Environmentally Safe Approaches to Crop Disease Control

Jack E. Rechcigl

• Publisher: CRC Press
• Year: 2018
• ISBN:
  9781351088725
• Edition: 1
• Topic: Biological Sciences
• Subtopic: Biology
• Index: Biological Sciences

The use of chemicals in agriculture and home gardens has become an area of concern due to improper use and negative environmental effects. Environmentally Safe Approaches to Crop Disease Control addresses alternative approaches for managing crop diseases. It gives a balanced overview of state-of-the-art environmentally safe approaches to crop disease control and discusses the latest trends.

Part I
Environmental Aspects

CHAPTER 1

The Influence of Environment on the Development and Control of Disease

H. Alastair McCartney

• I. Introduction
• II. The Pathogen and Environment
• III. The Crop Environment
  • A. Crop Architecture
  • B. Temperature
  • C. Wind
  • D. Humidity
  • E. Wetness
    • 1. Rain (Irrigation)
    • 2. Dew
    • 3. Guttation
    • 4. Measurement of Leaf Wetness Duration
• F. Estimating Crop Microclimate
• IV. Environment and Disease Control
  • A. Passive Measures
  • B. Active Measures
• V. Conclusions
• References

I. Introduction

Crop disease epidemics are the result of the complex interaction between the pathogen (or pathogens), the host, and its environment. What is meant by “environment” in the context of disease epidemiology? Environmental factors can have either a direct effect on the pathogen, for example, many fungal spores need water to germinate, or an indirect effect through their influence on the physiological status of the crop. For soil-borne pathogens the physical and chemical nature of the soil is obviously of paramount importance, but for foliar pathogens the microclimate of the crop plays the dominant role through its effect on leaf surfaces. When considering the dispersal of pathogens we may need to include the atmosphere near the ground in our definition of the appropriate “environment.” In the rest of this chapter the definition of “environment” will usually be restricted to that which has direct effects on pathogen development.

Since the Second World War crop disease in Western agriculture has largely been controlled with fungicides, pesticides, etc. Over the last few years there has been increasing pressure to reduce the use of phytochemicals in agriculture, both from environmentalists and from governments, for example, in Scandinavia and in Holland the aim is to halve their use by the year 2000. There are several reasons for this. Fungicides are perceived to be dangerous for human health either through direct exposure (during application or by spray drift) or through residues in drinking water or food. Thus, for high-value food products there is a demand for low levels of fungicide and pesticide residues and, as detection instrumentation sensitivity increases, the acceptable levels will continue to decrease. Since 1975 the European Union has issued several directives on the reduction of pesticide levels in drinking water (Regulations 75-440/EEC, 79-869/EEC, and 80-778/EEC). Intensive use of phytochemicals is considered to be detrimental to the environment. Pimentel et al. (1991) estimated that in the U.S. the costs of indirect damage due to long-term environmental pollution from agriculture was approximately $10⁹ (U.S.). In Europe, where intensive farming is common, the costs are probably at least equal to if not greater than this. The environmental consequences of phytochemical use include adverse effects on nontarget organisms including beneficial fungi pathogenic to insects; direct and indirect effects on insects, fish, and mammals; subtle perturbations on natural ecosystems; and the development of resistant strains of pathogenic organisms. The pressure to reduce the use of phytochemicals, particularly in the U.S. and Europe, is likely to intensify toward the end of the millennium.

The best way to control disease in crops is to eliminate the disease by growing resistant cultivars. A significant proportion of the effort of plant breeders is devoted to developing disease resistance in crops; but even with the advent of new molecular genetic techniques, it is likely that for the foreseeable future crop protection will still rely heavily on the use of phytochemicals. Thus, crop protection strategies need to be developed which minimize the use of phytochemicals while maintaining acceptable economic returns for the farmer. This means either the development of novel control measures, for example, based on biological control, or more efficient use of control chemicals. There are several options available for developing such control strategies, each requiring knowledge of the interactions between the pathogen, host, and environment. For example, reduction in phytochemical use can be achieved by applying control measures only at critical times during the development of an epidemic. This requires an understanding of how epidemics develop, including knowledge of the relationship between microclimate and pathogen growth. Alternatively, agronomic practices may be devised based on disease avoidance, for example, by the choice of a sowing date to avoid periods of weather which favor disease development or spread. Knowledge of the interactions between the pathogen and environment may suggest methods of manipulating crop microclimate through breeding or agronomic practice, which reduces the chances of disease. The reduction in phytochemical use could also be achieved by more efficient application of sprays, for example by targeting specific parts of the crop vulnerable to attack. Environmental factors play an important role in spray application and in the retention of spray on crop surfaces.

Although there is usually little we can do to control or manipulate those environmental factors which regulate disease development in crops, except perhaps for protected crops, it is clear that an understanding of how environmental factors affect crop pathogens is essential for the development of effective control strategies. The rest of this chapter will consider the effects of the major microclimate factors on the development of plant pathogens, the crop environment, and how this information can be used to control disease. The chapter will concentrate on foliar diseases caused by fungal pathogens, but the general principles should find applications in other crop/disease systems.

II. The Pathogen and Environment

The physical environment affects all stages in the life cycle of plant pathogens and much of the effort in plant pathological research is devoted to the study of these changes. Temperature and moisture are the two most important microclimatic factors in the direct interaction of host and pathogen, although radiation (light) can have also have an influence, while wind and rain play dominant roles in dispersal processes (including dispersal by insect vectors). The exact relationship between the pathogen and environmental parameters differs for each pathogen/host system and a comprehensive summary would fill several volumes. This section will illustrate some of these interactions, using selected examples taken mainly from foliar fungal pathogens of arable crops.

