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

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

No. metacercariae vs. host size 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. 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

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 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 budgets a. 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) - 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?