2. DISEASES AND TREES What exactly is a disease? It is the outcome of an interaction between a plant and the environment, resulting in an altered physiology of the host Sustained interaction=biotic Single event= abiotic

5. What is a pathogen? Strictly speaking a pathogen is the causal agent of disease Bacteria Viruses Nematodes Stramenopiles Algae Phytoplasmas Higher plants

6. And of course… fungi Fungi: saprophytic, symbionts, and pathogens Polyphyletic group in evolutionary terms –Basidiomycetes Ascomycetes Zygomycets Animals Plants Red algae Brown algae Myxomycetes

7. Fungi… again! Filamentous somatic (vegetative body) –High surface, good for extrogenous digestion –Good infection structures, infection peg, appressoria, rhizomorphs Chitin in cell wall Nuclear ploidy very unique Reproduction by spores: asexual mode very well represented Small nuclei, but with a lot of plasticity

8. Hyphae, sporangia, and zoospores of P. ramorum

9. Fungi do not photosynthesize Biotrophic: mycorrhyzae, rusts Endophites: clavicipetaceae, Necrotrophic; most pathogens Saprobes: primary (involved in litter decomposition)

10. Some pathogen roles in natural plant communities Selection of individuals best suited for the site Maintenance of genetic diversity and stability in host plant populations Establishment or maintenance of host geographic ranges Natural succession Regulation of stand density, structure, and composition

11. DISEASE!! Symptoms vs. signs; e.g. chlorosis vs. fruit- body The disease triangle

12. host-pathogen-environment Susceptibility of individuals or of portions of individuals Genetic variability Basic compatibility (susceptibility) between host and pathogen Ability to withstand physiological alterations

13. Genetic resistance in host Length of lesion (mm) Proportion of stem girdled (%) Nicasio\42.5 a 0.71 a China Camp40.5 a 0.74 a San Diego27.8 b 0.41 b Ojai25.0 b 0.47 b Interior live oak (Maricopa) 14.1 b 0.33 b

14. host-pathogen-environment Basic compatibility with host (virulence) Ability to maintain diversity: sex vs. no sex Size of genetic pool Agressiveness (pathogenicity) towards hosts Ability to survive without host

15. Chlamydospores of P. ramorum

17. West Coast Europe P. lateralis

18. host-pathogen-environment Temperatures Shading Relative humidity Free standing water pH and any potentially predisposing factors Nutrient status

19. Colony diameter (mm) at 13 days

20. Presence of free water Between 6 and 12 hours required for infection of bay leaves

21. 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.

23. Effects of fire exclusion

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

25. Effects of diseases on host mortality, growth and reproduction Young plants killed before reaching reproductive age Affect reproductive output Directly affect flowers and fruits

26. Complexity of forest diseases At the individual tree level: 3 dimensional At the landscape level” host diversity, microclimates, etc. At the temporal level

27. Complexity of forest diseases Primary vs. secondary Introduced vs. native Air-dispersed vs. splash-dispersed, vs. animal vectored Root disease vs. stem. vs. wilt, foliar Systemic or localized

28. Progression of cankers Older canker with dry seep Hypoxylon, a secondary sapwood decayer will appear

29. Stem canker on coast live oak

30. Cankers by P. ramorum at 3 months from time of inoculation on two coast live oaks

31. Root disease center in true fir caused by H. annosum

34. 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

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

36. 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

37. 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

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

41. 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

42. 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

46. 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

47. 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

49. 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

50. POPULATION DYNAMICS Species interactions and diversity

51. 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

52. 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)

53. 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

54. Diseases and succession Soil feedbacks; normally it’s negative. Plants growing in their own soil repeatedly have higher mortality rate. This is the main reason for agricultural rotations and in natural systems ensures a trajectory towards maintaining diversity Phellinus weirii takes out Douglas fir and hemlock leaving room for alder

55. Janzel-Connol Regeneration near parents more at riak 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

56. The red queen hypothesis Coevolutionary arm race Dependent on: –Generation time has a direct effect on rates of evolutionary change –Genetic variability available –Rates of outcrossing (Hardy-weinberg equilibrium) –Metapopulation structure

57. Frequency-, or density dependent, or balancing selection New alleles, if beneficial because linked to a trait linked to fitness will be positively selected for. –Example: two races of pathogen are present, but only one resistant host variety, suggests second pathogen race has arrived recently

58. Diseases as strong forces in plant evolution Selection pressure Co-evolutionary processes –Conceptual: processes potentially leading to a balance between different ecosystem components –How to measure it: parallel evolution of host and pathogen

59. Rapid generation time of pathogens. Reticulated evolution very likely. Pathogens will be selected for INCREASED virulence In the short/medium term with long lived trees a pathogen is likely to increase its virulence In long term, selection pressure should result in widespread resistance among the host

60. More details on: How to differentiate linear from reticulate evolution: comparative studies on topology of phylogenetic trees will show potential for horizontal transfers. Phylogenetic analysis neeeded to confirm horizontal transmission

61. Geneaology of “S” DNA insertion into P ISG confirms horizontal transfer. Time of “cross-over” uncertain 890 bp CI>0.9 NA S NA P EU S EU F

62. Phylogenetic relationships within the Heterobasidion complex Fir-Spruce Pine Europe Pine N.Am.

63. HOST-SPECIFICITY Biological species Reproductively isolated Measurable differential: size of structures Gene-for-gene defense model Sympatric speciation: Heterobasidion, Armillaria, Sphaeropsis, Phellinus, Fusarium forma speciales

64. Phylogenetic relationships within the Heterobasidion complex Fir-Spruce Pine Europe Pine N.Am.

65. SEX Ability to recombine and adapt Definition of population and metapopulation Different evolutionary model Why sex? Clonal reproductive approach can be very effective among pathogens

67. The “scale” of disease Dispersal gradients dependent on propagule size, resilience, ability to dessicate, NOTE: not linear Important interaction with environment, habitat, and niche availability. Examples: Heterobasidion in Western Alps, Matsutake mushrooms that offer example of habitat tracking Scale of dispersal (implicitely correlated to metapopulation structure)---two examples: Heterobasidion in California, and Coriolopsis in Panama

68. From Garbelotto and Chapela, Evolution and biogeography of matsutakes Biodiversity within species as significant as between species

69. S-P ratio in stumps is highly dependent on distance from true fir and hemlock stands.. San Diego

70. White mangroves: Corioloposis caperata

71. White mangroves: Corioloposis caperata Distances between study sites

72. Coriolopsis caperata on Laguncularia racemosa Forest fragmentation can lead to loss of gene flow among previously contiguous populations. The negative repercussions of such genetic isolation should most severely affect highly specialized organisms such as some plant- parasitic fungi. AFLP study on single spores

74. From the population level to the individual Autoinfection vs. alloinfection Primary spread=by spores Secondary spread=vegetative, clonal spread, same genotype. Completely different scales Coriolus Heterobasidion Armillaria Phellinus

75. Recognition of self vs. non self Intersterility genes: maintain species gene pool. Homogenic system Mating genes: recognition of “other” to allow for recombination. Heterogenic system Somatic compatibility: protection of the individual.