P P – 3 1 0 ( T ) 3 ( 2 – 1 )
Diseases
Epidemiology
Plant Disease
Epidemiology –
An Introduction
Epidemics
 When a pathogen spreads to and affects many
individuals within a population over a relatively large
area and within a relatively short time, the
phenomenon is called an epidemic
 Any increase of disease in a population
 the dynamics of change in plant disease in time and
space
Endemic
 When a disease is more or less constantly occurring
year after year in a moderate to severe form in a
country or locality then it is called as endemic disease.
 e.g.: wart disease of potato (Synchytrium
endobioticum) is endemic in Darjeeling, citrus canker
(Xanthomonas axonopodis pv citri)in Asia and
sorghum rust (Puccinia purpurea).
Pandemic
 When an epidemic disease spreads over continents or
subcontinents and involves mass mortality it is
considered as pandemic.
 The outbreak of black stem rust of wheat in India
during 1947 is best example for a pandemic disease.
Sporadic
 Diseases which occur at irregular intervals over limited
areas or locations are called sporadic.
 They occur relatively in few instances.
 e.g.: Fusarium wilt of cotton (Fusarium oxysporum f
sp. vasiinfectum) grain smut of sorghum (Sporisorium
sorghi ) and loose smut of wheat (Ustilago nuda).
Course of Epidemic
 Two phases
 Progressively destructive phase
 The decline phase
Epidemic types
 Slow epidemic (Tardive epidemic)
 Occurs in monocyclic diseases
 On perennial plants
 E.g. citrus tristeza; Dutch elm disease
 Fast epidemic (Explosive epidemic)
 In polycyclic diseases
 Annual crops
 E.g. rice blast, potato blight
Epidemiology
 Epidemiology can be defined as the study of population of
pathogen in the population of host and the resulting disease
under the influence of environmental and human factors
 The study of epidemics and of the factors that influence
them
 Epidemiology is concerned simultaneously
 Populations of pathogens
 Host plants
 Environment
 These three can be depicted in the form of a disease triangle
Disease Triangle
Epidemics of past
 The Irish potato famine of 1845–1846 was caused by
the Phytophthora late blight epidemic of potato,
 The Bengal famine of 1943 was caused by the
Cochliobolus (Helminthosporium) brown spot
epidemic of rice.
Elements of an Epidemic
 In fungal & bacterial diseases:
 The susceptible Host
 The virulent Pathogen
 favorable environmental conditions
 Human activity
 These four can be depicted in the form of a disease
tetrahedron
 In virus & virus like diseases
 The Virus
 The Host
 The Vector
 Environment
The disease tetrahedron.
Factors Effecting The
Development of
Disease Epidemic
 Host Factors
 Pathogen Factors
 Environmental Factors
 Effect of Human Cultural Practices and Control
Measures (Human Activities)
 Time factors
Factors
Schematic diagram of the interrelationships of
the factors involved in plant disease epidemics.
Host Factors
 Level of genetic resistance or susceptibility of host
 Degree of Genetic Uniformity of Host Plants
 Type of Crop
 Age of Host Plants
 Population Density and Structure
 General Plant Health
 Introduction of New Host
 Introduction of New Alternate Host
Level of Genetic Resistance or Susceptibility of
Host
 Highly resistant.
 Moderately resistant.
 Susceptible.
 Vertical resistance.(Monogenic, Host specific).
 Horizontal resistance.(Polygenic, More durable).
Development of Cylindrocladium black rot, caused by the fungus C.
crotalariae, on susceptible (Florigiant), resistant (NC3033), and
intermediate peanut varieties. The various genotypes maintain their
resistance rankings in both years (1986, 1987) and at all inoculum
density levels tested. [From Culbreath et al. (1991).]
Degree of Genetic Uniformity of Host Plant
 Monoculture (more likely hood).
 New strains are developed.
 e.g. Cochliobolus blight on Victoria oats,
 And in southern corn leaf blight on corn carrying Texas male
sterile cytoplasm.
 Rate of epidemic in response of genetic uniformity (Vegetative
grafting, self pollinated, cross pollinated hosts)
Types of Crops
 Annual crops.
