Wood Decay

Contents of this page :

Introduction to decay

Wood decay is a deterioration of wood by primarily enzymatic activities of microorganisms. For practical purposes, fungi are the only agents of wood decay. There are other kinds of deterioration, by insects, marine animals, UV, but this is not decay, nor is it quantitatively as important as decay.

Now you are ready to learn the basics of the decay types:

Types of Decay
Type Agent Color Texture Chemistry
White Basidiomycota ±bleached fibrous all components removed
Brown Basidiomycota ± brown fibrous texture lost early, cross-checking primarily carbohydrates lost, lignin mostly remains
Soft Asco- and Deuteromycota bleached or brown usually on surface, some fibrous texture lost, cross-checking in some cases carbohydrates preferred, but some lignin lost too

White rot

In white rot, all wood components are destroyed. The components remain in roughly the same proportion throughout decay as in the sound wood. White rot is fibrous because some cellulose remains intact until very late stages of decay. It is typically less fibrous in hardwoods than in softwoods because of the shorter fibers in hardwoods. It usually turns whitish because of bleaching by oxidation and loss of lignin, which is slightly brown. Color and texture vary among white rots caused by different fungi:

In some white rots, there is a phenomenon called selective delignification. All components are removed, but the relative rate varies. Lignin and hemicelluloses are selectively removed in early stages. This leaves enriched cellulose. This is what happens in the white regions of a mottled rot and in the pockets of a white pocket rot. There is a tremendous amount of interest in using these fungi in industry, because many uses of wood involve removing lignin (e.g., biopulping).



In Chile, selectively delignified wood of the genus Nothofagus occurs in large amounts.  It is mostly associated with decay by Ganoderma species and is called palo podrido.  Dr. Robert Blanchette reports that Indians in Chile have (had) a god called Trauco.  Trauco lives in the forest and looks like a man but has cloven feet.  Trauco represents fertility, perhaps in much the same way as Kokopelli of the Indians of southwestern North America. Unwed women who got pregnant often said that Trauco had visited them and he was responsible for their pregnancy. Trauco eats palo podrido, and there are reports that Indians did as well, perhaps to enhance fertility.

In selectively delignified wood there are often pockets of clear, gelatinous remnants of the wood. Armillaria species in particular often cause these gelatinous pockets. This may become colonized by yeast and may contain alcohol. We don't know what role this may play in the legend, but one noted forest pathologist who was trying to have kids ate some Armillaria jelly while on a trip and his wife became pregnant soon after!

Incidentally, the delignified wood is quite useful as fodder for ungulates. It can be readily broken down with the aid of microorganisms in their gut. Even in Alaska, I have seen evidence that moose have fed on logs decayed by Ganoderma applanatum!

Brown Rot

Brown rot is brown because carbohydrates are removed, leaving brownish, oxidized lignin. There is no fibrous texture because the cellulose is broken up early. The wood shrinks on drying and cross-checking is seen in later stages. It is often called "cubical" brown rot for that reason.

The initial stage of brown rot is non-enzymatic. The fungus produces some small chemical agent (involving oxalic acid and hydrogen peroxide) that zips around in the cell wall like a little pair of scissors, snipping chains of cellulose and hemicellulose into smaller pieces. This happens throughout the wall in fairly early stages. The carbohydrates become partly soluble, enzymes work on them, releasing sugars, and they are slowly absorbed by the fungus.

There are a handful of brown pocket rots. They only occur in living trees, and more specifically trees that have unusually durable wood, with otherwise effective antifungal chemicals in the heartwood. One can speculate that the occurrence of brown pocket rots in such tree species is probably related to the chemical protection of the wood, but how is a mystery that is yet to be solved.

Soft Rot

Soft rot is not known to occur in living trees. It is important in degradation of wood in service. The best known feature is the curious angular cavities in the secondary wall, but they are not always present.

Terms for position of decays

Decay terms by sapwood vs. heartwood involvement Decay terms by position in tree

In general, live trees tend to decay from the inside out and dead trees from the outside in. There are various reasons for this, but it is largely due to the fact that sapwood has a very effective active resistance when the tree is alive but virtually no resistance once the tree is dead.

