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CHAPTER 1 REVIEW QUESTIONS
1. Emergent properties refer to distinct attributes or phenomena that arise as a consequence of the interactions of two
components (such as a parasite and host). Describe some distinctive emergent properties that characterize the interactions between hosts and parasites.
Some emergent properties of parasitic interactions include:
• Colonization of a host
• Establishment within the host while evading the immune system responses
• Transmission to new hosts
• Altered host behavior
• Castration of the host
• Use of the host as transport or reservoir
• The ability of a parasite to infect a host and the resulting effects on the host (and parasite) are dependent on the
specific parasite-host interaction. Host specificity, virulence, and duration of infection will all depend on which
host the parasite is infecting. A parasite may be able to alter the behavior of one host but not another, while an
immunocompromised host may be susceptible to infection where a healthy host is not.
2. Definitions are elusive and it’s important to realize that exceptions or complications always occur. By considering parasites that defy simple categorization, we gain a deeper appreciation of the nature of parasitism. Consider the parasite
Trichinella spiralis referred to in Chapter 1. You may also want to look at the Rogues Gallery page referring to the life
cycle of this helminth. It is said the same host individual first serves as a definitive host and later an intermediate host.
How can this be?
The definition of a definitive host is one in which parasite undergoes sexual maturation and reproduction, while an
intermediate host is one in which parasite undergoes a required developmental step, but does not reproduce sexually.
In this example an individual first serves as a definitive host during the initial larval infection, through ingestion of
meat containing encysted Trichinella spiralis larvae, and the subsequent development and sexual reproduction of the
adult nematodes. The same individual then becomes the intermediate host for the resulting larval offspring which are
released into the circulation, encyst in the skeletal muscle tissue, and do not reproduce sexually in this host.
3. Consider the parasite Strongyloides stercoralis, an intestinal nematode of humans often called the threadworm. This
organism is also capable of free-living existence in the soil, with male and female adult worms present there that produce eggs. The eggs hatch and release larvae that undergo molts to become either larvae infective for people or that
develop into free-living adults that continue the soil-based part of the cycle. Look up the lifecycle of S. stercoralis in an
external source. Is it an obligatory parasite, a facultative parasite, or an opportunistic parasite?
All three definitions could apply to S. stercoralis. An obligate parasite is one which requires a suitable host to complete
its life cycle and, although S. stercoralis is capable of a free-living existence, it can be considered an obligate parasite
as infected human feces are needed to seed the soil-based cycle. It is also unclear how long the soil-based cycle can
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CHAPTER 1 QUESTIONS
persist without further seeding by infected feces so a host is required to enable this free-living existence. In addition
infection in the host can persist for a long time, and autoinfection can occur as eggs hatch and larvae mature in the
intestine producing more adult worms in the same host. S. stercoralis can also be termed a facultative parasite, one
which is usually free-living but can adopt a parasitic existence, as multiple rounds of worm reproduction can occur
in the soil-based cycle, producing some larvae which are infective for a new host and others which continue the
soil-based cycle. It could also be considered an opportunistic parasite, one which takes advantage of particular circumstances infect host it does not normally infect or cause disease in, when it infects an immunocompromised host,
as the chance of autoinfection increases in this case and this can be considered an opportunistic infection.
4. Parasitism is such a common, pervasive phenomenon that some kinds of structures and associations among species
depend on it for their existence. Provide some examples.
• Associations among species of cleaners, such as shrimp, fish or birds, and their hosts where the cleaners regularly
forage ectoparasites from infected hosts.
• The incisors of antelopes have evolved to be separated by spaces and function like a comb to remove ectoparasites.
5. List some examples in which a mutualistic (+/+) association between two different species might readily become a parasitic or other type of (+/-) association.
A mutualistic association may become parasitic when one of the individuals starts deriving a benefit to the detriment
of the other.
Examples include:
• Mycorhizal association is beneficial in a nutrient-limited environment where the mycorhiza provide essential
nutrients to the plant, but in an environment where nutrients are not limited the mycorhiza may be detrimental
by taking carbon away from the growing plant.
• Mycorhizal fungi may divert nutrients away from hosts to epiparasites such as Pterospora andromedea.
• Plasmodium chabaudi in rodents may cause a disruption in blood clotting resulting in an enhanced ability of
mosquitoes to locate blood and a shorter probing time. This could be considered mutualistic as it provides a
benefit to the mosquito in terms of providing food and, to P. chabaudi, in terms of enhanced transmission to
the mosquito vector. This then becomes a parasitic relationship once P. chabaudi has been transmitted and the
mosquito ceases feeding.
• Cleaners when they start feeding on the blood of the client e.g. yellow-billed oxpecker (Buphagus africanus).
6. Compare and contrast parasitoids, hyperparasites, cleptoparasites, brood parasites, and macroparasites.
A parasitoid spends a significant amount of its life on or within a single host, usually having a free-living existence
after leaving the host, and is usually more detrimental to the host than a parasite, often sterilizing, killing, and sometimes fully consuming the host.
Examples include:
• Larva of the wasp Aphidius smithi which parasitize the pea aphid Acyrthosiphon pisum.
• The fungus Harposporidum anguillulae which parasitizes soil-dwelling nematodes.
• Juveniles of Mermithid nematodes and horsehair worms which parasitize arthropods.
A hyperparasite is a parasite of a parasite. Examples include:
• The tapeworm Dipylidium caninum is a hyperparasite of the dog flea Ctenocephalides canis, itself a parasite of
dogs, cats and humans.
• Nested parasitism of the pea aphid (Acyrthosiphon pisum) by parasitoid wasp species. The aphid is parasitized
by a larva of the wasp Aphidius smithi, which is in term parasitized by larva of the wasp Alloxysta victrix
(hyperparasite), which can also be parasitized by larvae of another wasp, Asaphes californicus (hyperhyperparasite).
CHAPTER 1 QUESTIONS
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Cleptoparasites and brood parasites are types of exploiters. Cleptoparasites steal or scrounge food or other resources
obtained by another organism. Brood parasites are birds that surreptitiously deposit their eggs into nests of the same
or different bird species, with the result that the foster parents rear the progeny to fledging. In both cases the parasite
benefits from the exploitative interaction, but neither involves an organism living in or on another.
Examples include:
• The cleptoparasitic fly Milichia patrizii steals food from ants.
• The brown-headed cowbird is a brood parasite which lays its eggs in the nests of small passerine birds which then
feed and protect the cowbird fledglings, even at the expense of their own offspring.
Macroparasites are larger parasites such as worms, ticks or fleas, and are able to be counted. They are small and have a
rapid generation time relative to the hosts, but the disparity is less than between microparasites and hosts.
Examples include:
• The body louse, Pediculus humanus humanus, and head louse, P. humanus capitis.
• Blood-feeding mosquitoes (genera Anopheles, Aedes, and Culex) and tsetse flies (genus Glossina).
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CHAPTER 2 QUESTIONS
CHAPTER 2 REVIEW QUESTIONS
1. Why are studies of parasite diversity important and useful?
Studies of parasite diversity enable:
• Understanding how different groups of parasites have diversified and adapted to their hosts
• Prediction of which parasites may colonize new hosts, become invasive in new locations, or have the potential to
cause and emerging disease
• Determination of the full spectrum of parasites that might be involved in parasitic diseases and facilitate the
control of such diseases
• Development of more natural schemes of identification and classification of parasites
• Assessment of the rate that parasitic species are created and are going extinct
• Understanding of the unique biochemical capabilities of parasites which may be exploited for medicinal or other
purposes
• Understanding of the basic ecological and evolutionary processes that dictate how and why parasites have
diversified as they have.
2. The biological species concept is difficult to apply to some parasite groups. Which ones and why?
The biological species concept defines a species as a group of individuals with similar properties which are able to
interbreed with one another and produce fertile offspring and that don’t regularly interbreed with other species. The
concept can be difficult to apply in cases of cryptic speciation where morphologically similar species are genetically
distinct, and to those parasites which have reproductive systems involving infrequent, nonconventional, or cryptic
exchange of genetic information.
Examples include:
• Cryptic speciation in Trichinella species.
• Prokaryotic parasites which often have high levels of genetic diversity and that exchange genetic information by
horizontal gene transfer also further complicates this definition.
• Many protozoans in the genera Entamoeba, Leishmania, and Trypanosoma undergo infrequent, nonconventional
or cryptic reproduction.
• Giardia lamblia has distinct, but related, clonal lineages which may undergo genetic exchange when rare sexual
reproduction does occur.
• Trypanosoma brucei can undergo sexual recombination when different lineages come into contact in the same
host, this rare event may explain the exchange of the SRA gene among subspecies of T. brucei which may be
causative in epidemics of human sleeping sickness.
3. How many species of parasites are there, and what groups or factors make the answer particularly hard to quantify?
It is unknown how many species of parasite there are, in part due to the difficulty in estimating the total number of
species in general, and also due to factors such as the huge variety of parasitic lifestyles, the prevalence of cryptic species, hyperparasitism, and the range of host specificity. The amount of information available about specific parasite
groups, geographic areas, habitat types, and host species is also a factor. For example, there is a good general idea
of the number helminths of vertebrates but not for those that infect invertebrates or plants. There are difficulties in
quantifying the number of parasitic protozoans, algae, plants, fungi, and parasitic arthropods, and additional problems occur when trying to quantify the number of bacteria (not only due to difficulties in defining a species) and
other suborganismal entities, such as viruses and viroids, that are parasitic. Although it is clear an estimate of the
world’s parasite diversity is a long way off, assuming each free-living organism harbors at least one parasite species
and as parasites often harbor hyperparasites, there is a strong case for the existence of more species of parasites than
species of free-living organisms.
