|Forest and Shade Tree Pathology
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Canker: Localized necrosis of the bark and cambium on stems, branches or twigs. They are often sunken because the stem continues to get bigger elsewhere. Also, callus may be produced around the canker that makes it more sunken.
Pathogens are mostly Ascomycota. Many also have an asexual stage in the Deuteromycota.
There are some diseases usually considered with other groups that also involve cankers:
- Canker rots
- Some basidiomycetes that decay wood in the stem may also kill patches of sapwood and bark. We consider them along with stem-decay fungi.
- Stem rusts
- These cause cankers, but we consider them separately.
- Foliage diseases, shoot and tip blights
- Some of these kinds of diseases also can involve cankers of twigs, branches, and even main stems.
- Frost or sunscald
- These can kill patches of bark, causing cankers.
Often, cankers are centered around a wound or branch stub, suggesting that they were the infection court. But seeing a branch at the center does not tell us much. Did the pathogen colonize the branch or stub after it was dead, then attack the nearby living stem? Or did it infect the branch while it was alive (perhaps through some kind of wound?) and then grow down into the stem, killing the branch in the process?
Some people have trouble with this. Cankers are a good topic for examples. For example, the pathogen of coral-spot Nectria canker has both sexual and asexual fruiting structures that occur separately. The sexual structure is in the perithecial ascomycetes, characteristic of the genus Nectria, and the fungus is called Nectria cinnabarina.
The asexual structure is a sporodochium. Fungi with sporodochia are classified in the Deuteromycota. This particular sporodochium and conidia it produces belong in the genus Tubercularia, and this one is Tubercularia vulgaris.
So the fungus has two names, both referring to the same fungus. If we want to refer to the whole fungus (as we usually do), it is usually best to use the name for the sexual stage, because, as with plants, that is the stage usually used to indicate relationships. So we call this pathogen Nectria cinnabarina. But you may also hear people refer to the asexual stage by name.
For some fungi, though, we may just see the asexual stage. Cytospora canker is an example. We almost always only see pycnidia. So it is natural to call it by the stage that we see, Cytospora or Leucocytospora.
For some fungi, a sexual stage may never have been seen. Pitch canker is an example. All we see are sporodochia, so we can use only the name for the asexual stage, which in this case is Fusarium.
In other cases, there may be both stages, but the sexual stage is so consistently present that we don't need to use the name for the other stage and there may not be one. Hypoxylon canker is an example. There are conidia, but you never hear a name for that stage. There are almost always perithecia around to identify.
Additional categories that may be separated out for recognition are conditional cankers causing cankers under special conditions such as weakened trees and diffuse cankers. These categories can be somewhat subjective, but may be useful in considering host-pathogen relationships.
We'll consider at least one canker of each kind.
Fusarium canker of maples occurs in Northeast, maybe Midwest too. Cottonwoods get a Fusarium canker too, but the pathogen is different. From less than an inch to several feet long (vertically). Small ones are most common. One tree may have hundreds of these annual cankers. The cankers are evident as a ridge of bark after callusing over. The face may not open. Usually there is no impact on tree growth, but lumber is badly degraded. Fruiting is usually not seen.
The pathogen may get in through dead and dying shoots. It apparently grows during the dormant season. We think predisposition is involved, especially drought. So maybe this could go into the conditional canker category.
What do you think would be a good general approach to management of stands with these cankers? Take them out preferentially during any cutting operation. This may not be the greatest control but is all we have. In most cases it is sufficient. Good to recognize early stages of the cankers.
Canker face is usually free of bark, making it neat, but it may have bark on aspen.
We rarely see fruiting of the pathogen. It probably fruits mostly in certain years when weather is right, and then in the dormant season when we're not around to see it.
Butternut (Juglans cinerea) is naturally an uncommon tree through most of its range (US Northeast, Midwest and northern Southeast, and adjacent provinces of Canada). Beginning in 1967, increasing mortality was observed and soon linked to the disease. No other hosts are significantly affected.
Live butternut has decreased as much as 80 percent in much of its range. Most remaining trees are diseased. In many areas, it is anticipated that butternut will be nearly extirpated in a few decades.
