Principles of Plant Infection

Principles of Plant Infection investigates interactions among pathogens, host plants, the environment, time and space, and their role in plant infection. It describes the principles of infection, particularly of the root, stem, or leaf, as they apply to fungi, bacteria, or viruses. It also highlights the dual nature of resistance and suggests theories of host resistance.
Organized into seven chapters, this volume begins with an overview of the relation between the amount of inoculum and the amount of disease it causes. It then turns to a discussion of the disease/inoculum relations of tobacco mosaic virus; how obligate synergism restricts the transmission of pathogens; disease/inoculum relations in root disease; the independent action of spores as inoculum; variable factors other than the amount of inoculum that affect plant disease; and time as a determining factor of the degree of plant infection. The reader is also introduced to endemic disease of plants, the implications of endemicity for plant resistance to disease, the spread of disease via migration of pathogens, and the genetics of host-pathogen interactions.
Plant pathologists and plant breeders will gain valuable information from this book.

Inhalt

Preface
Chapter 1. The Relation Between the Amount of Inoculum and the Amount of Disease It Produces
1.1 The Question
1.2 The Simplest Relation: Disease Is Proportional to Inoculum
1.3 The Commonest Relation: The Ratio of Disease to Inoculum Decreases as the Amount of Inoculum Increases
1.4 The Effect of Antagonistic Interaction between Spores: As Inoculum Increases Disease Increases to a Maximum and Then Decreases
1.5 The Effect of Synergistic Interaction between Spores: as Inoculum Increases It Becomes Increasingly Effective
1.6 An Undemonstrated Relation: A Numerical Threshold of Infection
1.7 An Impossible Relation: Infection without Inoculum. Evidence against Recurrent Heterogenesis of Viruses
1.8 A Summary. The General Problem: What Chapters 1 and 2 Are About
1.9 Multiple Infection of Plants: The Problem of Assessing Data about the Percentage of Diseased Plants
1.10 The Theory of a Numerical Threshold of Infection. Evidence against It. Confusion with a Dilution End Point
1.11 The Experimental Law of the Origin. The Nature of Experimental Law
1.12 Curves Depicting Synergism between Randomly Dispersed Spores or Infection Sites. Relations near the Origin
1.13 Infection by Bacteria
1.14 Disputed Evidence for Obligate Synergism between Bacteria in Incompatible Host-Pathogen Combinations
1.15 The Complex Virus Story. Tobacco Mosaic Virus. Infection without Obligate Synergism
1.16 Sour Cherry Ringspot, Prune Dwarf, Cowpea Mosaic, Alfalfa Mosaic, and Tobacco Rattle Viruses. Obligate Synergism between Qualitatively Different Particles of the Same Virus
1.17 Incomplete Virus Particles That Infect without Obligate Synergism. Potato Spindle Tuber Virus. Satellite Viruses
1.18 Restrictions Imposed on the Pathogen by Obligate Synergism. Vector Transmission. Possible Benefits from Obligate Synergism
1.19 Disease/Inoculum Curves in Relation to Transmission by Vectors
1.20 Infectious Entities
1.21 A Basic Principle of Infection: The Probabilistic Viewpoint
1.22 Disease/Inoculum Relations near the Origin: Independent Action
Chapter 2. More About Disease/Inoculum Curves
2.1 The Scope of the Chapter
2.2 The Two Paths to Susceptibility and Their Relation to Curves A and B of Fig. 1.7. A Hitherto Neglected Factor in Epidemiology
2.3 The Relevance of the Two-Path Concept of Susceptibility to Models in Epidemiology
2.4 Curve C of Fig. 1.7. The Antagonistic Interaction of Spores
2.5 Curve D of Fig. 1.7. The Synergistic Interaction between Spores
2.6 A Short Summary of the Chapter So Far
2.7 Disease/Inoculum Curves in Root Disease
2.8 Tests for Independent Action of Spores
