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15° chestnut Blight ‘Simone Prospero and Daniel Rigting* ‘Swiss Federal Institute tor Forest, Snow and Landscape Research (WSL), Birmensdort, Switzeriand 15.1 Pathogen, Significance and Distribution The causal agent of chestnut blight, Cryphonectria parsition (Murrll) ME. Bary, is aan ascomycete fungus (Digporthales) that #8 native to eastein Asis (China and Japan) During the 20th century, this pathogen was, secidentally inireduced into North America and Lurope through infected Asian chest- rut plants (Griffin, 1986: Roane et a, 1966 Heisiger and Rigling, 1994), Within 50 years ofits first recovery in 1904 in the New York Bolanieal Garden, the fungus spread epi- demically ata rate of more than 30 km year (Evans and Finkral, 2010) throughout the native distribution range of the American chestnut (Castenco deninte (MMatsh.) Borkh,) in nortiveastem USA. In Europe, C.parmitice was offically frst discovered in 1938 in sly near Genoa, one of the main Italian commercial ports. Multiple nhioductions probably occurred both via North America and ditecily from Asia, and they lid not only target Italy but also evsthe western France and Spain.(Dutecheta!, 2010), [As in North America, chestnut blight spread -apidly in Europe, and by theend of the 1960s the disease had alzeady been recorded in mal: daril ising @ sich many countries such as Albania, Bosnia- Herzegovina, Crostia, France, Greece, Hungary, aly, Siovenia, Spain, Switzerland and Turkey (Heiniger and Righing, 19%; Nabi anc inigee, 2001). The pothoger successively colonized the more distant of isolated chostut stands in north-western Spain and Portugal, in norti- em Switzerland. in Germany, in northern France, in Austria, in eastern Burope (the Czech Republic, Macedonia, Romania and the Slovak Republic) and in the Aegean and Black Sea regions of Turkey (Heiniger and Rigling, 1 Haltofova etl, 2005; Akl ea, 2009; Brine etal , 2011). C. parasitica is also present in the most enstem distnbsshon range ofthe Kiwopoan ‘chestnut (Cestanexsutea Mil.) ancl has recently been offically reported in Iran (Kazempour tl, 2006) and Azerbaijan (Aghayeva and Harrington, 2008), In Asia, the impact of C. porasitica on the noative chestnut species is minor. Thanks te tie co-evolution wilh the pathogen, the two ‘main Incal host species, ie. the Chinese chest- nut (C, mollgsinia Blume) and the Japanese chestnut (C. crenata Siebolsi &e Zuce are highly resistant to C. parastis(Anagnostakis, 142). Ik North America, chestnut blight has had devastating consequences on the native American chestnut forests. The American 318 BAB International 2013, Infectious Fovest Dsewses (es P Gonthier and @, Nicolo) ). | Bosnia- ‘Mungary. nd Tukey 2Heiniget, colonized rstands in ‘in north- northern (the Czech, the Slovak flack Sea ing. 1994: 9; Prince seni the ¢ European pas recently azwmpour ayova and site on the “Thanks to en the two neces pe Japanese 2 ahighly sis 92 blight as nthe nate > Americ, ndG, Not) ‘chestnut Blight sna _ hostrut, a tree that could easily grow to be $38 m high and more san 1 m in ameter, has ‘been almost completely removed from the vertucey by the blight because ofits high Susceptibility tu the disease (Anagnostak's 1992), The eeamatic dicback of American chestnut has reslted in irreversible changes in the forest ecosystem struckute and AUNc- tioming (Griffin, 1992), In dition to such Genstic ecological impacts, chestnut blight has algo had major eronomic consequences, including the loss of 3 high-quality food resource for people who colleied chestnuts {Diamond ot, 2000) and dhe loss of valuable fsmbec (Holmes et, 2008). Chestnut light an North Ameria is considered textbook texampie of the impact of invasive palboens fon native ecosystems "Wher the C. pasta epidemics satied fn Europe, 2 high chestnut mortality was observed and there was serious concern Shout the survival of Eoropean chestt Fortunately later on, many chestwul stands in Burope recovered owing to the spontine- fous appearance of hypovizulence (Heiniger and Riging, 1994). The meidence ot the disease till ematned igh, hut healing cankers became dominant and the survival fale ofthe infected trees increased consid ably. Although at present some tree mor'al- jey is sll visible in chestmat stands, the survival of Europesn chestnut as @ major tree species does nat seum to be endangered fay more by chestnut Blight in areas with ‘widespread “hypovirulenee. Tx contrast, in rest of the regions at the epidemic front, fp. northeast Spain, Portugal and noth: fom Switzesland, swhere the incidence of hypovirulence 1 still very low, chestnut Diight still causes severe chestnut devine (Colinas and Useuphe, 1999; Bragana ear 2007, Hesriger and Righing, 2009) “the mais hosss of C. parasitica are spo~ ‘ces in the gens Casianen, particulasly the ‘American and the European chestrut, in Saaition,C. prastica hes been found un see feral ak species (Quercus spp) ant In a fess ‘ses also on other host plants (Gryvenkout ef ai, 2009). Generally, hosts other. than Covtenee spp. may be intected in areas where the disease preseure from: chestmut trees is high (Tasch and Mazes, 2108), 15.2 Diagnosis C. parasitica infects the stem and branches of its host plants (Heiniger and Riging, 1294; HPPO, 2005). On yours grafted trees, infec- tions are most frequent Ipcated in he regfon of the graft. In coppices, oll orchard tees and high forests, infections can be observed althe bose ofthe tuunk, along the rink 9: on branchesin he erawn, The symptomsanduces bby C. patitiea on European chestnut vary depending on te age of the infected stem/ branch and on the viwlence of the fungal strain involved, In its typical orm, chestnut Tight is always associated with extensive snecrusi (cankers) of Une bark, Qa young Trees