The terms relating to position of decay in the tree are just approximations; the fungi are not necessarily restricted to these regions.

In addition to the terms illustrated at the right (top rot, stem or trunk rot, butt rot, root rot), two that you run into are heart rot and sap rot. Heart rot is often defined as decay in living trees. Some define it as decay that develops primarily in the heartwood or inner wood of living trees. It is usually used to refer to decays that primarily develop in the stem rather than in the roots and butt. Sap rot may refer to saprobic decays or to those that develop in the sapwood. Usually sapwood decays extensively only in dead trees. But there are some fungi that commonly decay sapwood in living trees, usually causing cankers. Such diseases are known as canker-rots. Also keep in mind that saprobic fungi can and do decay dead wood in living trees.

Here we use the term stem decay for all diseases where the primary symptom is decay of stem wood, largely because 'heart rot' is thought by some some to imply that decay is restricted to heartwood, which is frequently not the case.

Another term you see is slash rot, simply referring to decay of dead material, particularly branches and tops that are left behind after logging.

Disease Cycle of Decays

Refer to the life cycle of a polypore, as it is closely related to the disease cycle. Two points need to be added. First, decay occurs for many years, between the stages of plasmogamy and fruiting, and fruiting may continue for many years. Second, dispersal and infection court are important issues:

Dispersal is by spores:

Infection court is invariably non-living wood

Fire scars:
Early studies suggested that fire scars are the most important, both in hardwoods of SE and in conifers of the west. That will be less true where fire scars are uncommon.
Broken tops (from glaze or snow storms, leading to top rot), treefall scars, animal damage (such as deer scraping off velvet, cattle damage to root collar, even bears in one case), logging scars, carving and hatchet marks. Logging injuries are an important infection court that we can manage to reduce butt rot and stem decay. Damage from pruning can be minimized by knowing how to prune (Forest Service on-line info).
Branch stubs:
Even dead twigs down to few mm diam. can be infection court for some fungi, such as Porodaedalea pini. The same fungus also can infect through white pine leaders killed by white pine weevil. Stubs/twigs also important for Stereum sanguinolentum and Echinodontium tinctorium.
Primarily root- and butt-rot fungi get in this way. See the page on root diseases for more details.
Cankers, mistletoe infections, necrotic galls:
These sites may eventually become infected by decay fungi, which may lead to stem breakage.

Tree resistance

Trees have several mechanisms of resistance against decay fungi. Bark is the first line of defense. No stem-decay fungi infect through intact bark. Wound response by trees

Sapwood is capable of active response to invasion. Parenchyma cells in sapwood sense the presence of the fungus and initiate a doomsday response. A terminal metabolism kills them, but results in conditions that are unfavorable for fungi. Chemicals limit the progress of the fungi. Second, in many conifers, resin is piped in to seal off the area. Third, the cambium responds to trauma by producing a fairly effective wall in the xylem at that point that often restricts an invader to the wood laid down before then. The wall may extend for some distance away from the invasion or wound.

Heartwood resistance is very different from sapwood resistance. Heartwood is dead and there is no active resistance. Instead, chemicals are deposited in heartwood as it forms by dying parenchyma. They render it more or less inhospitable to fungi. Species vary greatly in heartwood resistance. Redwood, cedars are very high; aspen, birch are very low. Nevertheless, every tree has at least a few fungi that have learned to live in its heartwood and cause heart rot.

Now, knowing the difference between sapwood resistance and heartwood resistance, you can begin to understand the difference in the pattern of decay in living and dead trees that we saw above.

Rate of growth in trees

Assume a tree is infected at a point in time. How fast does the fungus grow? There are two approaches to finding out: inoculate, wait about five years, then cut and measure; OR find trees with infection courts that can be aged, then cut and measure. What people have found is that decay develops slowly. Results are highly variable, from near 0 to 60 cm/yr. Average is much closer to 0, say 6-8 cm (about 3"). There is reason to believe that most figures overestimate the long-term average growth rate, because initial growth may be faster, perhaps due to better aeration.

