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Epidemiology Exam 3

3rd exam for Dr. Johnson's epidemiology PLP 551 WSU course.
What is the infection chain/disease cycle?
What information can be gained from a disease progress curve?
-Time of onset of epidemic
-Minimum, maximum, and final amount of disease
-Rate of disease progression
-Severity over course of epidemic
-Severity over host growth stages
-Shape of the curve
-Period of epidemic
-Single statistical value rather than repeated measures
Area under the disease progress curve was first used by who? How is a disease progress curve calculated? How can it be refined?
Van der Plank in 1963 to measure yield loss to stem rust, AUDPC was slow to gain acceptance. A disease progress curve is calculated by (x measurement + y measurement)/2 x interval between samples, then all measurements added together for final AUDPC. Remember that if there are 4 measurements there should only be 3 resulting numbers to add together Pay attention to time between sampling. Decreasing the time between sampling is an effective way to get a more refined AUDPC.
What are the three phases of an epidemic as shown by a disease progress curve?
Exponential phase (initial increase is exponential)
Logistic phase (middle of increase, growth is slower)
Terminal phase (end of increase, flattened out)
Graph shows disease severity over time, these phases are determined by the amount of disease present in the field overall.
Describe and explain the exponential phase further:
The exponential phase is also known as the lag phase between initial infection and lag before symptoms. It is also the point of greatest multiplication where the disease level can increase from 0.0005 to 0.5 very quickly. This is the point where chemicals are most effective and also disease forecasting.
Describe and explain the logistic phase further:
The logistic phase is from onset to about 50% disease. The increase is slower (0.05 to 0.5) showing only a 10 fold increase. The logistic phase has slower disease progress as spores land on already infected tissue and lowers the exponential progression. Many epidemics can be economically controlled at this point.
Describe and explain the terminal phase further:
The terminal phase is when most of the damage from the epidemic is already done. Control is difficult at this stage and treatment is next to useless. The terminal phase marks the time when sanitation and reducing inoculum for the next year is critical for diseases such as potato late blight.
Quantitative epidemiology was developed by who and used what kind of information, what was the result?
Van der Plank was responsible for starting quantitative epidemiology and the models were further developed by mathematicians. Analysis was based on infection rates, also the relation between amount of inoculum and the amount of disease it produced. The result was monocyclic and polycyclic disease classifications.
What is the analogy used between disease progression and money?
Principle-disease present in field
Interest-disease increase but dependent on principle
Simple interest- monocyclic disease (interest accrues but only on the principle rather than on the interest as well).
Compound interest- polycyclic disease (interest accrues based on amount of principle plus accumulated interest)
What are the 6 models for analyzing disease progress? (Only really need to 4 and see graphs in notes for better description).
According to Campbell and Madden they are:
1. exponential (J shaped)
2. monomolecular (like chemistry pH graph, saturation curve)
3. logistic (S shaped, exponential then flattens out)
4. Gompertz (population growth model, increases to max then declines to zero, not symmetrical around inflection point as it increases more rapidly than it decreases)
*5. log-logistic
*6. Richards
What is a Polyetic Disease and how is it different from mono and polycyclic disease cycles?
Polyetic disease is characterized by a pathogen that is capable of surviving long periods in a large population. The inoculum at the end of one season is closely related to the initial inoculum of the next season. Pathogen development over a number of years becomes exponential. An example disease is: Dutch Elm disease.
Define the characteristics that make up a monocyclic disease?
A monocyclic disease is characterized by only one cycle of infection in one cropping season. The development of the disease is limited by either the environment or the pathogen life cycle. The pathogen does not produce EFFECTIVE inoculum that functions during the same season and the inoculum present at the beginning of the season is the main source of disease (disease progress curve shows increase as roots expand through soil borne inoculum). High amount of initial inoculum over a large area can still be very devastating. An example disease is: vascular wilts such as verticillium dahliae.
Define the characteristics that make up a polycyclic disease?
