Effects of pathogens and disease on plant physiology

pathogenesis

process by which disease or disorder develops. infection and colonization of host, plus pathogen reproduction

plant parasite

organism that become intimately associated with a plant and multiplies/grows at expense of plant (not always harmful)

pathogen

organism that causes disease in host after infection

pathogenicity

ability of pathogen to interfere with host’s essential functions, causing disease (yes or no)

severity

degree of damage caused by pathogen, describes pathogen’s aggresiveness

if host-pathogen interaction is compatible, pathogen is ___

virulent

if host is resistant to pathogen strain, interaction is ___, and pathogen is ___

incompatible, avirulent

inoculum

pathogen that lands on plant or is brought into contact with it, refers to any part of pathogen that can initiate infection

monocyclic pathogen

completes only one disease cycle before growing season ends (soil-borne, stem, and root diseases)

polycyclic pathogen

completes multiple disease cycles during growing season, causes more infections (mildews, blights)

polyetic pathogen

takes more than one year to complete a disease cycle (tree diseases like vascular wilts)

pathogens in perennial plants

can survive regardless if plants are growing or dormant

pathogens in annual plants

host dies at end of season, so pathogens must survive without host

-fungi: mycelium/spores/sclerotia in soil, some are saprophytes

-bacteria: form biofilms in soil

-viruses, fastidious bacteria, mollicutes and protozoa need living plants

-nematodes: in plant roots or soil, juveniles in seeds or bulbs

what pathogens use vectors?

mollicutes, fastidious bacteria, protozoa, most viruses

-pathogens placed directly into plant cells

what pathogens don’t use vectors?

most fungi, bacteria and parasitic plants

-pathogens first brought into contact with plant’s external surface

how do pathogens become attached to the host surface?

-mucilaginous substances on surface (water soluble polysaccharides, glycoproteins, lipids, fibrillar materials)

-enzymes (cutinases)

-spores adhere with lectins, ionic interactins, hydrophobic contact

process of spore germination

-spore lands on leaf, recognizes host, produces germination tube and appressorium

-appressorium creates 40x more pressure than car tire to puncture cuticle plus cell wall (some also use enzymes)

-penetration peg forms, hypha enter apoplastic space, haustorium enter plant cells

what triggers spore germination?

contact w host, absorption of low molecular ionic materials, nutrient availability

pathogenicity factors

genes that enable pathogenicity on specific hosts, triggers non-specific plant defense (enzymes, toxins, growth regulators, polysaccharides)

effectors

pathogen secretions (mainly proteins) that manipulate host processes

race specific elicitor

encoded by avirulence gene, elicits host resistance in hosts with corresponding R gene (not corresponding = infection)

methods of plant penetration

Direct penetration thru plant surfaces (fungi, oomycetes, nematodes)

-nonobligate parasitic fungi use fine hyphae

-obligate parasitic fungi use penetration peg produced by appressorium

Penetration through wounds (bacteria, most fungi, viruses)

Penetration through natural openings (bacteria and fungi)

Natural openings for pathogen penetration

stomata, hydathodes, nectarhodes, lenticels

infection

process by which pathogens establish contact with susceptible cells or tissues of the host and procure nutrients from them

invasion

pathogens can spread into tissues of plant organs by growing directly through cells intracellularly or between cells intercellularly

pathogen dissemination by air

spores of most oomycetes and fungi, most parasitic plant seeds

pathogen dissemination by water

bacteria, nematodes, fungal structures in soil disseminated by rain and irrigation water

all bacteria and many fungal spores in sticky liquid, require water

pathogen dissemination by insects, mites, nematodes and other vectors

-viruses disseminated by aphids, leafhoppers and whiteflies

-leafhoppers main vectors of mollicutes, fastidious bacteria, protozoa

-fungi and bacteria stick to vectors, transmitted externally

photosynthesis

light converted to chem energy in thylakoids of chloroplast by PSI and PSII, reduce NADP+, oxidize water

pathogen effect on photosynthesis

-non-photochemical quenching: excited chlorophyll molecule returns to ground state by emitting heat energy (when light absorption exceeds utilization rates)

-disease limits NPQ, more reactive oxygen species are produced that damage the plant

pathogen effect on photorespiration

-photorespiration: O2 used as CO2 alternative for rubisco substrate, due to excess O2 that builds when a plant cant open its stomata

-temp/stomatal opening affects photorespiration/photosynthesis balance

pathogens that enter via stomata trigger stomatal closure, more H2O2 produced → chloroplast ROS production → defense response

pathogen effect on respiration

respiration produces sugars during photosynthesis. pathogens use more carbohydrates and nutrients, so respiration rate in infected areas increases

pathogen effect on membrane permeability

pathogens use toxins or digestive enzymes that cause cell loss of electrolytes and onset of necrosis, more soluble nutrient availability to pathogens

pathogen effect on transpiration

transpiration: process of losing water through leaf surfaces

most foliar pathogens reduce WUE

water use efficiency (WU

above-ground dry matter production per unit water transpired and evaporated per land area unit

pathogen effect on water translocation

canker or gall pathogens reduce translocation efficiency by destroying xylem vessels or clogging them with propagules/products