Joey M.

Terante
EDSCI 211
DR. MARY MAE M. CHEUNG

Behavioral Alterations and the Fitness and

Longevity of Infected Hosts
Despite an impressive repertoire of parasite avoidance techniques, animals
still acquire parasites. If behavioral alterations in parasitized animals were all the
result of natural selection favoring increased parasite transmission and therefore
increased R 0 for parasites, the world I am describing here would be uncomplicated.
Of course, most of the mechanisms by which parasites alter behavior remain a
mystery, and the evolutionary events that enabled them to seize upon these
mechanisms are equally unknown to us. These questions certainly lead into
complicated territory. Nonetheless, the general result, as far as basic reproductive
rate goes, would be fairly straightforward. R 0 simply would be larger than what one
would anticipate based on random encounters between propagules and
susceptibles, prey and predators. This is not always the case. In contrast to what
one might expect from polymorphids in amphipods sorting out altered habitat
preference by final host (Bethel and Holmes 1973), and digeneans increasing
mosquito vulnerability to voles and not to guppies (Webber et al. 1987a), not every
parasite has a happy ending not even those that alter host behavior. As noted
earlier, contact with susceptible animals has a large impact on microparasite R 0, as
does the proportion of immune hosts. For macroparasites, the number of successful
female offspring can be an indicator of R 0 . Altered behavior that enhances
transmission and parasite fitness essentially increases contact with susceptible
animals and increases numbers of successful female offspring. The host, however, is
also responding to selective pressures to minimize the negative effects of
parasitism and thus maximize its reproductive rate (see Hart 1990, 1994; Clark
1991; Lehmann 1993 for reviews of some costs of parasitism). Parasitism is an
ancient way of life perhaps as old as the origin of eukaryotes or older and the
happy circumstance of enjoying resources accrued by someone else is not recent. In
response, the ability to distinguish between self and non-self is pervasive among
living things. One of the end results of all of evolution is that organisms have quite
an arsenal with which to protect themselves if accosted by parasites. In so doing,
they can severely limit parasite reproduction and life span, parameters that, like
transmission, greatly affect Ro (table 5.1, p. 226). BEHAVIORS THAT REDUCE
PARASITE SURVIVAL When we consider this arsenal, the immune system and related
physiological responses usually spring to mind. Indeed, these are among those
phenomena that can heavily influence the probability of encountering susceptible
individuals, for instance, and ultimately determine if R 0 exceeds 1. Invertebrates as
well as vertebrates have elaborate physiological defense mechanisms, topics that

are fascinating, but well beyond what can be covered in this book. In turn, there are
remarkable adaptations on the parts of parasites to limit the influence of host
responses or even use those responses to benefit the parasite (Hayunga 1979;
Parker and Schneider 1981; Damian 1987; Loker 1994). There are also behavioral
defenses that can be strikingly effective behaviors that can engender or
accompany fever or chills, that can purge external or internal parasites, that can
protect kin (Hart 1988, 1990, 1994). These are behavioral responses that minimize
the success of parasites, perhaps as effectively as physiological defenses do. Hart
(1990, 1994) suggested two requirements for attributing defense against parasites
to a given behavior. First, the parasite should reduce host fitness; there should be a
cost associated with having the parasite. Second, the behavior should limit or
eliminate the parasite. The cost of the behavior would be offset by the benefit of
reducing the cost of the parasite. As discussed in chapter 4, such criteria are often
difficult to satisfy. Much like behaviors that are alleged to enhance parasite
transmission, behaviors that are alleged to enhance host defense frequently lack
rigorous experimental examination. This chapter covers aspects of behavior that do
not necessarily always meet Hart's criteria; some are even anecdotal. I include
them because they illustrate the broad scope of the possible, indeed perhaps even
the likely, if we only knew more about these interactions. One would do well,
however, to keep Hart's criteria in mind. In considering these defensive behaviors, I
limit them to behaviors that are prompted by the successful transmission/invasion
of a parasite (i.e., the behavior of the infected host) and that thus can truncate
parasite fecundity and/or life span within or upon the host. Behaviors that result in
parasite avoidance (thus reducing successful transmission itself) are discussed in
chapter 4. Many defensive behaviors have been recognized only recently as
important contributors to animal health, and I suspect more will be discovered in
the near future. Wakelin (1997) has suggested that the dangers of pathology
associated with immune response may result in moderate immunological responses
of limited effect. If this is the case, then behavioral avoidance and resistance may
be even more important in host defense than previously acknowledged.