 Biennial
 Perennial crops.
 Annual crops & foliar or fruits diseases develop much more
rapidly (in weeks).
 Perennial woody diseases take longer time to develop (in
years)
Age of Host Plant
 Plants change it resistance and susceptibility with age.
 Some plants are susceptible only during growth period & become
resistant during mature period.
 The change of resistance with age is known as ontogenic resistance.
 Pythium damping off and root rots, downy mildews, peach leaf curl,
systemic smuts, rusts, bacterial blights, and viral infections, the
hosts (or their parts) are susceptible only during the growth period
and become resistant during the adult period (adult resistance)
Change of susceptibility of plant parts with age
Change of susceptibility of plant parts with age.
 In pattern I, plants are susceptible only in the stages of
maximum growth (Ia) or in the earliest stages of growth (Ib).
 In pattern II, plants are susceptible only after they reach
maturity, and susceptibility increases with senescence.
 In pattern III, plants are susceptible while very young and
again after they reach maturity.
Effect of crop age on rate of infection. Cassava plantings of different ages
exposed to the whitefly-transmitted African cassava mosaic geminivirus
show increased resistance to infection as they age. [From Fargette and
Vie (1994). Phytopathology 84, 378–382.]
Population Density and Structure
 A Large Number of Host to the Pathogen
 A Large Area to Reproduce
General Plant Health
Introduction of Alternate Host
• Weaker the plant disease will be more
• Source of Primary Inoculum to the Next Crop
• Determine the Course and Intensity of an Epidemic
Pathogen Factors
 Presence of Pathogen
 Levels of Virulence
 Quantity of Inoculums Near Hosts
 Type of Reproduction of The Pathogen
 Ecology of The Pathogen
 Mode of Spread of the Pathogen
 Introduction of New Pathogen
 High birth and Low Death rate
 Adaptability
Levels of Virulence
 Highly aggressive
 High level of virulence more inoculum
 Disease epidemic faster
 Phytopthora infestans cause late blight of potatoes
 Moderately aggressive (disease spread moderately)
 Poorly aggressive
 Lesser inoculum
 disease spread in several years
 Xanthomonas axonopodis cause citrus canker
Quantity of Inoculums Near Hosts
 Greater the number of propagules greater will be the
rate of disease
 Greater the inoculum greater will be the disease
 Inoculum is less in quantity then the disease never
occurs
Effect of amount of soil
inoculum of Verticillium
dahliae on the amount of
vascular wilt on potato
plants at various dates
after planting. Disease is
expressed as a percentage
of stems (A)
and of main vascular
bundles (B) infected at the
base of the plants. , no
pathogen detected; , 1–5
propagules per gram (ppg);
, 6–10 ppg; and , more than
10 ppg. [From Nicot and
Rouse (1987).
Phytopathology 77, 1346–
1355.]
Type of Reproduction of The Pathogen
 Based on reproductive cycle
 Polycyclic
 Cause severe epidemics
 Produce many generations in a single growing season
 More inoculum production
 Monocyclic
 Takes many of years to develop in epidemic form (polyetic)
 Produce only one generation in a year
 complete only one life cycle in one year or growing season
 Based on type of reproduction
 Sexual (oospores, ascospores)
 Asexual (conidia, zoospores)
Schematic representation of a polyetic epidemic caused in a crop in a
field by a soil pathogen over a 4-year period.
Ecology of The Pathogen
Depends on the type of pathogen
 Ectoparasites
 Inoculum produce on the aerial parts of the host.
 Spores and seeds disperse with ease over a range of distances and
cause epidemics.
