Gremmeniella abietina (Brunchorstia disease)
- Taxonomic Tree
- Notes on Taxonomy and Nomenclature
- Distribution Table
- Risk of Introduction
- Hosts/Species Affected
- Growth Stages
- List of Symptoms/Signs
- Biology and Ecology
- Natural enemies
- Means of Movement and Dispersal
- Plant Trade
- Wood Packaging
- Environmental Impact
- Detection and Inspection
- Similarities to Other Species/Conditions
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- Gremmeniella abietina (Lagerb.) M. Morelet 1969
Preferred Common Name
- Brunchorstia disease
Other Scientific Names
- Ascocalyx abietina Schläpf.-Bernh. 1969
- Brunchorstia destruens Erikss. 1891
- Brunchorstia pinea (P. Karst.) Höhn. 1903
- Brunchorstia pinea var. cembrae M. Morelet 1980
- Brunchorstia pini Allesch.
- Crumenula abietina Lagerb.
- Crumenula pinea (P. Karst.) Ferd. & P.M. Jørg. 1939
- Exipulina pinea (P. Karst.) Höhn. 1903
- Godronia abietina (Ellis & Everh.) Seaver 1951
- Lagerbergia abietina (Lagerb.) J. Reid ex Dennis 1971
- Scleroderris abietina (Lagerb.) Gremmen 1953
- Scleroderris lagerbergii Gremmen 1955
- Septoria pinea P. Karst.
International Common Names
- English: canker of conifers; dieback of pine; scleroderris canker; shoot blight of pine
- Spanish: chancro de las resinosas; tristeza de las resinosas
- French: chancre des resineux; chancre gremmenielléen; deperissement des resineux; déssèchement des rameaux de pin
Local Common Names
- Germany: Kieferntriebsterben; Triebspitzenkrankheit: Kiefer; Triebsterben: Kiefer
- Sweden: Gremmeniella
- GREMAB (Gremmeniella abietina)
Taxonomic TreeTop of page
- Domain: Eukaryota
- Kingdom: Fungi
- Phylum: Ascomycota
- Subphylum: Pezizomycotina
- Class: Leotiomycetes
- Subclass: Leotiomycetidae
- Order: Helotiales
- Family: Helotiaceae
- Genus: Gremmeniella
- Species: Gremmeniella abietina
Notes on Taxonomy and NomenclatureTop of page Kirk et al. (2001) placed G. abietina in the order Helotiales and the family Helotiaceae.
Laflamme (2002) summarizes the recent taxonomic history approximately as follows: Dorworth and Krywienczyk (1975) recognised three pathological races on the basis of serology; the North American, European and Asian, but these serovars do not have any taxonomic standing. Petrini et al. (1989), using morphological, cultural and chemical characteristics, identified two varieties: G. abietina var. abietina with the known European (EU) and North American (NA) races from Pinus and the Asian race from Abies sachalinensis; and G. abietina var. balsamea on Abies balsamea and Picea spp. in Canada. The EU race has then been divided into three different amplitypes using PCR techniques (Hamelin et al., 1996). In Fennoscandia the pathogen has been divided into two different ecological types (large tree type/type A and small tree type/type B) (Uotila, 1983; Hellgren and Högberg, 1995). After several years of genetic analysis it has been suggested that the well-known races (NA and EU) of G. abietina might be regarded as separate species (Uotila et al., 2000; Laflamme, 2002), as well as the variety on Abies balsamea and on Picea.
DescriptionTop of page Conidioma (pycnidia) occur on stems and needles, are gregarious or solitary, dark-brown to black, stromatic, multilocular, without ostioles, up to 1 mm wide; the wall is several cells thick, composed of an outer wall of sclerotized and heavily pigmented cells and an inner wall of pseudoparenchyma. Conidiophores completely line the inside of the conidioma cavity, are hyaline and cylindrical. Conidia are hyaline, cylindrical, somewhat curved, tapering towards the apices, mostly three-septate (1-8 septa), not constricted at the septum, 25-40 x 3-3.5 µm.
