This disease occurs in Europe. The pathogen was apparently introduced from the Great Lakes region of North America, where it does not cause disease, to the UK shortly before 1945, when it was first noticed there. However, it has recently been found causing disease in Seattle, Washington, USA (see Distribution and Damage below).
Known as Rußrindenkrankheit in German, it should not be confused with sooty-bark canker of aspen. It’s interesting that these diseases have similar names, because it is for entirely different reasons. The ‘soot’ in the aspen disease is decomposed inner bark that fragments to dust. That of the maple disease refers to the incredible masses of airborne conidia released when the outer bark falls away. The conidia are a risk to forest workers around the dead and diseased trees, requiring mitigation.
The most prominent host is Acer pseudoplatanus, but there are additional maple species sometimes infected. All are European natives except A. negundo, A. rubrum, A. macrophyllum, and Cornus nuttallii from North America and A. palmatum from east Asia.
- A. pseudoplatanus. Known as sycamore maple in North America, sycamore in the UK, and Bergahorn in German. In addition to its use in parks and cities, it is used in forest plantations and in some areas is an important component of natural forests.
- A. campestre. Field maple in English, Feldahorn in German.
- A. platanoides. Norway maple in English, Spitzahorn in German.
- A. negundo. Box elder or Manitoba maple in North America, ashleaf maple in the UK, Eschen-Ahorn in German. Although its natural distribution overlaps with that of Cryptostroma corticale in North America, it is known to be attacked only in Europe.
- A. rubrum and A. macrophyllum. Red maple and bigleaf maple, native to North America, were found infected in the Pacific Northwest recently (see Emerging epidemic below). Like A. negundo, A. rubrum grows naturally within the distribution of the pathogen. It raises the question why there is disease only when planted out of the native range.
- A. palmatum, Japanese maple, also recently confirmed in the Pacific Northwest.
- Cornus nuttallii, Pacific dogwood, also recently confirmed in the Pacific Northwest.
- Aesculus hippocastanum, horsechestnut, also recently confirmed in the Pacific Northwest.
Cryptostroma corticale is the pathogen (this nice-sounding name means roughly “hidden stroma in the bark”). It was originally described in London, Ontario in 1898.
It does indeed produce stromata in the bark [11, 12]. The stroma splits parallel to the bark surface to form a roof and a floor. These are pushed apart by columns up to 1 mm long, making room for fruiting. The stromatal tissues blacken as they mature. From the floor, a blue-gray layer of conidiophores develops, producing conidia in chains. Shedding of the bark and outer stroma reveals the brown-black mass of conidia, as well as the persistent black columns (see featured image above, courtesy of Dr. Thomas Kirisits, IFFF-BOKU, Vienna). When the spores are dispersed, the conidiophores are blue-gray over the black stroma. Sexual fruiting is not known.
The stroma pushing up the bark is a little bit like Entoleuca mammata, which produces little pillars that push out the outer bark in salt-and-pepper canker. Also in oak wilt, the fungus produces “pressure pads” to crack the bark open, allowing insects to visit the inviting mycelial mat. And in butternut canker, the pathogen produces mycelial pegs that lift and rupture the outer bark where it is thin.
Nothing produces spores like this fungus, though. It’s a spore monster! A single stem 3 ft in diameter x 15 ft long can produce an estimated 5×1013 spores ! That’s 50,000,000,000,000, or 50 trillion!!
Using molecular phylogeny, the pathogen was found to belong in the genus Biscogniauxia (Xylariales: Graphostromataceae) . However, to date the name Biscogniauxia corticalis has not been formally published.
Increase in disease frequency following hot and dry summers has been widely observed. Some have even said that disease occurs only with such conditions . Soon after its introduction to Britain, the disease was most severe following hot summers of 1947, 1948, and 1955 . This suggests that host stress from such conditions increases susceptibility. However, the fungus grows in culture and in the host much faster at 25 C than at 10 C , so the pathogen is also favored directly by warm conditions.
Although it had been suggested that a threshold for disease outbreaks was at least one month of the summer (June/July/August) reaching a monthly average of daily maximum temperature of 23 C, Cech  noted that many places in Europe reach that threshold most of the time. He and others determined that the 23 C threshold applies better to the mean monthly temperature. For example, an outbreak in Gänserndorf (see Distribution and Damage below) followed 2015, when July and August exceeded that threshold.
The infection court is not known with certainty, but it appears that Cryptostroma corticale infects young shoots and branches, which may result in a largely inconspicuous twig or branch dieback . At the same time, however, the mycelium grows through the wood and into the heartwood without any further external symptom. Internally, there is a light green to brown stain that indicates where the fungus has grown. Colonization is mainly longitudinal, and the rate of growth is increased by heat and drought stress .
In hot summer weather, radial growth increases . When the fungus reaches the outside of the wood, it kills the cambium, invades the bark, and begins to develop the stroma, with its tremendous numbers of spores, as described above under Pathogen. The bark falls off, aided by pressure from the mycelial columns, and spores can be released.
