Past exam questions Flashcards
Mucor rot, caused by Mucor piriformis, is the main postharvest pathogen of apple in the United States. A group at Oregon State University has examined the impact of environment during the pre-harvest growth of the Granny Smith apple crop on the infection severity observed after storage of the apples at 0°C for 4 months. Table A (below) presents the results for when Granny Smith apples were grown in three different locations/environments (Hood River, Yakima or Wenatchee)
Answer the following questions using Table A and your knowledge from lectures about postharvest health and the disease triangle (that is, interactions between plant, pest and environment).
a) Describe the effect of environment on the development of Mucor rot in apple and briefly explain why you think there is an effect. Refer to the disease triangle in your answer. (6-7 mins)
b) Explain why there are differences in the infection severity between Royal Gala and Granny Smith. Your answer should briefly discuss the likely genetic/molecular basis of any differences. Diagrams may help you to answer this question (12 mins)
c) Describe at least three methods you would recommend to ensure Mucor rot does not develop during storage of apples and briefly explain why you would recommend them (6-9 mins)
QU 1 .A)
- Enviroment = Temp, Humidity, Wind, Light
- Increased humidity + temp promote fungal growth.
- Hood river has increasted humidity and temp.
- Yakima may have lower IS due to lower humidity from better conopy mamagement (better airflow).
- The 3 locations may have different disease load / control, stratagies = more or less hosts.
- Draw the disease triangle.
Qu B.
- Remove infected fruit from bins and orchard as it will decrease innoculum load.
- Sprey with fungacide or Gasses to prevent growth.
- Controlled enviroment (low temp, low humidity) prevents growth of fungas at storage.
Severity of powdery mildew (caused by the fungus Erysiphe necator syn. Uncinula necator on grape berries has been measured for most seasons since 1981 by Moyer and colleagues in New York State but in different cultivars (Table 1).
Using Table 1, describe any differences in disease severity between years and between cultivars (genotypes) and then explain the likely reasons for any differences. Reference the disease triangle in your answer.
10 marks
Of the pesticides used in Australia there are multiple modes of action of insecticides that target nervous system functions, fungicides that target membrane structure and herbicides that target photosynthetic processes.
Explain why so many registered products target each of these processes and any consequences this might have for pesticide use.
(Section one, Chris. 12 Marks)
Modes of action
Insecticides
- Kill the pest quickly (fast action)
- More toxic to humans
Types of insectacides
- Contact or stomach poisons (absorb or eat)
- Topical & systemetic (applied to surface, systemetic is absorbed by plant)
Herbicides
- (Nervous system & respiration)
- Effect photosynthesis, which kills the plant. Doesn’t have to be fast acting.
- Target something that only plants have.
Types of Herbicides
- Selective used within a crop to controll a weed species
- Non-selective damage all or most of the plants
- Pre- emergent applied to soil to stop plants germinating
- Post-mergent applied to foliage of unwanted plants.
Fungicides
- Target membrane structure to kill the fungus.
- They can all become resistant because there is a limited number of ways to attack the aspects to kill.
Types of fungacides
- Protectants stop germination of spores or entry of pathogen into plant.
- Only effective befor the pathogen has invaded the plant.
- Curative can stop groth of fungi after infection
Breeding for disease resistance is a high priority for all annual crops and vegetables.
Discuss, providing justification for your statements, the role of crop breeding in the management of plant pathogens including: why there is a continuing need to breed for disease resistance, whether plant resistance alone is a viable strategy for managing plant pathogens, and what other strategies, if any, should also be included in plant pathogen management strategies.
(Section one, Chris, 17 marks)
Disease resistance is the introduction of a disease resistant alleles (gene) into the crop.
Need to used crop breeding to get it in there
Loss of resistant (alleles) genes = because new genes and strains keep coming.
Mutations in pathogens = due to natural selection, resistant genes are doing the resistance.
Population size plays a big roll = If the population is low you won’t get resistance. If the population is high resistance will more than likely happen.
You wont get mutation because of the population alone.
It takes about 7 years to produce a resistant crop due to mutations. The pathogen in this time will have too many generations to build up resistance.
Multiple pronged strategies. Need to attack pathogens with multiple strategies. Use both cultural methods and fungicides. What are the justifications, of both of these aspects?
Key = Allow population to build up.
Pathogen resistance
Exploitation of natural resistance genes through conventional breeding
– Stacking of resistance genes to obtain wide resistance to pathogens.
– “Gene for gene” concept means that continual integration of resistance genes are required as new pathovars evolve or are imported.
• Introduction of novel resistance genes
– Viral coat proteins.
– Transgenic plants expressing viral genes are
tolerant of viral attack.
