The pathogens evolve virulence activities to retain the ability to infect, multiply in host plant and cause disease to which plant evolve new way to detect and combat defense attack. The virulence is the property of pathogens. Evolution of pathogen emerge from increased contact with their host. The common definition of virulence is the reduction in host fitness due to infection (Salvaudon et al., 2007). The evolution of more virulent pathogen is understood to be limited by the tradeoff between within- host-growth rate and transmissibility (Kubinak and Potts 2013). Sacristan and Garcia-Arenal (2008) define virulence as the degree of damage caused to a host by parasite infection, assumed to be negatively correlated with host fitness and pathogenicity as the qualitative capacity of parasite to infect and cause disease on a host. The transmission increased with increasing virulence among different host-parasite combination, as assumed by most models of evolution of virulence (Salvaudon et al., 2005). However, there was no general relationship between parasite and host fitness, estimated respectively such as transmission and seed production (Salvaudon et al., 2005). The factors that influence the evolution of virulence in plant pathogens are a) linkage between virulence and pathogen fitness, b) availability of alternative hosts and c) ability to reproduce on the dead plant material or produce long-term survival structures (e.g. oospore and chlamydospore produced by many Phytophthora species) (Parker and Gilbert 2004).
Pathogens evolving novel virulence activity is defined as anything that increases pathogen fitness with the consequence of causing disease in qualitative or quantitative sense including adaptation of pathogens to host immunity and physiology, host species, genotype or tissue or the environment (Sacristan et al., 2021). A non-virulent pathogen in an incompatible interaction do not infect and colonize plant hence no plant disease development. Whereas a virulent pathogen in a compatible (susceptible) interaction is not recognized by the host plant, even when the pathogen harbors an avirulence gene, the pathogen is successful in infecting a plant (Surico 2013). Novel plant-pathogen interaction occurs when a pathogen or plant species are introduced to regions outside the native range. Then for the pathogen to acquire a new host will depends on the genetic compatibility between the two, through either preadaptation of the pathogen or subsequent evolutionary change (Parker and Gilbert 2004).
Spread of disease depends on pathogens virulence, plant resistance mechanism and favorable environment. Parasites and pathogens should evolve reduced virulence to their host, because more virulent parasites and pathogens are more likely to drive their hosts and themselves to extinction (Lenski and May 1994). So, virulence can be linked to within-host multiplication, which is an element of pathogen fitness and would be a selectable trait. Another element of pathogen fitness is high virulence which will result in host mortality and morbidity, and this will negatively affect between-host transmission. Hence virulence results in trade-offs between within-host multiplication and between host transmission, the basis of so-called trade-off hypothesis (Sacristan and Garcia-Arenal 2008).
Plant can respond to infection through resistance (plants ability to control pathogen multiplication) or tolerance (plants ability to reduce effect of infection on its fitness regardless of level pathogen multiplication) (Pagan and Garcia-Arenal 2018). Fungal and bacterial pathogen when exposed to a resistant hosts evolve races that can overcome resistance (Dimond 1969). Van der Plank concept of two kind of resistance: vertical resistance and horizontal resistance. Vertical resistance is based on a few specific genes and horizontal resistance is based on many, the action of which may be indirect (Dimond 1969). In horizontal resistance plants are often disease-tolerant rather than hypersensitive and may successfully survive epidemic-favoring conditions (Dimond 1969).
Large fraction of plant pathogens are generalists, which can infect and multiply in wide range of host species belonging to different taxa, even to different kingdoms, whereas others referred to as specialists establish an intimate relationship with only a single-host species (Sacristan and Garcia-Arenal 2008; Baumler and Fang 2013). A generalist strategy provides the parasite with more opportunities for transmission and survival, but it is predicted that evolution would favor specialism: different hosts represent different selective environments and parasite-host coevolution could result in functional trade-off that would limit the generalist fitness in any one host (Woolhouse et al. 2001; Sacristan and Garcia-Arenal 2008).
It may be expected that evolution may favor pathogens that are more infectious or less lethal, everything else being equal (Kirchner and Roy 2002). These assumptions are borne, when genetic specificity of pathogen infection is low: though selection favors pathogen strains with higher intrinsic fitness (reproduction rate times longevity in the host). At higher degree of host-pathogen specificity, selection for these traits nullify or even reversed by the host-pathogen feedback (Kirchner and Roy 2002). The two components of pathogen virulence: a pathogen’s aggressiveness in transmitting itself from one host to another, is termed as infectiousness and the severity of its impact on host life span its termed as lethality. A pathogen that is more infectious will transmit itself more rapidly from one host to another and the one that is more lethal will kill host rapidly (Kirchner and Roy 2002). Host pathogen specificity means that an individual pathogen strain will be more infectious to some host strains than others and that other pathogen strain will exhibit different pattern of infectiousness across the different host strains (Kirchner and Roy 2002). The outcome of infection varies with plant resistance and tolerance to infection (Barrett et al., 2009).
Infectiousness is the ability to propagate from one host to another. Pathogen that can transmit themselves readily from one host to another has reproductive advantage. When host-pathogen specificity is high enough, the host-pathogen feedback regulates pathogen trait frequencies. High infectiousness will be disadvantageous for pathogen because it will put their preferred hosts at a competitive dis-advantage with other host strains. Thus, difference in specificity can reverse the direction of selection for pathogen virulence (Kirchner and Roy 2002).
Virulence is the measure of pathogenicity of an organism, and the degree of virulence is directly related to the ability of the pathogen to cause disease despite host resistance mechanisms (Peterson 1996). Whereas a virulence factor is microbial component that can damage a susceptible host (Casadevall and Pirofski 2009).
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