Conclusion Many internal and external factors affect the size of parasite populations ’Genes’ vs ’ecology’ hypotheses for determination of parasite population.

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

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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?