What is a canker?

A canker is an infectious disease of the phloem and cambium on stems, branches or twigs.  A patch of phloem and cambium is killed, the underlying wood dies as a result, and the killing often progresses over time. Cankers are often sunken if they grow slowly because the shoot continues to grow around it. Also, callus may be produced around the canker that makes it appear more sunken.

There are some diseases usually considered with other groups that are cankers, as well as injuries that can be confused with cankers:

  • Bacterial cankers.  These are covered with bacterial diseases.
  • Canker rots. Some basidiomycetes that decay wood in the stem may also kill patches of sapwood and bark. We consider most of them along with stem-decay fungi.
  • Stem rusts. These cause cankers, but we consider them separately with the rusts.
  • Foliage diseases, shoot and tip blights. Some of these kinds of diseases also can involve small cankers of twigs, branches, and even main stems; they are considered under foliage diseases.
  • Winter injury or sunscald. These kill patches of bark, and can be confused with cankers.  Also, canker pathogens can infect living tissues at the margins, so they can become cankers.

What causes cankers?

Pathogens are mostly in the phylum Ascomycota.

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?

What determines canker growth?

John Bier (1909-1967) was a brilliant forest pathologist.  He began his career with the Canadian Dept. of Agriculture, Division of Botany and Plant Pathology, and in 1956 accepted the position of Professor of Forest Pathology at the University of British Columbia [1].  During his career, he founded two forest pathology laboratories in Victoria and Toronto, then became the national leader of the forest pathology program in Ottawa.  His papers are written thoroughly and authoritatively.  His vision and insight can be seen from the fact that he was one of the first to appreciate the importance of endophytes (though he didn’t use that name) and their role in protecting trees from diseases.

His contributions are many and varied in the fields of nursery diseases, root diseases, cull surveys, and more.  But perhaps his biggest contribution was in determining what controls canker growth.  His findings apply to native, facultative parasites, primarily annual and diffuse cankers (see below).

Bier built on the work of Heinz Butin [4], who found that resistance of poplars to Cytospora canker was controlled by moisture content.  When the latter was reduced about ~20%  or more from maximum, the phloem could no longer produce wound periderm, and also became susceptible to the disease.  Bier recognized that resistance was more complex than that, and undoubtedly involved physiology, oxygen, biochemical changes, etc.  But he was able to use relative bark moisture content as a simple predictor of susceptibility.  And isn’t that the best science, simple and elegant?

Bier worked with a canker of willow caused by Cryptodiaporthe salicina [2].  He noted that during certain winters, when the plants were dormant, cankers developed.  They were initiated around nodes, lenticels, and insect wounds.

Bier found that, to overcome variation among samples in bark density, etc., the best measure was moisture content as a percent of that when saturated.  Eighty percent of saturation was the threshold.  It is interesting to note that this effect held also during dormancy, when the cuttings had no active response. Relative moisture content was also predictive of wound callus formation, effectiveness of endophytes at preventing disease, and rooting ability [3].  During some winters, willows in the field naturally fell below 80% of saturation, triggering canker development.

This work probably applies to most cankers except the perennial target cankers (see below).  It not only provided basic insight into canker epidemiology, it also:

  • resulted in concrete recommendations for handling cuttings so as to reduce losses before and after planting
  • emphasized the importance of moisture status of trees in winter in avoiding damage from dormant-season cankers
  • led to the realization that in breeding programs and testing for canker resistance, moisture status must be considered and controlled.

Types of cankers

Annual cankers

Annual cankers in various annual rings as seen in a cross-section.

As you might guess from the name, annual cankers last for (less than) a 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.

An example is Fusarium canker of maples in northeastern North America [6].  Cankers can extend from less than an inch to several feet long (vertically), but 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 never open through the bark. Usually there is no impact on tree growth, but lumber can be 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.  Cottonwoods get a Fusarium canker too, but the pathogen is different.

Following periods of drought or high temperature, annual cankers up to 7 m long may form on Fagus sylvatica (European beech).  Two facultative parasites are involved: Biscogniauxia nummularia on small trees and Eutypa spinosa on large trees [5].  Although it was suggested that cankers develop during the growing season, the evidence for that is unclear, and they may have formed during a dormant season.  The evidence does suggest that the pathogens may become established initially as latent infections, which only begin to kill and decay following moisture stress.


Perennial target cankers

A perennial canker with annual rings of callus as seen in face view and cross-section.

Perennial target cankers last for multiple years, but don’t usually girdle the stem unless it is very small when infected. They don’t expand rapidly.

Be sure you can relate the appearance of the canker face to the cross-section and understand how it develops over time. 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.

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.

Diffuse cankers

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. Most diffuse cankers are perennial, but there is no target formed from callus rings. Probably the difference between diffuse cankers and other perennial cankers is that diffuse cankers expand also during the growing season.

Diffuse cankers are often caused by facultative parasites, meaning they are normally saprobes, perhaps colonizing dead twigs or old sloughed-off bark, but 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.

Canker pages:

Alder heat canker

Aspen cankers

Beech bark disease

Butternut canker

Chestnut blight (have plenty of tissues ready, because this is a very sad story)

Other Cytospora cankers

Hypoxylon canker

Pitch canker

Some target cankers

Sudden oak death


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


Anonymous. 1967. Dr. John Ertel Bier (Obituary). Forestry Chronicle 43(1):104–105. [Source]
Bier JE. 1959. The relation of bark moisture to the development of canker diseases caused by native, facultative parasites.  I. Cryptodiaporthe canker on willow. Canadian Journal of Botany 37:229–238.
Bier JE. 1964. The relation of some bark factors to canker susceptibility. Phytopathology 54(3):250–253.
Butin H. 1955. Über den Einflüß des Wassergehaltes der Pappel auf ihre Resistenz gegenüber Cytospora chrysosperma (Pers.) Fr. Phytopathologische Zeitschrift 24:245–264.
Hendry SJ, Lonsdale D, Boddy L. 1998. Strip-cankering of beech (Fagus sylvatica): Pathology and distribution of symptomatic trees. New Phytologist 140(3):549–565. [Source]
Skelly JM, Wood FA. 1966. The occurrence and etiology of an annual canker of sugar maple in Pennsylvania. Canadian Journal of Botany 44(10):1401–1411. [Source]