2. Conclusion
Many internal and external factors affect the size of parasite populations
’Genes’ vs ’ecology’ hypotheses for determination of parasite population sizes
Interactive effects
D. Distribution of parasites in host populations
Terms
Recall parasite prevalence, intensity and abundance
sample mean and variance
3 general distribution patterns
patterns in nature

3. Frequency distributions of metacercariae in minnows
Prevalence = 98 %
Mean intensity = 26.9 (24.0)
Range = 0-77
Var-mean ratio = 21.6
N= 51
Prevalence = 62 %
Mean intensity = 1.8 (1.9)
Range = 0-8
Var-mean ratio = 1.8
N = 51

4. No. metacercariae vs. host size
Brain
Body cavity

5. Intensity ’brain’ vs. Intensity ’body cavity’
P =

6. Causes of aggregated distributions
distribution of infective stages (e.g. Leuchochloridium, Echinococcus)
distribution of vectors, larvae (e.g. clumping in Dermacentor)
inherent variation in hosts (Ascaris in pigs)
age, sex, behaviour, nutritional status
host genetics/immunity
P. falciparum and MHC alleles (west Africa)
S. mansoni in Brazilian villages (genes, not exposure to water)
Host genetics/not immunity
P. falciparum and sickle-cell gene
Recall genes vs ecology hypothesis for aggregation

7. Consequences of aggregated distributions
affects on ps population regulation
Density dependent regulation
Ps-induced host mortality
diagnosis

8. Parasites and host individuals
1. Parasite exploitation of host cell
e.g. Plasmodium and host rbc’s
recall life cycle
recall physiology of rbc
only infected rbc have a genome
e.g. recall Trichinella nurse cells
re-shaping of cellular environment is common
?  Parasites are often distantly related to their hosts. How can they command host morphology and physiology so precisely ?

9. 2. Parasite exploitation of host organism
recall definition(s) of parasitism
are all parasites pathogenic (i.e. cause detectable reduction in host fitness)?
‘reduced pathology vs absence of pathology’
recall classics

10. 1. Conspicuousness

11. 2. Growth

12. 3. Reproduction Case studies
1. Trematode larvae in snails cause castration
a. General
- biomass of ps relative to hs (1/4)
- asexual reproduction (= high metabolic demand)
- double-genome control
b. Double-phase of parasite development
- pre-patent vs patent
c. Biology
- infected snails never compensate for metabolic losses via increased feeding
- effects on reproduction differ depending on when snail is exposed

14. 2. Parasitoid/host interactions
e.g. Manduca sexta (sphingid) and its’ specialist wasp
extensive alteration of host endocrine system
host larval stage usually prolonged, via altered JH titres
Direct synthesis and secretions of JH by wasp
Secretion of wasp factors stimulate synthesis of host JH
Secretion of wasp-derived blockers

15. 3. Parasitic barnacles in crabs
recall life cycle of the rhizocephalans
100 % castration
‘parental’ care of ps eggs
feminization of male hosts

16. Adaptive significance of host fecundity reduction
recall fundamental hs/ps conflict
how can ps utilize hs resources without affecting host life-span?
the fundamental problem
By-product of infection (side effect hypothesis)
ps that feed directly on gonads
e.g. Fasciola in snails
hs produce fewer eggs due to ps-induced effects on food intake
no supportive evidence from trematode/snail interactions
but likely many examples of subtle side-effects
nutrient competition between hs and ps
some ectops/hs interactions, and some nematode/insect interactions
interaction between immunity, ps, and hs reproduction (i.e.energy allocation)

17. 2. Parasite in control (host manipulation hypothesis)
e.g. larval cestode in beetles (rat tapeworm)
developing larvae (but not encysted ones) produce a ‘manipulation factor’ that inhibits vitellogenesis
advantages to ps ?
re-distributed energy resources
increase in hs longevity (e.g. beetle tapeworm)
3. Host in control (host benefit hypothesis)
application of standard life-history theory
e.g. fecundity compensation
female beetles infected with cestode larvae produce a circulating hormone that reduces host fecundity
recipient uninfected beetles have reduced egg protein content

18. Summary:
some results suggest side-effect
both adaptive scenarios are not mutually exclusive, ie. both partners can gain by fecundity reduction

19. 4. Affects on host energy budgets
a. Acanthocephalan in starlings (Conners and Nichol, 1991)

21. - experimental design
- decreased basal metabolism (ca. 9%) and weight loss
- weight loss highest (ca. 20%) when exposed to cold temperatures
b. Ectoparasites in doves (Booth et al., 1993)
- manipulated lice loads in migratory doves (Illinois)
- results following recapture
- controls = 450 lice/bird
- treated = 100 lice/bird
- lower mass in controls and lower feather weight
- higher metabolic rate (9%) in controls (?)

22. Summary:
recall infections in minnows
the problem of subtle effects
field-based vs. lab-based tests (e.g. Booth et al.,)
evolution of host tolerance?