Forest and Shade Tree Pathology
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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.
It will first be helpful to know something about the chemistry and cell types in wood.
Now you are ready to learn the basics of the decay types:
|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 is fibrous because some cellulose remains intact till very late stages. 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 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.
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.
The initial stage is non-enzymatic. 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.
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 cavities in the secondary wall, but they are not always present.
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 at the left, 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. Also keep in mind that saprobic fungi can and do decay heartwood in dead 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, tops, and stumps after logging.
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:
Trees have several mechanisms of resistance against decay fungi. Bark is the first line of defense. No stem-decay fungi infect through intact bark.
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 very 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.
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.
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:
|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?
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.
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, Phellinus pini is more common in Douglas-fir in central and southern Oregon (dry) than in other parts of NW; 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.
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.
There are many approaches that can be used to reduce wounding:
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.
Yield tables are based on gross yield, but it is net yield that counts. Pathological rotation:
Pathological rotation may need to be factored into a manager's decision to determine the actual rotation based on all considerations. Usually other considerations in modern forestry call for a shorter rotation than the pathological rotation anyway, but in some species, such as aspen, pathological rotation is usually limiting. Here are some examples of fairly short pathological rotation ages:
|yellow birch||Nova Scotia||120|
|balsam fir||New York||70|
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 - take that to the bank. 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.
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!
|"So maybe it's a good thing when Mr. Burns calls me a fungus?"|