 Endoparasites
 Pathogen can be systemic in nature produce inoculum in the
system of host
 Spread of pathogen is rare without vectors
Mode of Spread of the Pathogen
 Survival Efficiency
 Air-borne
 Soil-borne
 Vector-borne
 Dispersal Efficiency
 Passive dispersal (may be in Km)
 Field tools and instruments
 Air
 Wind
 Irrigation Water
 Soil (etc)
 Active dispersal (may be in cm)
Lettuce heads infected by soil borne sclerotia of Sclerotinia
sclerotiorum
Large field of lettuce heads killed by infections with airborne
ascospores of the same fungus
Environmental Factors
 Aerial environment
 Edaphic Environment
 Some other factors
 Wind
 Air pollution
 Herbicide damage
Aerial environment
 Temperature
 Affects disease cycles of pathogens
 Can prolonged or shorten the disease cycle
 Moisture(Dominant factor in diseases caused by
oomycetes, fungi, bacteria & nematodes)
 Rainfall (duration and intensity)
 Dew (duration and intensity)
 Leaf wetness period
Edaphic Environment
 Concern with soil environment
 Soil temperature
 Soil pH
 Soil water content
 Soil fertility
 Soil organic matter content
Human Activities
 Have direct or indirect effect on disease epidemics.
 Favorable and unfavorable for disease epidemic
 Some of them are:
 Site selection and preparation.
 Selection of propagative material.
 Culture practices.
 Disease control measures.
 Introduction of new pathogen.
Site Selection and Preparation
 The following types of soil or fields are favorable for the
development of epidemics;
 Low lying soil.
 Poorly drained soil.
 Poorly aerated field.
 Field near the infected field
Selection of Propagative Material
 Diseased propagative materials
 Use of infected seed
 Infected nursery stock
 Infected root stock and scion
 Diseased suckers
 Diseased cuttings
Cultural Practices
 Cultural practices that increase the possibility and
severity of epidemics, are:
 Continuous monoculturing.
 Higher degree of uniformity.
 No-till culture.
 Dense planting.
 Overhead irrigation.
 Injury by herbicide application.
 Poor sanitation.
Effect of foliage density on development of Phytophthora infestans
during a period of partly favorable weather (May–June) and of
very favorable weather (November–December).
[From Rotem and Ben-Joseph (1970). Plant Dis. Rep. 54, 768–771.]
Disease Control Measures
 Some practices reduce or eliminate the possibility of an
epidemic, these may be:
 Chemical spray.
 Cultural practices.(Sanitation, Crop rotation etc.)
 Biological control.
 Use of resistant varieties.
 And some other control measures.
 Sometime certain control may develop virulent strain.
 These strain are:
 Either resistant to chemicals.
 Or can overcome the resistant of varieties.
 These control measures are:
 Excessive use of chemicals against pathogens.
 Monoculturing for a long time on large area.
Introduction of New Pathogen
 Possibility of introducing new pathogen
 Transportation of planting materials (seed, nursery
stock, tubers, cuttings, etc) and agricultural goods.
 Inability to produce resistance against new
pathogen.(Dainge in case of human)
 Pathogens cause severe epidemics.
 For example: chestnut blight, Dutch elm disease and
citrus canker caused by Xanthomonas compestris pv.
citri.
Time factors
 Season of the year
 Duration & frequency of favorable temp. & rains
 Appearance of vectors, etc.
Measurement of Plant Disease and Yield Loss
 Disease incidence
 The number of plant units that are diseased in relation to
 The total number of units examined
 Commonly used to measure the spread of a disease
 Disease severity
 The amount of plant tissue that is diseased
 Measured using assessment scales or by determining the
 Area under a disease progress curve (AUDPC)
 Yield loss
 The proportion of yield that the grower will not be able to
 harvest due to disease
 Results in economic loss
Pattern of Epidemics
 Interactions among the elements of epidemics, as
influenced over time by factors of the environment and
by human interference, are expressed in patterns and
rates.
 Disease-progress curve
 Disease-gradient or dispersal curve
Disease–progress Curve
 The progress of an epidemic measured in terms of the
numbers of lesions/ the amount of diseased tissue, or
the numbers of diseased plants plotted over time is
called the disease–progress curve
 Shows the progress of an epidemic over time, e.g.,
numbers of lesions, numbers of diseased plants, etc.
 Also allows disease forecasting & selection of the best
control strategy for the particular disease & time
Disease–progress Curve
 Basic epidemic patterns
 Saturation type of curve
Three monocyclic diseases of different epidemic rates.
 Sigmoid curve
Polycyclic disease, such as late blight of potato.
