Wound Decays by Stereum Species

Stereum species are basidiomycetes in the class Agaricomycetes, order Russulales, family Stereaceae. They are usually effused-reflexed (having a portion flat on the substrate and part that comes out to form a pileus) and have a smooth or irregularly bumpy hymenophore (fertile surface), having no pores or teeth. We’ll look at two that are important pathogens causing wound heart rot. They are both in a group called the “bleeders”. An excellent source for identifying North American species is Chamuris ​[4]​; in Europe Eriksson ​[6]​.

Wound heart rot of oaks caused by Stereum gausapatum

Coarse hairy (strigose-hirsute) nature of the cap of Stereum gausapatum.
Red-brown staining of the hymenophore of Stereum gausapatum after some rough handling. Arrows point to one of the areas that immediately stained at the formerly white margin.

Stereum gausapatum (feature image at top; thanks to George Chamuris for helping me identify this specimen) is practically restricted to Quercus spp. (oaks) ​[4]​ and causes the most common stem decay in that genus ​[11]​. The disease doesn’t appear to have a widely used name, so we just use the generic disease type and host. The fungus occurs in much of the northern hemisphere and South America. It colonizes, decays, and fruits abundantly on downed branches, logs, old stumps; and on wounds and branch stubs of living trees ​[2]​.

The pathogen has a coarsely hairy cap (best seen with a hand lens) and is one of three Stereum spp. called “bleeders” because actively growing basidiomata will stain red-brown and may even produce red droplets when bruised ​[4]​ (see photos). Such species were formerly put in a separate genus, Haematostereum. Stereum gausapatum is called the “bleeding oak crust”.

The disease type is a wound heart rot. The pathogen initially enters branch stubs and wounds, including fire scars. It colonizes and decays the dead sapwood behind wounds and progresses into the inner wood of the stem. From there it develops axially in the heartwood.

When trees are cut, many species will produce sprouts from the stumps. As these sprouts mature, S. gausapatum can grow from the stump into them, thus causing disease in the next generation. Even if the parent tree is not infected, the stump may be colonized after cutting and transmit the disease to its sprouts. Studies showed that sprouts originating high on stumps were most likely to be infected, and the lowest sprouts the least likely ​[10]​. Options for reducing sprout infection were developed on this basis:

  1. Burning just before or after cutting greatly reduces the number of high sprouts. However, this must be balanced against the possibility of creating fire scars as infection courts in residual trees.
  2. Cut stumps close to the soil line.
  3. After sprouting, remove high sprouts (about an inch or more aboveground.

Decay is a mottled white rot. In the early stage, white axial streaks appear in the wood. The early wood (spring wood) is decayed first, and eventually all the wood becomes bleached and easily fragmented ​[2]​. Decay columns elongate about 10 cm per year (one direction) in the South ​[12]​.

Red heart of conifers caused by S. sanguinolentum

Fruiting of Stereum sanguinolentum on Abies balsamea. New York, USA.
Fruiting of Stereum sanguinolentum on the base of a dead Abies lasiocarpa (subalpine fir). Colorado, USA.
Red heart of Abies balsamea. Decay is most advanced internally, but has progressed out to the cambium in the upper part of the section. New York, USA.
Red heart of Abies balsamea in freshly cut logs.

Stereum sanguinolentum occurs in much of world, wherever conifers are grown. It is often extremely common as a sap rot of dead branches, logs, and stumps of many species, and occasionally is even found on dead hardwoods ​[4]​. Like S. gausapatum, it is a “bleeder”. Similarly, the fungus is often called “bleeding conifer crust”. Fruiting is much more common on dead material than on living trees ​[2]​. It is less colorful than S. gausapatum (photos at right).

In many ways this disease is similar to the previous one, but it occurs on conifers. The species where the disease can be significant (and the disease name “red heart” is appropriate) is a much shorter list than those where it just decays dead material and causes localized decay of sapwood behind wounds. In North America, Abies balsamea is most affected, followed perhaps by Picea rubra (red spruce). In northwestern North America, it is important on Pinus, Picea, and Abies spp. ​[1]​. In Europe, Picea abies (Norway spruce) is the most important host, with extensive decay of living trees as well as stored logs.

Infection is through wounds of all sorts. Large wounds are often more likely to be infected than small wounds ​[2, 3]​, but severe infection has occurred in pruning wounds 1-3 cm diameter ​[9]​. In uneven-aged management, as more heavy machinery is used in logging, there are more logging scars to residual trees, resulting in more damage from red heart ​[3]​. In some cases after storms break tops, the fungus causes top rot. Decay is usually in the main and top parts of the stem, less often invading the butt. In Abies balsamea and other species, it generally progresses in the heartwood ​[1, 5, 8]​. In Picea abies, it is said to more often progress in the young annual rings ​[3]​ or the heartwood, but in some cases killing and decaying sapwood, and even whole trees (​[9]​, see below).