Some states have declared a moratorium on harvest of live butternut. It is now listed in category 2, under consideration, on the list of Endangered and Threatened Plants, it is a Sensitive species on National Forest System lands, and in Canada it was listed as Endangered in 2005.
The pathogen was previously unknown. Sadistic mycologists () gave it a tortured name that noone can pronounce: Sirococcus clavigignenti-juglandacearum. It produces pycnidia.
A new species such as this causing novel, severe damage to a host in its native range leads us to suspect that the pathogen is introduced, but there is no direct evidence.
Cankers may appear anywhere on the tree. They are common on the stem base and on exposed roots, presumably because spores are washed there in rain and accumulate. Cankers exude black liquid in spring, leaving a sooty residue. Older cankers are perennial and have successive callus layers.
There are many different Cytospora cankers on different hosts. See the "cankers on parade" page for details.
Normally not a big deal in natural stands. More for trees growing out of native range or off-site. During droughty periods, such trees can be hit pretty hard. Also severely pruned trees or cuttings in storage or in propagation beds can be attacked.
A wound or shedding twig is the infection court. Patch of bark is killed. May or may not get surrounded by callus.
Pycnidia are very abundant and appear as pimples in the bark surface. They have multiple chambers in a sort of pycnidial stroma, join up at the pore (like chestnut blight pathogen, to which it is closely related). When wet, they extrude spores, which often form a tendril. (May look like pus oozing out, completing the pimple analogy!) It looks like a curly thread.
The scale was introduced to Nova Scotia about 1890. It's first US find was in Massachussetts in 1929. The fungus was not found until 1929, but we don't know if it was introduced or just not noticed before. The disease has spread much more slowly than did chestnut blight. It is still moving south and southwest. The main front is about in Virginia and Ohio, but there are pockets in advance of that.
The disease requires a sequence. The scale appears first. Then the fungus appears, and the scale seems to be no longer necessary. In some way, the scale appears to block the defenses of the tree. Think of it as a local anasthetic, like a mosquito uses. The scale numbs the bark so the tree doesn't respond and slap it down. But then the fungus can get in, and it doesn't go away until the bark is dead in that patch.
Perithecia are red and superficial, in clusters, nice sign! See under Nectria canker above.
The canker may be diffuse, or there may be host response that stops the fungus. Irregular, blocky bark is an indication of some kind of resistance response.
As it began killing beech in large numbers, there was a flurry of interest in it. Pathologists sorted out the causal agents, determined how the disease was spreading and the response of the trees, etc. But interest soon dropped because foresters saw this as a good thing. Beech is an OK lumber tree, but very abundant, and maple and birch are usually more valuable. In fact, the reason beech was so abundant is that it was left behind when the more valuable birch and maples were harvested preferentially. (That practice of taking the most valuable trees and to hell with the rest is called high-grading, and is responsible for many of the modern problems in forest management.) Here was a pathogen helping the foresters for a change!
However, it soon became apparent that the disease was leaving behind, not stands of maple and birch, but stands of beech sprouts, thickets. Beech sprouts very well when the top is killed or when a stand is salvaged. Some old trees survive, but they are deformed and defective.
See the separate page on sudden oak death.
See the separate page on pitch canker.
This is a common disease of aspen. It is the most important aspen disease in many areas. It kills aspen, and in some cases can essentially make a stand worthless. Stands with up to 70% mortality have been reported. Wounds may be the infection court, but we don't know for sure. Stem infections often originate from small branches. Understocked stands have much higher incidence, and stand edges have higher incidence of cankers than stand interiors. Is that related to distribution of an insect that causes the wounds?
Near the margin of the canker, small pillars develop underneath the outer bark, lifting it off in small sheets. Conidia develop on and between these pillars, apparently functioning as fertilizing elements (spermatia). Later, small black stromata appear, each with about a dozen perithecia. These are abundant and easily seen.
The outer bark on aspen is light greenish; it turns yellow to orange at margin of canker. Inner bark turns black when killed, and gets exposed when the papery outer bark peels off. Also, the stromata are black. So cankers have a salt-and-pepper look.
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