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a pattern of reciprocal adaptation, caused by two
species evolving in close association.
coevolution is a change in the genetic composition of
one species (or group) in response to a genetic
change in another. More generally, the idea of some
reciprocal evolutionary change in interacting
species is a strict definition of coevolution
Coevolution, Coexistence, Conflict ?
Conventional thought: the good, or better adapted, parasite does
not unduly harm its host. Any exceptions can be viewed as new or
more recent associations compared with benign interactions
Therefore are all the parasites we have seen new associations?
When hosts encounter “harmful” parasites, that drain resources and
take actions to counter the effect of the parasites- is this peaceful
coexistence or a stalemate?
Should the relationship develop towards commensalism- or can a
certain level of pathogenicity be tolerated?
R0: The basic reproductive rate
The fundamental epidemiological quantity
R0 represents the average number of secondary
infections generated by one primary case in a susceptible
Can be used to estimate the level of immunization or
behavioural change required to control an epidemic
= βH
β =transmission rate, H= number of hosts
α = parasite induced host mortality (a measure of virulence)
µ= parasite mortality rate within the host, b=natural host death
Parasite-imposed and host-imposed selection can operate together
in determining features of parasite-host interactions.
Parasite virulence can incur costs for parasite and host- if parasites
incur too much suffering on their hosts. Anderson and May:
R0 =
Parasite net reproductive rate (R0) and virulence (α) are
inversely related
If parasite virulence brings no benefit to parasite, there is nothing to
stop virulence from evolving to zero (commensalism) or even a
positive relationship (mutualism). If the parameters were
independent of each other the predictions derived in this equation
would suggest that parasites to become benign.
Lizard malaria reduces clutch size.
Infected males interact less with
females and other males, results in
maintenance of inferior territories,
decreased ability to compete for
females, inability to attract females.
Infection may be associated with
significant reduction in fitness,
although no direct effect on
Genetically controlled resistance mechanisms also have a cost:
1) Immune responses may be harmful themselves
2) Structures for passive immunity or infrastructure for a response
(thymus and spleen) are expensive to produce and maintain
3) Mounting an immune response may be energetically expensive
Examine a scenario: R and S hosts in the presence and absence of a
1) Parasite present: R hosts should be fitter
2) Parasite absent: ?? Is R cost fixed or facultative?
What are the costs for developing an immune response? Does this
depend on the probability of encountering a parasite or the costs of
having a parasite?
Hypothetical differences in reproductive success between R and S hosts in
the presence and absence of parasites. A-D differ in whether the costs are
paid regardless of the presence of parasites (fixed) or only in the presence of
parasites (facultative)
Digenean infections of snails:
Snails are castrated: physiologically or physically
Selected snails to be S or R to a parasite:
R snails + parasite
S snails + parasite
R snails – parasite
S snails – parasite
Reproductive costs are paid by S snails - castrated
Reproductive costs are paid by R snails whether or not the parasite is present
How do parasites and hosts evolve?
Do parasites evolve to lose virulence? Should they?
Do parasites cause less disease because hosts mount counter
Are we in an arm’s race or in a negotiated settlement?
Can the parasite increase virulence and the host increase defences
indefinitely? Can this continue forever?
Should parasites be virulent or avirulent?
Can Virulence be altered easily…. or predictably, or on a regular
Parasite virulence can incur costs for parasite and host- if parasites incur too
much suffering on their hosts. Anderson and May:
R0 =
α = parasite induced host mortality (a measure of virulence)
Parasite net reproductive rate (R0) and virulence (α) are inversely
If parasite virulence brings no benefit to parasite, there is nothing to
stop virulence from evolving to zero (commensalism) or even a
positive relationship (mutualism)
Link between virulence and increased fitness is transmission.
If killing your parasites is expensive in terms of energy BUT your
parasites castrate you:
Where does the cost-benefit analysis kick in?
When is it better to expend large amounts of energy and when not?
Allocation of resources in mounting a strong response to a parasite
may reduce fitness. However the return- (survival, long term
reproductive output) should be justified even if it costs other fitness
= priority scheme
= tradeoffs.
Trade offs are linkages between traits that constrain the simultaneous
evolution of two or more traits.
Physiological trade offs: energy allocations between ≥2 functions requiring the
same energy
Evolutionary trade offs: are identified by manipulation experiments on
phenotype and by observed responses to selections on populations.
The effects of mating on longevity, fecundity on parental survival,
Reproduction on growth, offspring size vs offspring number
Some costs and benefits of high reproductive rates are known.