Ascoma (apothecia) appear on stems (on Pinus contorta highly concentrated to stem cankers) and axes of the needles, are gregarious, erumpent, superficial, about 1 mm diameter, with short stipes. Hymenium is cream-coloured, receptacle dark-brown to black, margin opaque. Excipulum is composed of several layers of polygonal cells, heavily pigmented and sclerotized towards the margin, and provided with irregular cell protuberances on the outside. Asci are subclavate, short-stipitate, inoperculate, eight-spored, 100-120 x 8-10 µm; ascus wall is bitunicate. Ascospores are biseriate, hyaline, ellipsoidal, sometimes slightly curved, with rounded ends; mature spores are three-septate, not constricted at the septum, 15-22 x 3-5 µm. Paraphyses are hyaline, filiform, septate (Punithalingam and Gibson, 1973).
DistributionTop of page A distribution map has been published by CMI (1989, No. 423).
The monitoring of 110 plantations of P. contorta in northern Sweden during 1987-1991, shows that this introduction was not problem-free (Karlman et al., 1994). In harsh areas (low temperature sum), an extensive epidemic of G. abietina caused severe damage and mortality in young plantations of P. contorta during the late 1980s. The damage was worst in topographic depressions within the regeneration areas and on sites where Picea abies was estimated to have a higher wood yield than Pinus sylvestris.
See also CABI/EPPO (1998, No. 203).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Georgia (Republic of)||Present||UK CAB International, 1989; EPPO, 2014|
|Japan||Present||UK CAB International, 1989; EPPO, 2014|
|Korea, Republic of||Present||La et al., 2007|
|Canada||Widespread||UK CAB International, 1989; EPPO, 2014|
|-Alberta||Present||UK CAB International, 1989; EPPO, 2014|
|-British Columbia||Present||UK CAB International, 1989; EPPO, 2014|
|-New Brunswick||Present||UK CAB International, 1989; EPPO, 2014|
|-Newfoundland and Labrador||Present||UK CAB International, 1989; EPPO, 2014|
|-Nova Scotia||Present||UK CAB International, 1989; EPPO, 2014|
|-Ontario||Present||UK CAB International, 1989; EPPO, 2014|
|-Quebec||Present||UK CAB International, 1989; EPPO, 2014|
|USA||Restricted distribution||UK CAB International, 1989; EPPO, 2014|
|-Maine||Present||UK CAB International, 1989; EPPO, 2014|
|-Michigan||Present||UK CAB International, 1989; EPPO, 2014|
|-Minnesota||Present||UK CAB International, 1989; EPPO, 2014|
|-New Hampshire||Present||UK CAB International, 1989; EPPO, 2014|
|-New York||Present||UK CAB International, 1989; EPPO, 2014|
|-Vermont||Present||UK CAB International, 1989; EPPO, 2014|
|-Wisconsin||Present||UK CAB International, 1989; EPPO, 2014|
|Austria||Present||UK CAB International, 1989; EPPO, 2014|
|Belgium||Present||UK CAB International, 1989; EPPO, 2014|
|Bulgaria||Widespread||****||UK CAB International, 1989; EPPO, 2014|
|Czech Republic||Restricted distribution||EPPO, 2014|
|Denmark||Widespread||UK CAB International, 1989; EPPO, 2014|
|Estonia||Present||UK CAB International, 1989; EPPO, 2014|
|Finland||Widespread||UK CAB International, 1989; EPPO, 2014|
|France||Restricted distribution||UK CAB International, 1989; EPPO, 2014|
|Germany||Restricted distribution||EPPO, 2014|
|Greece||Present||UK CAB International, 1989; EPPO, 2014|
|Iceland||Present||UK CAB International, 1989; EPPO, 2014|
|Ireland||Absent, confirmed by survey||EPPO, 2014|
|Italy||Restricted distribution||UK CAB International, 1989; EPPO, 2014|
|Lithuania||Present||UK CAB International, 1989; EPPO, 2014|
|Netherlands||Present||UK CAB International, 1989; EPPO, 2014|
|Norway||Widespread||****||UK CAB International, 1989; EPPO, 2014|
|Poland||Restricted distribution||UK CAB International, 1989; EPPO, 2014|
|Romania||Present||UK CAB International, 1989; EPPO, 2014|
|Russian Federation||Restricted distribution||EPPO, 2014|
|-Central Russia||Present||EPPO, 2014|
|-Northern Russia||Present||EPPO, 2014|
|Spain||Restricted distribution||EPPO, 2014|
|Sweden||Widespread||****||UK CAB International, 1989; EPPO, 2014|
|Switzerland||Widespread||****||UK CAB International, 1989; EPPO, 2014|
|UK||Restricted distribution||****||UK CAB International, 1989; EPPO, 2014|
|-England and Wales||Restricted distribution||EPPO, 2014|
|-Northern Ireland||Absent, confirmed by survey||EPPO, 2014|
|-Scotland||Restricted distribution||EPPO, 2014|
|Yugoslavia (Serbia and Montenegro)||Present||UK CAB International, 1989|
Risk of IntroductionTop of page G. abietina has not been classified as a quarantine pest by EPPO, but is of quarantine significance for NAPPO, and potentially in other regions. In Europe, it has generally been regarded as widespread and to have reached the limits of its natural distribution. Its absence from certain areas has been attributed to the fact that they lie outside the natural range of the fungus. There is certainly no strong suggestion that G. abietina has the potential to cause direct damage in such areas. However, its presence, even at relatively insignificant levels, could have indirect consequences for the export trade.
