.

0 (hodnocen0 x )

(3) Půjčeno:3x 

BK

1st pub.

Oxford ; New York : Oxford University Press, 2011

xviii, 516 s. : il. ; 25 cm

ISBN 978-0-19-922949-9 (brož.)

Oxford biology

Obsahuje bibliografii na s. 435-498 a rejstříky

000241515

Contents // Preface // 1 Parasites and humans 1 // 1.1 Mission impossible 1 // 1.2 Some lessons provided by yellow fever 3 // 1.2.1 The parasite life-cyde can be complex 4 // 1.2.2 Not all host and parasite strains are the same 4 // 1.2.3 Complex physiological and molecular mechanisms underiie // the infection 4 // 1.2.4 Parasites and hosts are populations 5 // 1.2.5 Parasites can be controlled when we understand them 5 // 1.3 Parasites in our times 6 // Summary 8 // 2 The study of evolutionary parasitology 9 // 2.1 The evolutionary process 9 // 2.2 Questions about host-parasite interactions 12 // 2.3 Selection and units that evolve 13 // 2.4 Life history 14 // 2.5 Studying adaptation: optimality and evolutionarily stable strategies (ESS) 14 // 2.5.1 Optimality 15 // 2.5.2 Evolutionarily stable strategies (ESS) 16 // 2.6 Comparative studies 16 // Summary 17 // 3 The diversity and natural history of parasites 18 // 3.1 The ubiquity of parasites 18 // 3.2 A systematic overview of parasites 20 // 3.2.1 Viruses 20 // vi CONTENTS // 3.2.2 Prokaryotes 21 // 3.2.2.7 Archaea 22 // 3.2.2.2 Bacteria 22 // 3.2.3 The basal Eukaryotes 24 // 3.2.4 Protozoa 24 // 3.2.4.1 Mastigophora 25 // 3.2.42 Sarcodina 25 // 3.2.4.3 Sporozoa 26 // 3.2.4.4 Ciliophora 26 // 3.2.5 Fungi 27 // 3.2.6 Nematodes (roundworms) 28 // 3.2.7 Flatworms 29 // 3.2.8 Acanthocephala 30 // 3.2.9 Annelida 30 // 3.2.10 Crustacea 31 // 3.2.ЮЛ Pentastomida 31 // 3.2.10.2 Copepods 31 // 3.2.10.3 Isopods 31 // 3.2.10.4 Branchiura

(fish lice) 31 // 3.2.10.5 Other groups 31 // 3.2.11 Mites (Acari), ticks, lice (Mallophaga, Anoplura) 32 // 3.2.12 Parasitic insects (parasitoids) 33 // 3.3 The evolution of parasitism 33 // 3.3.1 Evolution of parasitism in nematodes 34 // 3.3.2 Evolution of parasitism in trypanosomes 35 // 3.4 The diversity and evolution of parasite life-cycles 38 // 3.4.1 Steps in a parasite’s life-cycle 38 // 3.4.1.1 Step 1: finding a host 38 // 3.4.1.1.1 Passive dispersion 38 // 3.4.1.1.2 Active host-finding 39 // 3.4.1.2 Step 2: infecting and establishment in the host 39 // 3.4.1.3 Step 3: growth, multiplication 39 // 3.4.1.4 Step 4: reproduction 40 // 3.4.1.5 Step 5: transmission 40 // 3.4.2 Modes of transmission 40 // 3.4.2.1 Direct transmission 40 // 3.4.2.2 Transmission with paratenic hosts 40 // 3.4.2.3 Vector transmission 42 // 3.4.3 Trematode life-cycles 42 // 3.4.4 The evolution of complex parasite life-cycles 46 // Summary 51 // 4 The natural history of defences 52 // 4.1 The defence sequence 52 // 4.1.1 Pre-infection defences 52 // 4.1.1.1 Spatial avoidance 52 // 4.1.1.2 Temporal avoidance 53 // vii // 53 // 55 // 55 // 55 // 55 // 55 // 55 // 56 // 56 // 57 // 57 // 59 // 60 // 60 // 62 // 64 // 64 // 65 // 65 // 65 // 65 // 66 // 68 // 68 // 68 // 71 // 73 // 73 // 73 // 73 // 74 // 74 // 74 // 74 // 75 // 75 // 75 // 75 // 75 // 75 // 76 // 76 // 76 // 78 // 78 // 80 // 80 // 82 // 82 // CON 1 EN IS // 4.7.1.3 Avoiding certain diets 4 1.14 The selfish herd // 4.1.1.5 Mating