CHAPTER 2 QUESTIONS
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4. How do the patterns of inheritance implied by Darwin’s tree of life compare to those emerging from the concept of horizontal gene transfer, and how are parasites affected?
Darwin’s tree of life emphasized the inheritance of genetic information from an individual’s ancestors (vertical transfer) while the concept of horizontal gene transfer (HGT) involves the acquisition of genetic material from other
organisms or entities in the environment that are often entirely unrelated. Both modes of genetic material transfer
are important to parasites. In prokaryote parasites, HGT mediated by phage infection, transformation or plasmid
transfer, is important. Although HGT is thought to be less important in eukaryotes, due to their protection of cells
comprising the germ line, there are examples of where this has occurred. The genomes of some eukaryotic parasites including Blastocystis, Trypanosoma, Trichomonas, and Entamoeba show evidence of repeated and considerable
HGT from prokaryotes and viruses, especially from those sharing the same environments. Once genes are acquired
from bacteria and viruses they may be further shuttled serially among eukaryotes. HGT has also been found to have
occurred from fungi to the fungi-like oomycetes, such as in Phytophthora infestans, and genetic transfer from host
to parasite is seen in some members of the genus Rafflesia, which express hundreds of genes from their host plants.
5. Many of the parasitic protozoans have unusual cell biology that features peculiar organelles. Provide some examples.
Peculiar organelles found in parasitic protozoans include the hydrogenosome, mitosome, apicoplast, and kineoplast.
An additional example is found in Blastocystis hominis, which have an organelle that is intermediate in function
between a mitochondrion and hydrogenosome.
The hydrogenosome is an organelle which generates ATP from pyruvate giving off hydrogen (H2) as a by-product,
and an example is seen in Trichomonas species. The mitosome is a reduced version of a mitochondrion which has a
double-membrane and lacks mitochondrial DNA. Mitosomes in Giardia are incapable of aerobic respiration but are
still involved in ATP production, while those found in Entamoeba are among most reduced and do not appear to
participate in energy metabolism.
Apicomplexans, such as Cryptosporidium, Toxoplasma, and Plasmodium, have an apicoplast, which is a four-membrane structure containing a circular plastid genome. It is thought to have originated from a chloroplast through
secondary endosymbiosis, and although the genes for photosynthesis have been deleted, some functional genes have
been retained. Apicoplasts are thought to play a role in enabling penetration of new host cells, possibly due to synthesis of lipids used in the formation of parasitophorous vesicles.
A kinetoplast is a structure found within the single large mitochondrion of some excavates, such as Trypanosoma
and Leishmania. Kinetoplasts contain a network of concatenated circular DNA molecules. Some are maxicircles,
which encode the usual mitochondrial gene products but in a peculiar encrypted fashion, and many are minicircles,
encoding guide RNAs used to decode the maxicircles by either inserting or deleting uridine residues in maxicircle
transcripts. Kinetoplastids also sequester the enzymes of glycolosis within distinct, membrane-bound glycosomes.
6. Why do you suppose there have been many origins of parasitic species from free-living ancestors, but relatively few
examples of parasites evolving to become free-living?
Parasitic lifestyles, in many different forms, have evolved independently in organisms as diverse as bacteria, red algae,
fungi, and animals, suggesting that there are many advantages to adopting this type of lifestyle. When free-living
organisms adopt a parasitic lifestyle they often evolve adaptations to specialize them to parasitism and can lose genes
and structures which are no longer required as the parasite evolves to become dependent on the host for such functions. It is often thought that the move to parasitism is a one-way trip as this adaptation often results in the loss of
functions that are required for a return to a free-living existence. However, such losses are not ubiquitous, and especially in groups where adoption of parasitism is recent and has not yet been accompanied by extensive adaptation to
parasitism, reversals might be expected. Reversions to a free-living existence within groups that are parasitic have
occurred, and are particularly noteworthy in mites. For example, Mitonyssoides stercoralis is a predatory mite living
on other mites that feed on bat guano. It belongs to a family of mites (Macronyssidae) that is otherwise parasitic, and
is closely related to a species that is a parasite of bats. A plausible scenario is that some individuals of the parasitic
species adopted predatory feeding habits when they fell off or left their host.
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CHAPTER 2 QUESTIONS
7. What are metagenomics studies? Give some examples where they are relevant to the study of parasites in general.
Metagenomics is the characterization of genetic material recovered directly from a particular environment without
the need to culture the organism present. These studies offer a huge advantage in that they can reveal organisms
which might not be detected by any other means, and by collecting molecular signatures of the organisms present
can also determine how diverse the organisms are. For example, the sequencing of 18S rRNA genes directly from
seawater revealed an unappreciated diversity and abundance of parasitoid dinoflagellates which parasitize other dinoflagellate species that are involved in causing toxic blooms. Many of these parasitoids interact with their hosts in a
species-specific manner and contribute to the control of bloom-forming dinoflagellates.
Metagenomic approaches can also be used to reveal the full diversity of symbionts, potentially including previously
unknown parasites, found in vectors or intermediate hosts of medically important parasites such as mosquitoes or
snails. Many cryptic symbionts would not come to light without a metagenomics approach as they are too small to
be easily seen or recognized. Such studies may reveal the presence of natural enemies of the vectors which could be
developed or exploited to control the vectors. Metagenomics provides an important tool to further understanding the
full complement of parasites and other symbionts colonizing hosts in complex natural environments.
8. What is a monophyletic group and how does the process of homoplasy obscure relationships?
A monophyletic group is one that includes all the taxa derived from the most recent hypothetical common ancestor
of that group. Homoplasy refers to similarities that result from convergent evolution rather than common ancestry.
Homoplasy occurs when incorrect relationships are inferred among species exhibiting similar traits, such as morphological traits, when they originate from different lineages. This may be seen when a group includes taxa which are
not derived from the same most recent common ancestor (a polyphyletic group) or includes only some of the taxa
derived from the most recent common ancestor (a paraphyletic group).
Examples:
• Species in the phylum Myxozoa exhibiting the same spore morphology but differing genetically
• Three of the four morphologically derived subfamilies of flukes in the family Capsalidae were found not to be
monophyletic
Hypothetical example:
Consider a group of four taxa that is comprised of two pairs of sister taxa, taxa A and B, and taxa C and D. Suppose
all four taxa, A to D, are grouped together based on trait X, these form a monophyletic group as they all share the
same common ancestor and the group includes all descendants of that ancestor. Now suppose only taxa A to C are
grouped, they form a paraphyletic group sharing the same most recent common ancestor but the group does not
include all taxa derived from that ancestor. Now consider if taxa B and D are grouped, each is part of a separate sister
taxa group, so they do not share the same most recent common ancestor and therefore form a polyphyletic group.
Grouping of taxa B and D by trait X would be the result of homoplasy.
9. Differentiate between an isolate, a strain, and a subspecies. Use the example of Trypanosoma brucei to show why intraspecific diversity matters.
The term isolate describes a sample of a parasite species derived from a particular host at a particular time. A strain
refers to an intraspecific group of parasites that differs from other such groups in one or more traits, including traits
that might be relevant to control or treatment. Subspecies is used to identify a distinctive group of organisms within
a species that may occupy a particular region and that can interbreed with other subspecies. The importance of intraspecific diversity is highlighted by Trypanosoma brucei which consists of three subspecies, T. brucei brucei, T. brucei
rhodesiense, and T. brucei gambiense, each of which causes a specific disease and has a distinctive host range and geographical distribution. A relatively rare recombination event can introduce the SRA gene into T. b. brucei transforming
it into a human-infective parasite, and may be the cause of an epidemic of human sleeping sickness. Recombination
may be with T. b. rhodesiense as all human-infective isolates of this subspecies have this gene. However, this gene is
not the sole cause of human-infectivity in T. brucei as it is not present in T.b. gambiense.
CHAPTER 3 QUESTIONS
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CHAPTER 3 REVIEW QUESTIONS
1. Gnathostoma procyonis is a diecious, sexually reproducing nematode that parasitizes the stomach of raccoons. Raccoons,
which serve as definitive hosts, become infected when they consume either fish serving as second intermediate hosts
or paratenic hosts (other vertebrates that consumed the infected fish). Imagine a raccoon that is lightly infected
with this parasite early in the spring. As spring progresses the intensity of infection rises as the raccoon eats additional infected fish. How do you predict that this increasing parasite intensity will impact the reproduction rate of G.
procyonis?
In dioecious, sexually reproducing species such as G. procyonis, it would be expected that increasing parasite intensity
would make it easier to find a mate, and would therefore increase the rate of G. procyonis reproduction as spring progresses. This phenomenon is called the Allee effect, where individual fitness increases as population density increases.
In dioecious parasites with indirect life cycles, trophic transmission is thought to be an efficient way for parasites to
meet sexual partners, as it serves to concentrate parasites in a single location, and increasing parasite density should
therefor result in an increased rate of parasite reproduction.
2. Discuss the “hosts as islands” analogy. In what ways is it appropriate and in which ways is it inappropriate?
The “hosts-as-islands” analogy has been used to explain host colonization by applying the principles of island biogeography. In this case hosts are thought of as the relatively small, unevenly dispersed habitats, or “islands”, that can
only be reached by traversing “oceans” of intervening environment. This is appropriate in that hosts do form distinct
and separated habitats, however, there are numerous ways in which hosts differ from geographic islands. These differences include the ability of most hosts to move, the fact that they eventually die and that this may be accelerated by
the parasite, and that living hosts actively defend themselves against parasitic colonization.
3. You are studying a previously undescribed apicomplexan parasite, about which almost nothing is currently known. In
the course of your investigations you observe that the life cycle of this parasite includes a metabolically inactive “cystlike” stage. Which mode or modes of transmission can you likely rule out, based on this observation?