Factors affecting stem decay in stands (epidemiology)

Age of Stand

It is important to understand that stem decay increases with age of a stand. Obviously, the longer a tree stands, the more likely it is to become infected, and the longer the fungus has to do its thing. 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. But there are other reasons that make it more serious in older stands:

Examples: An example of a sound stand is Sitka spruce in BC:

At the other extreme, aspen in the Lake States:

But stands may vary tremendously. E.g., hemlock in Washington and Oregon:

Variation of decay in hemlock in Washington and Oregon
stand A 180 yr 14% decay of total volume
stand B (only 4 miles from stand A) 214 yr 61%

So there are obviously factors other than age that influence level of stem decay. What accounts for such variation among stands in the amount of decay?

Stand History

Events and conditions in the life of a stand, especially those that create infection courts, can cause dramatic increases in the level of stem decay.

basal scars
Ice and snow storms
top breakage, top rot
felling wounds, basal scars from skidders and logs
This factor is not so obvious. Assume a fungus gets in through large branch stubs. If the stand is dense, branches are shaded out while they are still small, and infection courts are not created. An open stand will have larger branch stubs. But remember that some fungi use small twigs as infection courts, so the dense young stand may favor them.
Remember ungulates can create infection courts, particularly when the stand is young. Therefore the history of animal management on the site can influence heart rot levels.

Stand Composition

As mentioned, species vary greatly in their susceptibility to decay, so stand composition is an obvious factor determining the level of decay. The percent of defect in a mixed stand should be roughly a composite of that expected for the species represented.

This has obvious management implications: we can influence the amount of decay in a stand by influencing composition. In the West, Douglas-fir is often clear cut. Clear-cut stands can come back to Douglas-fir, which generally has relatively low levels of decay. If we engage in partial cutting, as many argue we should for esthetic reasons, we leave an understory of hemlock and true firs, which are more susceptible to decay than Douglas-fir. Worse, the understory is often wounded by the logging. Obviously, a manager has many factors to consider, and decay is just one of them.


Relationships of stem decay to site are not very consistent, and no sweeping generalizations can be made. For root and butt rot, there are some, but for trunk rot there are few. There is a tendency for levels of stem decay to be greater in the drier parts of a tree's range. For example, Porodaedalea pini is more common in Douglas-fir in central and southern Oregon (dry) than in other parts of the Pacific Northwest; also more common on southern slopes than northern. The higher temperatures may be more important than moisture in these cases. Dichomitus squalens is much more serious on ponderosa pine in Arizona and New Mexico (10-50% cull) than in California. This is thought to be because the first states get summer rains with high humidities, allowing infection in the dead branches. In pine regions of California, summers are dry.


Here's another concept. We generally feel that the factors outlined above are more important in determining infection than the availability of spores. We assume that the spores will usually be there. However, in many cases, we do not have hard evidence for this.

Management to reduce decay

Decayed trees should be removed

An exception is in cases where wildlife, particularly endangered species, are a consideration. Many animals nest in decayed trees. For instance, red cockaded woodpecker in southern pines. One reason for their endangerment is the shortage of such trees in intensively managed forests.

In thinnings, decayed trees should be removed. This is less an issue of reducing inoculum than of improving the residual stand and giving healthy trees more room to grow.

Cuts whose main goal to remove such defective trees are called sanitation cuts. Those marking the trees, in fact for any cut other than clear-cut, should be trained to recognize indicators of decay in the particular tree species.

Also, salvage cuts after a fire or storm damage can be done to remove trees that have fresh infection courts that will certainly lead to decay.

A common practice in old days and no doubt still done in some cases today, was to leave decayed, defective trees as seed trees. The idea was that they weren't worth harvesting anyway, let's get some use out of them. But susceptibility to decay probably has a significant genetic component, so in doing that you reduce the quality of the next stand and future ones.

Wounding should be prevented

There are many approaches that can be used to reduce wounding:

Other infection courts

For cases where larger branch stubs are infection courts, maintain stand density to reduce their size, consider prunging. I'm not aware of any operational tests of this or actual cases where it was used, but it should be effective.

For cases where animal wounds are damaging, exclude or reduce cattle or deer.

For cases where fire scars are important, protect against fire.


Stump sprouts can be infected via heartwood through the stump. In pruning excess sprouts, favor lower sprouts that are less likely to be infected this way.