In early stages of decay there is a yellow, then red-brown discoloration, and the wood may appear water-soaked ​[2, 3]​. On the cut end of a log, there may be radial extensions of decay, as seen in red ray rot caused by Dichomitus squalens (see Fig. 10 in ​[8]​). As decay advances, thin, white mycelial felts may appear. The advanced decay is light brown and finely stringy.

A case study described severe disease following careless pruning in a Picea abies (Norway spruce) plantation in New York ​[9]​. Trees were pruned 19 years after planting, up to 2 m high, with branches 1-3 cm diameter. Some stubs were long and jagged, and stems were wounded. Five years later, S. sanguinolentum was fruiting abundantly on stubs and wounds. In 6 dissected trees, decay columns ranged from 1.0 – 3.3 m long. Although decay progressed mostly in heartwood, some trees were killed when the sapwood was attacked.

In Pinus strobus in eastern North America, pruning wounds can be infected if they are above about 5 cm diameter (see ​[2, 9]​).

Stereum sanguinolentum has also been implicated in “mottled bark disease” on planted conifer saplings in Idaho ​[7]​. The affected trees represented at least 7 species and many were 18-20 yr old. Infection apparently occurred through basal wounds. Trees died quickly during the growing season, and usually had resinosis on the root collar and butt. The inner bark of the butt and roots had a white mottled appearance. The underlying sapwood turned gray-brown and began to decay. Stereum sanguinolentum fruited on the butts, root crotches, and exposed roots. It was thought that drought stress may have precipitated the disease. I am not aware of further observations of this disease.


  1. 1.
    Allen EA, Morrison DJ, Wallis GW. 1996. Common Tree Diseases of British Columbia. Victoria, British Columbia, Canada: Natural Resources Canada, Canadian Forest Service, Pacific Forestry Centre.
  2. 2.
    Boyce JS. 1961. Forest Pathology, 3rd ed. New York: McGraw-Hill Book Company. 572 pp.
  3. 3.
    Butin H. 1995. Tree Diseases and Disorders: Causes, Biology, and Control in Forest and Amenity Trees. Oxford ; New York: Oxford University Press. 252 pp.
  4. 4.
    Chamuris GP. 1988. The Non-Stipitate Stereoid Fungi in the Northeastern United States and Adjacent Canada, Vol. 14. Berlin: J. Cramer. 247 pp.
  5. 5.
    Davidson AG, Etheridge DE. 1963. Infection of balsam fir, Abies balsamea (L.) Mill., by Stereum sanguinolentum (Alb. and Schw. ex Fr.) Fr. Can. J. Bot. 41(6):759–765 <10.1139/b63-063>.
  6. 6.
    Eriksson J, Hjortstam K, Ryvarden L. 1984. The Corticiaceeae of North Europe. Vol. 7: Schizopora – Suillosporium. Oslo, Norway: Grønlands Eskefabrikk. 167 pp.
  7. 7.
    Hubert EE. 1935. A disease of conifers caused by Stereum sanguinolentum. Journal of Forestry 33(5):485–489 <https://academic.oup.com/jof/article-abstract/33/5/485/4720471>.
  8. 8.
    Kaufert F. 1935. Heart rot of balsam fir in the Lake States, with special reference to forest management. University of Minnesota Agric. Exp. Station Technical Bulletin 110:1–27 <https://conservancy.umn.edu/bitstream/handle/11299/204039/mn1000_agexpstn_tb_110.pdf>.
  9. 9.
    Risley JH, Silverborg SB. 1958. Stereum sanguinolentum on living Norway spruce following pruning. Phytopathology 48(6):337–338.
  10. 10.
    Roth ER, Hepting GH. 1969. Prediction of butt rot in newly regenerated sprout oak stands. Journal of Forestry 67(10):756–760 <https://academic.oup.com/jof/article-abstract/67/10/756/4659226>.
  11. 11.
    Sinclair WA, Lyon HH. 2005. Diseases of Trees and Shrubs, 2nd ed. Ithaca, New York, USA: Cornell University Press. 660 pp.
  12. 12.
    Toole ER, Furnival GM. 1957. Progress of heart rot following fire in bottomland red oaks. Journal of Forestry 55(1):20–24 <https://www.fs.usda.gov/treesearch/pubs/42513>.