Summary of fourth lesson ASCOMYCETES, BASIDIOMYCETES, OOMYCETES DISEASE TRIANGLE+ humans Dominant/CO-Dominant/ Genotype

Disease triangle Effect of humans

Human activities affecting disease incidence in forests Introduction of exotic pathogens Planting trees in inappropriate sites Changing stand density, age structure, composition, fire frequency Wound creation Pollution, etc.

Effects of fire exclusion

DISEASE: plant microbe interaction 1-Basic compatibility need to be present 2- Chemotaxis, thighmotropy 3- Avirulence in pathogen matched by resistance in host according to the gene for gene model 4-Pathogenicity factors such as toxins and enzymes important in the infection process

1- Basic compatibility Size of infectious propagules Timing of susceptibility in host and production of infectious structures

2- Finding the host Chemotaxis: pathogen has receptor that detects food base: in oomycetes zoospores will all swim towards host Thigmotropy: recognizing morphological structures that indicate presence of host; prelude to production of infective structures such as infection pegs and appressoria

3- Infecting the host Pathogen will produce array of enzymes to infect host cells Upon identification of infection, host will produce array of antimicrobial compounds, or will kill some of its cells to halt infection process (hypersensitive response)

3- Infecting the host Plant that are resistant, must be able to react (dominant R resistant allele) Plants that cannot react (r allele) are always sensitive Pathogens that are not noticed by plant can infect (recessive avirulence allele) Pathogens that are noticed may be stopped (dominant A avurulence allele)

3- Infecting the host RA= no disease Ra=disease ra=disease rA=disease There will be a strong selection in favor of R alleles but R comes at a cost

4- Causing disease Correlated to ability of pathogen to invade plant cell, pathogenicity is usually a dominant trait

Categories of wild plant diseases Seed decay Seedling diseases Foliage diseases Systemic infections Parasitic plants Cankers, wilts, and diebacks Root and butt rots Floral diseases

Seed diseases Up to 88% mortality in tropical Uganda More significant when seed production is episodic

Stress cone cropBS on DF

Seedling diseases Specific diseases, but also diseases of adult trees can affect seedlings Pythium, Phytophthora, Rhizoctonia, Fusarium are the three most important ones Pre- vs. post-emergence Impact: up to 65% mortality in black cherry. These diseases build up in litter Shady and moist environment is very conducive to these diseases

Foliar diseases In general they reduce photosynthetic ability by reducing leaf area. At times this reduction is actually beneficial Problem is accentuated in the case of small plants and in the case other health issues are superimposed Often, e.g. with anthracnose,needle cast and rust diseases leaves are point of entry for twig and branch infection with permanent damage inflicted

Systemic infections Viral? Phytoplasmas Peronospora and smuts can lead to over 50% mortality Endophytism: usually considered beneficial

Grass endophytes Clavicipetaceae and grasses, e.g. tall fescue Mutualism: antiherbivory, protection from drought, increased productivity Classic example of coevolutionary development: Epichloe infects “flowers” of sexually reproducing fescue, Neotyphodium is vertically transmitted in species whose sexual reproductive ability has been aborted

Parasitic plants True (Phoradendron) and dwarf mistletoe (Arceuthobium) Effects: –Up to 65% reduction in growth (Douglas-fir) –3-4 fold mortality rate increase –Reduced seed and cone production Problem accentuated in multistoried uneven aged forests

Cankers, wilts, and die-backs Includes extremely aggressive, often easy to import tree diseases: pine pitch canker, Dutch elm disease, Chestnut blight, White pine blister rust Lethal in most cases, generally narrow host range with the exception of Sudden Oak Death

Root diseases Extremely common, probably represent the most economically damaging type of diseases Effects: tree mortality (direct and indirect), cull, effect on forest structure, effect on composition, stand density, growth rate Heterobasidion, Armillaria, Phellinus weirii, Phytophthora cinnamomi

Removing food base causes infection of roots of other trees Hyphae in plant tissue or soil (short- lived) Melanin-covered rhizomorphs will allow for fungus to move to new food Sources (Armillaria mellea)

Effects of fire exclusion

Floral diseases Pollinator vectored smut on silene offers an example of well known dynamic interaction in which pathogen drives genetic variability of hosts and is affected by environmental condition Puccinia monoica produces pseudoflowers that mimic real flowers. Effects: reduction in seed production, reduction in pollinators visits

Density-dependence Most diseases show positive density dependence Negative dependence likely to be linked to limited inoculum: e.g. vectors limited If pathogen is host-specific overall density may not be best parameter, but density of susceptible host/race In some cases opposite may be true especially if alternate hosts are taken into account

Counterweights to numerical effects Compensatory response of survival can exceed negative effect of pathogen “carry over” effects? –NEGATIVE: progeny of infected individuals less fit; –POSITIVE; progeny more resistant (shown with herbivory)

Disease and competition Competition normally is conducive to increased rates of disease: limited resources weaken hosts, contagion is easier Pathogens can actually cryptically drive competition, by disproportionally affecting one species and favoring another

Janzen-Connol Regeneration near parents more at risk of becoming infected by disease because of proximity to mother (Botryosphaeria, Phytophthora spp.). Maintains spatial heterogeneity in tropical forests Effects are difficult to measure if there is little host diversity, not enough host-specificity on the pathogen side, and if periodic disturbances play an important role in the life of the ecosystem