Improved prospects for transmission would be positive (unless all
parasites were successful- host killed)
If a parasite can kill its host then for a stable situation, overinfection should be
In evolutionary biology a trade-off between two traits is said to occur
when an increase in fitness due to a change in one trait is opposed
by a decrease in fitness due to a concomitant change in the second
The belief that evolutionary change is modulated and constrained
by such trade-offs is a central pillar of evolutionary thought. The
existence of trade-offs is not disputed, but there is still relatively little
understanding of how trade-offs evolve, or indeed if they can
Host Finding: How do you complete your life cycle?
As a parasite, how can you increase your chances of transmission?
As a parasite- can you alter your behaviour or the behaviour of your host so
as to get an advantage?
If everything else is the equal, then an increase in transmission rate results
in an increase in Ro.
If parasites induce such behavioural differences, they may be favoured by
natural selection.
If this occurs then several aspects of parasite epidemiology- including host
population levels required for their establishment may diverge from those
predicted in models.
Altered host behaviour can be found in direct and indirect life cycles, and
there are many transmission modes. Many involve predation on
intermediate hosts, direct transmission, or vector transmission.
The most dramatic is the ingestion of the intermediate host: when predators
eat the int. host- the cost to that int. host is very high.
Demonstrating the effect of altered behaviour on transmission is not easy,
representatives of every major taxon of predation-transmitted parasites
have been shown to enhance the risk of predation of the int. hosts.
Gastropods infected with digeneans may behave differently
Vectors infected with Plasmodia may feed differently
If this increases transmission, then Ro for these parasites will be greater than
if contact with their hosts was random
But can we prove that these behavioural modifications
1) actually increase transmission or
2) are “designed” to increase transmission
Parasite effects on host behavior
General issues
Extending "fitness effects of parasites on hosts" beyond simple mortality or
decrease in fecundity. Just as in the case of virulence and resistance, we
have to figure out which behavioral aspects of the host in the presence of
the parasite are caused by the parasite, which are caused by the host, and
which are accidental.
Parasites “wish” to increase their fitness by inducing host activities that
allow them to interact with potential hosts.
Host Space:
defined by the ecological requirements of the host
Host Time:
parasite emergence/existence should be timed to
coincide with the presence of a suitable host
(examples: cercariae from snails infected with Schistosoma at
noon- humans, night:rats. May be induced by photoperiod, host
signals, etc)
Adaptive value: enhance parasite transmission in placing the short-lived
cercariae in the Host space and Host Time
Should cercariae that penetrate hosts have a defined pattern?
Should cercariae that encyst on vegetation have a defined pattern or a
general emission from the snail host?
Categories of behavioral change
Change in activity (up or down): reduction in speed/distance travelled/etc. (mice
with Trichinella), increased activity, exploration etc.: increased predation (have to
be careful to test whether behavior leads to parasitism, rather than vice versa)
Many examples of changes in fish behavior
Acanthocephalans in invertebrates (good to test difference in activity patterns
rather than just increase/decrease, which can be caused by pathology)
Vectors can be affected: fly less (mosquitoes with filaria) or bite more, or change
host preferences
Conspicuous behavior:
height-seeking behavior: fish, ants side effect of pathology (e.g. hypoxia in fish)?
photophilia, heat-seeking behavior: "behavioral fever" (Hart, 1988; Boorstein and
Ewald, 1987; McClain et al 1988).
changes in color, changes in size
Changes in social behavior: castration, changes in mating behavior (host or
parasite or compensation?), changes in dominance; do parasites drive host
social behavior (group size, etc.)?
Testing hypotheses about parasite-induced behavior changes
Testing behavioral changes
Host behavioral changes in the presence of parasites are relatively easy to
document, and relatively well documented. One caveat, though, is that
ecological (correlational) studies might get the direction of causality wrong:
do hosts change their behavior when they are infected, or are they more
likely to be infected if they behave in a certain way? Possible solutions are:
laboratory studies of infection;
before-and-after studies of individuals;
parasitized behaviors that are completely outside the range of unparasitized
behavior (although this may still overestimate the size of behavior changes).
Testing effects on host and parasite fitness
A common assumption is that host behavior changes are driven by and for
parasites, to increase parasite survivorship and transmission. However, their
fitness consequences for the parasite or the host can be either positive, neutral,
or negative: these behavioral changes can constitute adaptations by either the
host or the parasite, or they can be "coincidental" side-effects of the hostparasite relationship. In many cases behavioral changes of hosts are sideeffects of parasite pathology, or host reactions, and do not necessarily enhance
parasite fitness.
For example: increased predation rates of parasitized hosts (assumed to be an
adaptation for transmission to the next host) is not necessarily by the right host.
Parasites may select particular host organs (that have strong effects on host
behavior) for reasons other than influencing host behavior. For example,
parasites in host CNS tissues are often isolated from host defenses:
`immunological privilege'.