behaviour and mate choice // 4.1.1.6 Self-medication // 4.17.7 Anticipatory defences // 4.11.8 Genetic defences // 4.1.2 Post-infection defences // 4 1 2.1 Behavioural changes // 4.1.2.2 Grooming // 4 12.3 Fever and chilling // 4.1.3 Social immunity Defence by the immune system Basic elements of the immune defence // 4.3.1 Humoral and cellular defences // 4.3.1.1 Phagocytosis // 4.3.1.2 Melanization, encapsulation // 4.3.1.3 Clotting, nodule formation // 4.3.1.4 Inflammation // 4.3.2 Innate and adaptive (acquired) immunity // 4.3.2.7 Innate immune defence // 4.3.2.2 Adaptive (acquired) immunity // 4.3.3 Signalling cascades // 4.3.3.7 Plants 4 3.3.2 Insects // 4.3.3.3 Mammals // 4.3.4 Proteolytic cascades // 4.3.5 The deployment of effectors Immune defence protein families // 4.4.1 Immunoglobulin-superfamily (IgSF) // 4.4.2 Leucine-rich repeats (LRRs) // 4.4.2.7 Toll and Toll-like receptors (TLRs) // 4.4.3 Lectins // 4.4 4 Other important families // 4.4.4.7 Tumour necrosis factor family (TNF) // 4 4.4.2 Cytokine receptor families // 4.4.4.3 Chemokine receptor family // 4.4 4.4 PGRfi GNBP // 4.4.4.5 NOD and other inlra-cellular sensors // 4.4 4.6 Scavenger receptors (SRCR) // 4.4.4.7 Down syndrome cell adhesion molecules (Dscam) 4Л.4.8 Fibrinogen-related protein (FREP) // 4.4.4Э Variable domain chitin-binding proteins (VCBPs) // 4.4.4.10 Anti-microbial peptides (AMPs) // The generation of diversity in recognition // 4.5.1 Polymorphism in the germ line // 4.5.2 Somatic generation

of diversity // 4.5.2 7 Alternative splicing // 4 5.2.2 Somatic rearrangement, copy choice // 4.5.2.3 Somatic (hyper-) mutation, gene conversion // viii CONTENTS // 4.5.3 The structure of immunoglobulins of В-and T-cells 83 // 4.5.3.1 B-cells 83 // 4.5.3.2 T-cells 87 // 4.6 The diversity of immune defences 88 // 4.6.1 Defence in prokaryotes 88 // 4.6.2 Defence in plants 88 // 4.6.3 Defence in invertebrates 89 // 4.6.3.1 Nematodes 89 // 4.6.3.2 Molluscs 89 // 4.6.3.3 Insects 89 // 4.6.3.4 Sea urchins 89 // 4.6.4 Early vertebrates 90 // 4.6.4.1 Cephalochordates 90 // 4.6.42 Urochordates (tunicates) 90 // 4.6.4.3 lawless vertebrates 90 // 4.6.5 The jawed (higher) vertebrates 90 // 4.7 Evolution of the immune system 94 // 4.7.1 Recognition of non-self 94 // 4.7.2 The evolution of adaptive immunity 94 // Summary 97 // 5 Ecological immunology 98 // 5.1 Variation in parasitism 98 // 5.1.1 Variation in parasite load 98 // 5.1.2 Variation in susceptibility and immune response 102 // 5.2 Ecological immunology: the costs of defence 105 // 5.2.1 General principles 105 // 5.2.2 Defence costs related to life history and behaviour 107 // 5.2.3 Cost of evolving immune defences 109 // 5.2.3.1 Genetic costs associated with the evolution of immune // defences 109 // 5.2.3.2 Physiological costs associated with the evolution // (maintenance) of immune defences 110 // 5.2.4 Cost of using immune defences 113 // 5.2.4.1 Genetic costs associated with the deployment of // immune defences 113 // 5.2.4.2 Physiological