 Bimodal curve
polycyclic disease, such as apple scab, in which the
blossoms and the fruit are infected at different, separate
times.
Schematic diagrams of disease–progress curves of some basic
epidemic patterns
Three monocyclic diseases of different epidemic rates
Schematic diagrams of disease–progress curves of some basic
epidemic patterns
Polycyclic disease, such as late blight of potato
Schematic diagrams of disease–progress curves of some basic
epidemic patterns
Bimodal polycyclic disease, such as brown rot of stone fruits, in which
the blossoms and the fruit are infected at different, separate times
Disease-gradient or dispersal curve
 The progress of an epidemic measured in terms of changes
in the number of lesions/ the amount of diseased tissue,
and the number of diseased plants as it spreads over
distance, is called disease gradient curve (spatial pattern)
 Disease–gradient curve: The percentage of disease and the
scale for distance vary with the type of pathogen or its
method of dispersal
 Being small for soil borne pathogens or vectors and
 Larger for airborne pathogens
 The amount of disease is greater near the source of
inoculum
 The amount of disease decreases with increasing distance
from the source
Schematic diagram of a disease–gradient curve. The percentage of
disease and the scale for distance vary with the type of pathogen or its
method of dispersal, being small for soil borne pathogens or vectors and
larger for airborne pathogens
Epidemic Rate Curves of Diseases
With a symmetrical epidemic rate
Epidemic Rate Curves of Diseases
With a high epidemic rate early in the season
Epidemic Rate Curves of Diseases
With a high epidemic rate late in the
season
Development of Epidemics
 For epidemic, specific combination of environmental
factors must occur constantly or repeatedly, and at
frequent interval over a large area.
 Epidemics occurs only when the combination of right
sets of condition occurs i.e. include
 Temperature
 Moisture
 Wind
 Insect vectors with susceptible stage of plant
Epidemics requires
 repeated infection cycles
 Presence of virulent pathogen
 considerable time before a pathogen produces enough
individuals
 set of favorable environmental conditions repeatedly
 Large area under genetically uniform crop
Development of Epidemics
 The most favorable combinations of conditions for
disease development do not occur very often over very
large areas
 Spectacular plant disease epidemics that destroy crops
over large areas are relatively rare
 However, small epidemics involving the plants in a
field or a valley occur quite frequently
 With many diseases, e.g., potato late blight, apple scab,
and cereal rusts, the environmental conditions seem
usually to be favorable, and disease epidemics would
occur every year were it not for the control measures
Modeling of Plant Disease Epidemics
 An epidemic is a dynamic process. It begins on a few
plants and then increase in severity and spreads over a
larger area.
 It stops when all host plants are killed , become
resistant or harvested.
 For our better understanding and prediction of
development of an epidemic, plant pathologists from
late 1960s have been developing models of common
and serious diseases.
Modeling of Plant Disease Epidemics
 Model?
 Models are generally crude simplifications of real
epidemics, roughly analogous.
 Construction of a model takes into account all the
components and sub-components of plant disease.
 Mathematical models;
 It provides a great information about amount and efficacy of
inoculum , effects of environment, disease resistance of host,
effects of management strategies.
Modeling of Plant Disease Epidemics
 For a model, a database of information is developed.
 Database contains information on:
 Crop
 The disease incidence
 The pathogen
 Location
 Crop canopy
 Rain fall
 Temperature
 Wind velocity
 Vector etc
Forecasting plant disease epidemics
 Being able to forecast plant disease epidemics is stimulating and
also an indication of the success of modeling of particular
disease.
 To develop a plant disease forecast, one must take into account
several characteristics of particular pathogen, host and
environment.
 In monocyclic diseases, disease development may be predicted
by assessing the amount of initial inoculum.
 In polycyclic diseases, disease development can be predicted by
assessing the rate of occurrence of infection cycles.
Forecasting plant disease epidemics
 Some points related to forecasting of plant disease
epidemics
 Disease diagnosis: The key to forecasting of any plant disease.
 Evaluation of epidemic Thresholds.
 Evaluation of Economic Damage Threshold.
 Assessment of Initial Inoculum and of Disease.
