*4.2. Climate Change and the Spread of Pathogens*

Climate change and changes in ecological conditions can promote the spread of pathogens, parasites and diseases, with the potential to seriously affect human health, agriculture and the environment [54–57]. They are one of the important stressors that can contribute to the extinction of many species. The IPCC estimates that 20–30% of plant and animal species assessed so far in climate change studies are at risk of extinction if temperatures reach levels projected at the end of this century [50].

Poland is one of the largest potato producers in the world, and it is one of the key edible and industrial plants. Unfortunately, its yields are almost half of those obtained in other EU countries. The main reasons are as follows: high susceptibility of genetically homogeneous cultivars to *P. infestans* and imperfect protection of plantations against pathogen and climate variability, which is favorable for the development and spread of this pathogen [11,56,57] and the ability to carry infectious material. Andrivon et al. [58] believed that the spores of Ph. infestans can spread to a distance of 70–80 km from the site of infection. Aylor et al. [59] state that the spores of the blight at wind speeds of 20–40 km h−1. They can spread from the site of infection to 80–160 km in 4 h. Moreover, the short infection cycle and the possibility of producing a large amount of infectious material creates favorable conditions for the development of blight, and 100,000 spores can be formed from one pathological lesion on a leaf. Fry [56] estimates the number of sporangia at 300,000 for 3 days, and sporulation may begin as early as one or two days after the onset of symptoms [58]. The amount of yield losses ranges from 30 to 60% [60], 70% [61,62] and 100% [57], and the growth of this pathogen, in the absence of protection, amounts to about 10–50% due to the premature destruction of the tops and 0–40% due to the destruction of tubers [12–14]. Haverkort et al. [63] estimate that, in Europe, the annual expenditure on combating potato blight amounts to EUR 900 million. In the USA, the amount of expenditure on protection against the plague is estimated at USD 3 billion per year. Global conservation costs and crop losses are estimated at USD 6.7 billion [5].

In the conducted research, the group of early varieties related to the resistance of cultivars to this pathogen had the greatest influence on the pace of spreading *P. infestans*. The influence of cultivar-related resistance on these plant health traits is confirmed by the studies of Croxall and Smith [64], Kapsa [61,62], Osowski [15] and Sawicka [12–14]. In Poland, where protection against late blight is carried out only on about 40% of potato plantations, the average yield loss was 20–25%. Losses on unprotected plantations are estimated at 70–80%. There are two phases in the development of late blight: early (hidden) and epidemic. During the first stage, the fungus multiplies, leading to local infections and the growth of primary infectious foci depending on the following: density and location of primary foci, susceptibility of the cultivars to late blight, plant physiological condition, weather conditions and changes in microclimate and ecoclimate [12,14].

The date of the outbreak in Polish conditions is usually June or July and depends mainly on the air temperature and precipitation patterns during the growing season. The development of the disease after reaching the epidemic stage is usually rapid, and usually, after a few or several days, the plants are almost completely destroyed by the plague. The date of the outbreak and the pace of its development determine the reduction in potential potato yields [11,13,15]. Over the past two decades, an increase in the infectivity

of *P. infestans* has been observed, which results from changes in the population of this pathogen. The result of these changes is an earlier onset of more rapid disease development, increased pathogenicity of the fungus, changes in epiphytotic the development of primary *P. infestans* infections and the breaking of genetic resistance of many potato cultivars and the ineffectiveness of traditional methods of plantation protection against the pathogen [17,18]. The increased severity of plague and the losses it causes justify the need to combat it. However, the goal of most potato blight control systems, due to their commercial nature, is a comprehensive plant protection strategy with the recommendation of specific chemical preparations and their dosage, while predicting the timing of an outbreak of *P. infestans* is only auxiliary or even switched off or is established only in case of occurrence through linear models. Almost all decision-making programs were developed on the basis of observations of the development of potato blight in Western Europe, which makes them completely unadjusted to other climatic conditions [2]. Therefore, there is an urgent need to monitor and predict the timing of an outbreak based on meteorological data and/or potato development phases.

Using the method of determining the upper and lower limits of the trait value for groups of varieties significantly different from each other, the cultivars tested were divided into three groups: cultivars with the lowest share of plants with symptoms of potato blight, in which the infection was less than 4%; cultivars with an average share of individuals with symptoms, where the paralysis ranges from 4.1 to 8.0%; and cultivars with a high proportion of plants infected with this pathogen, with an infection rate of > 8%. The late varieties showed the highest resistance to late blight; the lowest resistance was observed in very early and early varieties. It can be assumed that specific defense substances (socalled phytoalexins), which are activators of defense reactions to pathogenic factors, can trigger the trigger mechanism of resistance to plant infection by *P. infestans* in plants. Stark et al. [49] states that the compounds of this type can act as effectors of the expression of the plant resistance genome, as well as activate enzymes, transfer physiological stimuli from membrane receptors to the genome, etc., and, therefore, fulfill the function of the first informants in the pathogenesis and resistance of plants in establishing parasitic contact. The plant tries to preserve the species in this targeted way.