costs associated with the deployment // of immune defences 113 // 5.2.4.3 Costs due to self-reactivity 116 // 5.3 The nature of defence costs 117 // 5.3.1 What is the limiting resource? 118 // 5.3.7.7 Energy 118 // 5.3.7.2 Food and nutrients 120 // 5.3.2 Regulation of allocation 121 // 5.3.2.7 Hormones as mediators 121 // 5.4 ’Immunocompetence’and the benefits of defence 123 // CONTENTS і* // 5.4.1 Correlating immune response and fitness 123 // 5.4.2 Phenotype, immunocompetence, and fitness 124 // 5.5 Strategies of immune defence 124 // 5.5.1 Optimal defence to increase recovery rate 129 // 5.5.2 Specific vs. general defence 130 // 5.5.3 Constitutive vs. induced defence 130 // 5.5.4 Optimal memory 132 // 5.5.5 Robust defence 132 // 5.5.6 Optimal defence and host lifespan 135 // 5.6 Tolerance as defence element 136 // 5.6.1 Measuring tolerance 137 // 5.6.2 The evolutionary consequences of tolerance 139 // Summary 140 // б Parasites, immunity, and sexual selection 141 // 6.1 Differences between the sexes 141 // 6.1.1 Males are generally more prone to parasites 141 // 6.1.2 The role of sex hormones in vertebrates 144 // 6.2 Parasites and sexual selection 145 // 6.2.1 Female mate choice, immunity, and parasitism 147 // 6.2.2 Males indicate quality of resisting parasites 148 // 6.2.2.7 The Hamilton-Zuk hypothesis 148 // 6.2.2.2 Symmetry as an indicator of male quality 151 // 6.2.2.3 The immunocompetence handicap hypothesis 152 // 6.2.2.4 Immunosuppression to avoid self-damage 153

// 6.2.3 Male genotype and female self-reference 155 // 6.2.3.7 Heterozygosity advantage 155 // 6.2.3.2 Dissimilar genes 155 // 6.3 Sexual selection and immunity in invertebrates 159 // Summary 164 // 7 Specificity 165 // 7.1 Measuring specificity and host range 165 // 7.1.1 List of observed hosts 165 // 7.1.2 Screening with genetic tools 166 // 7.1.3 Experimental infections 166 // 7.2 Host-specificity of parasites 170 // 7.3 Evolution of the host range 170 // 7.3.1 Host range and ecological specialization 170 // 7.3.2 Factors affecting host range 173 // 7.3.2.7 Host range is limited by phylogenetic constraints 173 // 7.3.22 Host range depends on the phylogenetic age of the parasite group 173 // 7.3.2.3 Host range depends on transmission mode 173 // 7.3.2.4 Host range depends on the complexity of the life cycle 174 // x CONTFNTS // 7.3.2.5 Host range depends on the stages of the parasite’s life-cycie 174 // 7.3.2.6 Host range depends on the virulence of the parasite 174 // 7.3.2.7 Host range depends on the variation in host availability 175 // 7.3.2.8 Host range depends on parasite geographic distribution 175 // 7.3.2.9 Host range depends on immune defences 175 // 7.4 Specific defences of the host 177 // 7.4.1 Specificity beyond the immune system 177 // 7.4.1. J Behavioural defences 177 // 7.4.7.2 Physical and chemical barriers 177 // 7.4.2 Specificity of the adaptive immune system 177 // 7.4.3 Specificity of the innate immune system 179 // 7.5 Memory, immune priming, and trans-generational

transfer 179 // 7.5.1 Individual immune memory 180 // 7.5.2 Trans-generational protection 180 // 7.6 Adaptive diversity and cross-reactivity 184 // Summary 186 // 8 Parasite immune evasion and manipulation of host phenotype 187 // 8.1 Parasites manipulate their hosts 187 // 8.2 The diversity of immune-evasion mechanisms 190 // 8.2.1 Passive evasion 190 // 8.2.7.7 Hideaway 190 // 8.2.7.2 Becoming’invisible’ 190 // 8.2.7.3 Changing identity 190 // 82.7.4 Population escape by mutation 190 // 8.2.1.5 Molecular mimicry 197 // 8.2.16 Quiescence 191 // 82.7.7 Capsule formation 191 // 8.2.2 Active evasion 191 // 8.2.3 Targets of immune evasion 193 // 8.2.3.7 Escape recognition 196 // 8.2.3.2 Avoid complement attack 196 // 8.2.3.3 Avoid being killed by polymorphonuclear cells (PMNs) 196 // 8.2.3.4 Avoid being killed by macrophages and phagocytes 196 // 82.3.5 Manipulate the signalling network 197 // 8.2.3.6 Interference with the antigen presentation and processing // pathways 197 // 8.2.3.7 Avoid being killed by the effectors 197 // 8.3 Manipulation of the host phenotype to increase transmission 198 // 8.3.1 Manipulation of host behaviour 198 // 8.3.7.7 Site of transmission in space and time 198 // 8.3.1.2 Transmission from host to vector 203 // 83.7.3 Time of transmission 203 // 8.3.2 Change of host morphology 204 // 8.3.3 Affecting transmission routes 204 // 8.3.4 Affecting social behaviour 207 // 8.4 Manipulation of the host phenotype to increase infection lifetime 207 // CON 11 N I

