This is an introduction to stem decays. Related pages are:


Stem decay is decay of wood originating in the stems of living trees (excluding root and butt rots, although some of them can infect stem wounds as well as roots). Stem decays are an important disease category leading to economic loss, tree mortality, and wildlife habitat.  On developed sites and urban landscapes, stem decays are an important cause of tree hazard by creating tree defects that increase the likelihood of mechanical failure.

Such diseases are traditionally grouped into heart rots and sap rots. Here we deprecate that dichotomy because it implies that decay is restricted to that part, which is frequently not the case, and there is another important group to consider. See the next section for details.

Before this page, you should read the page on Wood Decay, which has necessary background information, including wood anatomy and chemistry, types of decay, terms for decays in various positions, disease cycle of decays, and tree resistance.

Some apparently consider decay of dead sapwood and heartwood not to be pathogenesis, i.e. not disease. Boyce argued that it is both parasitism and disease ​[4]​. I agree. If you had a microorganism destroying your fingernails, your hair, or feeding on your dead skin cells and turning them to mush, would you consider that a disease? Wood without living cells still serves a function for the living organism.

Types of Stem Decays

Heart vs. sap rot

Traditionally, decays in stems are grouped into heart rots, “any decay that becomes progressive in the central dead wood of a living tree”, and sap rots, “decays primarily of the sapwood” ​[22]​. The wording is important. If a wound removes bark (behind which the sapwood will die), and a fungus invades, decays and mostly stays there, that is a sap rot. But if it works through the dead sapwood into the heartwood, and progresses there, it is a heart rot.

But what about the disease in which a fungus is well established in the heartwood, then encroaches on the inner sapwood and begins to decay it? This is quite common (see references below under Disease Cycle: Invasion and the list of true stem decayers below). Some even grow in the outer sapwood, kill the cambium, and cause cankers. We can apply the term canker-rot in the latter case, but how do these fungi fit into the heart/sap rot dichotomy?

It has been suggested that the same fungus might simultaneously cause heart rot, sap rot, and canker rot ​[21]​. That’s fine, but to be clear, we’re then using the words like symptoms, to describe what a fungus is doing at a certain place and time. We’re not using them to group kinds of diseases.

True stem decays vs. wound decays

As information about novel infection courts began to become available (see Disease cycle below), a pattern began to emerge that characterized a group termed true heart rots or true stem decays ​[8, 18]​. True stem decays are highly specialized for infecting and decaying living trees. They are usually distinguished by:

  • consistently fruiting on living trees
  • may also cause punk knots
  • never invade slash, dead trees, or wood in service, but may continue to decay dead tree or log
  • mechanical injuries do not appear to serve as the principal infection courts

An additional feature that is often presented is that decay is usually confined to true heartwood. However, as discussed above under Disease Cycle: Invasion, it is not uncommon for them to attack and decay sapwood and, as shown in the list below, even kill the cambium (i.e., cause cankers).

Some of the true stem decays are listed here, mostly selected from ​[21]​. It is interesting to note that all but one of the pathogens are in the family Hymenochaetaceae.

  • Red ring rot of conifers caused by Porodaedalea pini (invades sapwood, cankers ​[4, 5]​)
  • Red ring rot of conifers caused by Porodaedalea chrysoloma (kills sapwood, cankers ​[11]​)
  • Rust-red stringy rot caused by Echinodontium tinctorium, the Indian paint fungus
  • White trunk rot of hardwoods caused by Phellinus igniarius (sapwood, cankers in inoculation ​​[20]​​)
  • White trunk rot of Populus tremuloides caused by Phellinus tremulae (cankers)
  • White trunk rot of Betula spp. caused by Phellinus laevigatus (cankers ​[4]​)
  • Robustus trunk rot of Quercus spp. caused by Fomitiporia robusta (sapwood, cankers ​[4, 21]​)
  • Trunk and branch rot of Juniperus monosperma caused by Fomitiporia texana (decays outer sapwood, kills trees ​[24]​)
  • Trunk rot of Tsuga heterophylla caused by Phellinus hartigii (spreads through sapwood, cankers ​[4]​)
  • Sterile conk rot of Betula spp. caused by Inonotus obliquus (cankers ​​[4]​)
  • Sterile conk rot of Acer and Fagus spp. caused by Inonotus glomeratus (sapwood, cankers ​[4, 20]​)

Other stem decays are simply called wound decays ​[13]​. Some fit the traditional definition of heart rot, primarily developing in heartwood, while others are more restricted to dead sapwood. They may infect through sapwood killed by cankers, sunscald, or other causes as well as mechanical injuries.