A polycyclic disease is capable of multiple infection cycles per season and inoculum increases throughout the growing season. It is continuous growth with overlapping generations and lesion expansion leading to increased inoculum levels. An example disease is: Phytophthora infestans which can germinate and sporulate in 4-6 days and repeat under ideal conditions.
What is the equation for simple interest or monocyclic disease?
Kt=K0(1+r*t) or I=Prt as in initial inoculum times rate times time.
What is the equation for compound interest or polycyclic disease?
Kt=K0(1+r)^t as in initial inoculum plus rate to the power of time.
What is the equation for compound interest or polycyclic disease when time becomes infinitesimally small?
Kt=K0^ert where e=2.71812 aka the base of natural logs. This equation represents exponential growth.
What are the differences between exponential and logistic growth curves?
Exponential curves are J-shaped and have uninhibited exponential growth whereas logistic growth curves are S-shaped and begin exponentially then flatten out due to a limiting factor such as food, space, or time. As less tissue becomes available for infection, absolute rate decreases.
What is the equation for a logistic growth curve?
dXt/dt= rXt(1-Xt) where X is the initial inoculum level, r is rate and t is time.
Van der Plank defined the logistic infection rate as:
the regression coefficient or the average value of r over all points in time.
What is the Threshold Theorem:
The continuity of any species requires that 1 individual produce at least 1 female offspring. Fungus: any lesion of 1 generation begets at least 1 lesion in the following generation and during infection the lesion should produce at least 1 effective spore.
Virus: infected plant material that gives rise to others
What controls epidemic speed?
Latent period (p) governs speed of an epidemic, the slope of the curve gradually decreases but the slope will never reach zero.
What are the different variables associated with rates and the resulting graphs/curves?
rl=exponential growth
r=logistic growth
Rc=corrected basic growth rate
Remember, an epidemic is a process of proceeding at a determinable speed or rate.
Define and characterize monomolecular models:
Saturation Curve
Straighten line to calculate slope and intercept, this provides a basis for comparisons, compare control treatments, and compare pathogen attributes
What does R summarize?
Effects of:
Host Resistance
Cultural Practices
Inherent ability of pathogen to induce disease
What does T summarize?
The amount of time for the interaction between the disease and it's environment.
What is a key aspect of disease modeling?
The model providing a good fit to the data does not necessarily indicate how the disease is increasing. An appropriate model may not be found for the data present. If models won't accurately fit another model, try using AUDPC. Also, remember that none of the 6 (*4) models were not developed specifically for plant pathology applications.
Application of the models are:
Select an appropriate model to describe disease progress data.
Parameters are estimated from the model.
Basis for statistical analysis
Comparison of disease progress curves.
Used to generalize the nature of an epidemic rather than to describe it in specific detail.
Severe disease can be induced by:
Both mono and polycyclic pathogens
If initial inoculum is large and rate is low:
Typical monocyclic disease and reducing initial inoculum is most effective strategy. Reducing rate and duration will also help, but not as much as reducing initial inoculum.
If initial inoculum is low and rate is high:
Typical polycyclic disease and reducing the rate is most effective strategy. Reducing initial inoculum and especially duration will also help, but reducing initial inoculum will help less compared to reducing the rate.
What are a few of the constraints of the exponential model?
Amount of initial disease must be small.
Environment, host resistance, pathogen aggresiveness, all must remain effectively constant
(1-X) adequately describes the suppressing effect of limited available host tissue.
Define Sanitation:
Process that reduces, excludes, or eliminates initial inoculum from which epidemics start. Generally aimed at decreasing the number of pathogen progagules before a crop is planted.
What are sources of initial inoculum?
Bacterial Cells/Slime
Virus particles (viroids too)
Infected Plant Material
All of the above in air, soil, water, equipment, and plant material.
What does CSSV SRRV QP stand for?
