Plant Pathology and Plant Pathogens. John A. Lucas

Figure 2.6 Relationships between host, pathogen, and disease reaction.

      In some instances, (see Chapter 9), pathogens penetrate their host only to be immediately prevented from further colonization by the death of the first living cells they enter. Such restricted development indicates that the host is resistant to the pathogen. Resistance, unlike immunity, is not an all‐or‐nothing property of the host. In practice, there may be a whole range of responses, varying from high resistance, where no visible symptoms are manifest, to low resistance, where the host succumbs completely to disease. Between these two extremes, resistance is described by a number of adjectives which, though imprecise, are of practical use in distinguishing between host reaction types.

      Alternatively, differing degrees of pathogen development may be described in terms of host susceptibility (Figure 2.6). For each degree of resistance, there is a corresponding level of susceptibility. For instance, high resistance is equivalent to low susceptibility. Complete susceptibility is of considerable biological interest, as it appears to constitute the exception to the general rule that plants exhibit a degree of resistance. However, in this book these complementary descriptions of host responses are mainly considered in terms of resistance. This approach has significant practical advantages in that it emphasizes the character which is selected for by plant breeders (see Chapter 12).

      The terms resistance and susceptibility describe conditions of the host. However, just as the host may vary in its ability to resist infection, so pathogens differ in their ability to invade and cause disease. Those microorganisms which cannot under normal circumstances induce disease in a host are regarded as nonpathogenic with respect to that host. Others which are able to penetrate but which have insignificant effects on the host may be termed avirulent; where the effects are more drastic, they are described as possessing some degree of virulence.

      It should be noted that there are still some problems with this terminology. In clinical microbiology, a distinction was originally drawn between nonpathogenic and pathogenic microorganisms. Pathogenicity was considered to be an absolute property. Virulence was used to describe differences in the extent to which different strains of a pathogen caused disease. These clear‐cut distinctions are valid for some pathogenic species, but it is now appreciated that the situation is more complex. Many microorganisms have the ability to acquire or lose traits which have a major effect on disease reaction type.

Ultimately, the phenomenon of pathogenicity needs to be analyzed in genetic terms, and the differences between species, strains, and pathotypes described in terms of the molecular interactions determining the disease phenotype. Avirulence, for instance, has a more precise meaning associated with the presence in the pathogen of a specific gene encoding a product which can be recognized by the plant, hence triggering resistance (see later in this chapter and Chapter 9). Hence some authors prefer to use the term aggressiveness to describe differences between pathogen strains in the amount of disease they cause in the host. Aggressiveness can only be measured under carefully controlled conditions where each pathogen strain is inoculated onto a defined host genotype in the same environment, allowing quantification of a range of different parameters (Table 2.2). Change in the aggressiveness of a pathogen is sometimes an important factor in the emergence of new invasive strains or increases in the severity of disease epidemics. For instance, the recent spread of yellow rust (Puccinia striiformis) to new regions has been linked to the appearance of strains with a more rapid disease cycle, greater production of spores, and the ability to cause epidemics under warmer conditions than those favored by previous strains.

Table 2.2 Some parameters used to measure aggressiveness

Length of latent period (time from inoculation to production of new inoculum)

Rate of multiplication of the pathogen in host tissues (used for bacteria and viruses)

Rate of lesion expansion

Number of lesions produced per amount of initial inoculum

Eventual lesion size or extent of host tissue infected

Number of spores or cells produced per unit area of host tissue

      Genetic Control of Resistance and Virulence

      In common with all other biological characteristics, host resistance and pathogen virulence are genetically determined. However, these two properties can only be assessed in the presence of the other partner. In the majority of cases, host resistance or pathogen virulence are not obviously correlated with other phenotypic characters. Features of the pathogen, such as rapid and extensive growth or the production of cell wall‐degrading enzymes, may or may not be related to virulence. Assessments of resistance and virulence are therefore based on disease reaction types. An interaction where symptoms are clearly expressed is described as a compatible disease reaction as opposed to an incompatible reaction where symptoms do not develop and the effect on the plant is minimal (Figure 2.6).

      Host resistance is controlled by one or a few genes whose individual effects may be easily detected, or by a multiplicity of genes, each of which contributes only a small fraction of the property as a whole. The practical implications of this are described in more detail in Chapter 12. In a few instances, disease reaction type has been shown to be controlled by factors inherited through the host's cytoplasm. The best‐known example of such cytoplasmic inheritance involves the reaction of maize to the leaf blight fungus Bipolaris maydis. In the past, the production of hybrid maize has involved the laborious task of detasselling by hand to avoid self‐pollination occurring. The discovery of a cytoplasmically inherited mitochondrial factor for male sterility (Cms), which meant that cross‐pollination was essential, removed the need for this operation. Because of this, cultivars possessing Cms came to predominate throughout the USA. Unfortunately, Cms was also correlated with susceptibility to a particular strain (race T) of B. maydis. As a result, the occurrence in 1970 of favorable conditions for the development of the pathogen resulted in a disastrous epidemic (see Chapter 5, Figure 5.1). In any breeding program, the possibility that the cytoplasm may be important in disease resistance must therefore be considered.

Although pathogen virulence, host resistance, and disease reaction types are genetically determined, the environment may modify the expression of any of these characters. For example, the Sr6 gene conferring resistance in wheat to black stem rust is effective at 20 °C, but is inoperative at 25 °C.

      Gene‐for‐Gene Theory

      From an evolutionary viewpoint, it is predictable that genetic systems determining virulence in the pathogen will be paralleled by genes conferring resistance in the host. This is because any mutation to virulence in a pathogen population will be countered by the selection of hosts able to resist this more aggressive pathogen. Evolutionary biologists describe such a dynamic process of complementary changes as an “arms race.” Thus, in an ideal world we might envisage a perpetual stalemate, with host and pathogen populations being closely matched in resistance and virulence. Hence over a period of several years disease would be neither completely absent nor would it