secretion system which amounts to
a syringe-like tube that can rapidly assemble and emerge from one bacterium to inject toxins into
another. Such an attack can be unilateral, one bacteria trying to kill and eat its neighbour. But the
victim can also sense the attack and rapidly deploy its own type six secretion system in a swift
counter attack, setting up a duel to the death. To successfully persist in the long run, bacteria that
inhabit us must generate defenses. Against many different types of attacks they face from the host
immune system as well as from other residents of our microbiome.
All of this complex competition that's already taking place among the resident microbiota. Provide
three levels of defense that protect us from invading pathogens. First it is the physical defense of the
biofilm layer covering our bodies. Second is the metabolic defense of the intense competition for
nutrients, leaving very little food to allow an invader to survive, much less grow. Third is the complex
inter-bacterial warfare that results in bacteria producing many molecules that are toxic to other
bacteria. And yet bacterial pathogens do invade. So they must have mechanisms to deal with the
defenses of the host and the host microbiome.
How do pathogens compete with the resident microbiome? And how does this affect their ability to
invade and infect a new host? This is one of the topics my lab has been focused on in the last few
years. Let's take a look. To understand how pathogens invade a host and what can stop them. We

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Basics of Ecology
study two organisms that are very closely related, but differ in their host ranges. Bordetella pertussis
causes whooping cough, which is highly infectious among humans but does not naturally infect other
animals, presenting a challenge when we need to study it in the laboratory. In contrast, Bordetella
bronchiseptica has a very broad host range. It efficiently colonizes the noses of mice. When we
simply add just a few bacteria to a drop of liquid and touch that drop to the tip of the mouse's nose.
We also noted that it depletes the many other organisms that usually live there in a stable
community. This is not just a minor or temporary disturbance. Many organisms are present before
we inoculate with B brochiseptica. But are gone thereafter, and don't come back.
Of course, this could have important implications. So we wanted to understand how it works. How
does one new bacterium introduce in very small numbers. Displace a resident community of
organisms that have lived there as a stable ecosystem? There are likely many mechanisms involved
in such a massive disruption of an eco-system like the nasal microbiome. But I'm going to talk to you
about just one of them - the type six secretion system- because it helped us to solve the riddle of the
host's specificities of these bacteria.
Type six accretion systems are actually derived from phages which are viruses that infect bacteria by
injecting their DNA or RNA into the bacterium. But bacteria have adopted this complex molecular
machinery and use it to inject toxins into adjacent bacteria. We observed that if we removed the
capacity to use its type six secretion system from B bronchiseptica. It was not able to displace the
various other nasal microbiota. So the type six secretion system appears to be required for this
effective competition with resident microbes. And this may contribute to the ability of b.
bronchiseptica to infect so many animals. By comparison, B pertussis, which is extremely contagious
among humans, is not very good at colonizing mice. Hundreds of thousands of bacteria have to get
deep into the lungs of mice for an infection to establish. When we looked closely at the genome of B
pertussis, we observed that it's missing the genes encoding the Type Six secretion system, the tool
that B bronchiseptica uses to efficiently compete with the resident bacteria. Based on these
observations we made the hypothesis that B pertussis fails to efficiently colonize the mouse nose
because it can't compete with the resident micro- organisms. To test this we treated mice with a
topical antibiotic that cleared the resident bacteria from the nasal cavity. This made the mice
hundreds of times more susceptible and allowed them to be colonized with less than one hundred B
pertussis in a tiny five microliter droplet on the tip of the nose. So it's not that B pertussis can't infect
mice. But rather it never gets the chance to, because it can't gain a foothold in the presence of all
the other members of the microbial community.
This answers the question, why is B pertussis unable to efficiently infect the noses of mice? It's not
because mice are so different from humans. And it's not that the B pertussis has a specific
mechanism to attach to human, but not mouse cells. Rather, what B pertussis lacks is the ability to
compete with the microbiota of the mouse nasal cavity. These experiments demonstrate how a
healthy host microbiome can protect against invading pathogens and the diseases they cause since
we are all highly dependent on defenses provided by our healthy microbiome. We should think very
carefully before doing something that disrupts them. Antibiotics may be helpful when we have a
serious infection. But can also remove all three types of defence conferred by a healthy microbiome,
leaving a potential breeding ground. For other invading pathogens, especially those are antibiotic
resistant. In general we should have a greater respect for the important functions of our healthy
microbiome. And be thoughtful to disrupt it, only when there is sincere danger of serious outcomes.