10 sanitation practices effective at reducing initial inoculum:
1. Crop rotations (blackdot on potatoes)
2. Seed treatment (barley loose smut)
3. Seed certification (golden nematode on potatoes)
4. Vertical resistance (stem rust of cereals, many cultivars have race specific resistance)
5. Soil fumigation (root knot nematode)
6. Removal of alternate hosts (stem rust of wheat reduced by barberry eradication)
7. Removal of cull piles (potato late blight)
8. Vine killing (potato late blight, reduces tuber infection)
9. Quarantines (potato cyst nematode)
10. Disease free root stock or seed (PVY and geranium cuttings free of bacteria)
What are 3 examples of heteroecious rusts?
Wheat stem rust (barberry-wheat)
White Pine blister rust (ribes-white pine)
Cedar Apple rust (cedar-apple)
Describe the situation provided in class concerning asparagus rust (autoecious):
Asparagus rust is autoecious meaning all pathogen life stages are on the asparagus. Organic crops can serve as islands for disease and should be isolated from other crops. One side of the field was planted and harvested earlier while the other was severely infected. Could have avoided this infection with chemical control, isolation of host, removal of host, prevention of spore spread and also getting rid of volunteers early in the season.
How can time be used to manage plant disease?
Early maturing cultivars (plant barley and rye in upper midwest, early season crop avoids disease)
Short season cultivars/crops (barley vs wheat/stem rust)
Sow early (Flax, pea and verticillium wilt prefers warm soil)
Avoid any slow down of crop growth (soil fertility also rhizoc on potatoes in cold soil)
Grow crop in environment that has limited duration of pathogen favorable weather (potato seed grown in cooler temps to prevent virus vector spread)
How can rate be used to manage plant disease?
Partial resistance slows disease progression
General resistance
Protective chemicals-applied repeatedly to reduce rate
Cultural practices (roguing, plant spacing, irrigation row orientation etc.)
What are the components of dilatory (aka partial) resistance?
Infection frequency
Lesion size
Quantity of sporulation
Latent period (not the same as incubation period)
Infectious period
High infection threshold
Reduce spore deposition
What are cultural practices that reduce the rate of an epidemic?
Sprinkler irrigation (apple scab and potato powdery mildew)
Plant spacing (white mold of potatoes)
Row orientation (wind blows spores down rows)
Plant nutrients (nutrient stress increases disease)
Rouging (cut down primary hops shoots to prevent powdery mildew infection)
Pruning (botrytis bunch rot of grapes)
Raised beds (strawberries and less soil/phytophthora)
Does sanitation affect rate in any way?
Sanitation practices performed during the course of an epidemic serve not to reduce initial inoculum, but act as a disease removal mechanism to reduce the substrate on which the pathogen can reproduce.
Reservoir of secondary inoculum is reduced and the rate is reduced.
What are the three epidemiological strategies to reduce plant disease?
Reduce initial inoculum
Reduce rate of disease progression
Reduce duration of the disease
Remember that sanitation only really delays the epidemic, but that they all work well together (differentiate between mono and polycyclic benefits in another question).
Equation for determining the benefit of sanitation?
Example from notes:
Sanitation ratio0.015/0.003 = 5
then log that number = log(5) = 0.6989
rate is 0.2
somehow = 2.3/0.2(log10 5)= 8 days
overall, remember that if R is halved it takes twice as long to reach same level of disease as if it was not. If santitation ratio is doubled it only delays the epidemic a small bit. Delay is long when r is small but delay is short when r is high.
Sanitation relative to rate?
The exponential basis of sanitation means that the returns diminish fast as sanitation is increase. Only so much sanitation is possible before the gain is too small to bother. However, a delay can be the difference of increasing yield as is the case with tuber bulking and late blight. Disease levels are directly related to yield.
Which is better, tolerant cultivars or partially resistant cultivars? Chemicals?
Tolerant cultivars do not reduce initial inoculum or rate and can in fact increase inoculum.
Vertical (race specific) resistance reduces initial inoculum.
Partial (dilatory) resistance reduces the rate and also delays an epidemic by reducing initial inoculum.
Chemical eradicants reduce initial inoculum.
Protective fungicides reduce the rate.
Cultural practices reduce the rate.
What are the differences between focal outbreaks and general outbreaks of late blight?
Focal outbreaks are often around cull piles or infected shoots from infected seed pieces. Obvious foci.