Based on the foregoing, I suggest the following terms and hierarchy. This is the traditional heart rot/sap rot dichotomy ​[22]​, except we pull out the true stem decays into a separate category. Seen another way, it follows the modern trend to recognize true stem decays and wound decays ​[13]​, except the latter is divided into two quite different groups.

  • True stem decays (as generally defined, without the feature that they are confined to the heartwood, because most are not)
  • Wound decays (do not have features of true stem decays; entering through mechanical injuries or otherwise dead sapwood)
    • Wound heart rots (become progressive primarily in the central dead wood)
    • Sap rots (primarily in dead sapwood)

Disease cycle


Stem-decay fungi must produce enormous numbers of spores because they are randomly dispersed in the air, and the chances of landing on and successfully colonizing a suitable infection court (along with a potential mate) are very small. One conk of Ganoderma applanatum produced over 30 billion spores per day for 6 months (yup, that’s over 5 trillion total), and that is just one year for a perennial conk ​[23]​. A field measurement of spore production of Fomes fomentarius gave 138 million per cm2 per day. For a large conk (770 cm2), that would be over 106 billion per day ​[6]​. But perhaps the world record goes to a conk of F. fomentarius that yielded over 300 billion spores per day (​[15]​, cited in ​[22]​).

Infection court: the “Hartig concept”

It is often said (e.g. ​[21, 25]​) that Robert Hartig ​[14]​ promulgated a concept of infection courts of heart rots. It is variously described, such as “all heart-rot infections occurred through the exposed heartwood in branch stubs” or “true heart rots . . . directly colonize heartwood exposed by natural injuries, such as broken large branches or tops, fire scars and stem cracks”.

In the cited work, Hartig was discussing one disease on one host. In the same chapter he criticized another author for extrapolating to another host, so clearly he was not making statements about heart rots in general. He apparently disliked generalizations and wrote about one disease at a time. I am not aware of any general pronouncements by Hartig about the infection courts of heart rots or stem decays. I don’t know where the “Hartig concept” came from, but it doesn’t seem to be from Hartig. If you know of any article or book where he did present such a concept, I would appreciate you letting me know.

Hartig presented red ring rot caused by Porodaedalea pini in Picea abies. He did not suggest that infection could occur through fire scars, broken tops, stem cracks, or abrasion wounds of the stem. He did suggest that freshly broken or cut branches can be important infection courts. There is still, as far as I know, no good evidence for or against this, although he noted high disease incidence in sites exposed to wind and near towns where people collected live branches. There are many later studies supporting Hartig’s conclusion ​[22]​, so it can’t be easily dismissed, despite other infection courts being implicated ​[12]​. Hartig also discussed the possibility that shade-killed twig and branch stubs could be infected, but thought that resin impregnation, competition from saprobes, and drying would make that an unlikely infection court.

Infection court: wounds and dead sapwood

Probably most decay fungi found in living trees enter through wounds and dead or dying sapwood. These include ​[22]​:

  • Mechanical injuries
    • breakage of tops and branches from wind, ice and snow
    • wounding from falling trees
    • wounding and shattering from lightning
    • wounding by humans from logging, vehicles, blazing, construction, etc.
    • animal damage
  • Frost cracks
  • Sunscald
  • Winter injury of bark
  • Fire scars
  • Branch stubs
  • Cankers, galls and swellings on the stem caused by fungi and mistletoes

Infection court: small, shade-killed twigs

Otherwise, early work focused on wounds as infection courts. However, it is not uncommon to find decay in a tree that has no evidence of a wound. The first evidence of another infection court was a study of Porodaedalea pini in Pinus strobus (eastern white pine) ​[12]​. Haddow showed that small dead twigs at the base of young trees (a few millimeters diameter) and leaders killed by the white pine weevil were common infection courts. These infection courts do not have heartwood. Growth progressed through the branch traces or down from the leader into the inner wood.

Evidence for an even more remarkable infection biology was presented in a study of Echinodontium tinctorium in Tsuga heterophylla (western hemlock) ​[9]​. Etheridge & Craig proposed that basidiospores infect primarily through shade-killed twig stubs ~1 mm diameter. After spore germination, mycelial growth continues until the twig stub is buried within the stem by radial growth. The fungus forms chlamydospores that can remain dormant for 50 years or more without causing decay. It is reactivated by increased aeration due to wounds or large branch stubs. This mode of infection was supported in Abies spp. by frequent isolation of E. tinctorium from clear wood not associated with stain or decay and not near wounds, but also from stain and decay near wounds ​[1]​.


