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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
Host size
Number Sp. B (body)
Number Sp. A (brain)
Frequency distributions of metacercariae in minnows
Prevalence = 62 %Mean intensity = 1.8 (1.9)Range = 0-8Var-mean ratio = 1.8N = 51
Prevalence = 98 %Mean intensity = 26.9 (24.0)Range = 0-77Var-mean ratio = 21.6N= 51
R2 = 0.1724
0
1
2
3
4
5
6
7
8
9
15 20 25 30 35 40
Host size
Number of metacercariae
No. metacercariae vs. host size
R2 =
0
10
20
30
40
50
60
70
80
90
15 20 25 30 35 40
Host size
Number of metacercariae
Brain
Body cavity
Intensity ’brain’ vs. Intensity ’body cavity’
P = 0.0015
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
Consequences of aggregated distributions
• affects on ps population regulation – Density dependent regulation– Ps-induced host mortality
• diagnosis
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 ?
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
1. Conspicuousness
2. Growth
3. ReproductionCase 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
QuickTime™ and a decompressor
are needed to see this picture.
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
3. Parasitic barnacles in crabs
• recall life cycle of the rhizocephalans• 100 % castration• ‘parental’ care of ps eggs• feminization of male hosts
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
1. 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)
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
Summary:• some results suggest side-effect• both adaptive scenarios are not mutually exclusive, ie. both
partners can gain by fecundity reduction
4. Affects on host energy budgetsa. Acanthocephalan in starlings (Conners and Nichol, 1991)
- 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)
- experimental design
- 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 (?)
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?