Cyst-like stages are typical of apicomplexans that spend at least part of their life cycle outside of the host as the cyst
enables the parasite to survive the unfavorable abiotic conditions in the external environment. The cyst represents
a transmission stage between hosts and cysts are most commonly associated with fecal-oral transmission. Vectorborne transmission could be ruled out, as when a parasite depends on the feeding of a biological vector it is not
usually subjected to the external environment, and a cyst-like stage is unlikely with this mode of transmission.
4. Parasites relying on vector-borne transmission are often among the most pathogenic. Can you think of a mode of transmission, for which selection might work to lessen pathogenicity?
Modes of transmission which might favor a lower pathogenicity are those which are less efficient or require the
host to be more active in seeking out the next host. Examples include sexual-transmission, which would require the
infected individual to remain healthy enough to engage in sexual contact, and vertical transmission, in which the
mother must be healthy enough to give birth to the infected offspring, and the offspring survive long enough for the
next stage of transmission to occur.
5. The R value, related to the basic reproduction number (R0) but taking into account the immune status of the population,
describes the average number of new cases in susceptible individuals derived from one infected individual. If members of the potential host population are immune to the infectious agent in question, they cannot become infected,
and this causes R to change as the proportion of individuals that are immune changes. In the following cases would R
be expected to rise or fall:
a) If a sudden influx of new potential host individuals who have not previously been exposed to the parasite in question
entered the population?
R would rise as the proportion of susceptible individuals would increase.
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CHAPTER 3 QUESTIONS
b) If a number of hosts became infected with the parasite, and subsequently became immune to later infections with the
same parasite?
R would fall as the proportion of susceptible individuals would decrease following the initial infections.
c) If a number of potential hosts were vaccinated against this particular parasite?
R would fall as the proportion of susceptible individuals would decrease as the number of vaccinated individuals
increased.
d) If a number of new babies are born.
R would rise as any new babies would be susceptible and would increase the proportion of susceptible individuals in
the population.
6. Onchocerca lupi is an emerging parasite of veterinary importance. Like the related O. volvulus, it can result in vision
loss for the definitive host. Whereas O. volvulus is a human parasite, O. lupi appears to affect mainly dogs and other
canines. The vector of this parasite has yet to be identified. Suppose that you wished to identify potential vectors, and
found that a species of biting fly was at least occasionally infected with larval stages of O. lupi. What would be your
next step, if you wished to further investigate the role of this fly as a potential O. lupi vector?
Although the fly can be infected with the larval stages of O. lupi, vector competence and vector capacity need to be
tested by determining first, whether the flies can transmit O. lupi to the canine hosts, and second, whether the flies
actually do transmit the parasite.
CHAPTER 4 QUESTIONS
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CHAPTER 4 REVIEW QUESTIONS
1. Based on recent findings, it has been suggested that even prokaryotes have an adaptive immune system. Upon what is
that argument based?
Many prokaryotes, 40–70% bacteria and 90% archaea, have been found to possess a type of defense from viruses and
foreign plasmids called the CRISPR/Cas system. This system enables the prokaryotes to cleave and then incorporate
exogenous short spacer DNA sequences from an infective phage into their own DNA, flanked by conserved repeat
units. These spacer-repeat units are later transcribed and used in a sequence-specific way to attack the DNA of a
comparable phage if encountered again. The stored phage sequences are an archive of previous exposure acting as a
form of immunological memory, and as such this system can be considered a type of adaptive (or acquired) immune
system.
2. How has the discovery and characterization of FREPs allowed us to at least partially answer an important question about
the ability of invertebrates to survive constant exposure to relatively fast-evolving parasites?
Invertebrates have generally been considered to have limited pattern recognition receptor (PRR) diversity. A key
question has been how they are able to survive in the face of parasites which would be expected to evolve rapidly to
circumvent limited PRR repertoires. The discovery of fibrinogen-related proteins (FREPS) involved in nonself recognition has provided a partial answer to this question. FREPS have been found to possess specific defense effector
functions including agglutination of parasite antigens and increasing the likelihood of phagocytosis or encapsulation
of the parasite by acting as opsonins. The organization of FREP-encoding genes in tandem arrays also allows for gene
conversion, which can result in diversification of the FREPS produced over an individual’s lifetime. This has shown
that invertebrates may not be as constrained in their ability to produce diverse PRRs as previously thought.
3. Why is it that complete elimination of eukaryotic parasites by the immune system is rarely achieved in vertebrate hosts?
Parasite persistence against the vertebrate immune response depends on the balance between pathology of the parasite, pathology and metabolic cost of the host immune response, and the parasites ability to evade the immune
response. Immune responses are energetically expensive and can cause their own pathology. If the parasites pathology
is not too severe a certain level of parasitism can be tolerated and may be less damaging to the host than immune-mediated damage. In addition parasites have evolved sophisticated immune evasion or manipulation strategies to ensure
persistence within the host long enough to complete the life cycle stages they undergo in that host. The combination
of the immune system providing host protection without too much collateral damage and parasites ability to avoid
complete immune destruction, explains why so many parasitic infections are persistent and long-lasting.
4. It has been demonstrated that the treatment of cutaneous leishmaniasis can be augmented by direct administration of
IL-12 into skin lesions. Based on what you have learned about the immune response to this parasite, and the role of
IL-12, explain the efficacy of IL-12 treatment.
Infection with Leishmania can result in either a localized or more serious disseminated form of cutaneous leishmaniasis depending on whether the host immune response is skewed towards a primarily cell mediated or humoral
response. The cytokine IL-12 is involved in activating the more protective cell mediated Th-1 response, and the parasite shifts the response towards a primarily humoral response by suppressing IL-12 release. Therefore treatment with
IL-12 should skew the immune response towards the cell-mediated response and result in the less serious localized
form of cutaneous leishmaniasis.
5. In what way does the phenomenon of premunition to Plasmodium infection impact our thinking about the possibility
of a fully protective malaria vaccine?
In Plasmodium infection, the immunity that develops does not eradicate all parasites in an infected individual and
is also of short duration. Regular and repeated infection is required to prevent the onset of more serious disease as
long-term immunological memory does not develop. This premunition means that a vaccine providing long-term
immunity to malaria would need to do something that does not happen in the course of a natural infection. As vaccines work by mimicking a normal infection, but without the associated pathology, this poses a substantial barrier to
the development of an anti-malaria vaccine. Novel strategies are needed to develop such a vaccine.
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CHAPTER 4 QUESTIONS
6. What problems might an individual with a deficiency of Natural Killer cells experience in terms of response to eukaryotic parasites?
Natural Killer (NK) cells play an important role in the early response prior full activation of an adaptive response.
They produce IFN-γ which stimulates a strong cell mediated response, is involved in class switching, and both actives
phagocytes and enhances the respiratory burst needed to kill ingested parasites. NK cells can also recognize and kill
certain infected cells such as Plasmodium infected erythrocytes. An individual with NK cell deficiency would have
a slower response to infection, allowing the parasite more time to replicate and consequently cause disease. These
individuals may be especially vulnerable to intracellular pathogens such as Leishmania, which are able to survive
in macrophages following phagocytosis, and Plasmodium, as NK cells mediate an initial innate response and are
involved in the lysis of Plasmodium infected erythrocytes.
7. We learned in this chapter that Toxocara canis encodes a protein that is similar in structure to a host protein called
CD23. The normal function of CD23 is to act as a receptor for the Fc region of IgE molecules on the surface of mast
cells and basophils. Its precise value to T. canis is unresolved. It may help to make the parasite appear more “host like”.
Alternatively, it may bind the Fc region of IgE antibodies that might ordinarily damage the parasite by binding it with
its Fab region. Can you describe an experiment which might allow a researcher to determine which of these two possibilities, if either, is more important?
It may be possible to develop a strain of T. canis in which the gene for production of the protein similar to CD23 is
inactive. Experimental animals might be infected with these worms and then inoculated with high levels of a soluble
form of CD23 which would bind up a large fraction of the available IgE. Since there would be little IgE available to
bind to the surface of the worms, any rapid destruction of the worms relative to controls could be attributed to the
inability to disguise themselves as “host like” rather than their ability to neutralize the effects of IgE.
An alternative would be to develop monoclonal antibodies against the Fc portion of the IgE antibody and administer
this to infected experimental animals that normally harbour the parasite. If the worms are destroyed it suggests that
the monoclonals interfered with the ability of the CD23-like protein to bind IgE Fc regions, and that it is Fc binding
that explains the protective value for the CD23-like protein for the parasite.
CHAPTER 5 QUESTIONS
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CHAPTER 5 REVIEW QUESTIONS
1. In Figure 5.1a, parasites with different thresholds of disease are illustrated. Two factors that may influence virulence,
and therefore whether the threshold is relatively high or low, are the mode of transmission utilized by the parasite
as well as its infective dose (the average number of infectious parasites to which hosts must be exposed, to infect
50% of those hosts). In general, as the ease of transmission goes up or as the infective dose goes down, the threshold
decreases. Explain these observations.
As the efficiency of transmission increases, and/or the number of parasites needed to provide an infective dose
decreases, the threshold for disease decreases as it becomes easier for the parasite to infect and colonize a new host.
In such cases, selective pressures to keep an infected host alive are reduced and pathogenicity increases. When
transmission is relatively inefficient, or if the infective dose is high, it is relatively difficult for the parasite to achieve
transmission and colonization. Consequently there is increased selective pressure to reduce pathogenicity so that
the host survives long enough to enable transmission, and in such cases the threshold for disease would be relatively
high.