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Basics of Ecology
2014 Ebola Outbreak
In early December, 2013, a child in a town in Guinea was infected with Ebola from an unknown
source and fell ill. She infected three family members, a nurse, and a midwife. All became ill and
some infected others in the community, including healthcare workers who transmitted infection to
hospital patients. And from this simple beginning, an Ebola epidemic developed that has resulted in
thousands of deaths and impacted the lives of millions.
This outbreak has now superseded 6,000 plus cases with about half as many fatalities. So 50 to 60%
case fatality rate. The challenge when we get a new condition in an area, is that we will treat it like
things that we have familiar with in ways that we're familiar, so. If it feels like the flu, it feels like
malaria, and then you would go to the clinic where you would normally get treatment without
knowing that there's something else isn't the area there's no reason to do anything differently.
Many of these emerging virus infections start with very similar disease symptoms. You don't feel
well, you may have muscle aches, and fever is typical of many of them. But this is just the first stage
of Ebola virus. The incubation period can be quite long before we see the classical symptoms of
haemorrhage. There have been 30 documented instances of at least one Ebola infection, since this
class of viruses was first identified in Democratic Republic of Congo, in 1976. The current outbreak,
which has largely been contained to Guinea, Sierra Leone, and Liberia, has resulted in more cases
than all of these combined leading to a variety of questions. Where has the virus been in-between
outbreaks? How do these outbreaks arise? And why is this outbreak so unusual compared to
previous outbreaks of Ebola? I think it's a really interesting question to ask, where is Ebola when it's
not in the human population? And it's clearly in wildlife somewhere. And it's spilling over. So the first
place you think of looking is in the primates. And in the animals that are closely related to us.
Look around to see if you can find the virus. But it's not found very commonly in those animals. Well
it is, but it is only when the animals are dead. The second obvious place to look is in the rodents. And
there have been lots of investigation and no sign of it. But with this instance, and this recent Ebola
outbreak, we're pretty convinced that it's actually coming through the fruit bats.
As the Ebola epidemic spreads, it has been revealed that transmission is highly variable from person
to person and setting to setting. It has also affected urban zones, which is hasn't in the past. These
outbreaks in previous history have really been restricted to very rural areas. This outbreak now in
Connie Creek, Freetown and Monrovia, these are all very populated urban settings. We needed to
know if there's been multiple points of introduction or if it's single.
We can use the genetic sequence data from the Ebola virus to get an idea of where it came from and
how it's being transmitted. Cause over the last decade the there's evidence from using what we call
phylogenetic trees. Think of them as family trees that there have been multiple -Independent crossspecies transmission events, that have occurred, that lead to these, smaller outbreaks. So the
outbreak that's currently going on, now, this 2014 outbreak, we can trace using, again, the virus
phylogenies. And if there is human to human transmission, we anticipate that the virus sequences
isolated from humans will be very closely related. And in fact that's the case. There's certainly
diversity that's occurring within the viruses because they're evolving within the individuals that they
all seem to be related to one emerging strain. That's quite distantly related to those that were
circulating about a decade ago in the DRC.

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Basics of Ecology
This is of scientific interest but also of practical importance, because it suggests that nothing
dramatic has changed about the interactions between humans and wildlife. And that control efforts
for this outbreak need to be focused on transmission from human to human.
Yes, this has become highly spatial. So it started in the village, it spread to other places. It's just like a
fire running through elements that will burn easily. So we'll get a fire breakout in one place and then
a spark, a person, will travel to another place and set off another epidemic. Unlike influenza, which
can be transmitted through coughing and sneezing, Ebola is transmitted through contact with blood
and other bodily fluids. And, of course, different behaviours, lead to different rates of exposure.
Unfortunately, funeral and burial practices in much of West Africa, involve washing and touching of
the body of the deceased, which can lead to transmission from those who have died of Ebola
infection to those handling the body. A further complication is that health care workers commonly
come into contact with bodily fluids while caring for patients. And the absence of strict sanitation
and protection guidelines, the doctors and nurses who are providing care are at higher risk both for
getting infected and for infecting others.
If you were to look at previous outbreaks of Ebola haemorrhagic fever, Ebola virus disease, most
health care workers get infected in health care facilities. They're coming in contact with patients that
are infected that are, that are symptomatic, typically not in the Ebola treatment units. We're talking
health care workers that are infected at primary care facilities which if you look back in history, or
look back in time for this current outbreak. The majority of the health care workers were infected at
these front line clinics.
Limited knowledge about the nature and transmission of Ebola virus has resulted in fear and
uncertainty about the current outbreak and may have contributed to behaviours that facilitate its
spread.
Something like just telling people about Ebola where 50 to 90% are likely to die. And it happening in
your area or you seeing somebody where it happens, fear is a likely result. And we've learned that
people will act on that fear. If we can convince people of recommended actions, people will often
use that fear and behave in those recommended actions.
The projections of the Ebola epidemic have ranged from thousands to millions of cases.
Unfortunately, predicting the Ebola outbreak is very difficult because we've only seen this initial
exponential growth phase. Most epidemics are limited, either because the conditions favouring
transmission change, control efforts like vaccination, isolation, and the use of protective clothing
slow the spread. Or the epidemic spread so far that it runs out of susceptible people to infect. Most
of the predictions so far have been high because we don't yet know which will be the factor that
finally limits Ebola transmission.
We are not even near the top of this, the tip of this outbreak. We're months and months away from
any effective intervention from a pharm, pharmacological perspective. So we really have to focus on
the non-pharmo, pharmacological interventions, that is, behavioural modification. Really, the only
way that we're going to stop this outbreak currently is getting the information out to individuals to
protect themselves.

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Basics of Ecology
I think there's several things that we can learn from this outbreak. One of those is how important it
is to have interdisciplinary teams. We have to be able to show people and tell people this is not a
good behaviour. We have to be changing people's behaviour in relation to transmission. So we need.
Epidemiologists, we need virologists, we need social scientists working on those issues together.
We need to invest in our communication strategies. And invest in the people and the time and the
resources to develop those communication strategies from the beginning so that we have something
that we can use in that environment that is going to be effective and appropriate for the audiences
that are there.
So while medical intervention is clearly needed, information and communication about the virus, its
transmission. And the best practices to limited spread are also critical tools in the fight against Ebola.

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