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Remarks (public):For a complete description including images see 
Remarks (internal):Asparagus rust was originally described from Europe in 1805 where it appeared localized and sporadic. It was first seen in North America along the Atlantic coast from N.J. to Mass. in 1896. By 1901 it had crossed the continent to Calif., its spread probably being due largely to the shipment of contaminated plants or soil. The disease reached epiphytotic proportions and caused heavy losses, particularly in localities subject to heavy dew. Dew is important as urediospores require soaking in water before germination, for a minimum of 3 hr., with opt. intensity of infection after 9 hr. (39: 526). It was early realized that the best hope for control lay in the use of resistant varieties, and pioneer work in this field was started by Norton (1913, 1919) in the eastern U.S.A. which led to the development of the Washington varieties. These proved resistant though not immune to the dicaryotic stage of the rust in infections arising from aeciospores or urediospores but were very susceptible to the haploid stage arising from sporidial infection. Despite the extensive cultivation of the Washington varieties severe epiphytotics of asparagus rust have been reported from Germany (13: 677), the U.S.A. (32: 58), and the Netherlands (33: 64) and the search for further sources of resistance continues (32: 58; 36: 81, 508). Chemical control measures have been attempted in seasons when heavy rust infection is experienced and disease resistance breaks down. Sulphur dusting was reported successful in the early years (Smith, 1905, 1906) but the use of Bordeaux was only partially successful (22: 509; 28: 560; 32: 58, 169). Zineb has given better control, in some instances superior to maneb, ferbam or captan (33: 64; 37: 619). Actidione-S or D-113 have proved as effective as zineb (38: 644). Some success has also attended the use of Elgetol and a maneb-NiSO4 mixture (dithane S-31) as eradicant sprays (21: 437; 43, 3080). Cultural methods for control include the destruction of wild and volunteer asparagus plants as well as unused beds near commercial plantings; the isolation of seedling beds from commercially producing beds and the avoidance of successive plantings of continuous blocks. Beds should not be sited in areas with poor drainage, wind-breaks should be avoided, and rows should be planted in the direction of prevailing winds for maximum air circulation.
Description type:Non-original description 
Description:Puccinia asparagi DC., in Lam. & DC., Flore Franc. Ed. 3, p. 595, 1805.
= Puccinia discoidearum Link var. asparagi (DC.) Wallr., 1833.
= Dicaeoma asparagi (DC.) O. Kuntze, 1898.
= Persooniella asparagi (DC.) Syd., 1922.
= Aecidium asparagi Lasch, 1848.Uredo asparagi Lasch, 1848.
Pyenia punctiform, brownish, preceding the aecia then surrounding or amongst them. Aecia caulicolous, gregarious, cupulate or short-cylindric. Aeciospores globose to oval, 15-21 x 18-27 µm; wall nearly hyaline, 1 µm thick, finely and closely verrucose. Uredia caulicolous, powdery, cinnamon brown. Urediospores globose to ellipsoid, 19-30 x 18-25 µm; wall golden, 2 µm thick, minutely echinulate; pores equatorial, generally 4. Telia caulicolous, blackish-brown. Teliospores 3-50 x 19-26 µm, rounded above, slightly constricted at the septum; wall chestnut-brown, to 10 µm thick at the apex; pedicel up to twice the length of the spore. Mesospores occasional, up to 35 µm long.
Hosts: On Asparagus officinalis (cult.), also on a few other species, including A. maritimus, A. plumosus and A. scaber; slight infections can be obtained on Allium cepa (see CMI Descript. 52).
Disease: Asparagus rust. Causing lesions on asparagus stems, either oval yellowish spots (aecia and pycnia) or blister-like pustules (uredia and telia), and producing premature desiccation with subsequent weakening of roots and crowns which reduces the yield of edible shoots in the following season. May also attack onion, shallot and chives.
Geographical distribution: Occurs in Africa, Asia, Australasia, Europe and North America wherever asparagus is grown (CMI Map 216, Ed. 2, 1950).
Physiological specialization: Apparently not known, though there is some evidence that new strains have developed as the formerly resistant asparagus variety Washington is now susceptible in some localities. Differences between resistant and highly susceptible populations appear to be determined by 4-5 genes (36: 508).
Transmission: Spore dissemination mainly by wind with rain contributing to spread on individual plants (33: 333). Also believed to be transmitted in shipments of contaminated plants or packing material and soil accompanying roots (Arthur 1929). Volunteer and wild plants may serve as sources of infection (32: 58).
Literature: The early history of the asparagus rust epiphytotic in North America is summarized by Arthur, The plant rusts, 1929. For rusts studies see Halstead, Bull. New Jers. agric. Exp. Stn 129, 1898; Smith, Bull. Calif. agric. Exp. Stn 165, 1905; Bull. New Jers. agric. Exp. Stn 172, 1906; Bremer, Gartenbauwissenschafr 10: 51-73, 1936; Kahn, Anderson, Hepler, & Linn, Bull. Ill. agric. Exp. Stn 559, 56 pp., 1952; Lubani & Linn, Phytopathology 52: 115-119, 1962. Work on breeding resistant varieties has been reported by Norton, Bull. Bur. Pl. Ind., U.S. Dep. Agric. 263, 1913; Norton, Circ. U.S. Dep. Apric. C.T. & F.C.D., 7, 1919; Thompson & Hepler, Pl. Dis. Reptr 40: 133-137, 1956; Hepler, Thompson, & McCollum, Bull. Ill. apric. Exp. Sta. 607 1-47, 1957 (143 refs).
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