Alder Heat Canker

Alder Heat Canker

Advancing margin of alder heat canker (white is paint).
Under moist conditions, conidia are squeezed out of conidiomata like toothpaste from a tube, forming orange cirrhi.

Although known since the late 1800s, this disease for a long time received little attention beyond acknowledgment of its existence.  But since the turn of the 21st century, the disease has certainly been noticed in the southern Rocky Mountains and in interior and southcentral Alaska.

Some may wonder at the name I have given this disease.  Such diseases are usually called “Cytospora canker of <host>”.  Disease names that include portions of pathogen names are deplorable for several reasons.  Since I have worked on this disease, I decided to point to the important role of temperature in contributing to canker expansion.


The hosts are Alnus spp. (alders).  The relative susceptibility of species is not well known.  In North America, Alnus tenuifolia (thinleaf alder, also known as A. incana ssp. tenuifolia) is the host of greatest concern [6–8].  In Alaska, it appears that A. sinuata (Sitka alder), A. crispa (green alder), and A. fruticosa (Siberian alder) are considerably less susceptible under normal conditions [3, 7].


The pathogen was described in the late 1800s (both the sexual stage, Valsa melanodiscus, and the asexual stage, Cytospora umbrina).   Since we are only using one name for a fungus now, the recommendation was made to select Cytospora for this group [4].  But we can’t call it Cytospora umbrina.  No, the older epithet, in this case melanodiscus, has to be transferred to the chosen genus, so Cytospora melanodiscus.  But that name does not exist until it is formally coined in a published paper, which it hasn’t been.  Catch 22.  So should we call it “The fungus formerly known as Cytospora umbrina“? 🙂

Koch’s postulates were completed, conclusively proving pathogenicity .  Alnus tenuifolia stems mechanically wounded and inoculated in Alaska formed cankers, as did plants in the greenhouse, where fresh leaf scars were inoculated.  When A. fruticosa was inoculated, only very small cankers formed [2, 3].  In Colorado, two sets of field inoculations of wounds in A. tenuifolia, one in late September and another in early August, resulted in no disease at all [10].  A Cytospora sp. in Oregon caused disease following wound inoculation, but not unwounded inoculation of A. tenuifolia [1].  However, it is uncertain what species that was.


The environment is the 800-pound gorilla for this disease.  More work is needed on how temperature and moisture determine susceptibility, but we know they can be very important.

Warm summer temperatures are conducive to the disease.  Canker expansion and killing of branches and stems occur almost exclusively in the warmest part of summer [10], and the effects of moisture stress on disease are greatest during periods of active growth [2]. However, many of the trees being killed during these warm periods in the Rocky Mountains are rooted directly beside year-round, perennial streams, and thus have continuous access to water.

Host age and vigor, as determined by changes in growth rate, had no influence on canker development [10].  Elevation and browsing level were unrelated to disease [8].  Disease decreased slightly as distance to streams increased, and alder in full sun was slightly more canopy loss than alder in full shade.  In Alaska, there is a variable but significant relationship between alder density and disease [5].

Disease Cycle

A very young canker on Alnus tenuifolia in Alaska. The canker started with no apparent wound and no twig stub. Possibly through lenticel? Notice lack of fruiting at the center, between the lenticels. Why?
The margin of alder heat canker seen under the bark surface.

The infection court remains unclear.  I have never seen a canker that appeared to start at a wound [8].  Some symptoms are initiated at shoot tips; others are initiated on clear, unwounded bark.  In a few cases it appeared that symptoms may have originated at lenticels.

Inoculum is often abundant on bark and bud surfaces, even in winter, but especially near diseased stems [10]. There are several lines of evidence that the pathogen is capable of inecting and growing in living tissue without causing disease.  We call these latent, biotrophic infections.  The evidence includes:

  • The pathogen can be isolated occasionally from healthy, asymptomatic internal tissues.    Inside healthy tissues, it occurred most frequently in dormant winter buds, and to a lesser extent in xylem and phloem.   In buds, it is possible that spores may have become embedded in the resin coating and thus been protected from surface sterilization, but this would not account for isolations from xylem and phloem.
  • It can be isolated routinely up to 5 cm beyond visible canker margins.  Isolation of the pathogen from xylem and phloem this distance from necrotic tissues indicates that the pathogen can grow in live tissues without causing immediate symptoms.
  • The initiation of cankers in the absence of wounding or twig stubs [8] could also be explained if the pathogen became established early in tissue development.

It is important to recognize that, if latent infections are common, the infection court may not be what is now the middle of a canker.  Infection may have occurred in a bud or leaf scar, then initiate disease years later on the surface of a large woody stem.  We also have no idea the extent of biotrophic growth.  Does the fungus get established and then remain dormant until the host is stressed, or is it able to grow substantial distances through the plant biotrophically?

In Colorado, the fungus produces primarily conidiomata in late winter and spring, and ascomata mature in late summer and fall [10].


Under the right circumstances, alder heat canker is an aggressive, devastating disease of Alnus tenuifolia.  Cankers expand during the growing season [10], when hosts are able to actively defend themselves, and cankers usually finish by girdling and killing the stem or branch [8].  In the southern Rockies, an epidemic apparently began in the 1980s, and by 2006 had killed 1/3 of alder stems and resulted in dieback on another 1/3.

In Alaska, A. tenuifolia is not restricted to riparian habitats.  The epidemic there caused damage on thousands of acres of alder in interior and southcentral Alaska [7].  Nitrogen fixation by bacteria in alder roots contributes up to 70% of the nitrogen in extensive Alaskan floodplains, raising concerns about the impacts of widespread mortality [5].  Disease intensification over just a few years was documented in the Tanana River floodplain [5].


There are several possibilities to explain the recent importance of this disease in alder populations:

1.  Why not?  The disease has always been doing this; it is part of the steady state of alder populations.

2.  The disease is cyclic or episodic, increasing to wreak havoc on alder populations, then settling down and allowing for recovery.

3.  Something has changed recently to cause an anomalous increase in disease.

There is ample evidence to rule out the first scenario [5, 10].  The second has been discussed [5, 10] and evidence for cycling of one of the dominant predisposing factors, high summer temperature, has been assembled [9, 10].  We also have good evidence that temperatures, and likely moisture stress, have increased directionally in recent years, supporting the third explanation.  In all likelihood, the second explanation is correct to some extent, but the directional change may now be erasing any past cycling of disease [5, 9, 10].


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