2.9 The Use of Logarithms in Disease/Inoculum Studies
2.10 Parameters in Disease/Inoculum Relations
Chapter 3. Effect on Disease of Variable, Limiting Factors Other Than Inoculum
3.1 The Scope of the Chapter
3.2 The Importance of Variation
3.3 Multiple Regression Analysis of Variables
3.4 The Relative Importance of Inoculum and Other Factors
3.5 Temperature and Moisture
3.6 The Interaction of Factors Other than the Amount of Inoculum. The Interaction of the Amount of Inoculum with Other Factors
3.7 Inoculum. Inoculum's Potential. Inoculum Potential
Chapter 4. Epidemics. The Time Dimension
4.1 Time as a Factor and a Dimension: How the Chapters Fit Together
4.2 The Basic Infection Rate R. The Periods of Latency and Infectiousness. Removals
4.3 The Apparent Infection Rate r. The Incubation Period
4.4 The Two Infection Rates Contrasted and Compared. Historic (Memory) Factors
4.5 Historic Factors That Increase the Variance of r. Cryptic Effects of Wavelike Variations. A Failing of Multiple Regression Analysis and a Simple Precaution
4.6 Historic Factors That Reduce the Variance of r. The Principle of Continuity
4.7 Simulation of Epidemics. Epidem and Epimay. Some Conclusions.
4.8 Equations for Infection Rates. Misuse of the Word Logistic
4.9 Continuous and Discontinuous Infection. A Simple Rule for Interchanged Estimates
4.10 The Period of Latency. Some Objections Considered
Chapter 5. When Time is Unimportant. Endemic Disease
5.1 Some Definitions. Endemic Disease of Perennial Tissues. Obligate Parasites Used for Illustration
5.2 Epidemic and Endemic Disease as a Continuum
5.3 An Equation for Timeless Disease
5.4 Loss of Infectiousness. Endemic Disease Likely to Be Underestimated. A Steady State Impossible with Obligate Parasites. Anti-Epidemics. Latent Viruses an Exception
5.5 Endemic Disease and Native Disease. Sporadic Epidemics of Disease Usually Endemic
5.6 The Implications of Endemicity. Horizontal Resistance in the Host Plants. Three Propositions
5.7 Adaptation in the Pathogen to Endemic Disease
5.8 The Rarity of Harmful Virus Infections in Forest Trees
5.9 The Constant Absence of Disease
5.10 Summary: Epidemic Disease, Endemic Disease, and No Disease. Host Population Immunity and Resistance Distinct from Individual Host Plant Immunity and Resistance
Chapter 6. The Spread of Disease. Time and Distance as Dimensions
6.1 The Spread of Disease and the Migration of Pathogens
6.2 Spread a Feature of Epidemic Disease
6.3 The Rate of Multiplication (the Infection Rate) and the Rate of Spread of Disease. Dispersal of Pathogens
6.4 Spread and Dispersal. Effective Dispersal
6.5 Foci of Disease
6.6 Varying Gradients of Dispersal. Migration and Colonization
6.7 The Multiplication and Spread of Phytophthora infestans Seen as Concurrent Processes
6.8 A Correlation between the Infection Rate and the Rate of Spread of Disease
Chapter 7. Genetics of Host-Pathogen Relations
7.1 Introduction
7.2 The Fundamental Classification of Resistance. Differential and Uniform Interactions between Host and Pathogen. Vertical and Horizontal Resistance
7.3 Flor's Gene-for-Gene Hypothesis
7.4 A Second Gene-for-Gene Hypothesis. Gene Identity and Quality
7.5 Potato Blight: The Resistance Genes R1 and R4, and the Frequency of Virulence on Them in Population of Phytophthora infestans
7.6 Wheat Stem Rust: The Resistance Genes Sr5, Sr6, and 5r9d, and the Frequency of Virulence on Them in Populations or Puccinia graminis tritici in Canada
7.7 A Theory of Leaky Mutants and Missense Mutation
7.8 An Essential Postulate. Some Light on Dominance and Allelism
7.9 The Commonness of Weak Resistance Genes
7.10 An Unsolved Geographical Problem
7.11 Four Arbitrary Categories of Adaptation in the Pathogen to the Host. Abundant Preexisting Virulence. Virulence by Adaptation. Restricted Virulence. Fo…