A general introduction to stem decays is another page. Here we focus on how fast (or slow) they progress in living trees and in stands. This is the kind of work pathologists did in days of yore, when they strode the forest like giants. So I had to dig into some pretty old sources to put this together.
Growth rate of decay columns
How fast does a wood-decay fungus grow axially in the stem? There are two approaches to finding out: inoculate, wait about five to ten years, then cut and measure; OR find trees with infection courts that can be aged, then cut and measure. The latter has the advantage of natural infection but the disadvantage that the time of infection could range from the time of wounding to the closing of the wound. Such studies have shown that rates are highly variable, even among trees of the same species with the same fungus (see table below; [2, 4–6, 8–10, 12–15]). The mean of all the means in the table is 10 cm yr-1 (in one direction).
There is reason to believe that the long-term average growth rate of natural infections may be somewhat less. Initial growth may be faster (e.g. in Celtis laevigata ), perhaps due to better aeration. Also, inoculation studies may overestimate early growth because natural infections likely have a much slower start. Generally, two sporelings of compatible mating type must grow near each other, fuse, and then slowly build resources like that of the artificial inoculum, which has much more inoculum potential. Indeed, growth rates based on natural infections tend to be lower than those from inoculation studies (see table).
Table: Growth rate of decay columns in living treesVertical spread (one direction, in some cases includes incipient decay) of decay in living trees, cm yr-1. For Toole & Furnival's data, the minimum and maximum represent the averages of the slowest and fastest identified fungus. Hirt & Eliason inoculated one tree each of 4 host species in which the fungus survived 10 years. The species with minimum and maximum spread are shown here; "average" is the average of growth up and down.
|Acer saccharum||Phellinus igniarius||1.8||0.6 – 3.0||Silverborg 1959|
|Betula alleghaniensis||Inonotus obliquus||2.1||0.6 – 3.7||Silverborg 1959|
|Fagus grandifolia||I. glomeratus||3.0||1.2 – 4.9||Silverborg 1959|
|Acer saccharum||I. glomeratus||8.5||7.9 – 9.8||Silverborg 1959|
|Fagus grandifolia||P. igniarius||15||7.9 – 20||Silverborg 1959|
|Fagus grandifolia||Ganoderma applanatum||17||9.7 – 21||Silverborg 1959|
|Populus grandidentata||P. igniarius||29||20 – 40||Silverborg 1959|
|Pinus strobus||Porodaedalea pini||11 up|
|3 – 35||Silverborg & Larsen 1967|
|Picea rubens||Fomitopsis pinicola||9.8||6 – 14||Hirt & Eliason 1938|
|Tsuga canadensis||F. pinicola||3||3 – 3||Hirt & Eliason 1938|
|Fagus grandifolia||Phellinus igniarius s.l.||3||2 – 4||Hirt 1949|
|Populus tremuloides||P. igniarius s.l.||15||6 – 35||Hirt 1949|
|Various||I. obliquus||19||0.4 – 38||Hirt 1949|
|Quercus spp. (black)||natural infection of aged fire scars||5.8||Hepting 1935|
|Fraxinus spp.||natural infection of aged fire scars||3.6||Hepting 1935|
|Liquidambar styraciflua||natural infection of aged fire scars||3||Hepting 1935|
|Celtis laevigata||natural infection of aged fire scars||1.4||(faster initially)||Hepting 1935|
|Quercus spp. (red)||natural infection of aged fire scars||4||3 - 20 (depending on fungus isolated)||Toole & Furnival 1957|
|Pinus sylvestris||Porodaedalea pini||14 – 28||Möller 1910|
|Picea abies||Heterobasidion annosum||28||19 – 63||Rennerfelt 1946|
Rate of decay in stands
Stand age is a consistently important factor in the amount of stem decay, across hosts, pathogens, and regions. Stem decay increases with age of a stand (first graph, ). Obviously, the longer a tree stands, the more likely it is to become infected, and the longer the fungus has to to colonize and decay it. Stem decay is not like a cold, it is more like arteriosclerosis: once you get it, you’ve got it the rest of your life, and it only gets worse.
This increase with time is true for individual trees and, in general, stands, but it has been observed that decay can actually decrease in old, decadent stands, even doing so in waves of decrease and increase [1, 2] (second graph). This is due to mortality of decadent trees, reducing the percentage of decay in the residual trees, followed by further increase in decay .
There are several reasons why decay generally increases as stands age:
- more infection courts in older trees (stubs, breaks, wounds, etc.)
- more heartwood in older trees
- wounds are closed more slowly in older trees so more likely to be infected
- older trees grow more slowly, so the fungus grows faster relative to the tree.