S xi // 8.4.1 Fecundity reduction 207 // 8.4.2 Changes of the social context 209 // 8.5 Mechanisms of host phenotype manipulation 210 // 8.6 Strategies of manipulation 213 // 8.6.1 What manipulation effort? 213 // 8.6.2 Multiple infections 214 // 8.7 Ecological significance of manipulation 217 // Summary 217 // 9 Infection and pathogenesis 219 // 9.1 Infection and dose 219 // 9.1.1 Analysing infective dose 223 // 9.1.1.1 Individual effective dose (threshold model) 223 // 9.1.1.2 Independent action model 223 // 9.1.2 The manipulation hypothesis 228 // 9.2 Similar parasites cause different pathologies 229 // 9.2.1 The common cold 229 // 9.2.2 Influenza 229 // 9.3 Pathogenesis: the mechanisms of virulence 230 // 9.3.1 Impairing host capacities 232 // 9.3.2 Destruction of tissue 232 // 9.3.3 Virulence factors 232 // 9.3.3.1 Adhesion factors (adhesins) 233 // 9.3.3.2 Colonization factors 233 // 9.3.3.3 Invasion factors (invasins) 233 // 9.3.3.4 Immune evasion factors 233 // 9.3.3.S Toxins 233 // 9.3.4 Toxins 234 // 9.3.5 Proteases 236 // 9.3.6 Pathogenesis by opportunistic infections 237 // 9.4 Immunopathology 237 // 9.4.1 Immunopathology associated with cytokines 238 // 9.4.2 Immunopathology caused by immune-evasion mechanisms 238 // 9.5 The genetics of pathogenesis 241 // Summary 243 // 10 Host-parasite genetics 244 // 10.1 The genetic architecture of host resistance 244 // 10.1.1 Number and location of host resistance genes 244 // 10.1.1.1 QTL-mapping 244

10.1.1.2 Genomic sequences 245 // 10.1.1.3 Comparative genetic studies 245 // 10.1.1.4 Resistance in plants and animals 246 // 10.1.2 Genetics of parasite virulence 250 // xii CONIENIS // 10.1.2.1 Genetics of virulence in bacteria 250 // 10.1.2.2 Example: genetics of virulence in Salmonella 253 // 10.1.3 Variation in gene expression 256 // 10.2 Evolutionary genetics of host-parasite interactions 259 // 10.2.1 Interaction between genotypes 259 // 10.2.2 Models of genotypic interactions 263 // 10.2.2.1 Gene for-gene interaction (GFGj 263 // 10.2.2.2 Matching specificities (matching alleles) 266 // 10.2.3 Epistasis 267 // 10.2.4 Inbreeding and heterozygosity 268 // 10.2.4.1 Genetically variable populations 268 // 10.2.4.2 Individual heterozygosity 272 // 10.3 Signatures of selection 272 // 10.3.1 Selection drives populations genetically apart 274 // 10.3.1.1 Phylogeny of haplotypes 274 // 10.3.1.2 Testing for genetic divergence 274 // 10.3.2 Selection affects non-synonymous mutations 275 // 10.3.3 Selective sweeps leave traces of linkage along the genome 275 // 10.4 Genetic structure of protozoan parasites 276 // Summary 278 // 11 Epidemiology 279 // 11.1 Population biology of host-parasitoid systems 279 // 11.2 Epidemiology of infectious diseases: microparasites 282 // 11.2.1 The SIR-model 285 // 11.2.2 Vaccination 288 // 11.2.3 Stochastic epidemiology 293 // 11.2.4 Spatial heterogeneity 295 // 11.3 Endemic infections and periodic outbreaks 295 // 11.4 Epidemiology of vectored

