"Review of fungal diseases in Poplar"
Gian Pietro Cellerino
1. Diseases caused by fungi p. 3
1.1. Root diseases p. 5
1.1.1. Root rot caused by Rosellinia necatrix p. 5
188.8.131.52. Symptoms and the damage caused p. 5
184.108.40.206. The pathogen p. 6
220.127.116.11. Biology and predisposing factors p. 7
18.104.22.168. Control strategies p. 8
1.1.2. Other root diseases p. 9
22.214.171.124. Root and butt rots caused by Armillaria spp. p. 9
– Heterobasidion annosum p. 11
– Ganoderma lipsiense p. 11
– Botryodiplodia palmarum p. 11
1.2. Diseases of stems and branches p. 12
1.2.1. Bark necrosis caused by Discosporium populeum p. 12
126.96.36.199. Symptoms and the damage caused p. 12
188.8.131.52. The pathogen p. 13
184.108.40.206. Biology and relations with the host p. 14
220.127.116.11. Control strategies p. 15
1.2.2. Necroses and cankers caused by Cytospora spp. p. 17
18.104.22.168. Symptoms and the damage caused p. 17
22.214.171.124. The pathogens p. 18
126.96.36.199. Biology and relations with the host p. 18
188.8.131.52. Control strategies p. 19
1.2.3. Canker caused by Hypoxylon mammatum p. 20
184.108.40.206. Symptoms p. 20
220.127.116.11. Incidence and the damage caused p. 21
18.104.22.168. The pathogen: taxonomy and geographical diffusion p. 22
22.214.171.124. Biology and relations with the host p. 23
126.96.36.199. Control strategies p. 24
1.2.4. Necroses ad cankers caused by other pathogens p. 25
188.8.131.52. Cankers caused by Phomopsis spp. p. 25
184.108.40.206. Necroses and cankers caused by Fusarium spp. p. 27
220.127.116.11. Sooty-bark canker caused by Encoelia pruinosa p. 29
18.104.22.168. Snake canker and wood decay caused by Cryptosphaeria lignyota p. 30
22.214.171.124. Black or target canker caused by Ceratocystis fimbriata p. 31
– Nectria galligena p. 33
– Rhytidiella moriformis and R. baranyayi p. 33
– Diplodia tumefaciens p. 34
– Phoma exigua var. populi p. 34
– Corticium salmonicolor p. 34
– Dothiorella gregaria p. 34
– Botryodiplodia populea p. 35
1.3. Diseases caused by Septoria spp. p. 35
1.3.1. Cankers and leaf spots caused by Septoria musiva p. 35
126.96.36.199. Symptoms and the damage caused p. 35
188.8.131.52. The pathogen p. 36
184.108.40.206. Biology and relations with the host p. 37
220.127.116.11. Control strategies p. 37
1.3.2. Leaf spots caused by Septoria spp. p. 38
1.4. Diseases of leaves and young shoots p. 39
1.4.1. Rusts caused by Melampsora spp. p. 39
18.104.22.168. Symptoms and the damage caused p. 39
22.214.171.124. Life cycle p. 40
126.96.36.199. The pathogens p. 41
188.8.131.52. Relations with the host p. 43
184.108.40.206. Control strategies p. 44
1.4.2. Leaf spots caused by Marssonina spp. p. 48
220.127.116.11. Symptoms and the damage caused p. 49
18.104.22.168. The pathogens p. 50
22.214.171.124. Life cycle and relations with the host p. 51
126.96.36.199. Control strategies p. 53
1.4.3. Leaf scab and blight caused by Pollaccia spp. p. 54
188.8.131.52. Symptoms and the damage caused p. 54
184.108.40.206. The pathogens p. 55
220.127.116.11. Life cycle and relations with the host p. 58
18.104.22.168. Control strategies p. 58
1.4.4. Other leaf diseases p. 59
22.214.171.124. Yellow blister of leaves and amenta caused by Taphrina spp. p. 59
126.96.36.199. Powdery mildews p. 60
188.8.131.52. Leaf blotch caused by Septotinia podophyllina p. 61
184.108.40.206. Leaf blight caused by Linospora spp. p. 62
– Ciborinia whetzelii p. 63
– Glomerella cingulata p. 64
– Sphaceloma populi p. 64
– Alternaria alternata p. 64
– Phyllosticta spp. p. 64
– Phoma exigua and P. macrostoma p. 64
– Phaeoramularia maculicola p. 64
– Cladosporium humile p. 64
– Cercospora populina p. 64
– Rhizoctonia solani p. 65
– Drechslera maydis p. 65
Essential bibliography p. 66
"Review of fungal diseases in Poplar"
Intensive poplar growing began to cover its most qualifying stages in the northern temperate zone since the beginning of the twentieth century. Massive employment of Populus nigra L. and some hybrids in south-central Europe, as well as of P. deltoides Bartr. in the warm areas and P. tremuloides Michx. in the cool ones of North America respectively, was in more recent times followed by the establishment of plantations in the Far East and in Australasia, where wider use was made of hybrids of different origin.