Planting material of tree species included in the host range of G. abietina should be chemically treated with the fungicide chlorothalonil prior to movement. Before export to countries free from the disease, Christmas trees should be inspected for canker and for shoot blight symptoms during the summer before trading. Immersion of diseased seedlings in warm water (55°C) and immersion or spraying with dilute sodium hypochlorite eradicated the pathogen with no apparent loss in needle colour or retention (Hudler and Neal, 1990). Regulatory action by the USA and Canada now prohibits the movement of Christmas trees and nursery stock from areas where the European strain of the pathogen is present.
In affected plantations, the optimum time to carry out sanitation fellings is the first winter after symptoms of the disease have appeared.
In Scandinavia there is a risk of secondary damage by the pine shoot beetle (Tomicus piniperda) which transfers blue stain fungi (Leptographium wingfieldii and Ophiostoma minus [Ceratocystis minor]) to already weakened Pinus sylvestris trees (Solheim et al., 2001). It has recently been shown that Pinus sylvestris defoliated by other insects by up to 90% may still manage to produce enough resin to avoid attack by Tomicus piniperda (Langström et al., 2001). This limit is, however, not applicable when the tree is defoliated by Gremmeniella. After the heavy Gremmeniella outbreak in Sweden, preliminary results indicate that Scots pines with less than 30% living crown in 2001 were dead in 2002 (M Vikholm and J Witzell, Swedish University of Agricultural Sciences, Umea, Sweden, personal communication, 2003).
Hosts/Species AffectedTop of page The five-needled pines seem to be more resistant than the two- and three-needled group (Skilling and O'Brien, 1979). For more information see Phillips and Burdekin (1985).
During the late 1970s and 1980s the North American species Pinus contorta was extensively introduced into northern Sweden, in order to increase forest yield. To date, P. contorta has been planted on more than 550,000 ha in Sweden. This pine species has a westerly distribution in North America, and therefore has not been exposed to G. abietina naturally. In harsh areas (low temperature sum), an extensive epidemic of G. abietina caused severe damage and mortality in young plantations of P. contorta during the late 1980s (Karlman et al., 1994). Populations attacking P. sylvestris and P. contorta in northern Sweden are probably identical genetically, suggesting that the fungus is not host-specific with regard to these two conifers. In view of the fact that the exotic P. contorta was severely infected during the late 1980s, the risk of spread from severely infected P. contorta plantations to adjacent plantations of indigenous P. sylvestris should be considered high (Hansson et al., 1996).
Recently, an even more severe outbreak of G. abietina has occurred in Sweden. The Forestry Board reported approximately 300,000 ha of at least moderately damaged Scots pine forests in 2001. The typical forest was a monoculture on sites formerly supporting Picea abies and the age was ca 50 years. The most effective sanitation action has been clear-cutting; sanitation thinning did not usually control the disease. About a third of the diseased forest area has been clear-cut.
Growth StagesTop of page Seedling stage, Vegetative growing stage
SymptomsTop of page Depending on the type of spores involved, infection (spore germination and establishment on the shoot) occurs at different times of the year. If conidia are involved, infection usually occurs in early summer, whereas ascospores infect later during the growing period and late in autumn (Skilling, 1972; Gibbs, 1984; Laflamme and Archambault, 1990). The killing of vascular tissue inside the shoots occurs during winter and when the temperature is between +5 and -6°C (Marosy et al., 1989).