2. Although the pathology caused by Entamoeba histolytica was discussed under the heading of “Trauma to host cells, tissues, or organs”, it might have been discussed under headings for different types of pathology as well. Under which
other headings might its discussion also have been appropriate and why?
Infection with Entamoeba histolytica might also have been discussed under the headings “immune response to infection” and “interference with host nutrient acquisition”. Some of the pathology associated with amoebiasis is a direct
effect of the host immune response as penetration of the intestinal epithelial layer by amoebae provokes an inflammatory response. In addition, damage to the intestinal epithelium and underlying tissues may impair nutrient absorption
while the resulting discomfort associated with the inflammatory response may reduce appetite.
3. Consider Figure 5.9. If the discussion of how malaria parasites prevent superinfection by stimulating the host to produce
hepcidin is confirmed, how might Figure 5.9 be different if all of the individuals portrayed in the figure were on iron
supplements?
Iron supplements would counteract the inhibiting effect of low iron concentrations on the growth of liver-stage
malaria parasites caused by hepcidin, and superinfection would occur sooner. In Figure 5.9, for young children
superinfection would occur after the first or second exposure to the new (red) strain rather than after the third exposure, for older children superinfection may occur after the first exposure rather than the second, while for adults
there would be no change.
4. After reading about how hemozoin contributes to the pathology of Plasmodium, do you think that this molecule merits
its traditional status as a true parasite toxin?
Hemozoin may not be a true toxin in the traditional sense as its pathogenic capacity can be attributed to both direct
effects on host processes and indirect effects stimulating host immunity. It has directly toxic effects on host cells and
processes, as once it is phagocytosed it cannot be digested in the endomembrane system, impeding phagocytosis and
resulting in immunosuppression. However, it also has indirect effects as a stimulator of innate immunity, as hemozoin bound to Plasmodium DNA has been found to bind with TLR-9 on phagocytes and result in an inflammatory
response.
5. In an experiment, mice that are FoxP3-/-are infected with Schistosoma mansoni. FoxP3 is an important transcription
factor expressed in Treg cells. Thus, a Treg response is absent in these mice. Predict the likely outcome of infection in
these mice, and explain this outcome, based on the lack of a Treg response.
Treg cells are thought to play an important role in preventing excessive and damaging Th-2 responses. Suppression
of the Th-2 response may be a key factor in the establishment of a chronic schistosome infection but may also reduce
the long-term morbidity of the host. Mice with FoxP3-/- would exhibit little or no Treg response, meaning that the
Th-2 response would not be suppressed, a greater immune response would be seen, and the mice would suffer more
serious symptoms of infection and increased morbidity.
12
CHAPTER 5 QUESTIONS
6. The hydatid cyst that forms in the intermediate host of Echinococcus granulosis can be filled with more than several
liters of liquid and can contain millions of larval stages called protoscoleces. When a hydatid cyst is removed from a
human, the cyst is often frozen with liquid nitrogen prior to its removal. Explain this necessary precaution, in light of
what you have learned about immunopathology.
Freezing the cyst prior to removal is necessary to prevent the release of any protoscoleces into otherwise sterile compartments of the body such as the peritoneal cavity. If release did occur, PAMPS on the surface of the protoscoleces
would interact with pattern recognition receptors leading to massive and systemic inflammation, ultimately resulting
in shock or death of the patient.
7. Suppose that a study is published in which it is shown that the cardiomyopathy associated with Chagas’ disease is worse
in those who have previously had a heart attack. What does this suggest about the possibility that Chagas’-associated
cardiomyopathy is due at least in part to autoimmunity and what does it suggest about the manner in which such
autoimmunity is initiated?
Chagas’-associated cardiomyopathy is thought to be autoimmune in origin, although how the loss of tolerance to
self-antigens occurs is unclear, it may be due in part to the release of sequestered antigens which are exposed by parasite-induced tissue damage. Increased severity of Chagas’-associated cardiomyopathy in those who have previously
had a heart attack may support this idea as previous damage to heart muscle during a heart attack may have also
released sequestered antigens. An autoimmune response to these antigens may add to the effects of parasite-induced
responses, resulting in the greater cardiomyopathy observed in these patients.
8. In our discussion of how parasites might alter host behavior as a way to increase the likelihood of trophic transmission,
we considered the example of Euhaplorchis californiensis, and the manner in which it might alter the behavior of killifish, making these fish more prone to predation by seabirds serving as definitive hosts. Why haven’t the birds evolved
to avoid killifish that are acting erratically and thus avoid becoming infected themselves? Can you think of a reason
why this has not occurred?
If the pathology caused by E. californiensis in the birds is not too severe then the extra nutrition gained by eating the
parasitized fish, especially as these fish represent an easy meal, may outweigh the negative effects of the resulting parasite infection. As such there would be no selective pressure for the birds to avoid predating on the parasitized fish,
and there may even be a net benefit to the birds.
CHAPTER 6 QUESTIONS
13
CHAPTER 6 REVIEW QUESTIONS
1. Think of the malaria parasite Plasmodium falciparum and all the different environments it inhabits. Starting from the
moment a sporozoite enters the human bloodstream, list in order all the distinct environments malaria parasites
must pass through as they complete their life cycle. You might want to consult the Rogues Gallery section to remind
yourself of the malaria life cycle.
•
•
•
•
•
•
•
•
•
•
Sporozoites enter the human bloodstream
Sporozoites migrate to the liver, penetrate a liver cell, and undergo merogany
Merozoites are then released into the bloodstream as the liver cell ruptures
Merozoites penetrate erythrocytes and undergo division
Merozoites then emerge into bloodstream and may repeat the cycle of penetrating erythrocytes and division
several times
Some merozoites enter erythrocytes and develop into gametocytes
Gametocytes are taken up in the blood meal of a mosquito ending up in the mosquito midgut. Here the
gametocyte forms gametes and fertilization occurs producing ookinetes
The ookinete migrates through the mosquito gut wall and forms a sporocyst on the outside of the gut wall.
Sporozoites are produced in the sporocyst.
Sporozoites are released into the mosquito’s hemocoel
Sporozoites migrate to the mosquito’s salivary gland, penetrate it and are now in a position to be injected into the
blood of another person when the mosquito takes a blood meal.
2. What is an encounter filter and a compatibility filter, and provide examples of each.
Encounter and compatibility filters are factors that limit the host spectrum occupied by a particular parasite. An
encounter filter is a factor which prevents contact between the parasite and host. These factors include the parasite and host living in different environments, being active during different seasons, and either organism exhibiting
behavioral preferences which prevent contact. An example of an encounter filter is seen in Dipozoon gracile, which
parasitizes the gills of four species of fish, but is never found in a fifth species, Barbus barbus, in the same streams.
Contact is prevented as the free-swimming oncomiracidia of D. gracile remain near the edges of habitats, where the
four other species occur, while B. barbus is found in deeper, central waters of larger streams.
A compatibility filter is a factor which, although infection is initiated, prevents the infection from succeeding. These
factors include the host not providing essential habitats or resources, and the host mounting an active defense
response. An example of this is seen with cercariae of Trichobilharzia species shed from snails in aquatic habitats.
When the cercariae penetrate human skin, instead of their usual avian hosts, they provoke pronounced immune reactions in the skin and are typically killed without further migration.
3. Why are studies to define the host specificity of parasites important?
There are several reasons why defining host specificity is important:
• The probability of emergence of new diseases may be greatly influenced by the likelihood that a parasite can shift
into new host species.
• The probability of extinction of a parasite species may be directly affected by its degree of host specificity. If a
parasite is host specific and its host is rare, it may face a risk of extinction.
• Specialist versus generalist parasites may require very different approaches from the standpoint of control
operations. It may be much harder to control a parasite with multiple host species.
• By understanding the molecular basis of host specificity, we can potentially devise new means, such as vaccines or
drugs, to control the parasites.
• Studies of host specificity provide essential foundation studies to help us understand the origins of parasite
diversity.
14
CHAPTER 6 QUESTIONS
4. Are parasites regulated in a density-dependent way in their hosts, and if so, how?
There are three ways in which parasite infrapopulations are subject to density-dependent regulation: decision-dependent, host death-dependent, and competition-dependent regulation. Decision-dependent regulation is when a
parasite avoids a particular host if the host is already infected. Host death-dependent regulation is when the most
heavily infected hosts succumb to their infection and die. This can be limiting as host death may occur before essential developmental stages or transmission can occur. Competition-dependent regulation is when parasite populations
are limited by the competitive interactions occurring among parasites. Intraspecific competition can occur in three
ways. First, interference competition occurs when there is active aggression between interacting individuals. Second,
resource or exploitative competition occurs when parasites compete for resources such as nutrients and space. High
parasite density can result in reduced per capita food supply and various crowding factors, and can lead to reduced
parasite size. Third, apparent competition is an indirect negative interaction which is mediated by a third party, such
as by the host immune response. Increasing parasite density increases the likelihood that an immune response is provoked and the immune response then limits the parasite population.
5. Are parasites important in the overall functioning of ecosystems? Identify some distinct lines of investigation that support your answer.
Parasites are important components of ecosystems and can affect overall ecosystem functioning in several ways.
Parasites can influence host population size and competitive ability, alter the probability of predation on infected
hosts, can be significant prey items both as free-living forms and within hosts, and may have a direct effect on species
richness and function as drivers of biodiversity. The importance of parasites in ecosystem functioning has been highlighted by food web studies which have shown that:
• Inclusion of parasites increases the connectedness of food webs, by 93% in one saltmarsh study, and this is
thought to increase food web stability.
• Parasites are a significant part of ecosystems. Parasite biomass exceeded that of predators in a study of estuarine
ecosystems, while annual biomass of termatode cercariae was also found to be greater than the biomass of birds in
the system.