microparasites 296 // 11.5 Epidemiology of macroparasites 297 // 11.5.1 The distribution of macroparasites among hosts 298 // 11.5.2 Population dynamics and models for macroparasites 299 // 11.6 Immuno-epidemiology 299 // 11.6.1 Effects of immune response on parasites 302 // 11.6.2 Effects of acquired immunity on epidemiological patterns 303 // 11.6.3 Effects of immunity on population dynamics 305 // 11.7 Epidemiology with evolutionary change 305 // 11.8 Within-host epidemiology 307 // 11.8.1 Within-host dynamics of parasites 308 // 11.8.2 Within-host competition between parasite strains 309 // Summary 311 // CONTENTS xiij // 12 Virulence 312 // 12.1 Virulence 312 // 12.1.1 Different meanings of virulence 312 // 12.1.2 Virulence as a non-adaptive phenomenon 312 // 7 2.7.2.7 Virulence as a side-effect 313 // 72.7.2.2 Short-sighted evolution 314 // 72.1,2.3 Virulence a negligible effect for the parasite 315 // 12.1.3 Virulence as an evolved trait 315 // 12.2 The evolution of virulence 319 // 12.2.1 Avirulence theory 319 // 12.2.2 Virulence as an adaptive trait 319 // 12.3 Concepts of virulence evolution 322 // 12.3.1 Basic principles of evolutionary theory 322 // 12.3.2 The recovery-virulence trade-off 323 // 12.3.3 The transmission-virulence trade-off 323 // 12.3.4 Horizontal vs. vertical transmission 327 // 12.3.5 Host density and background mortality 330 // 12.3.6 Host population size affected by parasitism 330 // 12.4 Within-host evolution 331 // 12.4.1 Within-host

replication and clearance of the infection 331 // 12.4.2 Multiple infections 331 // 12.4.3 Kinship among co-infecting parasites 334 // 12.4.4 Medical intervention and virulence 339 // 12.4.5 Obligate killers 344 // 12.4.6 Immunopathology and virulence 344 // 12.5 Life history of infection events 344 // 12.5.1 The timing of benefits and costs 344 // 12.5.2 A generalized theory: the sensitivity framework 346 // 12.6 Within- vs. between-host selection 348 // 12.7 Host population structure 350 // 12.7.1 Spatial structure 350 // 12.7.2 Variation in host types 350 // 12.7.3 Social structure 351 // 12.8 Non-equilibrium virulence 351 // Summary 352 // 13 Host-parasite (co-)evolution 354 // 13.1 Macro-evolution 354 // 13.2 Micro-evolution 359 // 13.2.1 Evolution of antibiotic resistance 360 // 13.2.2 Costs of antibiotic resistance 362 // xiv // CONTFNTS // 13.3 Micro-evolution: the maintenance of diversity 364 // 13.3.1 Antagonistic host-parasite co-evolution 364 // 13.3.2 Time-lagged negative frequency-dependent selection 365 // 13.3.3 Local adaptation 369 // 13.4 Antagonistic co-evolution, sex, and recombination 374 // 13.4.1 Sexual reproduction 374 // 13.4.2 Meiotic recombination 374 // 13.5 The evolution of sex and recombination under parasitism 375 // 13.5.1 The evolution of sex 376 // 13.5.2 The evolution of meiotic recombination 376 // 13.5.3 Empirical evidence: advantage for sex 379 // 13.5.4 Empirical evidence: advantage for recombination 383 // 13.6 Selective

sweeps 386 // Summary 389 // 14 Ecology 390 // 14.1 Parasites and host life-history 390 // 14.1.1 Changes in reproductive patterns 390 // 14.1.2 Gigantism 391 // 14.1.3 Group living 393 // 14.2 Host populations 395 // 14.2.1 Population regulation by parasites 397 // 14.2.2 Population decline and extinction 399 // 14.3 Host ecological communities 401 // 14.3.1 Parasite effects on host competition 401 // 14.3.2 Communities of hosts 401 // 14.3.3 Food webs 405 // 14.4 Parasite ecology 406 // 14.4.1 Geographical patterns 406 // 14.4.1.1 Species-area relationship 406 // 14.4.1.2 Species-isolation relationship 406 // 14.4.1.3 Latitudinal gradients 407 // 14.4.2 Parasite community assembly 409 // 14.5 Invasions 410 // 14.5.1 Host invasions 410 // 14.5.1.1 Escape from parasites 411 // 14.5.1.2 Characteristics of parasites 411 // CONTENIS // 14.5.2 Invasion by parasites (disease emergence) // 14.5.2.1 Biological processes // 14.5.2.2 Abiotic correlates of parasite invasion success // 14.5.2.3 Global patterns // 14.5.3 Climate change and disease emergence Summary // Glossary // List of Immunological Acronyms References Subject Index Taxonomic Index