Nevertheless, unceasing progress in terms of both quantity and quality was accompanied by an exponential increase in the toll exacted by diseases.
When exchanges between one region and another were few and far between, pathosystems were well defined and local. In the case of parasite fungi, for example, attacks on the part of two bark necrosis agents were the main concern: Septoria musiva Peck in America, Discosporium populeum (Sacc.) Sutton in zones with continental climate of both Europe and America. Rusts caused by Melampsora spp. were widespread almost everywhere, but the single species were confined to clearly identifiable geographical areas. With regard to Prokaryotes, the various parasites found on Salicaceae were restricted to even more circumscribed areas. Even today, the bacterial canker agent Xanthomonas populi (Ridé) Ridé et Ridé has not strayed from poplar districts of north-central Europe, including France north of the Loire. Agrobacterium tumefaciens (Smith et Town.) Conn only is a matter of exception, since it is found almost world-wide, presumably owing to its polyphagy; it is highly aggressive against some white poplar selections not yet employed in any great numbers.
Clones drawn from P. deltoides, P. × euramericana (Dode) Guinier and P. × interamericana Broek. attracted the greatest interest for high-profit poplar cultivation. They are often used as the bases for polyhybrids with species that are less suitable for planting, but possessing attractive genetic peculiarities.
These developments in the selection of clones and the intercontinental exchanging of plant material, itself an occasion for the unintended introduction of several parasites, also led to an unwanted evolution of pathosystems, sometimes with the appearance of epidemics attributable to pathogens new to particular poplar-growing areas. In the 1920s and 1930s, for example, a crisis was caused in the Entre Rios province of Argentina by the rust agent Melampsora medusae Thüm., as well as on both sides of the Alps by the leaf scab and blight provoked by Pollaccia elegans Serv. In more recent years, the wider diffusion of Euramerican hybrids proceeded together with the spread of the syndrome due to Marssonina brunnea (Ell. et Ev.) P. Magn. from the U.S.A. to Europe and then on to Asia and Australasia. The Poplar Mosaic Virus, too, moved from its original central European and Italian areale to other continents, due to the extensive use of its susceptible host P. deltoides.
The already fragile equilibrium in the various ecosystems was greatly disturbed both by the introduction of genetic improvements designed almost solely to boost production, with little regard for the question of tolerance or resistance to pathogens, and by the inevitable selection of different races or strains within certain pathogen species particularly aggressive towards some clones.
As a result of this co-evolution, the relative importance of individual diseases in poplar-growing areas also changed over time. Until the 1950s, for example, among leaf parasites were present Pollaccia elegans, especially in Italy, and P. radiosa (Lib.) Bald. et Cif. in northern Europe and North America; Marssonina populi (Lib.) Magn. and M. castagnei (Desm. et Mont.) Magn. in northern Europe, Italy, the United Kingdom and Iran. The bark necrosis and canker agents included Septoria musiva and Hypoxylon mammatum (Wahl.: Fr.) P. Karst. in North America, Discosporium populeum and Cytospora chrysosperma (Pers.: Fr.) Fr. in the cool and warm parts of the northern temperate zone respectively.
In the 1970s, attention was primarily centred on Marssonina brunnea in Europe, Melampsora larici-populina Kleb. and M. medusae in Oceania, Xanthomonas populi in north-central Europe, D. populeum in the cooler continental parts of the northern temperate zone (the existence in the former Jugoslavia of isolates with different aggressiveness was suggested), S. musiva in North America and – especially on account of its severe canker manifestations – in South America, and on H. mammatum in Europe, though here this is of less importance (being confined to some stands of P. tremula L.).
Since the 1980s to our days, despite the extra attention devoted to genetic improvements to achieve greater resistance to pathogens, in many regions there has been a recrudescence of attacks by some pathogens that have altered their aggressiveness genetically, such as M. larici-populina, through formation of several physiologic races. At the same time, new epidemics provoked by P. elegans and a recrudescence of D. populeum in Mediterranean Europe were observed, although the presence of new races has not yet been proved.
The renewed aggressiveness of some parasites, especially the cortical ones (D. populeum, C. chrysosperma), can be connected with a certain physiological vulnerability of new clones that, during a decade covering part of 1980s and 1990s, proved less suitable for particularly unfavourable soil and climate situations than the old selections. As observed on forest species such as oaks and beeches, a real decline spread which, on some Euramerican clones, was associated with the appearance of so-called “brown spots” and the consequent lowering of the value of ply-wood products.