Management of Pathogen Tolerant Crops
• Rotate Crops
– Pathogens build up in soil, on weeds, or on
stubble.
• Control other hosts
– Reduces population pressure and hence risk of resistance breakdown.
• Avoid high pathogen populations
– S or VS cultivars, alternative hosts, use
fungicides appropriately
• The higher the pathogen population that is exposed
to tolerant crops, the more likely that a new virulent variety of pathogen will evolve.
Erysiphe necator (powdery mildew) is a leaf and berry disease of grapevines that has recently evolved resistance to the strobilurin (activity Group 11) and the DMI (activity Group 3) fungicides in Australia. Grape berries are most susceptible to powdery mildew during the period between flowering to 4 to 5 weeks after fruit set. Powdery mildew spreads short distances by wind, so most infection occurs from sources within a vineyard. Powdery mildew is favoured under conditions that are mild, humid and cloudy and disfavoured by hot and dry conditions. Powdery mildew grows faster in shady situations and less well when exposed to direct sunlight.
Fungicides available for wine grapes for control of powdery mildew are listed in the table with fungicide action and withholding periods or last use. Sulfur applied under hot, humid weather conditions can cause damage to vines.
Mode of action Fungicide action Withholding period Group 3: (DMI) Protectant and curative 35 days to 60 days depending on product Group 5: (Amine) Protectant Not to be used later than 80% capfall Group 11:
(Strobilurins, Quinone outside inhibitor) Protectant and curative 63 days Group 13: (Aza-napthalenenes) Protectant only 42 days Group U6: (Phenylacetamide) Protectant only Not to be used later than berries at peppercorn size Group U8: (Actin Inhibitor) Protectant and curative Not to be used later than 80% capfall Group M2: (Sulfur) Protectant only 84 days
You have been asked to develop a management plan to deal with the resistance to Group 3 and Group 11 fungicides in powdery mildew for wine grapes. i) What practices would you include in the management plan? ii) Explain how the inclusion of each practice will help manage resistance in the vineyard.
(Section one, Chris 25 marks)
Cultural practices = trim the sides of the vine canopy to let in sunlight, increase airflow and decrease humidity.
Spray regime = using fungicides.
Forecasting = Use weather guides to decide what sprays to apply and when.
What order should we take action?
- Apply SO2 early in spring when it wont damage the vines
- Then apply a resistant protectant (group 3 or 11)
- Monitor the vines for disease. See if it is still there.
- Use the group 13 as a last resort
- removal of infected bunches by hand picking
How will these aspects help?
Pruning = population will stay down
Forecasting = use minimal spray, target the best time for application.
Protectant fungicide application early = Reduce population. Keep fungus away early
Group 3 and 11 = already resistant so use early and if it doesn’t work spray with something that’s not resistant.
Monitoring = know what’s happening, see if pesticides are working.
Hygiene = Last resort is removing the effected bunches
In the practical class on disease diagnosis, we focussed on visual assessment, sometimes aided by a hand lens or dissecting microscope. This approach does not always give us sufficient information to make a diagnosis. Outline the steps you might take to diagnose a plant disease you suspect to be caused by a bacterium or a fungus when visual inspection of symptoms and signs is insufficiently informative.
(Section one, Eileen, 13 Marks)
- Collect Back round information (management history)
- Record visual data (dissecting microscope
- Looks for signs and symptoms ( fungal structures, hyphae, spores ect.
YES = microscopic identification
Options. Moist incubation. Microscopic identification.
Culture fungus
Compare with prior knowledge, literature.
Look at spore colour, spore bearing and structure. Hyphae, aseptic and septic. Look at under dissection microscope.
NO
Turbidity test
Culture bacteria
If turbidity test positive the look at the shape, size, Bio chemical, molecular tests with compound microscope.
Note about mildew
Powdery = All on the surface
Downey = Inside the tissue
Long distance transport of flowers to markets (and in particular, roses) occurs at low temperatures but their ability to withstand storage is still affected by Botrytis damage. Many companies also store flowers in a moist environment to ensure they do not wilt. A recent study evaluated the impact of wet and dry transport storage (at low temperatures) on the development of Botrytis in cut roses from different cultivars.
Look at the data in the Table 1 and answer the following questions:
a) What is the effect of different transport and storage conditions on Botrytis development in cut rose stems and why do you think there is an effect?
b) Briefly discuss the likely genetic/molecular basis of any differences seen between Avalanche and Red Naomi.
c) What other methods would you recommend to ensure Botrytis does not grow on cut rose stems and why would you recommend those?