The basidiospores of most basidiomycetes have a single haploid nucleus. The mycelium developed from it is called a homokaryon, monokaryon (especially when it has one nucleus per cell), or primary mycelium. Most wood-decay fungi are heterothallic, meaning they must mate in order to reproduce sexually. Fusion of hyphae with a sexually compatible mycelium (plasmogamy) creates a heterokaryon, also called a dikaryon (especially when there are two compatible nuclei per cell) or secondary mycelium.

Based on typical isolation from wood almost exclusively of heterokaryons, it is apparent that plasmogamy occurs early in life, and that by far the dominant somatic phase is a heterokaryon. It is often thought that the secondary mycelium has better growth, combat, and decay abilities than a primary mycelium. For instance, 12 of 15 synthesized dikaryons of Gloeophyllum trabeum had higher decay ability than either of the component homokaryons ​[2]​. However, there are as many or more studies showing no relationship or even the opposite, e.g. ​[7, 10, 17, 19]​.

What, then, explains the dominance of the heterokaryon? Perhaps it is an advantage we are not measuring properly, or the sheer numbers of spores: a homokaryon is very likely to bump into a mate early in life.


Stem-decay fungi grow axially (i.e. vertically in an erect stem) much faster than radially or circumferentially. In part, this is due to the axially elongated tracheids (conifers) or fibers and vessels (hardwoods) that make up most of the xylem. Fungi encounter fewer walls they need to penetrate in a given distance. Another reason is the potentially less favorable environments they may encounter when they move radially. Heartwood may be protected by inhibitory chemicals formed when sapwood is converted to heartwood, or by wetwood. Sapwood has living tissues that can actively respond to stop or slow invaders. When intact, it may also be wet enough to prevent adequate oxygen from reaching the fungus ​[3]​ (although the host parenchyma and epithelial cells of resin canals are able to survive and function in the sapwood). Depending on the host and pathogen, growth may be best initially in the inner heartwood, outer heartwood, or in a few cases the sapwood.

Invasion of sapwood. Despite the obstacle posed by intact sapwood, it can be disrupted. It is sometimes assumed that ‘heart rot’ is restricted to heartwood, wood without living tissues and functional water conduction. However, many, if not the majority, of these fungi can kill and invade sapwood to some extent. Silverborg observed killing of sapwood and even cankers caused by Phellinus igniarius, Ganoderma applanatum, and Inonotus glomeratus ​[20]​. I have often seen P. tremulae decay columns in Populus tremuloides growing out very near to and even killing patches of cambium. Boyce & Wagg noted Porodaedalea pini commonly encroaching on sapwood of Pseudotsuga menziesii, resulting in reduced vigor and perhaps mortality ​[5]​ (p. 89); indeed, this fungus kills callus tissue to prevent it growing over punk knots. Vasaitis notes cases of Fomitiporia robusta invading and decaying sapwood and causing cankers in Quercus sp. ​[21]​ I have seen the same behavior by F. texana, which kills Juniperus monosperma when decay develops enough ​[24]​. A tree with a single conk may already have a thin crown, and dieback generally increases with the number of conks.


Fruiting may occur after the mycelium has colonized and decayed enough wood to provide the needed resources. Fruiting has been known to occur as early as 5 years after inoculation ​[20]​, but 6-10 is more common ​[16]​, and natural infections would take longer than inoculations. Some fungi delay fruiting until after the tree is dead, and fruiting may not occur at all. The fruiting body, especially when conspicuous, is commonly referred to as a “conk”.

Of course the function of fruiting is sexual spore production. See the typical life cycle for details. Spores are invariably windborne.

More stem decay pages:


  1. 1.
    Aho PE, Filip GM, Lombard FF. 1987. Decay fungi and wounding in advance grand and white fir regeneration. Forest Science 33(2):347–355 <>.
  2. 2.
    Amburgey TL. 1970. Relationship of capacity to cause decay to other physiological traits in isolates of Lenzites trabea. Phytopathology 60(6):955 <10.1094/Phyto-60-955>.
  3. 3.
    Boddy L, Rayner ADM. 1983. Origins of decay in living deciduous trees: The role of moisture content and a re-appraisal of the expanded concept of tree decay. New Phytol 94(4):623–641 <>.
  4. 4.
    Boyce JS. 1961. Forest Pathology, 3rd ed. New York: McGraw-Hill Book Company. 572 pp.
  5. 5.
    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 <>.
  6. 6.
    Buchwald NF. 1938. Om Sporeproduktionens  Størrelse hos Tøndersvampen, Polyporus fomentarius (L.) Fr. Friesia 2(1):42–69 <>.
  7. 7.
    Da Costa EWB, Kerruish RM. 1965. The comparative wood-destroying ability and preservative tolerance of monocaryotic and dicaryotic mycelia of Lenzites trabea (Pers.) Fr. and Poria vaillantii (DC ex Fr.) Cke. Annals of Botany 29(2):241–252 <>.
  8. 8.
    Etheridge DE. 1972. True Heart Rots of British Columbia. Canadian Forestry Service, Pacific Forest Research Centre. 14 pp.
  9. 9.
    Etheridge DE, Craig HM. 1976. Factors influencing infection and initiation of decay by the Indian paint fungus (Echinodontium tinctorium) in western hemlock. Canadian Journal of Forest Research 6(3):299–318 <10.1139/x76-041>.
  10. 10.
    Fryar SC, Kirby GC, Hyde KD. 2002. Interspecific competitive ability of homokaryotic and heterokaryotic wood decay basidiomycetes. Austral Ecol 27(3):343–349 <10.1046/j.1442-9993.2002.01186.x>.
  11. 11.
    Gilbertson RL, Ryvarden L. 1986. North American Polypores, Vols. 1 and 2. Blindern, Norway: Fungiflora A/S. 885 pp.
  12. 12.
    Haddow W. 1938. The disease caused by Trametes pini (Thore) Fries in white pine (Pinus strobus L.). Transactions of the Royal Canadian Institute 22(1):21–80.
  13. 13.
    Hansen EM, Lewis KJ, Chastagner GA. 2018. Compendium of Conifer Diseases, 2nd ed. St. Paul, Minnesota: APS Press, the American Phytopathological Society. 224 pp.
  14. 14.
    Hartig R. 1874. Wichtige Krankheiten der Waldbäume. Beiträge zur Mycologie und Phytopathologie für Botaniker und Forstmänner. Berlin, Heidelberg: J. Springer Berlin Heidelberg. 164 pp. <>.
  15. 15.
    Hilborn MT. 1942. The biology of Fomes fomentarius. Bulletin of the Maine Agricultural Experiment Station 409:161–214.
  16. 16.
    Hirt RR. 1949. Decay of certain northern hardwoods by Fomes igniarius, Poria obliqua, and Polyporus glomeratus. Phytopathology 39:475–480.
  17. 17.
    Hiscox J, Hibbert C, Rogers HJ, Boddy L. 2010. Monokaryons and dikaryons of Trametes versicolor have similar combative, enzyme and decay ability. Fungal Ecology 3(4):347–356 <10.1016/j.funeco.2010.02.003>.
  18. 18.
    Hunt RS, Etheridge DE. 1995. True Heart-Rots of the Pacific Region. Victoria, B.C: Canadian Forest Service, Forest Insect and Disease Survey, Pacific Forestry Centre. 8 pp. <>.
  19. 19.
    López SC, Theelen B, Manserra S, Issak TY, Rytioja J, Mäkelä MR, de Vries RP. 2017. Functional diversity in Dichomitus squalens monokaryons. IMA Fungus 8(1):17–25 <10.5598/imafungus.2017.08.01.02>.
  20. 20.
    Silverborg SB. 1959. Rate of decay in northern hardwoods following artificial inoculation with some common heartrot fungi. Forest Science 5(3):223–228.
  21. 21.
    Vasaitis R. 2013. Heart rots, sap rots and canker rots. In: Infectious Forest Diseases, eds Gonthier P, Nicolotti G, pp. 197–229. Wallingford: CABI <,%20sap%20rots%20and%20canker%20rots%20CABI.pdf>.
  22. 22.
    Wagener WW, Davidson RW. 1954. Heart rots in living trees. The Botanical Review 20(2):61–134 <>.
  23. 23.
    White JH. 1919. On the biology of Fomes applanatus. Transactions of the Royal Canadian Institute 12:133–174.
  24. 24.
    Worrall JJ. 2016. Stem decays. In: Diseases of Trees in the Great Plains. Gen. Tech. Rep. RMRS-GTR-335, eds Bergdahl AD, Hill A, pp. 105–128. Fort Collins, CO: U.S. Department of Agriculture, Forest Service, Rocky Mountain Research Station <>.
  25. 25.
    Zabel RA, Morrell JJ. 1992. Wood microbiology: decay and its prevention. San Diego: Academic Press. 476 pp.