It appears that, aside from some initial twig or branch killing after infection, the fungus can become latent in the tree. If temperatures are cool and the host is not stressed, there may be longitudinal growth but little radial growth, so external symptoms do not develop. Thus, a tree may be colonized from the roots to the twigs, so that when stress and heat trigger radial growth, it is rapid and devastating, with spore masses developing up and down the stem and branches.
This widespread latent infection suggests that the distribution of the pathogen and the frequency of infected trees may be much greater than indicated by disease .
Distribution and Damage
Cryptostroma corticale was described in 1898 from London, Ontario, Canada. It is common in the Great Lakes region of North America, mostly on maples, but is considered a saprobe and does not cause tree disease  (but does it infect trees asymptomatically, as an endophyte?). It has been known since 1932 that it can be dangerous to humans, however  (see below).
Elsewhere in North America, it was collected near Poncha Springs, Colorado in 1898 on Populus angustifolia (narrow-leaf cottonwood) , but there is no indication it was associated with disease. Similarly, it was collected in 1969 in eastern Washington on a young standing dead Acer pseudoplatanus (sycamore maple) .
The fungus was apparently introduced to Europe from North America. it was first noticed in 1945 in northeast London . It spread quickly, causing a devastating wilt and mortality of sycamore maple. It has been suggested that it came to Great Britain in timber imported into London docks. The large-scale shipment of men and materiel from North America to England during World War II may be a likely route and time.
Sooty-bark disease of maple is now well established in the UK, France, Germany, and Austria [3, 12, 14] and was found more recently in Switzerland, the Netherlands, Bulgaria, and the Czech Republic [2–4].
In Austria, the disease was initially scattered and never affected more than 5% of the potential hosts . However, in 2018 the disease was found in the Gänserndorf area, northeast of Vienna near the Slovakian border, with an estimated 60% of the sycamore maple trees infected.
Emerging epidemic in northwestern USA
In early 2020, a damaging disease was observed in A. pseudoplatanus trees in one location in Seattle, Washington. As the symptoms and signs appeared to fit sooty-bark disease, samples were sent to Bartlett Tree Research Laboratories. There, DNA sequencing confirmed the presence of Cryptostroma corticale (personal communication, Chris Rippey, Seattle Parks and Recreation; and Megan McConnell, Bartlett Tree Research Laboratories). This is the first report of the disease in North America.
Later in 2020, the disease was found at three additional sites in Seattle, and two samples were sequenced, confirming the pathogen again (personal communication, Chris Rippey and Megan McConnell). These new sites included two new hosts: Acer rubrum (red maple, native to eastern and central North America) and Acer macrophyllum (bigleaf maple, native to northwestern North America). Acer rubrum grows naturally in the native distribution of C. corticale, but the disease has not been reported there. The fact that the disease appears to be spreading and infecting native Acer spp. raises concern.
By 2021, the disease was appearing in more locations in Seattle, and the list of hosts expanded (personal communication, Mark Malone, Seattle arboriculturist). Using molecular methods, the disease was confirmed on Acer palmatum (Japanese maple), Cornus nuttallii (Pacific dogwood), and Aesculus hippocastanum (horsechestnut). The latter two are alarming because they expand the host range outside the genus Acer and because Pacific dogwood is a native species in the Northwest (like A. macrophyllum).
If we weren’t transporting fungi all over the world, this never would have happened. Now, prevention can only be accomplished by reducing the amount of the host. In dry-warm sites of Austria outside of the Alps, A. pseudoplatanus should be incorporated into new stands only as a mixture and in limited numbers . Similarly, in southern Britain, where temperatures often favor the disease, it is recommended to reduce the proportion of A. pseudoplatanus where it is used at all .
However, Phillips & Burdekin suggested that, in Britain, the temperature requirements for disease would restrict it to the south, and greater London in particular . They felt that suitable conditions would be infrequent and that, “Unless there is a dramatic change in the summer temperatures in Britain active measures to control the disease would therefore seem to be unnecessary.”
The spores are hyper-allergenic; they can cause severe asthma  and hypersensitivity pneumonitis . Maple bark disease, or maple bark stripper’s disease, is an uncommon condition caused by exposure to the spores of C. corticale. The disease has been found among workers in the paper industry employed to debark, cut and chip maple logs. The symptoms include breathlessness, fever, night sweats, chills and weight loss . In North America, it has only been an issue when logs have been stored for at least 6 months , but where it is a pathogen, large numbers of spores can be released even before the tree dies, and removing or harvesting dead standing trees can endanger workers.
Forest workers must wear personal protective equipment when working around dead and diseased maples . It is recommended to keep the public away while working on trees, and preferably to use machine felling rather than chainsaws. It is also advised to work during wet weather to reduce the number of airborne spores. Wood should not be used for firewood. It should be covered during transport and burned. Personal protective equipment includes:
- Protective suit with hood
- Protective gloves
- Closed shoes or boots that are easy to clean
- Disinfection should not be needed, since it doesn’t infect humans. The goal is to avoid inhaling large numbers of spores.