An infection of G. abietina might be detected in several ways. By early spring, before the start of bud flushing, the needles on infected shoots are easy to detach due to their dead vascular tissue. The shoot blight symptom occurs after the time of normal shoot elongation; typical reddish-brown needle bases (more brown on Pinus sylvestris and more red on P. contorta), gradually extending to the tip, followed by needle-cast as the result of dieback of these shoots. The shoot blight symptom is usually concentrated in the lower parts of the crown, but in Sweden the disease appears in the top of the tree. A characteristic yellow coloration of the xylem tissues can be seen (Read, 1967). In early summer, new stem cankers might occur; typically recognized as oval 'thumb marks' on the young pine bark (Witzell, 2001). Stem cankers might occur despite no other symptoms being present (Kaitera and Jalkanen, 1994). Old cankers grow quite fast, especially vertically, and some might be >20 cm long. At least on Pinus contorta, they are often covered with apothecia (Witzell, 2001). In early spring, cryptopycnidia (which are smaller than conventional pycnidia) can sometimes be found under the thin bark (Cauchon and Lachance, 1980). During spring or early summer the vegetative fruiting bodies (pycnidia), which are about 1 mm in diameter and shiny black or dark-brown, can be seen on the recently killed shoots. Two years after infection the sexual fruiting bodies, apothecia, are formed. These are sometimes seen on the same twigs where pycnidia occur, as the pycnidia are produced both one and two years after infection. The size of apothecia is about the same as for pycnidia, but the colour is more brownish and the structure somewhat hairy (at least not shiny). When air humidity is high (during or after rain) the apothecia open up and the light grey hymenium is exposed.
On Picea abies, pycnidia only develop on needle cushions. No apothecia have been found on this host. In northern Sweden, extreme abundance of apothecia on the introduced Pinus contorta is reported (Karlman et al., 1994; Hansson et al., 1996).
Adventitious buds sometimes occur at the base of dead shoots. If the attack is not too heavy, this might mean that the trees survive and adventitious buds develop below the point of dieback to provide new growth (Gremmen, 1972). However, in the heavy epidemics of 2001 in Sweden, entire Scots pine stands were rapidly killed without having any chance to recruit adventitious shoots.
Pine seedlings in the nursery should be inspected for orange to brown discoloration at the base of needles in early May. By July, needles and branch tips become brown. Needles fall from branch tips when the slightest pressure is applied. In young pine trees, green discoloration appears beneath the bark of dead branches. Stem cankers are rare but small branch cankers are commonly found. Throughout the year, but mostly in spring and early autumn, black pycnidia or light-brown apothecia should be visible at the base of dead needles or on dead branch tips.
List of Symptoms/SignsTop of page
|Growing point / dead heart|
|Growing point / dieback|
|Leaves / necrotic areas|
|Stems / canker on woody stem|
|Stems / internal discoloration|
|Whole plant / discoloration|
|Whole plant / plant dead; dieback|
Biology and EcologyTop of page Life Cycle
The fungus enters the apical buds and developing shoots by germinating conidia or ascospores, especially during cool and wet conditions (see section on Symptoms). The presence of free water has been found to be necessary to induce the discharge of both conidia and ascospores (Skilling, 1969). In addition, the ambient temperature at this time influences both the number of ascospores that are discharged per apothecium and how soon dispersal commences. Maximum spore discharge takes place at about 17°C. If free water is available in the form of rain for 4-8 h at about 17°C, major spore release will take place (Skilling, 1972). Experiments in Finland show that relative humidity is more important for conidial dispersal earlier in the season, and rainfall later in the season (Petäistö et al., 2000).
