This is an introduction to stem decays (also known generally as heart rots). Related pages are:

Stem decay in Sequoia sempervirens (coast redwood), California, USA.


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.

Modern Myths

Two myths about stem decays have become widespread in recent years. These are discussed in more detail in the appropriate sections below.

  1. Stem decays traditionally known as heart rots are restricted to heartwood. To my knowledge, pathologists of yore never said this, because they knew it to be false. There is much incontrovertible evidence to the contrary in many papers by good scientists.
  2. True stem decays do not use branch stubs, wounds, fire scars, etc., as infection courts. The demonstration of alternate infection courts for some of our stem decays led to this. It may be true for some true stem decays, but much evidence indicates that it is not true for all.

Types of Stem Decays

The pattern of fruiting of Trichaptum abietinum indicates that it is decaying sapwood in this Picea engelmannii log, initiated after the tree was cut. Fomitopsis pinicola is also fruiting.

Traditional: 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.

If a fungus is well established in the heartwood, then encroaches on the inner sapwood and begins to decay it, the disease is still a heart rot by these definitions. This is quite common (see references below under Disease Cycle: Invasion). Some such heart rots can even progress to and kill the cambium, thus causing cankers. Other pathogens grow primarily in the outer sapwood (and thus cause sap rots), kill the cambium, and cause cankers. In these cases, both the heart rot and the sap rot are a special type of disease called canker-rot. It has been suggested that the same fungus might simultaneously cause heart rot, sap rot, and canker rot ​[21]​. This is not characterizing disease types, this is using the words as symptoms to describe what a fungus is doing at a certain place and time. To summarize, the traditional grouping of these diseases is:

  • Heart rots – become progressive primarily in the central dead wood/heartwood, but may then attack sapwood and even cambium
  • Sap rots – any decay primarily in dead sapwood, including when the fungus kills the sapwood, but also including sapwood of dead trees (in this case of course it is not a disease).

Newer: True stem decays vs. wound decays

As information about novel infection courts became 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:

  • often 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 may not 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 below under Disease Cycle: Invasion, it is common for them to attack and decay sapwood and sometimes even attack the cambium (causing cankers).

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 sapwood and are thus traditional sap rots. They may infect through sapwood killed by cankers, sunscald, fire, or other causes as well as mechanical injuries.

Four types?

That gives us two types of stem decays: true stem decays (true heart rots) and wound decays. A proposed system ​[21]​ breaks them into four types, including sap rots. Sap rots are not clearly defined in that proposal, first considered as a case of heart rot where sapwood is attacked, but then as decay by saprotrophic fungi in dead trees or dead portions of trees. These definitions of sap rot are incompatible, and neither fits the traditional definition above. Here’s the breakdown ​[21]​:

  1. True heart rots entering an “intact tree” through “natural courts of infection.
  2. True heart rots that “directly colonize heartwood exposed by natural injuries” (e.g., broken large branches and tops, fire scars, stem cracks).
  3. Wound heart rots entering through “exposed dead sapwood”. Also defined as “associated with artificial mechanical damage”.
  4. Apparently sap rots constitute a fourth type of stem decay.

This confuses me. What is “an intact tree”? Presumably it is one that is not wounded, but then, what is a wound? Are leaf scars, twig scars, included? If not, where do you draw the line? What if a disease can employ infection courts described in both 1 and 2 above, which almost certainly happens? The terms “natural” and “artificial” are also murky. If a tree falls in a storm and breaks the top out of a neighbor, that would seem to be natural. But an identical infection court could be made by a logger while felling a tree. Is that artificial? I think artificial vs. natural source of infection courts is not a sound basis for classification.

The distinction between entering through exposed heartwood vs. dead sapwood is puzzling too. Heartwood is dead wood that was once sapwood, and in many species there is little difference between it and dead sapwood.

Conclusion: two types of stem decay

Based on the foregoing, I suggest sticking with the modern dichotomy of disease types ​​[13]​, but using the term stem decays instead. Traditional heart rots and sap rots ​​[22]​ occur in both types (see Disease Cycle > Invasion below for an example of a true stem decay that is a sap rot).

  • True stem decays – as defined above, without the feature that they are confined to the heartwood, because most are not:
    • often 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 may not serve as the principal infection courts
  • Wound decays – do not have features of true stem decays; usually entering through mechanical injuries or otherwise dead wood

Disease cycle

Dispersal is by spores

  • Spores may be released for a few days (mushrooms) or for six months or more per year (perennial conks).
  • The spores are carried by wind. They are in suspension in air and can travel many miles even in light breeze.
  • Some decay fungi have a conidial stage in culture but those are rarely found in nature and their importance is unknown.

