Forest Pathology - Cankers

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What is a canker?

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.
What causes cankers?

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.

How do canker pathogens get in (what is the infection court)?
It is amazing for how few of them we really know how the pathogen gets in. We think that generally none of them penetrate intact bark.

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?
Sexual vs. asexual stages

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.
Types of canker diseases
The most straightforward division of cankers is into annual and perennial.

* Annual canker diagram Annual cankers last for only one year, and the host then puts an end to them. The necrotic areas are callused over. Sometimes evidence can be seen on the bark surface for years afterward as an irregularity over the callus. In a cross section of the stem (right), annual cankers show up as small dark lines that follow an annual ring for a short distance and are covered by a bit of callus.
* Perennial canker diagram Persistent perennial cankers last for multiple years, but don't usually girdle the stem unless it is very small when infected. They don't expand rapidly. Sometimes, a layer of callus is produced and killed each year. When the host is active, it makes a roll of callus to try to heal; the pathogen lays low. When the host is dormant, the pathogen grows and kills the callus and perhaps a bit more. This leads to concentric rings of callus, giving the appearance of a target, and the name target canker. The diagram at right shows the target appearance of the canker and a view of the cross-section.

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.

* Conditional cankers (sometimes referred to as saprobic canker fungi although they are not strictly saprobes) are actually facultative parasites. They are normally saprobes, perhaps colonizing dead twigs or old sloughed-off bark. Under certain conditions that we usually interpret as stressful to the host, these fungi are able to overcome the host defenses and cause cankers. This does not mean they are not damaging. For instance, they may kill a host that otherwise might recover from temporary stress.
* Diffuse cankers are those in which necrosis spreads fairly rapidly so that the host does not build barriers (wound periderm) and callus to stop and heal it. These are not exclusive categories, because a weak pathogen may cause a diffuse canker. Certainly most diffuse cankers are perennial. Probably the difference between diffuse cankers and other perennial cankers is that diffuse cankers expand also during the growing season.

We'll consider at least one canker of each kind.
Annual cankers
Fusarium canker

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.
Persistent perennial cankers
Most persistent perennial cankers have the appearance that give them the term target canker. Remember how these cankers forms? Be sure you can relate appearance of canker face to cross-section and understand how it develops over time. These lessen value of trees by interrupting log length (cull). For low stem infections, that can be 50% loss. They also can serve as infection courts for decay fungi. They also can predispose the tree to snapping, even without decay.

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.
Nectria canker
Nectria sp. This is the most characteristic target canker, the best example. Usually get nice annual roll of callus, lasts for many years. Don't usually kill trees. Many hardwoods susceptible.

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.
Eutypella canker
This is another persistent perennial canker. It differs from Nectria canker in several respects:

* It is primarily restricted to maples
* The target appearance is usually not so clear. Cankers often have flaring margins, like a cobra (why not call it cobra canker?); and the bark tends to stay on.
* Fruiting can usually be found. Black perithecia embedded in the bark with long necks sticking out.
* Under the bark at the advancing margin of an active canker, mycelial fans can be found.

Butternut Canker - Goodbye Butternut?

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.
Pathogen:

The pathogen was previously unknown. Sadistic mycologists (joke) 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.
Disease:

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. How-to logo
Conditional cankers
Cytospora canker

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.

Cytospora sp.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.

Beech bark disease
Another introduced disease. But this is a bit more complicated than the others as far as the causal agent goes. There are two organisms that must occur for beech bark disease. One is a scale insect, the other is a Nectria.

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. FIDL icon
Diffuse cankers
Chestnut blight
See the separate page on chestnut blight, but have plenty of kleenex ready, because this is a very sad story.
Sudden Oak Death

See the separate page on sudden oak death.
Pitch Canker

See the separate page on pitch canker.
Hypoxylon 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?

Hypoxylon mammatum 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. FIDL icon
Want the nitty-gritty on more canker diseases (table of diseases)? Go for it.



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