Moore, J. (2002). Oxford Series in Ecology and Evolution :

Parasites and the Behavior of Animals. Cary, US: Oxford University
Press. Retrieved from http://www.ebrary.com

Historically, infections with nematode parasites have been

among the most common parasitisms affecting laboratory animals. Like
other parasitisms, the range and number of nematode infections of
laboratory animals have markedly decreased with improvements in animal
husbandry and the predominating use of laboratory-raised animals. In spite
of these improvements, some nematode infections, particularly those with
direct life cycles, may still commonly be found in laboratory animals. In
contrast, infection of laboratory animals with acanthocephalans has always
been uncommon, and is even more so today. This chapter briefly describes
the taxonomy, general life cycles, and morphology of the nematodes and
acanthocephalans one may encounter in the laboratory setting. Specific
parasites are discussed in the relevant host chapters.
CLASS NEMATODA The class Nematoda (roundworms) contains the
largest number of helminth parasites of endothermal animals. Worms in this
class are cylindrical, unsegmented, and elongated. These worms have a
pseudocoel (body cavity derived from the embryonic blastocoel) containing
an alimentary canal. Histologically, this arrangement appears as a tube
within a tube. In most cases, the sexes are separate. The life cycles may be
direct or indirect 1 3 . The class Nematoda is further divided into five orders
and fourteen superfamilies. With relatively little training, nearly anyone can
learn to differentiate worms by superfamily, and so facilitate arrival at
parasite identification (Figure 5.1). Order Rhabditida Most members of the
order Rhabditida are free-living, but a few are parasitic. Worms in the order
are so named because of the shape of the esophagus, which in free-living
forms includes a long, cylindrical portion that terminates in a posterior bulb
with a valvular apparatus, which appears refractile under light microscopy.
These worms are very small and have small lips and a reduced or absent
buccal cavity. Spicules are of equal length. For parasitic species, parasitic

and parthenogenetic females inhabit the small intestine. Eggs passed from
the host can produce either parasitic female larvae (homogonic life cycle) or
free-living male or female worms (heterogonic life cycle). The latter can
produce either infectious parasitic or free-living forms. Infection occurs when
larvae enter the host either by ingestion or by penetration of the skin, after
which they migrate into blood vessels and are carried to the lungs, where
they enter the alveoli. They are then carried up the airways to the trachea
and are swallowed. In the intestine the larvae develop into mature females
within the intestinal crypts. Vertebrate parasites are found only in the
superfamily Rhabditoidea. Superfamily Rhabditoidea Members of this
superfamily are commonly associated with soiled living conditions.
Vertebrate parasites are found in the families Rhabditidae and
Strongyloididae.
Baker, D. G. (Ed.). (2008). Flynn's Parasites of Laboratory
Animals (2). Hoboken, US: Wiley-Blackwell. Retrieved from
http://www.ebrary.com

Introduction
Valerie T. Eviner
While many studies demonstrate that pathogens can have dramatic
impacts on their hosts, substantially fewer studies have explored the
ecological consequences of these pathogeninduced changes in hosts.
Pathogen effects on host behavior, reproduction, and mortality can infl uence
community interactions such as competition, facilitation, predation, and
invasion. These pathogeninduced changes in host individuals and
communities can have strong impacts on ecosystem pro cesses (e.g.,
productivity, nutrient cycling) and landscape structure and function (e.g.,
disturbance regimes, land use, landatmosphere interactions). While we know
that pathogens have the potential to shape communities, ecosystems, and
landscapes, we still have poor ability to predict the magnitude and duration
of the impacts of any specifi c pathogen, or how the impacts of that
pathogen will vary depending on biotic and abiotic factors. Our goal in this
section was to incorporate the role of disease into our conceptual models for
community, ecosystem, and landscape ecol ogy in order to enhance our
ability to predict and manage ecosystems and pathogens. Such an endeavor
requires going beyond the expertise of any one research group, integrating

many different perspectives. A rough roadmap of how these different areas

of ecol ogy intersect (fi gure II.1) was provided at the outset, and each
author was charged with synthesizing knowledge on how pathogens impact a
subset of the boxes and arrows in fi gure II.1. In chapter 6, the fi rst chapter
of this section, Sharon Collinge and colleagues discuss the impacts of
pathogens on keystone species, dominant species, and feedbacks between
hosts, communities, and pathogens. This chapter highlights how spatial
variation in the ecological role of keystone species can cause spatial
variation in disease dynamics. Keith Clay and colleagues in chapter 7 explore
how the role of pathogens in fostering host diversity depends on host
frequency, density, and distance, and temporal oscillations due to factors
such as time lags, pathogen cycles, and selection. Both chapter 7 and
chapter 8 point out that pathogens can strongly infl uence the fate of a new
species arriving in an ecosystem, and how a new species interacts with the
resident community. This is particularly relevant to the topic of invasive
species, addressed in chapter 8 by Sarah Perkins and colleagues. Although
considerable recent attention has focused on how invasions may be
facilitated by escape from pathogens, this chapter addresses the tough
questions: which pathogens are likely to be lost and gained during invasion,
and how that infl uences the magnitude and duration of invasive species
release from pathogens. These authors also discuss how invasive species
may alter pathogen dynamics in native host communities. Kevin Lafferty in
chapter 9 shows that parasites play an integral role in determining a large
suite of community interactions, including competition, predation,
parasitism, and mutualism. The explicit inclusion of parasites in our
conceptualization of communities thus greatly increases the connectivity and
complexity of these communities. Spencer Hall and colleagues in chapter 10
explore the extent to which pathogenhost interactions and predatorprey
interactions mirror one another or are unique, carefully detailing key life
history characteristics that can be used to group consumerresource
interactions into qualitatively distinct pro cesses.
Ostfeld, R. S., Keesing, F., & Eviner, V. T. (Eds.). (2010).
Infectious Disease Ecology : Effects of Ecosystems on Disease and of
Disease on Ecosystems. Princeton, US: Princeton University Press.
Retrieved from http://www.ebrary.com