This is a disease primarily of aspen species (Populus section Populus): Populus tremuloides (trembling aspen) and P. grandidentata (bigtooth aspen) in North America and P. alba and P. tremula in Europe . Some hybrid poplars can also be infected. The fungus has been found as a saprobe on a wide range of woody plants in other genera.
Known over the years as Hypoxylon pruinatum and H. mammatum, this pathogen was moved some years ago into the genus Entoleuca, giving the combination E. mammata . The authors wanted to restrict the scope of the genus Hypoxylon to a core group that our species did not belong to. The move was based on morphological characters, and could well be revised again on molecular bases.
The disease is traditionally known as Hypoxylon canker. When the pathogen was moved to the genus Entoleuca, the forest pathology community did not change the disease name to follow, as they have with other diseases. Perhaps it is more obvious in this case that the genus may change again, and it is a pointless pursuit. But still, the “Hypoxylon” part of the disease name is now meaningless, nothing more than an historic legacy. Therefore, I believe the changing of the pathogen name should trigger a move away from a pathogen-based disease name. I like “salt-and-pepper canker”. This name reflects how we recognize the disease at a distance, consistent with the “mottled” appearance described by many authors.
The role of the environment in the disease is complex and there are many contradictions . Like many characters in aspen, there is likely genetic variation in disease response to environment. In general, the disease has been associated with open stands. Consistent with this, in one study, disease was greater in thinned than in unthinned stands. Multiple studies indicate that moisture stress increases susceptibility.
Infection often occurs through small wounds . Ascospores are the likely inoculum , although many inoculation attempts with ascospores have failed . There are some indications that wounds into the xylem are best, as the pathogen is better able to invade bark when it is already established in the wood . These may be galls or oviposition wounds made by various insects and other types of wounds.
The fungus is able to decay wood and does so while it also expands in the cambium and phloem. As the canker grows, it may progress down a branch into a larger branch or stem. Typically the tree dies when it is girdled (killed all the way around) or it snaps due to the wood decay.
Within a few years, near the margin of the canker, small pillars develop underneath the outer bark, causing it to loosen and blister and lifting it off in small sheets. Conidia develop on and between these pillars, apparently functioning as fertilizing elements (spermatia) to cross-fertilize mycelia between cankers. In another year, hard, gray-black stromata are formed on the same spot, each with about a dozen or more raised perithecia. These are abundant, durable, and easily seen (see also the featured image above). Ascospores are forcibly ejected from the perithecia immediately following rain  and during moist conditions throughout the year .
Symptoms and Signs
The outer bark on aspen is light green to white; 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. The blistered bark, conidial pillars, and stromata occur in small patches. All these colors and patterns give the canker a very mottled, salt-and-pepper appearance as seen from a distance. At the canker margin, beneath the bark, the fungus advances with white to gray mycelial fans.
Distribution and Importance
This is a common disease of aspen in eastern and central North America. Here it is often the most important aspen disease. It also occurs in the southern Rocky Mountains but is uncommon to rare. It appears to be absent from the middle Rocky Mountains of the US and Alaska.
The disease can be found in northern Europe, and the fungus has been collected in the Alps of Italy and Switzerland . Study of genetic variability indicate that the pathogen is native to North America and was introduced to Europe several centuries ago .
It kills aspen, and in some cases can essentially make a stand worthless. Stands with up to 70% mortality have been reported. It is most damaging in young aspen. Understocked stands have much higher incidence, and stand edges have higher incidence of cankers than stand interiors. This may be related to preferences of the insects cause the wounds, and the increased availability of young branches for oviposition in open stands and stand edges .
- 1.Bier JE. 1940. Hypoxylon canker of poplar. Publication 691; Technical Bulletin 27., Vol. III Ottawa: Canada Dept. of Agriculture, Division of Botany and Plant Pathology.
- 2.Kasanen R, Hantula J, Ostry M. 2004. North American populations of Entoleuca mammata are genetically more variable than populations in Europe. Mycological Research 108(7):766–774.
- 3.Manion P, Griffin D. 1986. Sixty-five years of research on Hypoxylon canker of aspen. Plant Disease 70(8):803–808.
- 4.Ostry ME. 2013. Hypoxylon canker. In: Infectious Forest Diseases, edsGonthier P, Nicolotti G, pp. 407–419. Wallingfork, UK: CAB International.
- 5.Ostry ME, Anderson NA. 1998. Interaction of Insects, Woodpeckers, and Hypoxylon Canker on Aspen. Research Paper NC-331. St. Paul, Minnesota, USA: USDA Forest Service, North Central Research Station.
- 6.Rogers J, Ju Y-M. 1996. Entoleuca mammata comb. nov. for Hypoxylon mammatum and the genus Entoleuca. Mycotaxon 59:441–448.