General outbreaks spread over whole field, spread from field to field, and change is often dramatic.
Compare Late blight and stem rust as major plant disease epidemics:
Potatoes supply own inoculum in spring, wheat inoculum blown up the puccinia pathway from south to north or from barberries.
Both have a fast rate (0.46 unit/day) with favorable weather.
Late blight weather most favorable during all season, stem rust favorable during end of season.
Late blight completes S-shaped curve in Main, stem rust only a partially shaped S curve in upper midwest (inoculum from south delays duration a bit).
Potatoes can survive if tubers set early enough to be affected by killed foliage, but yields are often reduced.
Wheat yield is hugely affected if foliage is killed before grain is ripe.
Barberries and wheat stem rust:
Barberries are alternate host for wheat stem rust. They are responsible for local epidemics and destructive regional epidemics. Barberry eradication efforts helped to reduce outbreaks and limited the number of new genetic races of stem rust as the sexual stage of the pathogen was on barberries (aeciospores). However, inoculum from the south negated some of these efforts and still cause outbreaks (only a few urediniospores required to initiate infection). There has been breakdown of race specific resistance that has been directly linked to barberry bushes.
Fusarium wilt on Tomato:
Monocyclic disease managed with reduced initial inoculum. Clean seed and treated seed also helped. Crop rotation and race specific resistance. Shows a simple proportional relationship between number of spores and number of infections.
What are some of the lessons from Vertifolia and late blight resistance?
Vertifolia was a potato cultivar with vertical resistance to a few races of late blight. Intentionally selected away from partial resistance and the resistance broke down. So, selecting for R genes when all races are not present may reduce partial resistance. Best way to select for partial resistance is to make sure all races (high genetic variety) are present during testing. Test over many years and many plots to increase exposure.
Give an example of an early/susceptible cultivar?
Russet Norkotah is susceptible to late blight and verticillium among other diseases. They increase inoculum levels and speed up epidemics.
Tell me more about wheat stem rust, specifically what did removing barberries accomplish?
Early onset of disease is correlated with increase in losses due to disease. The effects of removing barberries were:
Reduced frequency of epidemics
Delayed disease about 10 days
Reduced initial inoculum level
Decreased number of pathogenic races
Stabilized current pathogenic races (and R genes)
What are the steps in wheat stem rust infections? (heteroecious)
Teliospores (on straw)
Basidiospores (from wheat to barberry)
Pycniospores (barberry)
Aeciospores (barberry to wheat, can travel but to infect, farther distance from bush to wheat require higher inoculum levels)
Urediniospores (wheat to wheat and then into telio-)
What are the steps in white pine blister rust? What is the alternate host?
5 stage lifecycle (similar to wheat stem rust TBPAU with aeciospores and urediniospores on ribes aka gooseberry or currant). A very serious disease for forests as the urediniospores can be disseminated up to a mile and have a long infectious period of 185 days. Pine is infected by the basidiospores and has a long latent period. The aeciospores can be disseminated up to 350 miles(!).
What about management of white pine blister rust?
Infected saplings only live up to a year, older trees can survive three years. The Eastern US has two highly susceptible species (more susceptible=more spores) but eradication of ribes species were slow moving although somewhat effective. Western US had 5 susceptible species and even more space to eradicate ribes, complete eradication is considered necessary for best control. Rust epidemic came in waves with some years better than others, and when eradicating need to have protective zone around pine stand of up to 420 yards.
What were some of the major problems with managing the white pine blister rust epidemic?
Stands of pine were inaccessible due to rugged terrain.
Regrowth of Ribes from 'crown' tissue
Long latent period of infection in pine
Several susceptible pine species
Complete eradication is needed
Non-uniform spread of rust
Labor intensive
Inaccurate assumptions about rust epidemiology
Interagency/governement problems
Panic caused mis-applied fungicides that did not work
Is lesion expansion a component of an epidemic?