• Parasites significantly influence food web structure, and by influencing the likelihood of predation of some hosts
by others, may increase the strength of some links in the food web.
• Parasites commonly serve as prey for other species. This is important in terms of understanding food web
construction and energy flow through ecosystems, and how parasite abundance and diversity are regulated.
6. Describe circumstances in which parasites might be expected to change the behavior of their hosts. What are some of
the ecological consequences of manipulation?
Behavioral manipulation is when a parasite alters the behavior of the host, often increasing its conspicuousness and
the likelihood of predation. This is especially likely for trophically-transmitted parasites which require the host they
are currently in to be eaten by the next host in their life cycle for transmission to occur. Some of the ecological consequences of such manipulation are:
• Manipulative parasites can increase the strength of links in food webs between some prey and predator species by
increasing the likelihood of predation.
• Manipulative parasites may facilitate creation of new trophic linkages within an ecosystem by increasing the
likelihood of predation by inappropriate hosts.
• Manipulated hosts may be more energy-rich than those that are not infected, with the parasitic infection affecting
energy flow between trophic links.
• Ingestion of manipulated hosts may lead to more definitive host species becoming infected. If the definitive host
is a top predator, it may then exert other cascading effects on prey species in the ecosystem.
• If the cost of acquiring another parasite is low relative to the food value of the infected prey item, then a predator
may actually benefit nutritionally from the ease with which it can capture manipulated prey.
CHAPTER 6 QUESTIONS
15
7. What is ecological immunology and how does it apply to parasitism?
Ecological immunology considers the influence biotic and abiotic features in the environment have on the evolution
and function of immune responses, and how the nature and extent of these immune responses influences an organism’s ecology. Understanding the factors which affect host and parasite ecology and immune response, and how these
interact, is central to determining how host-parasite relationships evolve and are influenced by ecological conditions.
Many factors potentially influence the immune response a particular host mounts against its parasites, including the
many trade-offs an organism must contend with and the complex environment in which the host lives. Some examples of how these factors may influence host-parasite relationships are:
• The host immune response may be influenced by other symbionts, which may contribute to the defense or may
exacerbate the infection.
• Hosts may engage in behaviors that minimize the risk of parasitism, thereby minimizing the downstream
expenses associated with infection, but that might limit access to good forage or increase risk of predation.
• Host immune response may be influenced by how well fed the host is and how much energy it has to apportion to
defense as opposed to other vital activities such as reproduction.
• Reproductive success of a host may depend on the extent to which it can elaborate ornaments needed to attract
mates without compromising its ability to respond to infection.
• A vigorous immune response may require modulation to reduce associated pathology to the host, and this may
result in tolerance to some level of parasitic infection rather than complete elimination of the infection.
8. How are ecology and epidemiology similar, and different?
Ecology and epidemiology are similar in that both fields seek to understand patterns in the distribution and abundance of organisms, and reveal the processes that underlie such patterns. Both fields also have a strong emphasis on
modelling, which can offer powerful predictive insights into parasite biology and transmission. They differ in that
the goal of epidemiology is focused on identifying risk factors, and anticipating and preventing disease outbreaks.
In terms of parasitism, epidemiology is interested in a triad of factors, host, parasite and environment, and how they
intersect to create the opportunity for disease transmission.
9. Provide some ideas for how the basic mathematical models we discussed can be expanded to be made more realistic.
Basic mathematical models of parasite biology and transmission can be improved by incorporating spatial and
temporal variation in factors such as host and parasite population dynamics, environmental conditions and host
behaviors that affect the likelihood of host-parasite contact, and heterogeneity in individual parasite infectivity or
host susceptibility. Model accuracy would be increased by the incorporation of spatiotemporal variation in host and
parasite population distribution, including within host parasite aggregation and host aggregation within the environment, and in host population structure, including age-related factors such as immune competence, and whether
a population is on average young or ageing, expanding or contracting. Temporal variation is also an important component of transmission, including seasonality in vector abundance and in host behaviors such as children returning
to school en masse and host aggregation around smaller water bodies during dry seasons. Incorporation of annual
and long-term climate changes would also increase the accuracy of model predictions. Another important aspect to
include is the heterogeneity among individual hosts in terms of susceptibility to infection and likelihood of transmission, especially in the case of superspreaders. Incorporation of the spatiotemporal variation in these factors would
produce a more realistic model of parasite transmission, increasing model accuracy and the ability to forecast future
events.
16
CHAPTER 7 QUESTIONS
CHAPTER 7 REVIEW QUESTIONS
1. With respect to parasites, identify some factors expected to increase the genetic differentiation (structure) among
populations.
Factors that would be expected to increase the genetic differentiation among parasite populations include:
• Hosts that are immobile or asocial may result in parasites becoming isolated and can lead to accumulated
differences
• Host or free-living stages of the parasite life cycle living in unstable or heterogeneous external environments can
lead to fragmentation of parasite populations.
• Parasites with complex life cycles with specific obligate hosts are more likely to become fragmented and
differentiated, depending on where the specific hosts are found.
• A patchy distribution of suitable parasite niches, for example, when free-living larvae require a particular type of
soil to survive and there is a patchy distribution of this soil type.
• Small effective population sizes can result in higher levels of genetic drift and inbreeding.
• A highly aggregated distribution among hosts can result in more isolation for some parasites.
• Parasites that are mostly self-fertilizing may create localized, genetically differentiated populations, as low levels of
sexual reproduction occur.
• Frequent extinctions and reestablishments can increase spatial and temporal separation from other populations,
and result in significant founder effects due to reestablishments from few individuals.
• Parasites with high host specificity have a greater vulnerability to variation in host abundance and this can result
in greater isolation among parasite populations.
• Parasites with low mobility, including vertically from host to offspring, are more likely to become isolated.
2. Recall the example of Plasmodium falciparum and its varying abundance in different parts of the world. Explain how
this abundance affects the amount of genetic recombination and gene flow that occurs in this species, and why understanding gene flow and recombination frequency matters.
Plasmodium falciparum shows varying abundance with a high prevalence in Africa and Papua New Guinea and
low prevalence in South America. In high prevalence areas P. falciparum exhibits high levels of genetic variability
and low levels of genetic differentiation suggestive of high gene flow. In these areas, it is more likely for mosquitoes to acquire multiple parasite genotypes and for sexual recombination to occur among these, maintaining genetic
diversity and gene flow. In areas of low prevalence mosquitoes are less likely to be infected by multiple parasite genotypes, with increased levels of selfing as recombination occurs among gametes from the same asexual lineage. Lower
genetic diversity, higher levels of population subdivision, and lower levels of gene flow are observed in these areas.
Understanding this population composition and structure is important as it has implications for potential control
measures. In low prevalence areas there is likely to be a lower diversity in variant surface antigens, which is potentially relevant to vaccine efficacy, and it is likely that vaccination may be more effective in these areas. In comparison,
the high levels of diversity and gene flow in high prevalence areas mean that vaccine efficacy is likely to be lower, and
that any resistance which develops is also more likely to spread among these populations.
3. What is coevolution, and what are some of its outcomes? How does coevolution differ from “evolution”? Hint: don’t
confuse this term with cospeciation.
Coevolution is the reciprocal evolution between two species in which each species imposes selection on the other. It
is a dynamic process of ongoing reciprocal change where a parasite population imposes a selective influence on a host
population which responds to the selection, in turn imposing a selective influence on the parasite population, with
this cycle potentially repeated over and over. Coevolution may involve traits like parasite infectivity, host resistance,
parasite host-finding ability and parasite avoidance behavior by the host. The key difference between evolution and
coevolution is the reciprocity of selective pressure and change occurring in the parasite and host.
Possible outcomes of coevolution include an arm’s race, negative frequency-dependent selection, and local adaptation. An arm’s race occurs when a successful innovation in the parasite population results in a selective sweep where
CHAPTER 7 QUESTIONS
17
the old trait is replaced by the new trait which increases to fixation, and is then followed by development of a new
innovation in the host population to counter the parasite which undergoes a similar selective sweep. This directional process continues, with both partners continually being “improved” by selection that favors innovations as
they appear.
Negative frequency-dependent selection is a cyclical and non-directional coevolutionary change where parasite-mediated selection leads to an advantage of being rare, and where the parasite present has also coevolved to be infective
to the most common host genotypes. Parasite induced selection leads to increasing frequency of a rare host genotype,
which is then mirrored, with a time lag, by an increase in the frequency of a parasite genotype infective to that host
genotype. As this parasite genotype becomes common it has the effect of creating a selective pressure favoring a different, rare host genotype, resulting in a decline in the original rare host and parasite genotypes, and an increase in
the new rare genotypes. This is a cyclical change in genotype frequencies, where at any one time polymorphisms in
both host and parasite alleles are expected, and the same host and parasite alleles may keep recycling.
Another important potential outcome of coevolution is local adaptation, where parasites have become adapted to,
and perform better in or on, hosts from the same geographic area (parasite and host are sympatric) compared to
hosts from different geographic areas (parasite and host are allopatric). Local maladaption may also occur, when allopatric combinations of host and parasite are more compatible, but observations of this may actually represent a time
lag in parasite’s response or a locally well-adapted host.
4. What is virulence and what is meant by the trade-off hypothesis with respect to parasite virulence?
Virulence is a measure of likelihood that an infectious agent can cause disease, pathology, harm, damage or fatality, and can also be the considered in ecological or evolutionary terms as the ability of a parasite to reduce its host’s
fitness. In terms of parasite virulence, the trade-off hypothesis is the idea that selection should act to favor the combinations of the two linked traits, virulence and transmission to a new host, that maximize the overall fitness of the
parasite. An increase in fitness in one of these linked traits may lead to a reduction in fitness in the other, such as an
increase in virulence leading to earlier mortality of the host, which results in a reduction in transmission. In most
cases the essential trade-off is between how fast and for how long the parasite can be transmitted. High rates of progeny production can be beneficial, but may be expected to increase virulence and this may induce strong immunity,
limit infection duration, limit host mobility, and cause host mortality, all potentially limiting the interval that transmission is possible. A lower rate of progeny production may diminish the immune response, extend host longevity,
and enable transmission to persist longer, but produce fewer offspring per unit time. Depending on the peculiarities
of the system in question, any level of virulence could potentially evolve.