 Monitoring Weather Factors That Affect Disease Development
 THANKS 
Prepared by:
Ahsan Abdullah
2011-ag-3149
Plant Pathology

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Plant diseases epidemiology

  • 1. P P – 3 1 0 ( T ) 3 ( 2 – 1 ) Diseases Epidemiology
  • 3. Epidemics  When a pathogen spreads to and affects many individuals within a population over a relatively large area and within a relatively short time, the phenomenon is called an epidemic  Any increase of disease in a population  the dynamics of change in plant disease in time and space
  • 4. Endemic  When a disease is more or less constantly occurring year after year in a moderate to severe form in a country or locality then it is called as endemic disease.  e.g.: wart disease of potato (Synchytrium endobioticum) is endemic in Darjeeling, citrus canker (Xanthomonas axonopodis pv citri)in Asia and sorghum rust (Puccinia purpurea).
  • 5. Pandemic  When an epidemic disease spreads over continents or subcontinents and involves mass mortality it is considered as pandemic.  The outbreak of black stem rust of wheat in India during 1947 is best example for a pandemic disease.
  • 6. Sporadic  Diseases which occur at irregular intervals over limited areas or locations are called sporadic.  They occur relatively in few instances.  e.g.: Fusarium wilt of cotton (Fusarium oxysporum f sp. vasiinfectum) grain smut of sorghum (Sporisorium sorghi ) and loose smut of wheat (Ustilago nuda).
  • 7. Course of Epidemic  Two phases  Progressively destructive phase  The decline phase
  • 8. Epidemic types  Slow epidemic (Tardive epidemic)  Occurs in monocyclic diseases  On perennial plants  E.g. citrus tristeza; Dutch elm disease  Fast epidemic (Explosive epidemic)  In polycyclic diseases  Annual crops  E.g. rice blast, potato blight
  • 9. Epidemiology  Epidemiology can be defined as the study of population of pathogen in the population of host and the resulting disease under the influence of environmental and human factors  The study of epidemics and of the factors that influence them  Epidemiology is concerned simultaneously  Populations of pathogens  Host plants  Environment  These three can be depicted in the form of a disease triangle
  • 11. Epidemics of past  The Irish potato famine of 1845–1846 was caused by the Phytophthora late blight epidemic of potato,  The Bengal famine of 1943 was caused by the Cochliobolus (Helminthosporium) brown spot epidemic of rice.
  • 12. Elements of an Epidemic  In fungal & bacterial diseases:  The susceptible Host  The virulent Pathogen  favorable environmental conditions  Human activity  These four can be depicted in the form of a disease tetrahedron  In virus & virus like diseases  The Virus  The Host  The Vector  Environment
  • 14. Factors Effecting The Development of Disease Epidemic
  • 15.  Host Factors  Pathogen Factors  Environmental Factors  Effect of Human Cultural Practices and Control Measures (Human Activities)  Time factors Factors
  • 16. Schematic diagram of the interrelationships of the factors involved in plant disease epidemics.
  • 17. Host Factors  Level of genetic resistance or susceptibility of host  Degree of Genetic Uniformity of Host Plants  Type of Crop  Age of Host Plants  Population Density and Structure  General Plant Health  Introduction of New Host  Introduction of New Alternate Host
  • 18. Level of Genetic Resistance or Susceptibility of Host  Highly resistant.  Moderately resistant.  Susceptible.  Vertical resistance.(Monogenic, Host specific).  Horizontal resistance.(Polygenic, More durable).
  • 19. Development of Cylindrocladium black rot, caused by the fungus C. crotalariae, on susceptible (Florigiant), resistant (NC3033), and intermediate peanut varieties. The various genotypes maintain their resistance rankings in both years (1986, 1987) and at all inoculum density levels tested. [From Culbreath et al. (1991).]