Table 1. Percentage of rose stems rejected due to Botrytis at the start of vase life (when the rose has reached the marketplace) or after 7 days of vase life (in water at 20°C after transport). Stems were transported for 11 days at 0.5°C in either wet storage (in buckets of water) or dry storage (in cardboard boxes). Humidity was maintained at 95%. Adapted from 1. Cultivar of rose Storage conditions Start of vase life (after transport) After vase life (storage for 7 days after transport) Dry Wet Dry Wet Avalanche 0 20 20 70 Red Naomi 10 53 100 100
Amanda 2013 question 12
A )Avalance never has as much disease
wet enviroment
Control host and pathogent remove dead wood
B) Avalanche is capable of activating defence genes and inducing resistance against botrytis.
It prefers dry conditions for switching on its defence genes.
Red naomi seems to have no defence against botrytis.
Effectors ( botrytis)
Recognition (R-gene - R proteins)
Guard = hypothesis
C)
Roses should be packaged seperating them from each other.
Reduced humidity will reduce the risk of botytis
sprey with fungacide
choose resistant variety
- Resistant plants induce a range of defence responses when challenged by pests or pathogens. Explain in detail how resistant plants detect or recognise a challenge by a pathogen and how we can use that knowledge to breed for disease resistance.
Amanda 2015 question 2
Firs layer of defence
Basal layer = pattern recognition receptors
- Recognise any generaly pathogen molecule
- Receptors recognise (pattern recognition)
- host evolved to have resistance genes
- Makes resistant proteins
- Molecular patterns
- Gene expression produces an imune responce
- Pest produce ffectors which damage the host and reduce immune responce
2nd Layer
Guard hypothesis (effector triggerd immunity)
- R guard proteins receptor can change in the host and turn on a defence responce to increase immune responce
- Specific r protiens guards a specific pest/pathogen
- Resistant guard proteins detect change in the host protein
- Guard cell deflects it if protein changes
- virus induce resistance ( trick plant)
- Introduces a pretend effector to host (turns on) (chitanase)
Breeding for resistance
Multiple r genes should be displayed to make it harder for the pest pathogen to overcome these genes. GM breeding
Molecular marker to screen offspring to make it quicker
Tinv coat proteins PR proteins
Myaram 2015
- Choose ONE (1) of the following production systems:
20 marks i.
A citrus orchard ii.
A tomato production greenhouse iii.
A vineyard
a) Explain SIX (6) main steps in the development of an IPM program in that production system.
b) What is the key IPM principle when you are making decisions to apply pest management practices?
Section A)
- Identify the causes of loss in yield and decline in the quality of a crop - Diagnosis
- Elucidate the biology, ecology and economics of the pests • Inspect, • Identify, • monitor pest problems
- Set action thresholds
- Formulate strategies for reducing losses to pests
- Utilise crop protection practices in pest management
- Evaluate the IPM program in terms of: • Economic returns, • Environmental consequences • Social consequences
Section B)
Is it a real pest problem or a percieved pest problem?
Diagnosis options = Nutrient stress, Insects, Disease, Herbacide damage, Wind damage, Frost, Mites, Birds, Water stress, Weed competition, Salinity,
Key is number 2 above
- Pest life cycle?
- Economics of damage?
- Weak links in life cycle that can be targeted for control? • What is the spatial distribution of the pest? How can numbers be accurately determined?
- Interactions with other pests, natural enemies and antagonists?
- Seasonal activity? Dormancy? Movement?
- How does weather affect the pest?
- Sources of nutrients?
- Nature of damage it causes?
Choose ONE (1) of the following production systems:
i. A citrus orchard
ii. A tomato production greenhouse
iii. A vineyard
Explain at least THREE (3) useful ways that IPM could be improved in the pest management for that production system.
Myram
- Reduce selection for resistance => sustainability
- Integration of control tactics against multiple pests in a crop=> profitability and sustainability
- Multiple control strategies => more robust control => more effective
- Protecting the biological control agents => contribute to ongoing pest management program => profitability and sustainability
Key principle, Use the most toxic controll method as a last option
a) Draw a graph of the population density of a hypothetical pest over time with appropriate labels. Show the Economic Injury Level (EIL) and Economic Threshold (ET).
b) List TWO (2) key factors that determine the Economic Threshold.
Amanda
A) see immage
B) A regression of yeild vs
- Pest population levels
- levels of damage
- An action threshold for native budworm attacking chickpea in Northern Australia has been reported as 6 larvae per square metre, assuming the price is $500/tonne and the cost of an insecticide spray is $80/ha.
a. How could the accuracy of this threshold be verified?
10 min
b. What would happen to the threshold if the cost of an insecticide spray dropped to $60/ha? Explain.
5 min
Amanda
What are the steps for identifying a plant pathogen?