G. abietina infects through stomata on bracts subtending the short shoots. Germ tubes penetrate between the guard cells and the bract tissue is sparsely colonized by late summer or autumn. Only after mid January-early February of the following year does the fungus extend from the bract and begin to colonize the short shoot and surrounding cortical tissue, producing a resinous, brown, necrotic area of cortical parenchyma and phloem beneath the bract as the first visible symptom of infection (Skilling, 1972; Patton et al., 1990). The death of vascular tissue inside the shoots occurs during winter and when the temperature is between +5 and -6°C (Marosy et al., 1989; Petäistö, 1993). After entry, the fungus kills the bud and proceeds downwards into the stem and needle fascicles. Shoots start dying in the following spring from the tips. Needle bases turn orange to brown while the tip may still be green, and finally fall off. Small, black pycnidia (vegetative fruiting bodies) appear at the base of dead needles or on dead shoot tips throughout the year but more commonly in spring and early autumn. The sexual fruiting bodies, apothecia, occur in the same place as pycnidia but 1 year after the shoots die (and 2 years after initial infection). The entire crown may be infected, which causes significant loss of foliage, further weakening of the trees due to secondary attack by other fungi and insects, and finally death. In Sweden, during the heavy epidemics of 2001, tens of thousands of hectares of middle-aged Scots pine stands were rapidly killed within some mild winter months and without having any chance to produce adventitious shoots.
The fungus overwinters as mycelium in the conifer host or as immature fruiting bodies. It is capable of infecting the host while it is actively growing, but rapid development of disease symptoms can take place while the host plant is dormant. Mortality incurred during the development of an epidemic depends on the size of the host plant at the time of infection. Very small trees, such as nursery seedlings, are susceptible and die soon after infection, usually in the first year. Most larger trees take several years to succumb, usually dying one branch at a time.
Experiments indicate that Gremmeniella abietina has the ability to degrade celloluse and pectin within cell walls (Ylimartimo et al., 1997).
Causes of Epidemics
Climatic conditions such as wet spring and cool summer months, high precipitation, high humidity and fog are reported to favour serious outbreaks of the disease (Butin and Hackelberg, 1978; Karlman, 1986; Uotila, 1988; Karlman et al., 1994). In Japan, the epidemic of 1970 is thought to have been favoured by unusually low (freezing) air temperatures from late September to early October 1969 and a subsequent long period of deep snow (Yokota, 1975). In Sweden the most severe epidemic ever (300,000 ha of Scots pine) was presumably predisposed by the very wet summer and autumn of 2000 and the following very mild winter.
Plantations in topographic depressions, on north-facing slopes and fertile, moist sites (in Scandinavia known as 'spruce sites') often suffer from an increased risk of disease (Dorworth, 1973; Uotila, 1988; Witzell and Karlman, 2000). Heavy snow loads, especially if combined with bad root development (instability), are extremely dangerous since the pathogen has perfect conditions under the snow (Karlman et al., 1994; Hansson and Karlman, 1997).
At stand level, dense stands seem to be more affected (Read, 1967; Nevalainen, 1999). The origin of plant material is also important; there is less infection on northerly provenances (Karlman, 1986; Dietrichsson and Solheim, 1987; Hansson, 1998). In Sweden, during the epidemics of 2001, provenances of Pinus sylvestris transferred two degrees or more to the north were significantly more affected than local or more northern provenances (M Wikström and P Hansson, Swedish University of Agricultural Sciences, Umea, Sweden, personal communication, 2003).
Natural enemiesTop of page
|Natural enemy||Type||Life stages||Specificity||References||Biological control in||Biological control on|
Means of Movement and DispersalTop of page Conidia liberated from infected tissues are dispersed under wet conditions by a water splash mechanism (Uotila, 1985). Long-distance dispersal of the fungus is thought to occur largely through wind-borne ascospores. The previously thought absence (scarcity) of ascospores in the European race has been re-evaluated. Enormous numbers of apothecia (see Pictures) produced on diseased Pinus contorta plantations in northern Sweden (Karlman et al., 1994) have been reported. This population is genetically identical to the population on adjacent P. sylvestris (Hansson et al., 1996). It is suggested that the high apothecial production in this northern amplitype of the European race of the pathogen may be favoured by a long-lasting and deep snow cover (Hamelin et al., 1996).
Transport of infected nursery stock or movement of infected Christmas trees of P. sylvestris may provide alternative means of long-distance dispersal. Magasi and Manley (1974) showed that G. abietina can survive for 10 days in branches of 9-year-old P. sylvestris trees cut for the Christmas tree trade, regardless of whether they are left outdoors or brought indoors and subjected to dry, warm conditions.