The interaction between fungal pathogens and host broadly follows three phases: infection, development, and sporulation — each of which may be limited by environmental factors.

Infection usually includes spore germination followed by penetration and invasion of the host tissue. Some spores, referred to as resting spores, remain dormant for a period after their formation (Hawker and Madelin, 1976; Manners, 1982). In some cases, dormancy can be broken in response to environmental cues. For example, alternate wetting and drying or freezing and thawing will stimulate the germination of teliospores of Puccinia graminis, while spores of Tilletia species require exposure to temperatures below 10°C before they will germinate (Manners, 1982). Many spores do not have a dormant period as their function is to propagate the pathogen quickly. Nevertheless, their germination is often mediated by environmental factors. However, it must be remembered that spore germination can be stimulated or inhibited by other factors related to the host and the pathogen (Macko, 1981).

As with all biological functions, spore germination is temperature dependent. For all spores there is a minimum and maximum temperature range, outside of which the spores will not germinate (Table 1). The rate of germination tends to increase to a maximum at an optimum temperature, then decline as the temperature increases. For example, Harthill and Cheah (1984) found that germination of conidia of Pyrenopeziza brassicae on cauliflower (Brassica oleracea) increased almost linearly from 6°C to about 16°C before declining with higher temperatures until ceasing at 26°C; similar results were found by Figueroa et al. (1995a) on oilseed rape (Brassica napus). Rust basidiospore germination usually takes place over a wide range of temperatures, but thermal death occurs in some species at temperatures greater than 30°C (Gold and Mendgen, 1991). Temperature can also affect the rate of penetration of the pathogen into the host. In epidemiology this is often quantified as the incubation period: the time taken between spore inoculation and appearance of visible symptoms (Manners, 1982). The temperature response of incubation periods tends to reflect that for germination, with the shortest periods found near the optimal temperatures for germination. Further development of the pathogen within the host can be quantified, in epidemiological terms, by the latent period: the time between inoculation and the production of spores (Manners, 1982). Both infection and latent periods are influenced by temperature (Table 1). Latent periods tend to decrease with increasing temperature, providing other factors are favorable. For example, the latent period for Erysiphe graminis decreases from about 14 days at 5°C to 3 days at 18 to 25°C, and that for Puccinia hordei decreases from 60 days at 5°C to 6 days at 25°C (Polley and Clarkson, 1978). The effects of temperature on pathogen/host interactions may be moderated by other environmental factors such as light and moisture.

Light can stimulate germination in some fungi and inhibit it others (Leach and Anderson, 1982), but the mechanisms are poorly understood. Most basidiospores are released at night or early morning; however, darkness is not necessary for germination and when other conditions are favorable light has either no effect or a marginal negative effect (Gold and Mendgen, 1991). The effects of light on germination can be complex: for example, germ-tube elongation of Alernaria linicola conidia on linseed under wet conditions was interrupted by exposure to light periods of up to 12 h immediately after inoculation, but resumed on return to darkness (Vloutoglou et al., 1996). However, if the light period started 6 h after inoculation germ-tube elongation was unaffected, suggesting that the germ-tubes had started penetration and were no longer sensitive to light. Similarly, exposure to light reduced the probability of infection of wheat leaves by Mycosphaerella graminicols (Septoria tritici) early in the infection process but stimulated it later (Shaw, 1991). Schuh (1993) found that 12 h dark/12 h light was more conducive to germination of Cercospora kikuchii on soybean than, in descending order, 24 h dark or 12 h light/12 h dark or 24 h light. The importance of light on the development of epidemics in the field has been little studied and is poorly understood.

Moisture is probably the most crucial environmental parameter affecting spore germination and infection of fungal pathogens. Most fungal spores require high relative humidities to germinate and some need the presence of free water (Polley and Clarkson, 1978). The presence of free water inhibits the germination of Erysiphe graminis, and is generally inhibitory to basidiospores or leads to the formation of secondary basidiospores (Gold and Mendgen, 1991). The duration of wetness needed to promote germination and infection is usually dependent on temperature (Grove et al., 1985) to greater than 100 h (Diaporthephaseolorum on soybean, Damicone et al., 1987) have been reported. Huber and Gillespie (1992) list the wetness requirements for a number of foliar pathogens from studies done between 1985 and 1991. In some fungal pathogens which require free water for germination and infection, discontinuous wet periods will still initiate infection (Stuckey and Zadoks, 1989; Chakrabortry et al., 1990), and in recent years there has been an increasing interest in the effects of intermittent wetness on infection and sporulation processes (e.g., Shaw, 1991; Mridha and Wheeler, 1993; Schuh, 1993; Sah, 1994; Butler et al., 1994; Wadia and Butler, 1994b; Hong and Fitt, 1995; Vallavieille-Pope et al., 1995; Vloutoglou et al., 1996). Intermittent wet periods can reduce the efficiency of infection; for example, fewer Pyrenophora tritici-repentis lesions developed on wheat plants exposed to different periods of dryness after an initial 6-h wetness than on plants exposed to continuous 24-h wetness (Sah, 1994). Butler et al. (1994) found that intermittent wetness enhanced infection efficiency of Phaeoisariopsis personata in groundnut (Arachis hypogaea) compared to continuous wetness. Intermittent wetness produced more germ-tubes per conidium and increased branching, which may have increased the chances of stomatal penetration (Wadia and Butler, 1994b). Interruption of wetness also enhanced infection of soybean by Cercospora kikuchii, but only when the relative humidity during the dry period was >95% (Schuh, 1993). There are suggestions that for some pathogens wetness periods may be partially cumulative (Stuckey and Zadoks, 1989; Wadia and Butler,...