Favor sprouts that are alone. When sprouts are large (>3") clumps of very close sprouts should be treated as a unit, either all cut or all left.

Pathological rotation - curves of gross volume and decay vs. stand age
Total and merchantable wood volume of balsam fir over the life of a stand in the Lake States. Each measure of wood volume is separated into gross, decay, and net (gross minus decay/cull). Based on data from Kaufert 1935 (®).

Yield and Rotation Age

Yield tables are often used in forestry to predict wood volume produced in a stand of given species, age, and site quality. They usually predict gross yield. However, yield may be much less when you account for decay. At right is an example, shown in terms of both total volume and merchantable volume (or what would be merchantable without decay).

In addition, the practical length of time a stand should grow for timber production (rotation age) may be influenced by decay. This is referred to as pathological rotation. The concept was first presented in 1916 by Meinecke (®), although he did not present supporting data. The data of Kaufert (®), using balsam fir, provide a good example (data are graphed at right). Pathological rotation may be defined variously:

Pathological rotation may need to be factored into a manager's decision to determine the actual rotation based on all considerations. In some species, such as aspen, pathological rotation is usually limiting. Here are some examples of fairly short pathological rotation ages:

Examples of short pathological rotation ages
Species Location Pathological
aspen Minnesota 40-50
  Utah 80-90
yellow birch Nova Scotia 120
balsam fir New York 70

Decay of wood in service, stains

Products deterioration

Buildings, decks, railroad ties, utility poles, bridges, ladders, horticultural uses, etc.

Losses: no good figures, but it is said that 10% of annual cut goes to replace decayed wood. Doesn't include cost of replacement, liability, cost of preservative treatment.

Moisture content: dry wood won't decay (and you can take that to the bank: "dry rot" is a misnomer). If you add water to dry wood, it goes to satisfy need of walls, which absorb water. Up to moisture content of 28% (that's dry weight basis, so 28 g water per 100 g dry wood), added water goes into wall. Above that, you get free water in the lumens. That point is called fiber saturation point. Decay fungi require free water. So wood must be above FSP to decay. For practical purposes, a value of 20% is used as a cutoff, leaving a margin for error. Thus, processors and users should keep wood below 20% moisture content to avoid decay.

Control - 3 approaches

  1. Keep wood dry. For practical purposes, and a margin of error, the rule is keep it at below 20% moisture content (dry-wood basis). Good construction practices with this in mind are important in buildings, but many construction people and even architects do things wrong.
  2. Use durable wood. But it must be heartwood!
  3. Use preservatives. Ideally they should be pressure-impregnated. Painting/dipping are much less effective. Not all wood species treat well, some won't accept it.


There are many different wood conditions grouped under the term stain, with many different causes. The only one we need to really be concerned with here is blue stain.

This is a blue-grey stain of wood that can tend to being black. It is caused by ascomycetes or deuteromycetes that have dark brown hyphae. The way light goes through the wood, it ends up looking bluish grey.

The most common and well-known form of blue stain is found in conifers, especially pines, that have been invaded by bark beetles. The beetles either kill the tree or invade it as it is dying. They carry with them a fungus in a group we will just call by the genus Ophiostoma.

When the beetles attack, they inoculate the tree with their fungus. The fungus invades the wood, but especially the rays and the resin canals. The rays are heavily colonized. When you look closely at the wood, you can often see dark streaks where the resin canals were stuffed with hyphae. Such wood is common after salvage operations (harvesting recently killed trees), and when logs are stored after cutting under conditions that permit beetle attack.

One hypothesis on the relationship is that the fungus helps the insect by killing cells in the sapwood such as rays and resin canal cells. This reduces the host reaction against the beetle. Another is that the fungi may produce chemicals that are important in beetle maturation. Other things may be involved. In turn, the beetles provides the fungus with vectoring services. This is a symbiosis.

The fungus does not decay the wood, although some strength may eventually be lost. It is used for many purposes such as plywood, rough lumber, etc. It may even be sold as special decorative wood ("blue pine").

Ready to learn some specific decay fungi? Go for it!

Funny picture "So maybe it's a good thing when Mr. Burns calls me a fungus?"

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Last modified 22 Feb, 2015