Plant TradeTop of page
|Plant parts liable to carry the pest in trade/transport||Pest stages||Borne internally||Borne externally||Visibility of pest or symptoms|
|Bark||fruiting bodies; hyphae; spores|
|Flowers/Inflorescences/Cones/Calyx||fruiting bodies; hyphae; spores||Pest or symptoms usually invisible|
|Leaves||fruiting bodies; hyphae; spores||Yes||Yes||Pest or symptoms usually visible to the naked eye|
|Seedlings/Micropropagated plants||fruiting bodies; hyphae; spores||Pest or symptoms usually invisible|
|True seeds (inc. grain)||spores||Pest or symptoms not visible to the naked eye but usually visible under light microscope|
|Plant parts not known to carry the pest in trade/transport|
|Growing medium accompanying plants|
Wood PackagingTop of page
|Wood Packaging not known to carry the pest in trade/transport|
|Loose wood packing material|
|Processed or treated wood|
|Solid wood packing material with bark|
|Solid wood packing material without bark|
ImpactTop of page Brunchorstia dieback, caused by G. abietina, was reported to have devastated Pinus nigra var. maritima [P. nigra subsp. laricio] in Scandinavia in about 1880. In the UK, it occurs mainly on P. nigra var. maritima and only occasionally on P. sylvestris. It has also caused loss to Picea abies in continental Europe over the last century. G. abietina was first identified in North America in 1962 and since then has been an increasing threat to Picea, Pinus resinosa and P. sylvestris forests.
In Sweden the most severe epidemic ever started in 2001 and has seriously affected the forest industry regionally. Approximately 300,000 ha of managed productive Scots pine stands were severely affected. An economic evaluation of the early harvest of these only half-grown productive forests indicates that the net losses were over 100 million euro (M Persson and P Hansson, Swedish University of Agricultural Sciences, Umea, Sweden, personal communication, 2003). This figure does not include the losses due to the expected long-term depression in yield on moderately affected stands that were only thinned.
In a Finnish study, volume growth in slightly damaged Pinus sylvestris plots decreased by 22-42%, depending on disease severity (Riihinen and Uotila, 1992).
P. contorta logs with occluded cankers caused by the pathogen G. abietina gave kraft pulp with poor paper properties: it required more beating energy and resulted in paper with a low tear strength, air permeability, tensile stiffness, burst strength, and poor light-scattering properties (Ahlqvist et al., 1996). Thus, wood damaged by G. abietina should be separated and classed as low-grade raw material.
The disease is typified by death of the growing point and the apical needles of the lower branches of pine and spruce (although the disease started in the top of the crowns in Sweden in 2001). Under severe conditions all the foliage of the host may be affected and die. Thousands of hectares of 30- to 50-year-old, and some 70- to 80-year-old, Pinus sylvestris trees were killed during the 2001 epidemic in Sweden. It is most damaging to species that are grown towards the limit of their range and attacks are favoured by shaded conditions, by dense, badly aerated plantations in which humidity is high, and by weather damage, such as temperature oscillations during shoot elongation. The disease may kill young trees as well as reducing growth and causing distortion of older trees. It can also cause serious nursery loss.
Environmental ImpactTop of page Most severe epidemics of G. abietina occur in monocultures of introduced pine species or in monocultures of too optimistically transferred provenances of native species. Therefore, there is a risk that well-adapted natural conifer stands might be infected due to the increased inoculum produced in infected less-adapted stands.
Detection and InspectionTop of page
Under field conditions G. abietina is easiest to detect when the shoot blight symptom is fresh, during the first summer after initial infection. At this stage the diseased stands are bright reddish-brown. Affected stands might be recorded from aerial inspection (helicopter or small aircraft), and also from satellites (Olsson, 1990). This inspection is harder to perform if the disease is concentrated in the lower part of the crown. With satellite remote sensing there is a risk of confusion with the colour patterns of recently thinned stands which have wilting logging slash on the ground.
Using PCR techniques it is possible to detect latent infection and differentiate the North American and European races (Hamelin et al., 2000; Zeng et al., 2005). This could be useful in nurseries.
Detection based on symptoms on host plants and identification based on the morphology of the isolate are detailed in OEPP/EPPO (2009).