With higher summer temperatures, more frequent extremes, and increased frequency of drought, it is clear this disease will become more severe, and the disease distribution will increase. But there is an additional point of pain with this disease. In Europe, maple species, especially Acer pseudoplatanus, have been regarded as the reservoir of hope for deciduous forests in the face of climate change . This species was considered a likely substitute for the species more obviously endangered by climate change. Now it appears that these hopes are dashed.
If you have looked at much of this web site, you will think I’m a broken record. Well, this tragedy is repeated around the world, hundreds of times, often with devastating consequences. We’ve got to stop moving wood and plant materials around the world without regard for creating new tragedies.
Type of disease
Is this really a canker, as I have placed it, or a wilt disease? Well, it attacks and kills cambium and bark, so by definition it is a canker. Growth in and stain of wood is unusual for cankers, but it is similar to Cryptosphaeria (snake) canker of aspen in this respect. The stain pattern is not typical for wilts. So for now, we’ll consider it a canker.
Thomas Kirisits (IFFF-BOKU, Vienna) kindly provided the main references on this disease. I also thank him and Thomas Cech (Dept. of Forest Protection, Federal Forest Research Center, Vienna) for providing the photos and permission to use them.
- 1.Anonymous. 2019. Arbeitssicherheit & Gesundheit, Biologische Arbeitsstoffe, Loseblatt B.01.18: Schutzmaßnahmen bei Tätigkeiten an Ahorn mit Rußrindenkrankheit. Sozialversicherung für Landwirtschaft, Forsten und Gartenbau, Kassel, Germany <https://cdn.svlfg.de/fiona8-blobs/public/svlfgonpremiseproduction/bbb58ebb5c9760d3/3aa2ce9f2c9a/b_01_18-bio-arbeitsstoffe-russrindenkrankheit>.
- 2.Bencheva S. 2014. First report of Cryptostroma corticale (Ellis & Everh.) P.H. Greg. & S. Waller on Acer platanoides L. in Bulgaria. Silva Baltanica 15(2):101–104 <https://www.researchgate.net/publication/275823623>.
- 3.Cech TL. 2018. Rußrindenkrankheit bedroht Ahornbestände in Laubwäldern im Osten Niederösterreichs. Forstschutz Aktuell 65(4):1–6 <https://bfw.ac.at/rz/bfwcms.web?dok=10373>.
- 4.Cochard B, Crovadore J, Bovigny PY, Chablais R, Lefort F. 2015. First reports of Cryptostroma corticale causing sooty bark disease in Acer sp. in Canton Geneva, Switzerland. New Disease Reports 31:8 <10.5197/j.2044-0588.2015.031.008>.
- 5.Emanuel DA, Wenzel FJ, Lawton BR. 1966. Pneumonitis Due to Cryptostroma corticale (Maple-Bark Disease). New England Journal of Medicine 274(25):1413–1418 <10.1056/NEJM196606232742504>.
- 6.Farr DF, Rossman AY. Fungal Databases. U.S. National Fungus Collections, ARS, USDA. <https://nt.ars-grin.gov/fungaldatabases/>.
- 7.Goree H. 1969. Occurrence of Cryptostroma corticale in northwestern United States. The Plant Disease Reporter 53(1):87 <https://babel.hathitrust.org/cgi/pt?id=uc1.31175002384181&view=1up&seq=95>.
- 8.Gregory PH, Waller S. 1951. Cryptostroma corticale and sooty bark disease of sycamore (Acer pseudoplatanus). Transactions of the British Mycological Society 34(4):579–597 <10.1016/S0007-1536(51)80043-3>.
- 9.Kessler J Kenneth J, Ohman JH. 1965. Cryptostroma corticale–allergen, plant pathogen, saprophyte. Phytopathology 55(7):811–812.
- 10.Koukol O, Kelnarová I, Černý K, Woodward S. 2015. Recent observations of sooty bark disease of sycamore maple in Prague (Czech Republic) and the phylogenetic placement of Cryptostroma corticale. Forest Pathology 45(1):21–27 <10.1111/efp.12129>.
- 11.Peace TR. 1962. Diseases of Maple and Sycamore – Sooty bark disease. In: Pathology of Trees and Shrubs – With Special Reference to Britain, pp. 411–413. London: Oxford at the Clarendon Press.
- 12.Phillips DH, Burdekin DA. 1982. Diseases of Bark and Trunk – Sooty bark disease caused by Cryptostroma corticale. In: Diseases of Forest and Ornamental Trees, pp. 254–256. Houndmills, Basingstoke, Hampshire: The Macmillan Press Ltd.
- 13.Spoerke DG, Rumack BH, eds. 1994. Handbook of mushroom poisoning: diagnosis and treatment. Boca Raton: CRC Press. 456 pp.
- 14.Strouts RG, Winter TG. 2004. Sooty bark disease of sycamore. In: Diagnosis of Ill-Health in Trees: Research for Amenity Trees vol., pp. 257–258. Norwich, UK: Her Majesty’s Stationery Office. 2nd ed.
- 15.Towey JW. 1932. Severe bronchial asthma apparently due to fungus spores found in maple bark. Journal of the American Medical Association 99(6):453 <10.1001/jama.1932.02740580021005>.