  • 20. Degree of Genetic Uniformity of Host Plant  Monoculture (more likely hood).  New strains are developed.  e.g. Cochliobolus blight on Victoria oats,  And in southern corn leaf blight on corn carrying Texas male sterile cytoplasm.  Rate of epidemic in response of genetic uniformity (Vegetative grafting, self pollinated, cross pollinated hosts)
  • 21. Types of Crops  Annual crops.  Biennial  Perennial crops.  Annual crops & foliar or fruits diseases develop much more rapidly (in weeks).  Perennial woody diseases take longer time to develop (in years)
  • 22. Age of Host Plant  Plants change it resistance and susceptibility with age.  Some plants are susceptible only during growth period & become resistant during mature period.  The change of resistance with age is known as ontogenic resistance.  Pythium damping off and root rots, downy mildews, peach leaf curl, systemic smuts, rusts, bacterial blights, and viral infections, the hosts (or their parts) are susceptible only during the growth period and become resistant during the adult period (adult resistance)
  • 23. Change of susceptibility of plant parts with age Change of susceptibility of plant parts with age.  In pattern I, plants are susceptible only in the stages of maximum growth (Ia) or in the earliest stages of growth (Ib).  In pattern II, plants are susceptible only after they reach maturity, and susceptibility increases with senescence.  In pattern III, plants are susceptible while very young and again after they reach maturity.
  • 24. Effect of crop age on rate of infection. Cassava plantings of different ages exposed to the whitefly-transmitted African cassava mosaic geminivirus show increased resistance to infection as they age. [From Fargette and Vie (1994). Phytopathology 84, 378–382.]
  • 25. Population Density and Structure  A Large Number of Host to the Pathogen  A Large Area to Reproduce General Plant Health Introduction of Alternate Host • Weaker the plant disease will be more • Source of Primary Inoculum to the Next Crop • Determine the Course and Intensity of an Epidemic
  • 26. Pathogen Factors  Presence of Pathogen  Levels of Virulence  Quantity of Inoculums Near Hosts  Type of Reproduction of The Pathogen  Ecology of The Pathogen  Mode of Spread of the Pathogen  Introduction of New Pathogen  High birth and Low Death rate  Adaptability
  • 27. Levels of Virulence  Highly aggressive  High level of virulence more inoculum  Disease epidemic faster  Phytopthora infestans cause late blight of potatoes  Moderately aggressive (disease spread moderately)  Poorly aggressive  Lesser inoculum  disease spread in several years  Xanthomonas axonopodis cause citrus canker
  • 28. Quantity of Inoculums Near Hosts  Greater the number of propagules greater will be the rate of disease  Greater the inoculum greater will be the disease  Inoculum is less in quantity then the disease never occurs
  • 29. Effect of amount of soil inoculum of Verticillium dahliae on the amount of vascular wilt on potato plants at various dates after planting. Disease is expressed as a percentage of stems (A) and of main vascular bundles (B) infected at the base of the plants. , no pathogen detected; , 1–5 propagules per gram (ppg); , 6–10 ppg; and , more than 10 ppg. [From Nicot and Rouse (1987). Phytopathology 77, 1346– 1355.]
  • 30. Type of Reproduction of The Pathogen  Based on reproductive cycle  Polycyclic  Cause severe epidemics  Produce many generations in a single growing season  More inoculum production  Monocyclic  Takes many of years to develop in epidemic form (polyetic)  Produce only one generation in a year  complete only one life cycle in one year or growing season  Based on type of reproduction  Sexual (oospores, ascospores)  Asexual (conidia, zoospores)
  • 31. Schematic representation of a polyetic epidemic caused in a crop in a field by a soil pathogen over a 4-year period.