5. How are new species of parasites formed?
New species of parasites are formed by speciation events. Speciation occurs when populations of the same species diverge, become separated by isolating mechanisms which precluding cross-fertilization among the divergent
populations, such that their gene pools become and remain distinct. There are three main mechanisms by which
speciation is thought to occur: allopatic speciation, where populations become physically isolated to an extent that
prevents genetic interchange; peripatric speciation, where small populations at the periphery of a large geographic
range become isolated and genetic drift or inbreeding result in divergence from other populations in the broader
range; and sympatric speciation, which occurs without any physical or geographic barriers to isolate the populations.
Allopatric parasite speciation could occur if a population of host and associated parasites was divided by a major
geological event, such as the emergence of a mountain range or the changing course of a river. If the populations
remained separate for long enough to accumulate sufficient differences such that if they intermingled again the parasites associated with each host population would remain distinct. Speciation may also have occurred among the
associated host populations. Peripatric parasite speciation might occur during the process of host switching, where
one or a few parasites colonize a new host species, essentially forming a peripheral population. If this colonization
was followed by divergence and isolation, it could form a new species-host combination. In parasites, sympatric speciation would require speciation to occur among sympatric members of a single host species. It could occur if a
population of parasites occupying one host individual changed in such a way that they became genetically isolated
from the original parasites without any geographical separation. However, it is difficult to determine exactly what
would constitute sympatric speciation in parasites, as what initially appears to be sympatric is often actually better
defined as a form of allopatric or peripatric speciation.
18
CHAPTER 7 QUESTIONSS
6. Why do parasites often have such complex life cycles?
Parasite life cycles are often complex and result from a complicated interplay between phylogenetic constraints, the
exploitation of predictable trophic links, a tendency to buy time and population stability in the form of resistant resting stages, and the use of innovations such as extra rounds of reproduction or the production of stages that actively
seek hosts. They reflect the action of natural selection on all life-cycle stages, at times with contradictory effects on
different stages, such that those parasites able to maximize their production of progeny are favored in their competition with conspecifics. One aspect which may explain why so many parasites exhibit complex life cycles is the
ongoing ‘natural experimentation’ that occurs, such that some parasite propagules will always find themselves in an
unexpected host or new locality which, if circumstances are right may allow for transmission, and the attainment of a
new host and the development of new life-cycle stages.
7. What concrete evidence can be mustered that parasites have an impact on host evolution?
Evidence of parasite-driven host evolution can be seen in immune system genes and with malaria-driven polymorphisms in humans. Genes of the immune system are often under intense selection and exhibit striking
polymorphisms, such as the high levels of polymorphism in the major histocompatibility complex in vertebrates.
Increased MHC II polymorphism has been associated with high helminth species richness in rodents, while regional
differences in MHC I diversity has been associated with intracellular pathogen richness in humans. An increased
frequency of MHC alleles associated with protection against parasites has also been shown to occur following imposition of a parasite burden on some populations. Malaria-driven polymorphisms provide evidence for the impact of
parasitism in altering the genetic composition of host populations. These polymorphisms include sickle-cell anemia
and loss of the Duffy antigen on erythrocytes, both of which confer some protection against malaria. Heterozygotes
for the sickle-cell trait exhibit enhanced resistance to Plasmodium falciparum, although homozygotes have a high risk
of developing sickle-cell anemia and early mortality. Increased frequency of the sickle-cell trait has been selected for
independently at least five separate times in different locations in Africa and Asia, with distribution corresponding
to the geographic regions with the most intense malaria transmission, especially from P. falciparum. A high prevalence of Duffy blood group antigen loss in West Africa is thought to account for the lack of Plasmodium vivax in that
region, while heterozygotes for Duffy-negativity in Papua New Guinea have been found to be less susceptible to P.
vivax.
8. How do parasites influence mate selection?
Parasites can have direct and indirect effects on mate selection. Direct effects include when a potential mate is avoided
due to a visible infection, or chosen due to appearing visibly healthy and vigorous. Indirect effects include parasites
affecting production and elaboration of ornaments, used as an indication of mate quality, and indirectly affecting
mate choice. Ornaments can be energetically expensive to produce and parasite burden could be expected to diminish the energy available to grow and maintain such ornaments. In addition, elaboration of ornaments often requires
androgens such as testosterone, which are typically immunosuppressive, or diet-acquired pigments such as carotenoids, which also play a role in immune function. These represent a trade-off between maintaining immune defense
and elaborating an ornament. Production of a superior ornament by an evidently healthy potential mate can be considered a reliable indicator of mate quality. An example is the decrease in carotenoid content and coloration of the
supraorbital comb in red grouse associated with increasing parasite abundance. Non-ornament based factors, such
as MHC diversity, may also have parasite-related effects on mate choice. Some degree of heterozygosity at MHC loci
is considered advantageous as it increases the number of MHC alleles available and the breadth of parasite-derived
peptides that can be recognized. Selecting a mate that can provide a maximal or intermediate level of MHC heterozygosity, or that has a particular MHC allele effective against a very common local parasite, may be advantageous. This
mate choice may be based on odors associated with particular MHC alleles, possibly with the involvement of other
odor-producing genes that augment MHC gene effects.
9. Do hosts have sexual systems of reproduction because of parasites?
One hypothesis is that the pressure imposed by fast-evolving parasites results in selection on hosts to adopt sexual
rather than asexual reproduction. Genetic recombination following sexual reproduction is expected to produce more
diverse progeny than would be obtained with asexual reproduction and this greater diversity should increase the
CHAPTER 7 QUESTIONS
19
chance that some progeny were able to withstand the onslaughts of parasites. The nematode Caenorhabditis elegans
and bacterial parasite Serratia marcescens provide an example of a coevolving parasite resulting in selection for biparental sex in the host. The proportion of sexual reproduction in C. elegans was found to increase from 20% to 80–90%
after 30 generations in the presence of S. marcescens. In addition, C. elegans lines incapable of outcrossing were found
to go extinct within 20 generations. Coevolution of parasite and host also occurred with ancestral nematodes 2–3
times more vulnerable to the bacteria that had interacted with the worms for 30 generations, and the nematodes that
had interacted with the bacteria for 30 generations much better at withstanding their contemporaneous bacteria than
their ancestors.
20
CHAPTER 8 QUESTIONS
CHAPTER 8 REVIEW QUESTIONS
1. Why is it often supposed that parasites will not be a factor in causing extinction of host species?
Parasites are often considered to be less likely than other factors, such as habitat destruction or fragmentation, to be
responsible for host species extinctions. This is because if a parasite diminishes the host population to a low level, it is
expected that the parasite will disappear before the host. If host population density drops to below the threshold host
population size needed to support the parasite, the parasite may have difficulty infecting new hosts or finding mates
within the host, so that the parasite will drop out while the host population persists.
2. Why do we see present day examples, such as with chytrid Batrachochytrium dendrobatidis, that seem to be responsible
for causing extinctions? Identify some particular properties of this species that might lead to this result.
Parasite-specific factors that can contribute to host extinction include very fast transmission and high virulence,
long-lived free-living stages which continue transmission even in the absence of actively infected hosts, and common
host species which serve as a steady source of infection to other less common and more susceptible species. The first
and last of these are key in the example of the chytrid fungus Batrachochytrium dendrobatidis that infects amphibian
species, and is a major cause of decline in nearly half the world’s amphibian species. The spread of B. dendrobatidis is
dominated by a single lineage, thought to be more virulent than other known lineages, and has been aided by global
trade in two host species, the North American bullfrog (Rana catesbeiana) and African clawed frog (Xenopus laevis).
These species are infected with B. dendrobatidis, are tolerant to its effects, and act as a steady source of infection for
other species. The virulence of B. dendrobatidis and the transmission due to these tolerant host species has contributed to the decline in many amphibian species, although other factors such as habitat fragmentation and destruction,
climate change, and land-use change also play a role. Parasite infection in more vulnerable species which are also
under threat from other drivers of extinction may have a greater impact and tip the balance against the host more
than would normally be expected.
3. One of the most famous examples of how parasites can cause extinctions of host species, and thereby pose considerable concerns for conservation biologists, is provided by the indigenous birds of Hawaii and their exposure to avian
malaria.
a) What is particularly noteworthy about the honeycreepers found in Hawaii?
Parasite-mediated extinction is thought to have occurred for 17 endemic honeycreeper species, with another 14 species listed as endangered or critically endangered. Significant reductions in abundance in these species followed the
introduction of mosquitoes, avian malaria and avian poxvirus to Hawaii.
b) Why are they so susceptible to avian malaria?
Mosquitoes were not present on the islands until 1826, so the endemic bird species had no evolutionary history
dealing with mosquitoes, or the avian malaria that they transmitted once it too was introduced with imported bird
species in the early twentieth century. Honeycreepers have been found to be susceptible to both avian malaria and
avian pox, and infection with both introduced pathogens may have further weakened infected individuals.
c) What additional factors have favored the continued persistence of avian malaria in Hawaii?
