Pathogenesis Flashcards

1
Q

What is pathogenesis?​

A

The process of development of a disease​
Symptoms​
Biological underpinning – mechanism​

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2
Q

what is Pathogenicity?

A

Pathogenicity describes the ability of a pathogen to produce pathogenesis and is associated with the ability of the pathogen to complete (relevant stages of) its life cycle in a host (c.f virulence) ​

virulence=degree at which it is pathogenic

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3
Q

What is it about the presence of a pathogen that causes pathogenesis?​

A

Linking symptoms and biological mechanism can sometimes be very straightforward​

Damage may caused directly by the pathogen, indirectly as a consequence of pathogen action or may be self-inflicted damage caused by the host​

It might help you to think about competing strategies of host and pathogen​

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4
Q

What is the damage directly caused by the pathogen​

A

Strategic damage​ is the direct outcome of their infection strategy
Penetration and progression through the host​ (physical damage done to cell wall)
Cell wall degrading enzymes​ (cellulases, pectinases etc.)​
Toxin Triggered Immunity​

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5
Q

Plant responses to necrotrophic pathogens​

A

There are few known R genes that confer resistance to necrotrophic pathogens, therefore breeding resistance to necrotrophs is more challenging than to biotrophs​
(fungus)

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6
Q

Damage indirectly caused by the pathogen​

A

The ash dieback fungus is called Hymenoscyphus fraxineus (sexual) also called Chalara fraxinea (asexual)​
Major tree pathogen​
Fungal hyphae block the vasculature of the ash tree causing death of tissues above this point​ as it cant get nutrients

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7
Q

Changes in plant biotic and abiotic plant responses have a physiological basis​

A

Case study​

Infections with the vascular pathogens Verticillium longisporum and Verticillium dahliae induce distinct disease symptoms and differentially affect drought stress tolerance of Arabidopsis thaliana

Both Verticillium longisporum (VL43) and Verticilium dahliae (VDJR2) can infect Arabidopsis and both inhibit growth and have an associated pathology​

after induced you gte leaf curling, senescence

Vascular effects differ between VL43 and VDJR2​
VDJR2 shows typical cell wall thickening​
VL43 shows cellular proliferation in the plant vasculature​

Cell walls autofluoresce which makes them easy to visualise​
> 6 times more new xylem (vascular) cells in VL43 infected plants ​
this means that if these plants go through drought stress those inoculated with the pathogen are more likely to survive and recover and this is due to an increase water content in the plant due to proliferation of cells in the presence of longisporum

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8
Q

Some effectors alter plant behaviour and development​

A

bacterial pathogens e.g P.syringae ( uses molecules that it produces to mimic phytohormones that plants use to open and close stomata) and X. citri (uses necrosis and cankers which breaks open to give rise to infected particles). Both of these use physiology of plant for their own benefit.
G. fujikuroi is a fungal pathogen of rice which produces lesions that produces lots of spores to spread. It produces extra gibberellin which is responsible for the vertical growth of plants. more growth of seedlings so when spores are produced they are broadcasts more efficiently.
Therefore manipulation of the plant physiology

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9
Q

Some pathogens take advantage of the defense signal cross-talk​

A

Pseudomonas syringae producing coronatine ​
Coronatine is an excellent mimic of JA-Ile, the active jasmonate hormone. By suppressing biotrophic defenses coronatine production significantly enhances the pathogenicity of the bacteria that produce it​.#
makes a molecule that is the opposite to confuse the plant

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10
Q

Defense pathways intersect with other signaling pathways​

A

Defense responses reduce growth rate. Drought stress and abscisic acid (ABA) accumulation suppresses responses to pathogens​

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11
Q

Salicylate and jasmonate are mutually antagonistic​

A

biotrophs go through the salysiclic pathway whereas necrotrophs go the the jasmonate pathway

Perhaps because the pathogenicity of necrotrophs is enhanced by the hypersensitive response, so HR should be suppressed in the presence of necrotrophs…​

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12
Q

Many organisms manipulate plant hormone action​

A

Eriophyes tiliae is a mite which chemically induces nail galls on lime (linden) tree leaves.​
This isn’t too harmful to the plant.​

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13
Q

what do some insects do?

A

Some insects use microbial pathogen effectors to interfere with host phytohormone signalling and gene expression​.

bites switches off genes and makes it a better place to live

phytoplasma can reprogram flowers to be in a vegetative site
Aster leafhopper Macrosteles quadrilineatus demonstrates oviposition preference for plants with leaf-like flowers.​

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14
Q
  1. Plant responses to pathogens contribute to pathogenesis​
A

Callose, ROS and phytoalexins can arrest pathogen attack ​

Callose, a polysaccharide, acts as a barrier, and ROS and phytoalexins are toxic to pathogens​

you get thickening of cell walls (callose)
Callose is laid down by the plant to physically block pathogens – local immune responses and at plasmodesmata​

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15
Q

Senescence and cell death are normal, actively controlled processes​

A

Nutritional senescence​
Pathogen-induced cell death​
Reproductive senescence​
Autumnal senescence​
Developmental cell death​ (deliberate)

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16
Q

What are senescence and cell death? Our definitions…​

A

We are defining cell death as a localized process that culminates in the death of the cell, and is often quite rapid​. We are defining senescence as a slower, systemic process that includes nutrient remobilization, and under most conditions culminates in the death of cells​

17
Q

Defensive action – Programmed Cell Death​

A

The hypersensitive response (HR) is a defense mechanism. Infected and adjacent cells are killed through PCD​.

18
Q

HR cell death is mediated by ROS signals and salicylic acid (SA) ​

A

ROS is generated in the apoplast, in chloroplasts, and mitochondria . ROS and SA act synergistically.
PCD in plants involves ROS production and hormone signals​.
The vacuole is very important in plant PCD​.

Lytic enzymes are stored in the vacuole​
The vacuole can rupture and release lytic enzymes into the cytoplasm​
Cytoplasmic components can be delivered into the vacuole through the process of autophagy​​

19
Q

Caspase-like VPE is necessary for hypersensitive cell death​

A

TMV infected leaf shows HR cell death​
Vacuolar Processing Enzyme (VPE)-silenced TMV infected leaf shows no HR cell death​.

HR cell death requires autophagy ​
Note appearance of autophagosomal-like vesicles​

20
Q

Summary I​

A

Affecting growth and development of plants can have a great effect on physiology​

Possible because of overlap in biochemical pathways and manipulation by pathogen and host​

Both plant and pathogen cause pathogenesis​

Pathogens cause pathogenic symptoms via direct (CWDEs) and indirect (physical) means​

Plants produce phenolic compounds, thicken cell walls, use ROS and PCD​