This document discusses key concepts in plant disease epidemiology. It defines epidemics as widespread disease affecting many individuals over a large area in a short time. Endemic diseases constantly occur year after year, while pandemics involve mass mortality over continents. Sporadic diseases occur irregularly over limited areas. Epidemics follow disease progress curves from an initial destructive phase to a decline phase. They are influenced by factors like the pathogen, host, environment, and human activities. The interaction of these factors forms the basis of disease triangles and tetrahedrons.

1. P P – 3 1 0 ( T ) 3 ( 2 – 1 )
Diseases
Epidemiology

2. Plant Disease
Epidemiology –
An Introduction

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

10. 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

13. The disease tetrahedron.

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