- Identify the host species
- Perform preliminary examination of the host and/or specimen
- Prepare a list of possible causes
- Collect background information (soil condition, management history, local pest/disease outbreaks, etc.)
- Perform thorough visual examination of the specimen and record observation
- Perform low-power examination (hand lens or dissecting microscope), looking at/for:
- Fungal
- hyphae
- reproductive structures (conidia/ophores, sporangia/ophores)
- growth habit
- Nematodes
- Colour
- Size
- Any other diagnostic features
- Perform high power examination (compound microscope); look for the same things previously stated.
- Perform advanced tests
- Fungi:
- moist incubation to encourage sporulation
- culture (view under low- and high-powered microscopes)
- septa
- reproductive structures (conidia/ophores, sporangia/ophores)
- size, shape, and colour of spores
- the presence of rhizoids
- perform metabolic analysis
- Bacteria
- Culture (view under compound microscope)
- Morphology (shape, size, elevation, etc)
- Biochemistry
- Gram stain
- Culture (view under compound microscope)
- Infect a healthy host to confirm symptoms are a result of the pathogen
- Depends on the value of the crop/pathogen.
If no pathogen was found, the problem is environmental/nutritional/etc
When a pathogen is identified, research and prepare recommendations for management
At each stage of the process, attempt to identify the pathogen by comparing the diagnostic features observed with diagnostic information in relevant reference material.
Exam question 2015:
- Why is it important to use a forecasting model in order to control fungal pathogens?
- Primary infection occurs in Spring when spores are released
- Sporulation depends on leaf wetness and temperature
- Effective control depends on minimising primary infection in the Spring with well-timed fungicide applications
Predicted sporulation of apple scab
• The need for fungicide treatment is based on
spore load, so sampling with spore traps or by
other means is important for spray decisions
• Use the degree-day model to predict the date of
98% spore trapping, i.e, the end of the period
when primary infection can occur
General infection model for foliar fungal plant pathogens
• Model fits the response of a wide range of pathogens to
wetness and temperature
• The time required for spore germination and penetration
depends on a wetness period that is modified by the
response to temperature
– There are minimum and maximum temperature
thresholds and a non-linear response curve between
these extremes
• Can be used as the foundation for disease forecasting
Of the pesticides used in Australia there are multiple modes of action of insecticides that target nervous system functions, fungicides that target membrane structure and herbicides that target photosynthetic processes. Explain why so many registered products target each of these processes and any consequences this might have for pesticide use.
Chris Exam
Insectacides
How?
Kill the pest quickley, Fast action, lots of them have this.
Herbacides
- Modes of action effect photosyntheis
- Want to kill plants
- Dont have to kill them quickley
- Target membrane structures (in fungasides)
Why?
- Combination of what the users want
- Insecacides = Fast action
- Fungasides = Membrabe structure
- Herbacides = Kill plants
Insectacides can effect humans = concequence , more toxic to humans than pestacides
Resistance = limited number in ways to target things
Erysiphe necator (powdery mildew) is a leaf and berry disease of grapevines that has recently evolved resistance to the strobilurin (activity Group 11) and the DMI (activity Group 3) fungicides in Australia. Grape berries are most susceptible to powdery mildew during the period between flowering to 4 to 5 weeks after fruit set. Powdery mildew spreads short distances by wind, so most infection occurs from sources within a vineyard. Powdery mildew is favoured under conditions that are mild, humid and cloudy and disfavoured by hot and dry conditions. Powdery mildew grows faster in shady situations and less well when exposed to direct sunlight.
Cultural practices
- Trim sides of the vines to open up the conopy
- Manage sprey ragime - Fungasides
- Start with a protectant - SO2 early in spring = cooler conditions which wont hurt the vines
- Forecasting early on, tells us when conditions are ok for spreying
- When its too hot SO2 cant be spreyed
- Sprey group 3 or 11 first after the protectant (resistance groups)
- The use group 13 ( no resistance) along with cultural processes (pruing)
- Always monitor the vine yard
- Last resort if hygene (removal of bunches)
How will these actions help?
Pruning = Population down (good)
Forecasting = targets what spreys and when. dont waste sprey or damager plants
Protectant (fungaside) early = Reduced population size, fingacude wont get hold early
Other fungasides = Group 11,3 have resistance, is it doesnt work we can use something with no resistance
Monitoring = Know whats happening and see if fungasides are working
see photo
Volterra’s Principle
Following simultaneous harvest of a predator and its prey, the predator population will always take longer to reach its original population size than the prey.
- Many insectacied are more toxic to natural emamies than the insect pests
- Predators are way more susaptable
- some herbacides and fungacides also kill insects
- use the least toxi one first to avoid killng the natural emamies
