Many fungi, bacteria, viruses, and nematodes are plant pathogens. A plant pathogen is an organism or agent that incites ifectious disease. A distinct sequence of events occurs in the developement of a plant disease; these events are known as the disease cycle.
This chapter describes basic facts about the disease cycle: development stages of the pathogen and effects of the disease on the host plant. It also discusses pesticide resistance and it's management.
The main events of stages comprising the disease cycle include the following: production and dissemination of the primary inoculum, primary infection, growth and developement of the pathogen, secondary infection, and overwintering.
The primary inoculum is the part of the pathogen (that is, bacterial or fungal spores or fungal mycelium) that overwinters (over-seasons) and causes the first infection of the season, known as primary infection. An example of primary inoculum is the cells of the fire blight bacterium, Erwinia amylovora, that overwinter in infected bark tissue along the margins of cankers. In spring, the bacteria multiply and are spread by rain or insects to suculent tissue of apples or pears where primary infection occurs. In gerneral, the greater the amount of inoculum and the nearer it is to its host, the greater the potential for a disease epidemic.
Dissemination refers to the spread or dispersal of the pathogen from an inoculum source to a host. Dissemination can occur by wind, splashing rain, insects, infested pruning tools, infected or infested transplants, and other means. Spread can occur over short distances within the tree canopy or from distant sources. For example, conidia of the bitter rot fungus are primarily dispersed by rainwater within the tree canopy, but basidiospores of the cedar apple rust fungus can be carried more than 1/2 mile by the wind. Some pathogens have multiple means of dispersal. Erwinia amylovora can be spread by rain, wind, insects, and infested pruning equipment.
Primary infection occurs when the pathogen comes into contact with a susceptible host under favorable environmental conditions. Pathogens penentrate the surface of a plant directly or enter through wounds or natural openings. The bitter rot fungi, Colletotrichum spp., generally penetrate the apple fruit directly whereas the white rot fungus, Botryosphaeria dothidea, enters through cracks in the cuticle or through lenticels on healthy twigs. Most fungal and bacterial pathogens require free water for spore germination; consequently, infection is favored by prolonged warm, wet periods with high relative humidity.
Growth and development of a pathogen usually occurs on or within infected plant tissue. Fungi grow and spread within their host by means of mycelium. Most fungi produce spore-producing structures such as pycnidia or perithecia on or within infected tissue. These structures give rise to secondary inoculum which eventually causes additional, or secondary, infections during the season. Bacteria spread by rapidly increasing in numbers. Spread of bacterial cells usually occurs when fissures or cracks develop on infected tissue exposing the cells (secondary inoculum) to the environment. Each pathogen has it's own optimal conditions for growth and development which usually coincide with optimal condition for infection.
Secondary infection results from spores or cells produced following primary infection or from other secondary infections. The secondary infection cycle can be repeated many times during the growing season. The number of cycles is dependent on the biology of the pathogen and its host and the duration of environmental conditions needed for infection. Apple powdery mildew, caused by the fungus Podoshpaera leucotricha, passes through many secondary cycles during the growing season until terminal buds set wheras cedar apple rust has no secondary cycle. Erwinia amylovora continues to cause infection as long as young succulent growth is available and warm, wet, and humid conditions prevail.
Overwintering or overseasoning is the ability of a pathogen to surivive from one growing season to the next. Pathogens of apple survive the winter in a number of different ways. The fire blight bacterium overwinters in infected branch and trunk cankers. Verturia inaequalis, cause of apple scab, Mycosphaerella pomi, cause of Brooks spot, and Alternaraia mali, cause of Alternaria blotch, survive from one season to the next in leaves on the orchard floor. Botryoshpaeria dothidea, cause of white rot, overwinters in dead wood in the tree and on the ground and in mummied apples in the tree. Gymnosporangium jumiperi-virginianae, cause of cedar apples rust, survives as a parasite of cedar trees, its alternate host.
For a plant disease to occur, a susceptible host, a pathogen (casual agent), and favorable environmental conditions must be preseint and interact with one another. If any one of these requirements is not met, a plant disease will not occur. At present, our ability to manipulate the environment is limited to only a few practices such as pruning to promote drying, bedding to improve soil drainage, and scheduling of irrigation. Severe disease outbreaks can be prevented by manipulating the host -- through the use of resistant cultivars -- and the pathogen -- through cultural practices and fungicidal or bactericidal sprays.
Edward J. Sikora
Resistance of plant pathogens to pesticides was not a widespread concern until the early 1970s. Prior to that time most of the fungicides used were broad spectrum protectants that affected multiple sites within the target fungi. However, in the late 1960s, fungicides were developed that had systemic activity and could control some fungi after infection occurred. These fungicides had specific sites of action and resistant populations of fungi developed, causing diseases on many crop plants. The selection and subsequent increase of resistant forms of the pathogens occurred similarly to that described previously for arthropods. (See Chapter 1, Pesticide Resistance And Its Management.)
So far, resistance has become a problem in the United States to only two pathogens that affect apples during the growing season: Venturia inaequalis, cause of apple scab, and Erwinia amylovora, cause of fire blight.
Resistance of V. inaequalis to the benzimidazole fungicides became widespread in the mid and late 1970s throughout the Southeast. Consequently, the benzimidazole fungicides are no longer recommended for apple scab control in most southeastern states. Resistance of V. inaequalis to dodine has been reported from several northern apple producing states but has not been reported from the Southeast. Similarly, there have been reports from other countries of the world concerning resistance of V. inaequalis to the demelthylation inhibiting fungicides (DMI fungicides), but resistance has not been reported in the United States. Resistance of the fire blight bacterium, E. amylovora, to streptomycin has been reported from California, Michigan, and several other states, but not in the Southeast.
Several strategies are available for minimizing the likelihood of resistance development. These strategies involve reducing the selection pressure on the pathogen in one of several ways: by minimizing the use of a particular pesticide or by combining it with another pesticide, which has a different mode of action and broad-spectrum activity .
To avoid the development of dodine resistance, limit dodine use to two or three applications a year. In areas of the United States where dodine resistance is a problem, dodine was often used ten to twelve times through the growing season. Historically in the Southeast, dodine has been used only two to four times, early in the season. A similar strategy should be used to avoid resistance to streptomycin. Applications of streptomycin should be made only when needed during periods favorable for infections. (See Chapter 5, Fruit and Foliar Disease, Fire Blight.) To avoid development of resistance to the DMI fungicides, apply these fungicides only in combination with a broad spectrum, protectant fungicide such as captan or the EBDC fungicides (metiram or mancozeb).
Turner Sutton