rancis, the smooth burk at the site of the infoctcn tums fcom olive-green to bright ‘brown, orange brown, yellow brown, or red brown, When older treeo/beanches become infucted the discoloration caused by the can ers is usually less pronounced. Vizwlent fun gal strains prow in the ceanbium and in she bork tisste, and develop characteristic pale ‘brown, flat yeetial fans that are wsible afler removing he outer bark. The cambivmn under the infocted bark is killed and the bark sinks inwards, The cankers may enlorge rapidly and girdle the stem or branch, which induces the death ofthe plant pasts distal to Phe infee- tion. The leaves weit ond typically somain hanying on the inlocted branch, sometimes even unt winter, Below the cankers, 3265 typically produce numeres epicorvie (adventitious) shoots (ate 194). When infections are caused by hypoviw tent fungal strains, cankers may initially show similar chanscleristics to those induced by Yirulent fungal strains, but their expansion ray successively slow down anid new layers fof bark may form under dhe affected. ances, causing a swelling and cracking of the outer ack Tlealed, inactive conkers are typically superficial, callused or swollen (Plate I9B) and Iryeclil ‘are are less frequent than in active cankers. Because the cambiuah snot colonized ‘and killed by the fungus, the plant pars distal fo the infection survive and no epicormic shoots are formed belons the canker. Masses of yellow orange to reddish brown pustules (stromata) hacbouring the sexual (pecthecia) and ssexual (pycnidi 'S Prospara and 0. Piging fruiting bodies of the fungus may develop on the infected bark, especialy if the infection i caused by a virulent C. parwition stain. On bolder sees/branches with a rough bark, stro- saat often form in the longitticinal cracks of the bark, even in the absence of a clearly vis bie lesion, The bark of recently dead or cut chestnut wood is also a favourable substrate for the development of stromata (Pros2ero ‘et al, 2006), Perithecia can be reengnized by their ostisles, which appeas, when using a hand-magnifying lens, ay blaes dois on papillate protuberances on the surface of ‘he stroma, As the ostioles of perithecia and prenidia can look sivilar, the presence of peritrecia should be confirmed ‘samples of suromata under a dissecting, micro scope. Asexual spores (conidia) are extrucied asupto Lom long yellow tendrils during moist weather, but sexual ascospores are actively slischarged into the air from the flask shaped penithevia, On oak species, symptoms are localized and consist of slow-developing, cankers that only rarely ‘ill infected trees orbranches. The fruiting structures of C. paresitca can be microscopically characterized in the laboratory. The yellow to dark orange stto- mats (0.5-4 mm in diameter, up to 25 mm high) are embedded in the bark with only the upper part protruding from the surface. Pycnidia (100-300 jm in cbameter) are for- ‘med asirreguloc cavities within the stromatic tissue and, in moist conditions, exiruce the yellow tendrils of hyaline conidia through the pyenidial ostioles. Perithecia (800-400 jm indiameter)re globose and deeply mumersed inthe stromatic tissue. Fach has along, cylin- ddrical neck. For details on these macromor- phological and micromorphological features refer to EPPO (2008). In the absence of ériting bodies, ar for confirmation, C. parusitian may be identified after isolation in pure culture (EPPO, 2003). ‘On potato dextrose agar (PDA), virulent iso Tates produce an initially white mycelium, which becomes subsequently yellow orange and, after 1-2 weeks, red orange. In hypovire Ulentisolates, the mycelium typically remains “white, After about 5 days of incuhotion in the light at room temperature (20°C), pyenidia, begin to form in cetureand appear asa dense, cerange pigmented globose mat. Viralent s0- lates show an aburelont prediction of pyctidin. seich aze typically formed on concentric rings ifeultutes are incubated in a light-ask cece. is hypovitulent isolates, pyenicial pro- duction is Inegely reduced! under low light conditions, but can be considerably stimulates swith more intense light conditions (Filiman st al, 1980). Perithecia are sot produced in culture either in the virulent or the hypovine Tent strains. DNA-based identiication of pre cultures mainly rely on the sequence analysis of conserved DNA regions, for example, of the internal tarscribed spacer (ITShregion or the Berubulin gene, Beside €. parusiten, the genus Crupho- vctria includes onher species (see Gryaenhout, Cupier 16, this volume). OF these, three saprotzophic species are frequently fourd when attempting to isolate C, parasfiat from stromata on the bark of dead chestnut er oak wood, namely C. rails Schwein.) ME. Bact in Burope and North Amezica, C- aterciae MAH, Braganga. E. Diogo & AJL. Phillips (probably 3 eynoayra of C. decipiens Gry 8 MJ. Wingt) in Europe, and C. japonica (Tak Kobay. & Kaz. ltd) Gryzenh, & MJ. Wingf. in Japan. For details on how to distinguish these ther Crypkoneatria spp. (rom C. parastica tefee to Hoegger of al. @U2), Gryzenbaut ef al (200 and Brayanga es! 201, 15.3. Infection Blology . parasitica isa averotcophic pathogen thet equites dead host tissue to penetrate into the stems and branches of healthy chestast trees (Fig. 15.1), Although the early stage of inéostion has been poorly dacumented, it is generally assumed that conidia or asco- spores germinate in fresh woundsor growth cracks where an initial lesion 1s formed ‘Roane etal, 1986). Besides wouncs in the bark, moribund chesimat hesue might also serve as an entry point for C. parasitica (Prospero ef gt, 2006). Such tissue can be generated by tre natural eath of a tree's lower twigs vr beaches due to shading from the upper canopy or by sprout mortality resulting from competition,