Stem Decays – Growth Rate

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 ​[4]​), 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 trees

Vertical 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 saccharumPhellinus igniarius1.80.6 – 3.0Silverborg 1959
Betula alleghaniensisInonotus obliquus2.10.6 – 3.7Silverborg 1959
Fagus grandifoliaI. glomeratus3.01.2 – 4.9Silverborg 1959
Acer saccharumI. glomeratus8.57.9 – 9.8Silverborg 1959
Fagus grandifoliaP. igniarius157.9 – 20Silverborg 1959
Fagus grandifoliaGanoderma applanatum179.7 – 21Silverborg 1959
Populus grandidentataP. igniarius2920 – 40Silverborg 1959
Pinus strobusPorodaedalea pini11 up
14 down
3 – 35Silverborg & Larsen 1967
Picea rubensFomitopsis pinicola9.86 – 14Hirt & Eliason 1938
Tsuga canadensisF. pinicola33 – 3Hirt & Eliason 1938
Fagus grandifoliaPhellinus igniarius s.l.32 – 4Hirt 1949
Populus tremuloidesP. igniarius s.l.156 – 35Hirt 1949
VariousI. obliquus190.4 – 38Hirt 1949
Quercus spp. (black)natural infection of aged fire scars5.8Hepting 1935
Fraxinus spp.natural infection of aged fire scars3.6Hepting 1935
Liquidambar styracifluanatural infection of aged fire scars3Hepting 1935
Celtis laevigatanatural infection of aged fire scars1.4(faster initially)Hepting 1935
Quercus spp. (red)natural infection of aged fire scars43 - 20 (depending on fungus isolated)Toole & Furnival 1957
Pinus sylvestrisPorodaedalea pini14 – 28Möller 1910
Picea abiesHeterobasidion annosum2819 – 63Rennerfelt 1946

Rate of decay in stands

Gross merchantable volume and that lost to decay in Abies balsamea over time. Tree growth slows after 100 years while decay continues at the same rate. By age 160 there is no merchantable wood left. Almost all of the decay was butt rot caused by Perenniporia subacida and Postia balsamea; and top rot caused by Stereum sanguinolentum. This is rapid and severe decay, but there are worse examples. Data from Kaufert 1935, table 3.

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, ​[7]​). 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.

Gross volume and loss due to Porodaedalea pini in old-growth stands of Pseudotsuga menziesii on good sites (site II). The wave pattern is caused by increase of decay over time followed by death of decadent trees. Overall, P. pini caused about 80% of decay. Data from Boyce & Wagg (1953), Table 19 and Fig. 23. This depiction uses 2nd order polynomial curve fitting for gross volume and spline interpolation for decay volume.

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 ​[15]​.

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 ​[1]​:

  • 200 yr: 0.7% decay of merchantable volume
  • 750 yr: 27%

At the other extreme, Populus tremuloides in Minnesota ​[11]​:

  • 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 ​[3]​.

stand A180 yr14% decay of board-foot volume
stand B (only 4 miles from stand A)214 yr61%

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. 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. 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. <>.
  3. 3.
    Englerth GH. 1942. Decay of western hemlock in western Oregon and Washington. Bulletin 50. Yale University School of Forestry.
  4. 4.
    Hepting GH. 1935. Decay following fire in young Mississippi Delta hardwoods.  USDA Technical Bulletin 494. Washington DC: US Department of Agriculture. 32 pp. <>.
  5. 5.
    Hirt RR. 1949. Decay of certain northern hardwoods by Fomes igniarius, Poria obliqua, and Polyporus glomeratus. Phytopathology 39:475–480.
  6. 6.
    Hirt RR, Eliason EJ. 1938. The development of decay in living trees inoculated with Fomes pinlcola. Journal of Forestry 36(7):705–709 <>.
  7. 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 <>.
  8. 8.
    Möller A. 1910. Der Kampf gegen den Kiefernbaumschwamm. Zeitschrift für Forst- und Jagdwesen 42:129–146.
  9. 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 <>.
  10. 10.
    Risley JH, Silverborg SB. 1958. Stereum sanguinolentum on living Norway spruce following pruning. Phytopathology 48(6):337–338.
  11. 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 <>.
  12. 12.
    Silverborg SB. 1959. Rate of decay in northern hardwoods following artificial inoculation with some common heartrot fungi. Forest Science 5(3):223–228 <>.
  13. 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 <>.
  14. 14.
    Toole ER, Furnival GM. 1957. Progress of heart rot following fire in bottomland red oaks. Journal of Forestry 55(1):20–24 <>.
  15. 15.
    Wagener WW, Davidson RW. 1954. Heart rots in living trees. The Botanical Review 20(2):61–134 <>.