  • 32. Ecology of The Pathogen Depends on the type of pathogen  Ectoparasites  Inoculum produce on the aerial parts of the host.  Spores and seeds disperse with ease over a range of distances and cause epidemics.  Endoparasites  Pathogen can be systemic in nature produce inoculum in the system of host  Spread of pathogen is rare without vectors
  • 33. Mode of Spread of the Pathogen  Survival Efficiency  Air-borne  Soil-borne  Vector-borne  Dispersal Efficiency  Passive dispersal (may be in Km)  Field tools and instruments  Air  Wind  Irrigation Water  Soil (etc)  Active dispersal (may be in cm)
  • 34. Lettuce heads infected by soil borne sclerotia of Sclerotinia sclerotiorum
  • 35. Large field of lettuce heads killed by infections with airborne ascospores of the same fungus
  • 36. Environmental Factors  Aerial environment  Edaphic Environment  Some other factors  Wind  Air pollution  Herbicide damage
  • 37. Aerial environment  Temperature  Affects disease cycles of pathogens  Can prolonged or shorten the disease cycle  Moisture(Dominant factor in diseases caused by oomycetes, fungi, bacteria & nematodes)  Rainfall (duration and intensity)  Dew (duration and intensity)  Leaf wetness period
  • 38. Edaphic Environment  Concern with soil environment  Soil temperature  Soil pH  Soil water content  Soil fertility  Soil organic matter content
  • 39. Human Activities  Have direct or indirect effect on disease epidemics.  Favorable and unfavorable for disease epidemic  Some of them are:  Site selection and preparation.  Selection of propagative material.  Culture practices.  Disease control measures.  Introduction of new pathogen.
  • 40. Site Selection and Preparation  The following types of soil or fields are favorable for the development of epidemics;  Low lying soil.  Poorly drained soil.  Poorly aerated field.  Field near the infected field
  • 41. Selection of Propagative Material  Diseased propagative materials  Use of infected seed  Infected nursery stock  Infected root stock and scion  Diseased suckers  Diseased cuttings
  • 42. Cultural Practices  Cultural practices that increase the possibility and severity of epidemics, are:  Continuous monoculturing.  Higher degree of uniformity.  No-till culture.  Dense planting.  Overhead irrigation.  Injury by herbicide application.  Poor sanitation.
  • 43. Effect of foliage density on development of Phytophthora infestans during a period of partly favorable weather (May–June) and of very favorable weather (November–December). [From Rotem and Ben-Joseph (1970). Plant Dis. Rep. 54, 768–771.]
  • 44. Disease Control Measures  Some practices reduce or eliminate the possibility of an epidemic, these may be:  Chemical spray.  Cultural practices.(Sanitation, Crop rotation etc.)  Biological control.  Use of resistant varieties.  And some other control measures.  Sometime certain control may develop virulent strain.  These strain are:  Either resistant to chemicals.  Or can overcome the resistant of varieties.  These control measures are:  Excessive use of chemicals against pathogens.  Monoculturing for a long time on large area.
  • 45. Introduction of New Pathogen  Possibility of introducing new pathogen  Transportation of planting materials (seed, nursery stock, tubers, cuttings, etc) and agricultural goods.  Inability to produce resistance against new pathogen.(Dainge in case of human)  Pathogens cause severe epidemics.  For example: chestnut blight, Dutch elm disease and citrus canker caused by Xanthomonas compestris pv. citri.
  • 46. Time factors  Season of the year  Duration & frequency of favorable temp. & rains  Appearance of vectors, etc.
  • 47. Measurement of Plant Disease and Yield Loss  Disease incidence  The number of plant units that are diseased in relation to  The total number of units examined  Commonly used to measure the spread of a disease  Disease severity  The amount of plant tissue that is diseased  Measured using assessment scales or by determining the  Area under a disease progress curve (AUDPC)  Yield loss  The proportion of yield that the grower will not be able to  harvest due to disease  Results in economic loss
  • 48. Pattern of Epidemics  Interactions among the elements of epidemics, as influenced over time by factors of the environment and by human interference, are expressed in patterns and rates.  Disease-progress curve  Disease-gradient or dispersal curve
  • 49. Disease–progress Curve  The progress of an epidemic measured in terms of the numbers of lesions/ the amount of diseased tissue, or the numbers of diseased plants plotted over time is called the disease–progress curve  Shows the progress of an epidemic over time, e.g., numbers of lesions, numbers of diseased plants, etc.  Also allows disease forecasting & selection of the best control strategy for the particular disease & time
  • 50. Disease–progress Curve  Basic epidemic patterns  Saturation type of curve Three monocyclic diseases of different epidemic rates.  Sigmoid curve Polycyclic disease, such as late blight of potato.  Bimodal curve polycyclic disease, such as apple scab, in which the blossoms and the fruit are infected at different, separate times.