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 . 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 sometimes 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 that 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 even the stubs of dead branches. He did suggest that freshly broken or cut branches can be important infection courts. 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, leading to top rot
    • pruning (damage and resulting decay can be minimized by knowing how to prune)
    • wounding from falling trees
    • wounding and shattering from lightning
    • wounding by humans from logging, vehicles, blazing, construction, etc.
    • animal damage such as deer scraping off velvet, cattle damage to root collar, even bears
  • Frost cracks
  • Sunscald
  • Winter injury of bark
  • Fire scars. Early studies suggested that fire scars are the most important, both in hardwoods of SE and in conifers of the west. Of course that is not the case where fire scars are uncommon.
  • Branch stubs
  • Cankers, galls and necrotic swellings on the stem caused by fungi and mistletoes

All the work showing the role of branch stubs, wounds, and dead wood as infection courts for true stem decays has been summarily dismissed with generalizations like, “This assumption was based on the simple fact that the fruiting body of a heart rot fungus is typically formed on or in the vicinity of a branch stub.” ​[21]​ However, these were not assumptions. They were conclusions based on years of work by many competent investigators who spent a lot of time making careful observations and studies and analyzing decay columns in thousands of dissected trees. I don’t think scientists of an earlier era were such simpletons; quite the opposite. Beginning with Hartig and carrying into the 20th century, their powers of observation and careful logic were at a higher level than those of some scientists today.

Thus, other infection courts and processes notwithstanding, the importance of these infection courts cannot simply be dismissed. A conclusion on their relative importance must be based on comprehensive evidence.

Infection court: small, shade-killed twigs

It is not uncommon to find decay in a tree that has no evidence of a wound or even large branch stubs. The first good evidence of another infection court was a study of Porodaedalea pini in Pinus strobus (eastern white pine) ​[12]​. Haddow showed that small dead twigs (a few millimeters diameter) at the base of young trees 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. Haddow also found that white pine leaders killed by white pine weevil can be an infection court. There is no heartwood in a leader.

An even more remarkable infection biology was proposed 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]​.

Much is made of these small, obscure infection courts in discussions of true stem decays ​[21]​. However it is important to note a few things:

  • There are really only a few studies that point toward these ‘novel’ infection courts, but they are not the only infection courts. There are scores of studies supporting the traditional branch stubs and wounds as infection courts.
  • Even Haddow ​[12]​, author of the pioneering work on P. pini, wrote, “Infection originating at large branch stubs in the mid-trunk section of older trees has long been recognized, and that it is of common occurrence cannot be doubted.”


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 thought that the secondary mycelium often 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.

A nice vertical section through Echinodontium tinctorium conk, decay, and branch in Abies sp. The decay column is encroaching into the sapwood. Photo by Kelly Burns.

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 (see the list of true stem decays below with evidence of killing live tissue). 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.

Some of the true stem decays are listed here, mostly selected from ​[21]​, along with evidence of their attacking living sapwood and inner bark. 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 sensu lato (invades sapwood, cankers ​[4, 5, 12]​)
  • 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 (see photo).
  • 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]​)

Example of aggressive sapwood invasion

Here is a gallery of Juniperus monosperma (one-seed juniper) infected by Fomitiporia texana in Whitby Canyon, Comanche National Grassland, Colorado, USA ​[24]​. The fungus is part of the Fomitiporia robusta complex, which is considered to cause a true stem decay ​[21]​. I did not see any wounds on infected trees and don’t know the infection court.

All photos are from the same tree, which had eight conks. This aggressive pathogen attacks the sapwood at an early stage, leading to crown thinning and dieback of branches. It eventually kills cambium and can kill the tree. Trees with a single conk may already have thin crowns, several conks are usually associated with dieback, and trees are often near death when the number of conks approaches ten. This fits the traditional definition of sap rot because it progresses more in the sapwood than in heartwood. It is the most aggressive case of sapwood killing from stem decay that I have seen.


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. This takes us back to Dispersal, where we started above. See the typical life cycle for another, briefer description.

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 <10.1111/j.1469-8137.1983.tb04871.x>.
  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 <>.
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    Zabel RA, Morrell JJ. 1992. Wood microbiology: decay and its prevention. San Diego: Academic Press. 476 pp.