The presence of both introduced and native bird species that are tolerant hosts, which support persistent malaria
infections without succumbing and serve as an ongoing source of infection, has contributed to the persistence of
avian malaria in Hawaii. Other factors such as the feeding behavior of another introduced species, feral pigs, which
create additional mosquito habitats in fallen tree ferns, and human-mediated modification of aquatic habitats, has
also favored the persistence and multiplication of mosquito populations.
d) What factors have enabled some indigenous bird species to survive?
Some indigenous bird species are tolerant to avian malaria, while others have persisted at higher elevations
(>1500m) where mosquito populations and absent or rare, and where low temperatures preclude malaria sporozoite
development.
CHAPTER 8 QUESTIONS
21
e) How does climate change figure into this example?
Climate change has the potential to cause increased temperatures leading to an upward elevational shift in suitable
habitats for mosquito populations and conditions suitable for malaria sporozoite development. This would further
reduce, or even totally eliminate, the high elevation refugia in which have enabled some endemic species to persist.
f) Is there any hope for the native birds? If so, why?
There is the potential for adaptation of native birds to avian malaria and avian pox. Some endemic species, such has
the Hawaii ‘amakihi’ (Hemignathus virens virens), have become more common even in the mosquito-rich lowlands,
and may have sufficient genetic variation to favor the emergence of individuals resistant to the pathogenic effects of
malaria or avian pox. There is also the potential for range expansion in such species, and the possibility of speciation
events occurring.
4. What is spillover? Distinguish it from spillback.
Spillover is when an introduced parasite, usually introduced along with their original host, beings to exert effects on
indigenous host species. This is also used to describe the transfer of a parasite from a domestic or commercial population of hosts into a wild host population. Spillback is when a native parasite is acquired by an introduced host and
thrives in the new host, then comes to spillback and have a greater detrimental effect on the original indigenous host
species.
5. What advantages do invading hosts have with respect to parasitism, and how might we diminish these advantages to
help control the invasive host?
An invading host can have an advantage in being released from parasite pressure and may have greater success in the
new environment, including a competitive advantage over native counterparts which still have their parasite load.
Introduction to a new habitat has been found to halve parasite load, including loss of existing parasites and gain of
new parasites, and lower the intensity of infection compared with that experienced by the host in its native environment. This reduced level of parasitism may occur due to the absence of some parasites in the founding individuals of
the new host population, difficulties in parasite transmission if hosts are initially rare in the new environment, and
a lack of suitable alternative hosts or habitats required to complete the parasites life-cycle. One way to diminish the
advantage of lower parasite burden in introduced species is to introduce that species’ parasites from its original range.
However, this requires great care as it is difficult to predict what will happen when parasites are introduced into new
habitats, especially ones containing indigenous species that are closely related to the invasive host species.
6. How can parasites help us to understand if an ecosystem is intact, or is losing species?
Parasites are potential biological indicators for ecosystem integrity and gauging the extent to which indigenous parasites are maintained can be used to determine and monitor ecosystem health. A healthy ecosystem can be considered
one that persists through time, retaining productivity and diversity, and is resilient to change, and parasites can provide an indication of species diversity and food web stability that can be used to assess this. Parasites are important
components of ecosystems with many trophic links in natural food webs involving parasites and their hosts, with
most hosts harboring at least one or more parasite species. In addition, many parasites exhibit complex life-cycles
that require several different host species to complete and the presence of such parasites can provide an indication
that all the component hosts are present and the tropic links among them are intact. Parasites may also be used to
indicate the continued presence of otherwise elusive host species, without which the parasite would not persist in that
ecosystem, but which may be difficult to monitor in other ways. For example, a snail species may harbor the larval
stages of a parasite known to infect a rare shorebird, and infection in the snails can serve as an indicator of the continued presence of that shorebird in the ecosystem.
Parasites can also be indicative of other environmental impacts such as reductions in parasite abundance associated
with increasing pollution, or used to monitor pollutants such as heavy metals which can accumulate in parasites.
Parasites can also be indicative of environmental problems and changing ecosystems such as the occurrence of parasites associated with humans, agriculture, and domestic animals in marine animals. This is associated with changes
in marshland extent, areas which would have previously filtered out many terrestrial parasites, which has led to parasite-laden freshwater runoff entering the ocean directly, contributing to changing marine ecosystems.
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CHAPTER 8 QUESTIONS
7. Consider Dracunculus medinensis, a human-infecting nematode now on the verge of extinction. Can you think of any
factors that might prevent its extinction? Can you make an argument explaining why it would be desirable to figure
out how to preserve this species?
A key factor that has favored the success of control measures and brought Dracunculus medinensis close to extinction
is that there are no known prominent reservoir hosts. However, there is some evidence to suggest that fish or frogs
may serve as paratenic hosts and dogs can be infected by adult worms. It is possible that the paratenic hosts may
connect copepod infection with dogs or people, but it is not clear if this is a pathway for human infection. The ability
to use alternative hosts represents a significant factor that may prevent eradication of this species. Additional factors
such as civil unrest in places such as South Sudan may also make it difficult for eradication efforts to succeed in some
of the final known transmission foci. Re-emergence of D. medinensis has also been observed, where it appeared in
Chad after an apparent absence of 10 years. It is difficult to argue for this species to be allowed to persist in nature as it
causes true misery, pain and suffering for those infected. However, it is also a spectacular example of biodiversity and
although other species of Dracunculus exist, this is the only species with a preference to infect humans. It has been
part of the human experience for thousands of years and a palpable connection with our past will be lost when it is
eradicated. We should ensure that samples of the worm, including its genome, are preserved for posterity to study.
8. What factors favor parasite extinction?
Factors that can favor parasite extinction include co-extinction with host species, high host-specificity, poor dispersal ability, and a lack of intermediate or definitive hosts involved in a complex parasitic life-cycle with multiple
hosts. Host-specific parasites will go extinct if their host species are extirpated, but may also go extinct if the host
populations become too small or fragmented. Interactions among these factors also frequently occur. For example,
a host-specific parasite achieving low prevalence in a host species with small or fragmented populations has a much
poorer chance of survival than a generalist parasite attaining high prevalence in large host populations.
CHAPTER 9 QUESTIONS
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CHAPTER 9 REVIEW QUESTIONS
1. Compare the relative difficulty of control via a reduction in transmission for the three most important human schistosomes, Schistosoma mansoni, S. japonicum, and S. hematobium. Which factors render each species relatively easy or
difficult to control?
S. hematobium would be the easiest to control as it is the most specific to humans and does not have any significant
animal reservoir hosts. S. mansoni would be more difficult to control as it can on occasion infect wild primates as well
as humans. S. japonicum would be the most difficult to control because of the broad range of mammalian species,
including dogs, rodents, and water buffalo, that can serve as determinant hosts.
2. Yellow fever, caused by the yellow fever virus, utilizes a variety of primates as reservoirs. In the early twentieth century, when it was first realized that mosquitoes transmitted yellow fever, mosquito control was implemented in both
Panama and Cuba. Yellow fever was effectively eradicated from Cuba. In Panama, while the number of cases declined
dramatically, eradication efforts were never completely successful. Explain this difference, considering that Panama
had large populations of wild primates, while Cuba did not.
Mosquito control methods, such as placing screens on windows and utilizing bed nets, drastically reduce the
likelihood of mosquito-to-human transmission of yellow fever virus. In Cuba, once transmission to humans was sufficiently interrupted, as no additional wild primate reservoirs were present, the virus went locally extinct. In Panama,
although the incidence of yellow fever was greatly reduced it was never eradicated as there was always a reservoir
for the virus in the wild primate populations. It much more difficult to control transmission to animal hosts than to
human hosts, especially transmission to non-domestic animals such monkeys. Unless transmission to wild primates
is also interrupted, these animals will continue to provide a reservoir for the yellow fever virus in Panama.
3. In considering the control of parasite-transmitting mosquitoes through the use of insecticides, what is the logic of rotating different insecticides?
Using different insecticides in rotation decreases the likelihood that resistance to each insecticide will develop.
Selection pressure on the mosquitoes to favor resistance to any one insecticide will decrease while that insecticide is
not being used. Rotating the insecticides will also rotate the selection pressures so that mosquitoes resistant to any
one insecticide do not have enough of a selective advantage to perpetuate and result in widespread resistance.
4. Why is a higher therapeutic index considered to be a favorable attribute when considering an anti-parasitic drug? Why
in general is a higher therapeutic index more important when considering a drug for prophylaxis as opposed to one
for treatment of a sick individual?
The therapeutic index of a drug is a comparison of the amount of the drug that is toxic to the host to the amount that
will effectively destroy the parasite. The higher the therapeutic index, the larger the dose that will result in toxicity to
the host and the lower the effective dose needed to eliminate the parasite. A higher therapeutic index is important to
reduce the likelihood of toxic side effects, and ideally, a large dose would be required to cause host cell toxicity, while
only a small dose would be required to treat the parasite. This is especially important when considering anti-parasite
drugs for prophylactic treatment as the level of acceptable side effects is lower in a healthy individual trying to avoid
infection, than may be acceptable when treating an already infected, sick individual.
5. Imagine a newly developed drug that is highly lethal against all stages in the life cycle of Toxoplasma gondii. The drug has
been found to be safe and effective both for human and for veterinary use. Although the drug can eliminate infection
in both humans and cats, its use in humans will have very little impact on overall prevalence of human toxoplasmosis. Its use in cats, alternatively, could, at least in theory, reduce prevalence in both humans and cats. Explain this
difference.
Humans are intermediate hosts for T. gondii and are effectively a dead end host, as to complete transmission to the
definitive host a cat would have to eat an infected human. As there is essentially no transmission from human to
cat, use of the drug in humans may clear the infection but would have no impact on transmission. However, as
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CHAPTER 9 QUESTIONS
transmission occurs from cat to human, through human contact with infective oocysts present in cat feces, treatment of cats would not only reduce prevalence in cats but would also block this route of transmission to humans.
