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Remarks (public):For a complete description including images see 
Remarks (internal):Infection can take place on the upper or lower surface of the leaf, but is more frequent on the upper. Germ tubes penetrate the cuticle directly, spreading subsequently in the subcuticular tissues. Very young leaves are not infected. Conidia germinate over the range of 0-33°C, optimum 18°C (24, 508) and require contact with free water. Infection (42, 27) can take place at RH 85-100% and 6-33°C, optimum 24°C (42, 27; 17, 821) but below 18°C the pathogenicity of the fungus decreases sharply. Lesions are apparent about a week after infection and sporulation occurs a few days after this. Some control is possible by removal and destruction of infected foliage when it is dry, but this is laborious and persistent stem lesions can compromise these measures (45, 3562). There is considerable variation in susceptibility between rose varieties but numerous races of the pathogen exist (34, 301) and symptom expression varies with environment and host condition (42, 731; 49, 2511). Thus, the use of resistant varieties for control of black spot is limited to a regional basis. A wide range of funcicides has been successfully used for control among which benomyl (51, 2588, 2589; 49, 2890), cycloheximide (45, 1650g, 1989h, 3459c), chlorthalonil (50, 715; 45, 3459c) and maneb preparations (51, 2589; 50, 715; 48, 3526) have recently shown promise. Timing of spray treatments depends on the epidemiological pattern of the disease. In the UK build up of inoculum in August may lead to rapid spread in September (42, 3562) and application of protectants should be timed to anticipate this. The use of eradicants for control of latent inoculum over winter months is said to have little value (40, 333). Germination of the conidia of is inhibited by low concentrations of sulphur dioxide; black spot of roses is, therefore, rare in areas with significant levels of industrial pollution (45, 3562).  
Description type:Non-original description 
Description:Diplocarpon rosae Wolf, Botanical Gazette 54: 231, 1912.
= Fabraea rosae (Wolf) Seaver, 1951.
Conidial state: Marssonina rosae (Lib.) Died., Kryptogamenflora Pilze 9: 830, 1915.
= Asteroma rosae Lib., Memoires de la Societe Linneane Paris 5: 405-406, 1827.
Apothecia epiphyllous, globose to disc-shaped, sunken, subcuticular, up to 300 µm diam.; wall composed of dark brown pseudoparenchymatous cells. Asci inoperculate, oblong cylindrical, short-stalked, 8-spored, 70-80 x 12-18 µm, with a pore staining blue in iodine. Ascospores oblong elliptical, hyaline, unequally 1-septate, constricted at the septum, 20-25 x 5-6 µm. Paraphyses numerous, filiform, septate, enlarged at the tips. Conidial state in amphigenous spots, dark brown to black, confluent. Mycelial strands of numerous hyphae forming a subcuticular network; internal mycelium intercellular with simple, bulbous haustoria. Acervuli subcuticular, erumpent, black. Conidiogenous cells phialidic, enteroblastic, cylindrical to ovoid. Conidia hyaline, oval to elliptical, 1-septate, constricted at the septum, 18-25 x 5-6 µm. Spermogonia subcuticular, epiphyllous, in dark spots on old decaying leaves. Spermatia hyaline, rod-shaped, 2-3 µm long, formed terminally on sterigmata in a dense layer of spermatiophores. Sometimes normal 1-septate conidia are formed in spermogonia; Some apothecia may produce conidia in the presence of abundant moisture. Acervuli on leaves and young shoots in summer, apothecia and spermogonia on decaying over-wintered leaves.
Hosts: Confined to members of the genus Rosa.
Disease: Black spot of roses. More or less circular black lesions up to 1,5 cm diam. with radially fringed margins usually on the upper side of the leaf, which may be followed by chlorosis and leaf cast. Severe leaf cast may be followed by a further flush. Stem lesions occur as small indistinct black areas without a fringed margin and symptoms may occur on floral parts.
Geographical distribution: Worldwide in temperate and tropical zones (CMI Map 266, ed. 2, 1968).
Physiological specialization: There is evidence that a number of races exist, varying in their host reactions (34, 301).
Transmission: Mainly by splash dispersed conidia formed in acervuli on infected leaves on the host or after they have been cast. A microconidial state (spermagonia) with a similar dispersal mechanism may occur on fallen leaves in the spring and autumn. Conidia lose viability rapidly, few surviving more than one month (24, 508). Overwintering is by saprophytic mycelium in cast foliage or infected stem tissues.The perfect state has been reported from Britain, North America and the USSR (51, 2590 and IMI 185129), where it is formed on infected cast foliage in the spring. Ascospores are forcibly ejected; they do not appear to be essential for the survival of the pathogen.
Literature: Palmer & Semeniuk, American Rose Annual 46: 125-133, 1961 (susceptibility); Palmer, Semeniuk & Stewart, Phytopathology 56: 1277-1286, 1966 (pathogenicity, seasonal variation and host susceptibility); Saunders, Annals of Applied Biology 58: 103-122, 1966 (toxicity of sulphur dioxide and epidemiology); Saunders, Annals of Applied Biology 60: 129-136, 1967 (host-parasite interactions); Saunders, National Rose Society's Rose Annual 1970: 118-128, 1970 (resistance); Shirakawa, American Journal of Botany 42: 379-384, 1955.

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