L17 - Epidemiology (3) Flashcards
Describe Rhizomania (“root madness”):
Include:
- the pathogen and any vector
- It’s infection cycle
- effects
- Caused by BNYVV (Beet Necrotic Yellow Vein Virus)
- Vectored inside Polymyxa betae (fungal-like protist)
- Primary infection by swimming zoospores
- Mature plants produce cystosori, germinate in later years
- Several cycles of infection + release within season
- Soil infested almost indefinitely
- Small amounts of soil movement spreads it e.g. on farm machinery
- Alters root architecture
- Occurs worldwide
- in UK by mid 1980s
Draw a sketch of the infection cycle of rhizomania.
Include both the survival and multiplication phase
- See diagram on pg 2 of L3
Give an overview of why control of Rhizomania is needed and the why this is a challenge
- Yield loss of 80% makes control necessary
Challenges:
- Extensive cryptic infestation in fields
- 2-3 crops (decade) from initial infection of field to widespread symptoms
- Large amplification of virus during growing season
- No resistant beet varieties when virus first discovered in the UK
- No effective control of vector P. betae
What was the initial method pursued in the UK to control the spread of Rhizomania?
What was the growing system at this time
“Field scale strategy”:
- DEFRA declared Rhizomania a notifiable disease in 1990s:
- Annual surveys
- Field w/ infected sugar beet crops destroyed
- No further growth on fields
- Waste not left on arable land
- Strict quota system controlled amount of sugar beet grown
Give an overview of the model used to assess if the “field scale strategy” of controlling Rhizomania should work
- Amount of virus in each field modelled
- Amount amplified only when sugar beet grown (3-4 year rotation)
- Model within farm transmission from infected soil/workers
- Model between farm transmission via sharing of machinery/workers
- Determine BNYVV density required to detect infection = symptomatic farm
- Apply field-scale control only to symptomatic farms
What were the conclusions from the “field-scale strategy” model
Applying field scale control to symptomatic farms gives no containment of spread:
- Crop rotation + delay before symptoms means control starts almost decade too late
- Virus already moved to neighbouring fields
- Culling symptomatic fields pointless
What alternative idea was used to try to control the spread of Rhizomania whilst maintaining sugar beet production?
Stewardship Scheme altered:
- Growers concerned about Rhizomania risk allowed to denote some/all of quota to other growers
- Controlled by growers, not centrally
- Introduced by British Sugar
Outline how a model can be developed to optimise the Sugar Beet stewardship scheme
- Model a network of farm-farm contact
- Create two degrees of freedom for stewardship:
1) Order: how many contacts to track
e.g. n = 0 (respond to disease on
own farm etc…
2) Sensitivity: π = risk aversion of
growers - Grower redistributes quota if average fraction of symptomatic fields within n th order radius exceeds 1 - π
What does the optimisation of the stewardship scheme model for Sugar Beet show the optimum “order” is.
Sketch a diagram showing the effectiveness of n = 1,2,3 against π
n = 2 order best (n = 3 increases spread again)
See diagram - spread controlled under certain parameters
What control for Rhizomania actually happened in the UK after the field scale strategy?
- Stewardship performed but adhoc
- Resistant varieties introduced in early 2000s
- Significant faith put in resistant varieties
- Legislation for stewardship repealed
- Amplification of inoculum in soil continued
What is the current state of Rhizomania in the UK?
- Resistance breaking reported recently
- Infestation now more widespread
- Rhizomania still a threat
Describe Sudden Oak Death (SOD):
Include:
- the pathogen and any vector
- It’s infection cycle
- effects
- Invasive exotic pathogen in NW Europe, UK and USA, especially California from 1990s
- Caused by Phytophthora ramorum (oomycete)
- Generalist: infects many native forest species
- Some species die quickly e.g. oak
- Many species don’t transmit
- Others survive indefinitely, pump out inoculum + propagate epidemic
- Millions of oak killed
What key questions did the modelling of the P. ramorum epidemic in California seek to address?
1) Where will pathogen be in 20 years?
2) Areas to prevent the pathogen spreading to
3) Can the epidemic be controlled?
What problems were associated with modelling SOD and how were these overcome?
Challenges:
- Multiple host species that respond differently is complex
- Very large area, can’t include individual trees
Solutions:
- CA divided into 250x250m squares
- Produce single “host index” per square based on host density (satellite imagery) and knowledge of host response
- Environmental factors affecting sporulation + infection included
Once CA had been divided into squares and a host index had been applied to each square what was then required to create a model of SOD
Dispersal kernel between squares had to be characterised
- Kernel estimated from data using Markov chain Monte Carlo
What was discovered about the dispersal kernel of SOD?
- Short and long-range component of dispersal kernel observed
1) Short range (wind blown rain/splashes) has 93% dispersal within 250m of cell
2) Long range dispersal (hikers/nurseries) has 95% dispersal within 100km of parent cell
What were the conclusions of the SOD model for California?
- Huge area at risk of SOD
- Explosive increase in area infected imminent, especially upon reaching of NW coast (high host + environment suitability)
- Epidemic not even halted w/ implausibly large removal now
- Earlier control could’ve been successful at large cost - optimal control radius method
- Focus now on containment