Yes, lesion expansion is directly related to the development of new infectious inoculum. However, spore production does not always estimate the sum of all the parts of an epidemic (resistance and disease development), lesions may continue to expand even if the environment no longer favors infection. Lesion size is used to determine the severity and aggressiveness of an epidemic as well as cultivar resistance. Lesion expansion contributes to the shape of the disease progress curve.
Rate of lesion expansion may vary based on:
Leaf position
Age of lesion
Age of host
Inoculum concentration
Lesion density
Dew period
What factors make Phytophthora infestans a possibly ultimate pathogen?
Fast lesion expansion rate
Short latent period
Ample number of effective spores
Small initial lesion size, but expands quickly
Infects hosts with numerous susceptible sites
Latent infection (tubers in storage)
Compared to Pi, another pathogen with a combination of these features on the other end of the spectrum would only cause mild and slow epidemics
What pathogen causes leaf rust?
P. recondita, more successful at infections, wider temp range, shorter latent period, slightly more severe overall.
What pathogen causes stripe rust?
P. striiformis, fast lesion expansion, more spores per lesion, narrow temp range for infection, more progeny per adult,
What pathogen causes corn rust?
Puccinia sorghi, faster infection efficiency, more spores, higher disease severity and way more efficient but overall less severe than E. turcicum
What pathogen causes northern corn leaf blight?
Exserohilum turcicum, fast rate of lesion expansion, and lower everything else, but still has overall more severity.
What are the expected characteristics of a successful pathogen?
Wide host range
Wide adaptation to environmental conditions
Rapid rate of increase
Effective dissemination
Allow host to reproduce
What are the optimum conditions for epidemic development of a disease (fungal, bacterial, other)?
Abundant viable inoculum early in season near plant hosts and virulent
Abundant and timely liberation of inoculum
Rapid and widespread dissemination of inoculum
Concentrated and extensive population of susceptible hosts (crowded, monoculture, aggregation, etc.)
Optimum moisture and temps for pathogen germination, penetration, growth, and sporulation
What is the population concept?
Individual usually not too important except:
Initial stage of an epidemic
Exotic pathogen
Exotic genotype
Valuable host individual
According to Whetzel what are the main management practices for disease control?
What is exclusion?
Preventing to a profitable degree the entrance and establishment of a pathogen in a non infested area. This is accomplished using quarantines etc.
What is eradication?
The more or less complete elimination or destruction of a pathogen after it is established in a given area. This is accomplished using soil fumigation, bio fumigation etc.
What is protection?
The interposition of some effective barrier between the susceptible host parts and the inoculum of the pathogen. This is accomplished with chemical control or altering planting time (warm soil versus cold soil)
What is resistance?
The development by natural or artificial means of a highly resistant plant population in the area infested with the pathogen to be combated.
What are the control methods are related by Dr. Johnson?
Avoid the causal agent (quarantines, disease free stock, certifications etc.)
Reduce the population of the causal agent (sanitation, soil fumigation, rotation, etc.)
Protection (seed treatment, chemical control, irrigation management, row/plant spacing etc.)
Vector management (insecticides, nematacides, weed control)
Therapy (Heat treatment of seeds -loose smut- systemic fungicides)
Genetic resistance (R genes, partial or race specific)
Disease management and control depends on knowledge of what?
Crop economics
Population dynamics (host, pathogen, environment)
Disease control technology
What is the economic threshold?
The amount of injury which will justify the cost of artificial control measures. Changes from season to season and area to area. Depends on:
Price of commodity
Price of pest control
Distance to market
What is the action threshold?
The severity of the disease at which control measures should be implemented to prevent disease progressing to the damage threshold. Some yield loss may occur before action threshold reached.
What are some considerations for the thresholds?
Must know:
Production costs
Control costs
Quantitative effects of disease on yield and quality
Future prices of commodities vary
Can't just turn off an epidemic
Must begin control in exponential phase of disease
What are the goals of a good IPM or IDM program?
Social responsibility
Production efficiency
Environmental compatitbility
Economic viability
What is the epidemic sextuplet?
Initial disease
Latent period
Infectious period
Daily spore production/lesion
Spore effectiveness
Lesion expansion