Similarities to Other Species/ConditionsTop of page The ascoma of G. abietina are similar to those of Cenangium ferruginosum, which, at least in Scandinavia, is saprobic. On recently killed plant material there is usually no difficulty in identifying G. abietina, since no saprobic fungi have yet invaded. The ascoma of G. abietina are somewhat smaller, less aggregated (clustered) and, most important, not so obviously concentrated on the needle-scars on the twigs as those of Cenangium.
Prevention and ControlTop of page
Due to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.The disease may be controlled in the nursery using the fungicide chlorothalonil applied about seven times from May to mid-August (Skilling and Waddell, 1970, 1974). In Swedish nurseries the fungicides propiconazole and azoxystrobin are used. On the forest scale, however, once G. abietina is established in a plantation it is almost impossible to control. The use of chemicals is not practical in plantation crops where careful selection of disease-free planting material, as well as selection of planting sites at some distance from infected plantations, are important considerations.
Systematic pruning of the lower four whorls in diseased red pine (Pinus resinosa) plantations in Quebec, Canada, reduced the incidence rate of the disease from 67% to 22% (Laflamme, 1999). To avoid many successive interventions, pruning the lower half of the crown whorls and even two-thirds, if necessary, is recommended in infected plantations less than 20 years old.
ReferencesTop of page
Dietrichson J; Solheim H, 1987. Differences between provenances of Pinus contorta var. latifolia in resistance to attack by Gremmeniella abietina. Scandinavian Journal of Forest Research, 2(3):273-279
Dorworth CE, 1973. Epiphytology of Scleroderris lagerbergii in a kettle frost pocket. European Journal of Forest Pathology, 3(4):232-242.
Dorworth CE; Krywienczyk J, 1975. Comparisons among isolates of Gremmeniella abietina by means of growth rate, conidia measurement, and immunogenic reaction. Canadian Journal of Botany, 53(21):2506-2525
EPPO, 2014. PQR database. Paris, France: European and Mediterranean Plant Protection Organization. http://www.eppo.int/DATABASES/pqr/pqr.htm
Gibbs JN, 1984. Brunchorstia dieback in Europe. In: Manion, PD, ed. Scleroderris Canker of Conifers. The Hague, Netherlands: Martinus Nijhoff/Dr. W. Junk Publishers, 32-41.
Gremmen J, 1972. Scleroderris lagerbergii Gr.: the pathogen and disease symptoms. European Journal of Forest Pathology, 2:1-5.
Hamelin RC; Bourassa M; Rail J; Dusabenyagasani M; Jacobi V; Laflamme G, 2000. PCR detection of Gremmeniella abietina, the causal agent of scleroderris canker of pine. Mycological Research, 104(5):527-532; 28 ref.
Hansson P; Karlman M, 1997. Survival, height and health status of 20-year-old Pinus sylvestris and Pinus contorta after different scarification treatments in a harsh boreal climate. Scandinavian Journal of Forest Research, 12(4):340-350; 51 ref.
Hansson P; Wang XR; Szmidt AE; Karlman M, 1996. RAPD variation in Gremmeniella abietina attacking Pinus sylvestris and Pinus contorta in northern Sweden. European Journal of Forest Pathology, 26(1):45-55; 37 ref.
Jurc D, 2007. Diseases of shoots, branches and trunk. Gremeniella abietina, Cronartium flaccidum, Melampsora pinitorqua. (Bolezni poganjkov, vej in debla. Gremeniella abietina, Cronartium flaccidum, Melampsora pinitorqua.) Gozdarski Vestnik, 65(2):89-104. http://www.dendro.bf.uni-lj.si/gozdv.html
La YJ; Kim YH; Kim SG; So J; Kwon YD, 2007. Outbreak of Scleroderris canker of Korean pine (Pinus koraiensis) in Korea. In: Proceedings of the 2007 Summer Meeting of the Korean Forest Society. Korea Republic: Korean Forest Society, 53-56.
Laflamme G, 2002. Taxonomy of the genus Gremmeniella, casual agent of scleroderris canker. In: Uotila A, Ahola V, eds. Proc. of IUFRO WP 7.02.02 Shoot and Foliage Diseases, Meeting at HyytiSla, Finland, June 17-22, 2001. Finnish Forest Research Institute, Research Papers 829, ISBN 951-40-1809-5.
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