An exceptionally sound example is Picea sitchensis (Sitka spruce) in Queen Charlotte Islands, British Columbia :
- 200 yr: 0.7% decay of merchantable volume
- 750 yr: 27%
At the other extreme, Populus tremuloides in Minnesota :
- 20 yr: 8% decay of total volume
- 80 yr: 34%
But these are large-scale averages. Individual stands may vary tremendously, e.g., Tsuga heterophylla in Washington and Oregon .
|stand A||180 yr||14% decay of board-foot volume|
|stand B (only 4 miles from stand A)||214 yr||61%|
What can account for such a big difference between stands that are of similar age? See the page Stem Decays – Epidemiology and Management for some ideas. Also, for more on the Kaufert data in the first graph above, see the discussion of pathological rotation on that page.
- 1.Bier JE, Foster RE, Salisbury PJ. 1946. Studies in Forest Pathology. IV. Decay of Sitka spruce on the Queen Charlotte Islands. Ottawa, Ontario, Canada: Department of Mines and Resources, Lands, Parks and Forests Branch, Dominion Forest Service, Canada Department Agriculture, Division of Botany & Plant Pathology.
- 2.Boyce JS, Wagg JWB. 1953. Conk Rot of Old-Growth Douglas-fir in Western Oregon. Bulletin 4. Oregon Forest Products Laboratory and Oregon State Forestry Department. 96 pp. <https://ir.library.oregonstate.edu/downloads/k35695737>.
- 3.Englerth GH. 1942. Decay of western hemlock in western Oregon and Washington. Bulletin 50. Yale University School of Forestry.
- 4.Hepting GH. 1935. Decay following fire in young Mississippi Delta hardwoods. USDA Technical Bulletin 494. Washington DC: US Department of Agriculture. 32 pp. <https://doi.org/10.22004/ag.econ.164668>.
- 5.Hirt RR. 1949. Decay of certain northern hardwoods by Fomes igniarius, Poria obliqua, and Polyporus glomeratus. Phytopathology 39:475–480.
- 6.Hirt RR, Eliason EJ. 1938. The development of decay in living trees inoculated with Fomes pinlcola. Journal of Forestry 36(7):705–709 <https://academic.oup.com/jof/article-abstract/36/7/705/4721217>.
- 7.Kaufert F. 1935. Heart rot of balsam fir in the Lake States, with special reference to forest management. University of Minnesota Agric. Exp. Station Technical Bulletin 110:1–27 <https://conservancy.umn.edu/bitstream/handle/11299/204039/mn1000_agexpstn_tb_110.pdf>.
- 8.Möller A. 1910. Der Kampf gegen den Kiefernbaumschwamm. Zeitschrift für Forst- und Jagdwesen 42:129–146.
- 9.Rennerfelt E. 1946. Om rotrötan (Polyporus annosus Fr.) i Sverige. Dess utbredning och sätt att uppträda [Über die Wurzelfaule (Polyporus annosus Fr.) in Schweden]. Meddelanden Från Statens Skogsforskningsinstitut 35(8):1–89 <https://pub.epsilon.slu.se/9895/1/medd_statens_skogsforskningsinst_035_08.pdf>.
- 10.Risley JH, Silverborg SB. 1958. Stereum sanguinolentum on living Norway spruce following pruning. Phytopathology 48(6):337–338.
- 11.Schmitz H, Jackson LWR. 1927. Heart rot of aspen with special reference to forest management in Minnesota. Technical BuIlletin 50. University of Minnesota Agricultural Experiment Station <https://conservancy.umn.edu/bitstream/handle/11299/203990/mn1000_agexpstn_tb_050.pdf?sequence=1>.
- 12.Silverborg SB. 1959. Rate of decay in northern hardwoods following artificial inoculation with some common heartrot fungi. Forest Science 5(3):223–228 <https://academic.oup.com/forestscience/article-abstract/5/3/223/4763968>.
- 13.Silverborg SB, Larsen MJ. 1967. Rate of decay in Pinus strobus following artificial inoculation with Fomes pini. Plant Disease Reporter 51(10):829–831 <https://www.google.com/books/edition/The_Plant_Disease_Reporter/5KL8l7pXtLoC?hl=en&gbpv=1&pg=PA831>.
- 14.Toole ER, Furnival GM. 1957. Progress of heart rot following fire in bottomland red oaks. Journal of Forestry 55(1):20–24 <https://www.fs.usda.gov/treesearch/pubs/42513>.
- 15.Wagener WW, Davidson RW. 1954. Heart rots in living trees. The Botanical Review 20(2):61–134 <https://pdfslide.net/documents/heart-rots-in-living-trees.html>.