Behavioral changes may be host-driven, either as part of host defense or just
as compensation for parasite-caused pathology.
Behavioral changes can be completely coincidental (although if they affect
parasite or host fitness in any way they should be subject to selection)
Beyond a certain point, it's very hard to disentangle causality evolution. For
example, suppose a parasite species inhabits the CNS and changes host
behavior. Is the parasite in the CNS to avoid host defenses, with changes in
behavior being a coincidental result of tissue damage, or are they actively
changing host behavior? Probably the best way to answer these questions is
simply to look at the changes in parasite and host fitness.
Parasite fitness
+ (transmission)
+ (survivorship)
-- (transmission)
Host fitness
Parasite manipulation
Parasite site selection
Host behavioral resistance
Host inclusive-fitness reactions?
Host pathology?
Host compensation
This field is famous for "just-so stories" - host behaviors that are just too weird
and incredible to believe are anything but parasites driving their hosts to do
things that enhance parasite fitness - but we have to figure out where and
how to draw the line. Intuitively, behavioral changes that are complex and
ones that we have a hard time explaining as simple pathogenic effects are the
ones that we usually ascribe to parasite manipulation.
Transmission by intermediate hosts
Immature stages of parasite ingested with intermediate host
Amphipod intermediate hosts: uninfected amphipods avoid bright light, and
burrowed if disturbed, to escape predators.
Amphipods infected with juvenile Polymorphous paradoxus (acanthocephalan)
demonstrated similar behaviour
Amphipods infected with infective stages of the parasite showed behavioural
changes: stayed in lighted areas, stayed at the surface, and grasped
floating objects – eaten by ducks. Infected int. hosts eaten at 4 fold
increase over uninfected int. hosts
Behaviour only altered when parasite is infective. This is a case where if a
parasite can kill, weaken, or derange its int. host it may be favoured by natural
Transmission by vectors:
Bloodfeeding insects that contain parasites in salivary glands may have trouble
probing to get a blood meal- stay longer to feed, will jump off one host onto
This may lower fitness: vectors may not get enough nutrients, fecundity
decreases, longer feeding means more danger
Transmission to vectors:
Enhanced transmission if host shows decreased defensive responses,
increased attractiveness
Lethargy: conserves energy- docile host more easily fed upon
reduced defensive behaviour (slapping) reduces vector mortality
Transmission of parasite propagules:
The right Place:
In Aedes sierrensis: infected by a ciliate L. clarki:
Mosquito induced to have behaviours that mimic oviposition: ciliate released into
water- infects larvae
The right Time:
Emergence of cercariae from a snail to coincide with host presence
Movement of microfilariae (Brugia malayi) from visceral to peripheral blood to
coincide with the feeding behaviour of a suitable vector
Swim (energetically costly, reduces longevity) or stay (competition?)
Swim=dispersal from habitat of first int. host
Highly elaborate host finding is required
Swim towards host signals
How can parasite conserve energy- yet ensure it emerges to coincide with the
presence of its next host?
Bring a host to a site suitable for parasite emergence
Make an intermediate host more susceptible to predation
Interfere with the chemical communication in hosts- aberrant behaviour
Evolutionary origins of host manipulation go back as far as the origins of
complex life cycles: changing the existing conditions to favour your
transmission would be favoured over conspecifics by natural selection.
The cercaria are released from the snails embedded in the snails mucus
slime balls which form in the snails respiratory chamber and are eventually
deposited on vegetation.
Ants eat the slime balls. Within the ant most of the cercaria encyst in the ant's
abdomen. However, one or two of the cercaria first undergo a migration to the
head of the ant to the sub-oesophageal ganglion where they encyst. These
metacercaria do not become infective but instead substantially alter the
behaviour of the ant, such that when the temperature drops as evening
approaches, the infected ants, instead of returning to their nests, climb to the
top of the vegetation and clamp on to the leaves with their mandibles. They
stay there immobile until the next morning. When the temperature warms up
the ants then resume there normal behaviour. This very strange behaviour
places the ants in a region where they are likely to be eaten by browsing
"zombie ants".
1) Describe how this happens
2) Are some cercariae altruistic? How selected?
3) How would this have developed?
4) What benefits are there for brain metacercariae?
5) What costs are there for brain metacercariae?
6) What benefits are there for abdominal metacercariae?
7) What costs are there for abdominal metacercariae?
Can Parasites alter behaviour in other ways?
Do parasites influence sex?
Why do animals have sex?
Can parasites affect mate selection?
Can one gender determine the parasite status of a potential mate before
males usually larger, more colorful, loud...
typically costly in males