  • 51. Schematic diagrams of disease–progress curves of some basic epidemic patterns Three monocyclic diseases of different epidemic rates
  • 52. Schematic diagrams of disease–progress curves of some basic epidemic patterns Polycyclic disease, such as late blight of potato
  • 53. Schematic diagrams of disease–progress curves of some basic epidemic patterns Bimodal polycyclic disease, such as brown rot of stone fruits, in which the blossoms and the fruit are infected at different, separate times
  • 54. Disease-gradient or dispersal curve  The progress of an epidemic measured in terms of changes in the number of lesions/ the amount of diseased tissue, and the number of diseased plants as it spreads over distance, is called disease gradient curve (spatial pattern)  Disease–gradient curve: The percentage of disease and the scale for distance vary with the type of pathogen or its method of dispersal  Being small for soil borne pathogens or vectors and  Larger for airborne pathogens  The amount of disease is greater near the source of inoculum  The amount of disease decreases with increasing distance from the source
  • 55. Schematic diagram of a disease–gradient curve. The percentage of disease and the scale for distance vary with the type of pathogen or its method of dispersal, being small for soil borne pathogens or vectors and larger for airborne pathogens
  • 56. Epidemic Rate Curves of Diseases With a symmetrical epidemic rate
  • 57. Epidemic Rate Curves of Diseases With a high epidemic rate early in the season
  • 58. Epidemic Rate Curves of Diseases With a high epidemic rate late in the season
  • 59. Development of Epidemics  For epidemic, specific combination of environmental factors must occur constantly or repeatedly, and at frequent interval over a large area.  Epidemics occurs only when the combination of right sets of condition occurs i.e. include  Temperature  Moisture  Wind  Insect vectors with susceptible stage of plant
  • 60. Epidemics requires  repeated infection cycles  Presence of virulent pathogen  considerable time before a pathogen produces enough individuals  set of favorable environmental conditions repeatedly  Large area under genetically uniform crop
  • 61. Development of Epidemics  The most favorable combinations of conditions for disease development do not occur very often over very large areas  Spectacular plant disease epidemics that destroy crops over large areas are relatively rare  However, small epidemics involving the plants in a field or a valley occur quite frequently  With many diseases, e.g., potato late blight, apple scab, and cereal rusts, the environmental conditions seem usually to be favorable, and disease epidemics would occur every year were it not for the control measures
  • 62. Modeling of Plant Disease Epidemics  An epidemic is a dynamic process. It begins on a few plants and then increase in severity and spreads over a larger area.  It stops when all host plants are killed , become resistant or harvested.  For our better understanding and prediction of development of an epidemic, plant pathologists from late 1960s have been developing models of common and serious diseases.
  • 63. Modeling of Plant Disease Epidemics  Model?  Models are generally crude simplifications of real epidemics, roughly analogous.  Construction of a model takes into account all the components and sub-components of plant disease.  Mathematical models;  It provides a great information about amount and efficacy of inoculum , effects of environment, disease resistance of host, effects of management strategies.
  • 64. Modeling of Plant Disease Epidemics  For a model, a database of information is developed.  Database contains information on:  Crop  The disease incidence  The pathogen  Location  Crop canopy  Rain fall  Temperature  Wind velocity  Vector etc
  • 65. Forecasting plant disease epidemics  Being able to forecast plant disease epidemics is stimulating and also an indication of the success of modeling of particular disease.  To develop a plant disease forecast, one must take into account several characteristics of particular pathogen, host and environment.  In monocyclic diseases, disease development may be predicted by assessing the amount of initial inoculum.  In polycyclic diseases, disease development can be predicted by assessing the rate of occurrence of infection cycles.
  • 66. Forecasting plant disease epidemics  Some points related to forecasting of plant disease epidemics  Disease diagnosis: The key to forecasting of any plant disease.  Evaluation of epidemic Thresholds.  Evaluation of Economic Damage Threshold.  Assessment of Initial Inoculum and of Disease.  Monitoring Weather Factors That Affect Disease Development
  • 67.  THANKS  Prepared by: Ahsan Abdullah 2011-ag-3149 Plant Pathology