Therefore, treatment of cats could reduce prevalence in both species.
6. Suppose that resistance of schistosomes to Praziquantel were to become a reality. Currently, Praziquantel is the only
drug widely used to treat humans infected with schistosomes. Imagine that a new anti-schistosome drug has been
developed that is just as safe and effective as Praziquantel. How could these drugs be used together to reduce drug
resistance to either drug?
There is always a probability that an occasional mutation will occur that renders a small number of schistosomes
resistant to the drug in use. Worms that develop this resistance will have a large selective advantage over more sensitive worms, and over time may come to represent a substantial proportion of the parasite population. If both drugs
are utilized, any parasite that becomes resistant to one of the drugs will likely be killed by the other drug, and as the
likelihood of acquiring mutations for resistance to both drugs at the same time is much lower, this reduces the overall
likelihood that a completely resistant strain will emerge.
7. Explain the following statement; “Part of the difficulty in developing a vaccine against many eukaryotic parasites is that
the vaccine would have to do something that does not occur in the course of a natural infection”.
Successful vaccines mimic natural, primary infections but without the associated disease. Vaccines use a modified
form of the infectious agent, usually either killed or attenuated, to provoke a primary immune response in which
immunological memory to the infectious agent is established. If the vaccinated individual is later exposed to the
living, virulent strain of the infectious agent the immune system will respond with a secondary response, due to
memory established in response to the vaccine, and the parasite will be eliminated before it is able to cause disease.
In the case of many eukaryotic parasites, including protozoa and helminthes, which naturally establish long term
chronic infections, solid immunological protection is never established. Therefore, any vaccine against such parasites,
if it is to result in long-lasting, protective immunological memory, must be able to do so in a way that a natural infection does not.
CHAPTER 10 QUESTIONS
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CHAPTER 10 REVIEW QUESTIONS
1. An important issue for the future is food security. Discuss how parasites pose major challenges to our ability to adequately feed everyone in a future world with well over 7 billion people.
Parasites have major impacts on the health of both plant and animal food species, and many parasites have already
developed resistance to the chemical defenses used to treat them. This poses a serious threat to food security, especially in a future world where population increase places severe pressure on global resources and food production.
Present day examples compromising the health of food species include oomycetes (Phytophthora) in potatoes, and
fungi in wheat (Puccinia), corn (Ustilago), bananas (Fusarium), and coffee (Hemileia). Significant problems for wool,
meat, and milk production are posed by the antihelminthic resistance in nematodes of small ruminants (Teladorsagia,
Trichostrongylus, Haemonchus), and to a lesser extent in cattle (Haemonchus, Cooperia). Farming practices can also
increase the impact of infectious disease. For example, the dense rearing conditions used in fish and crustacean aquaculture favor rapid transmission of infectious diseases such as salmon lice in farmed salmon.
2. Of what use is having complete genome information for parasites?
Obtaining complete genome information for parasite species will help achieve a much deeper understanding of
host-parasite interactions, how parasite life cycles are deployed and genes required of each life cycle stage regulated, and will enable an improved understanding of the origins and diversification of parasite lineages by providing
definitive molecular phylogenetic interpretations of their evolutionary history. The genomes of parasite species also
represent an enormous store of potentially useful genetic information which could be exploited for practical purposes such as determining new drug or vaccine targets, and the discovery of modulators of immune responses, novel
synthetic pathways, innovative new structural materials, and genes encoding factors that suppress the growth of other
parasites.
3. Molecular parasitology also has a great deal to offer us in the future. Provide some examples.
Molecular parasitology can provide insights into how anti-parasite drugs attack and disable their targets, how
mutated versions of drug targets minimize the effects of drugs, why particular parasite antigens are better stimulants
for successful immune responses, and how immune cells interact at the molecular level to generate responses able to
kill parasites. Molecular-level studies can help identify new targets for drug development by revealing significant new
details of the molecular from which complex parasite structures such as flagella, apicoplasts, cytoskeletons, suckers,
or even nervous systems are constructed.
Molecular studies can help understand why some parasites can infect several species whereas other closely related
species cannot. An example is the comparison of generalist Toxoplasma gondii and more specialist Neospora caninum,
where less genes of the surface antigen encoding SRS gene family were expressed, despite a greater diversity of such
genes, and an inactive ROP18 gene, thought to result in a lower ability inactivate host defenses as it enters the hosts
cells, were found in N. caninum. Such studies can also provide details of basic gene expression and gene control,
particularly when the systems are unusual, as in the case of RNA editing in trypanosomes. In addition, these studies
can help understand how complex life cycles are orchestrated, providing clarification of which genes are involved
in determining the transition among life cycle stages. For example, identifying the genes involved in determining
whether malaria parasites continue to produce more erythrocyte-infecting merozoites or begin to produce gametocytes instead.
4. How is the study of climate change relevant to parasitology? For instance, if the climate is warming, can we expect that
vector-borne parasitic diseases of the tropics will invade more developed countries?
Each parasite species has its own optimum environmental conditions, including temperature ranges, and climate
change is important as it will affect the occurrence and distribution of such conditions, and therefore parasite distribution. The nature of change in parasite distributions, such as range shifts, contractions or expansions, will require
rigorous consideration on a case-by-case basis to account for factors such as variation in global temperature rise, with
temperate and arctic regions expected to see a greater effect, and the complexity of interactions involved in many
parasitic life cycles.
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CHAPTER 10 QUESTIONS
It is often assumed that increases in global temperature will increase the range of tropical diseases, particularly those
that are vector-borne, into temperate regions and increase the global areas where such diseases occur. Vector-borne
parasites are believed to be particularly responsive to warming climates as invertebrate vectors are directly exposed to
the effects of increasing temperatures, which can increases rates of vector development and of parasite development
within vectors. In the case of malaria, increased temperature can speed up the rate of malaria development in mosquitoes, but if temperatures become too warm other critical rates such as mosquito fecundity and survivorship begin
to fall. This trade-off between increased rates of development versus lower survival time with rising temperature
is often encountered among parasites and their vectors, and these factors suggest that the optimal temperature for
malaria transmission may be lower than that predicted by several climate models.
The potential spread of vector-borne parasites, such as malaria, to more temperate areas is alarming as human populations in these areas lack experience with such diseases. However, developed countries have better means at their
disposal to combat the spread of such diseases, and transmission may be mitigated by a lack of suitable aquatic habitats for the vectors, and by behaviors such as individuals living in urban areas where vectors are not particularly
common, and spending much of their time indoors so they may not be commonly exposed to infection.
5. Drug resistance is a huge problem in our ongoing battle to control parasites. Outline some approaches for how we overcome it.
Key to all the strategies for slowing and/or preventing development of drug resistance in parasites is a thorough
understanding of the targets and mode of action of the drugs involved, and the evolutionary and population biology
of parasites including how they respond to human-imposed selection from drug pressure or other control measures.
Some approaches for overcoming drug resistance are:
• Minimize the selective pressure imposed on the parasites
• Slow the development of resistance by maintaining some parasites in “refugia” that are not exposed to drug
pressure, such that genes for susceptibility are maintained within the population
• Adopt strategies to preserve the useful lifespan of anti-parasitic drugs such as rotation or simultaneous use of
multiple drugs with different modes of action
• Combine two drugs that target the same parasitic enzyme, but which would then select on their own mutually
incompatible combinations of mutation
• Identify new drug targets utilizing information provided from genome projects, high throughput screening and
genome-wide association analyses
• Improve mathematical models for predicting fluctuations in parasite abundance resulting from drug control and
the impact of drug resistance
• Identify and understand the consequences of the cost of resistance and to develop strategies to manage mixed
infections with alternative treatment strategies
• Develop new categories of drugs
• Screen existing drugs already approved for other purposes for anti-parasite activity
6. Why does integrated control represent a smart way forward with respect to coping with the burden of parasites?
Integrated control capitalizes on intimate knowledge of the target organisms and utilizes a variety of control measures
in a well-coordinated manner to minimize the parasites present and future impacts on the hosts being protected, but
does not place excessive reliance on any single control measure. Integrated parasite control could include:
• Implementing behavioral changes to minimize transmission opportunities
• Utilizing other organisms, such as predators of larval stages, which can interrupt transmission
• Judicious use of the available drugs, including rotation or simultaneous use to prolong efficacy
• Improvements in host health to increase resistance to parasite infection
• Maintenance of refugia to protect drug sensitivity by selective drug treatment
• Education to improve awareness of how infection is acquired and how it can be prevented
• Continued development of new control approaches including new drugs and vaccines
CHAPTER 10 QUESTIONS
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7. What is the difference between elimination and eradication of a particular parasite?
Elimination is when transmission of a parasite ceases in a particular area due to deliberate control efforts, such that
the incidence of new cases in that area is zero. Eradication is the permanent global reduction in the incidence of new
infections to zero, with no danger of re-introduction. This is essentially an extinction event for the parasite unless it is
maintained in confined and protected settings such as government laboratories.
8. What do parasite control programs need to succeed?
A range of factors are important for the success of parasite control programs including:
• Adequate funding to implement the control program, including the purchase of drugs and equipment, and for
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logistical aspects such as labor and transportation
Suitable training and experience for those implementing the control programs so that they can work effectively
often under difficult circumstances
Continual interaction with local populations while maintaining sensitivities to religious, cultural and social issues,
to enable education of the target population to the benefits of control
Support and cooperation of those people most affected by the control program, specifically those receiving drugs
or implementing other control measures
Ongoing surveillance and education to enable persistence of control measures, and the identification and
treatment of any disease re-emergence
The development of new tools and technologies, especially those that enable better diagnosis of parasite infection