Compendium of Potato Diseases - (PDF, 101 mb) - USAID

More documents

Recommendations

Info

Virus diseases, although seldom lethal. reduce plant vigorand yield potential of seed tubers. Identification is complicated by wide symptom variation attributable to virus strain differences, plant response in relation to maturity and duration of infection, potato cultivar. and environmental influences. l)ifferentiation of viruses may involve purification, electron microscopy, comparison of physical properties, clectrophoresis. serology, and possibly other techniques. Recent developments in serology using the ELISA (eniyme-linked immunosorbent assay) ,echnique provide an extremely sensitive test for virus presence and identity and have for the first time permitted serology with certain viruses difficult to detect in potato. General References BODE. 0. 1958, Die Virosen der Kartoffel und des'Tahaks. Pages 1-30 in: M. Klinkowski, ed. i'lianliche Virologie. Vol. II. Akademie- Verlag. Berlin. 393 pp. CI.ARK. M. F., and A. N. ADAMS. 1977. Characteristics of the microplate method of eniime-linked immunosorbent assay for the detection of plant viruses. .1.Gen. Virol. 34:475-483. de BOKX, J. A.. ed. 1972. Viruses of Potatoes and Seed-Potato Production. Pudoc, Wageningen, The Netherlands. 233 pp. FERNANDEZ VAI.IEI.A, M. V. 1969. Introducci6n a la Fitopatologiii. Vol. I. Virus, 3rd ed. Pages 764-845. Inst. Nac. de lecnol. Agropecuaria. Buenos Aires. 1,011 pp. GIBBS. A.. and B. HARRISON. 1976. Plant Virology: The Principles. .Joh n Wiley and S o ns, New Y o rk. 292 pp . KI.INKOWSKI. M.. and 1H.KEGI.ER. 1962. Viruskrankheiten der Kartoffel. pages 1025-1138 in: R. Schick and M. Klinkowski. eds. Die Kartoffel, Vol. II.2.112 pp. MATItEWVS, R. E. F. 1970. Plant Vir,',,gy. Academic Press, New York. 778 pp. SMITH. K. M. 1972. A texlbook of .< virus diseases, 3rd ed. Longman, Iondon. 684 pp. Potato Leafroll Virus Potato leafroll, an aphid-transmitted disease is one of the most serious in potato and is responsible for high yield losses throughout the world wherever potatoes are grown. In Colombia and the Andes, the potato leafroll virus (PLVR) occurs in Solanum andigena potatoes: the disease has been known as "enanismo amarillo" for many years. Symptoms Primary symptoms (Plate 55) follow transmission by aphids Symptoms appear mainly in the young leaves, which usually stand uprigh:, roll, and turn slightly pale. In some cultivars, young leaves are pink to reddish starting at tile margins. Rolling sometimes affects only the base of the leaflet rather than the whole leaflet. These symptoms may spread later to the lower leaves. Primary symptoms may be lacking with late season infection, making diagnosis in seed stocks a major problem. Secondary symptoms (Plate 56) become evident when an infected tuber produces a plant. Lower leaflets are rolled and higher leaves are slightly pale. l.eaves are stiff,dry, and leathery and make a crisp, somewhat paperlike sound when touched. Older leaves of some cultivars are i..ak and or severely necrotic, especially at the margins. Plants are often noticeably stunted and rigid. Symptoms are less pronounced in the top of a plant with secondary infection than in one with primary irfection, and secondary infection is more damaging to the plant. Severity of symptoms depends on the isolate of the virus, the potato cultivar, and the growing conditions. In S. tuherosumssp. antdigena cultivars. secondary symptoms (enanismo amarillo) tend to be somewhat different from those in S. tuherosum ssp. tuherosutm, consisting of a marked upright habit of growth. stunting, and a marginal and interveinal 68 Viruses chlorosis of leaflets (Plate 57), especially of' dwarfed upper leaves. Rolling of lower leaves is often lacking. Secondary symptoms in hybrids of S. tuherosum ssp. andigena X S. tuherosum ssp. tuherosum consist of the rolling of lower leaves typical of S. tuherosuim ssp. tuherostni cultivars. In some cultivars, however, distinct interveinal and marginal chlorosis occurs as in S. tuherosumn ssp. antdigena cultivars. Internal net necrosis (Figs. 28B and 73A), visible to the unaided eye when the tuber is cut, is particularly marked in certain American cultivars such as Russet Burbank, Green Mountain, and Norgold Russet. This net necrosis is found in tubers from plants with primary, secondary, or tertiary infection. The color may vary from light translucent to dark. A definite trend toward a less severe type of infection from primary to tertiary has been found in tubers of Russet Burbank. Causal Agent PI.VR has icosahedral particles 24 nm in diameter(Figs. 73D and E). 'ransmission is successful only by aphids and grafting; artificial inoculation by mechanical means has never been accomplished. The virus is transmitted by aphids in a persistent (circulative) manner (i.e.. after an aphid has fed on an infected plant it normally transmits the virus for the rest of its life). Isolates have not been differentiated by serological, physical, or chemical properties nor by vector specificity or transmission e mical No per ti ano r no All tra ns i ssi on efficiency. No differential plants are known. All strains give the same type of symptoms. Isolates vary in severity of symptoms on potato cultivars and on Ph'salisfloridana, but existence of strains has not been well defined. Some workers refer to three strains called severe, moderate, and mild; others refer to four strains called No. 1,2, 3, and 4. A fifth isolate, differing in symptom severity from No. I on P.floridana but not on other hosts, has been isolated. Histopathology From the moment of symptom appearance, infections are always accompanied by phloem necrosis, which consists of thickening of the walls of the primary phloem cells in the stem and petioles (Fig. 73B). Accumulation of callose is often pronounced around the sieve plates in the phloem oftubersand stems (Fig. 73C). Stiffness of leaves in primary and secondary infections isaconsequence of starch accumulation in leaf cells. Epidemiology SThe virus istuberborne and isalso efficiently persistent transmitted manner in by a aphids that colonize potatoes, My'zus persicae being the most efficient. Infection efficiency increases with the length of feeding. The virus is spread over long distances by windborne winged aphids and over short distances by nonwinged aphids moving from plant to plant. Aphid transmission occurs from tuber t(. tuber during seed storage, especially in tropical countries. Plants from infected tubers and diseased volunteer potato plants also serve as virus sources. Moderate temperatures and dry weather favor spread. Plants become resistant to infection with age, and occasionally some tubers of plants infected late in the season escape infection. Other Hists Several plant species, mostly in the Solanaceac, are known as hosts. P.floridana is asuitable indicator, test, and propagation host that reacts with interveinal chlorosis, darkening of the veinal areas, and a slight cupping at the first two or three true leaves. Infections at a later stage cause plants to become somewhat pale. Datura siraionium is favored by some workers, especially in the more tropical regions, as a test and propagation host in which chlorosis develops. In Brazil, alternative hosts to PI.VR
have been demonstrated, including tomato, D. stranionium, and a Physalis species. D. stramoniutm also seems to be a reservoir for the virus in the Andean region, where it is a common weed. No evidence indicates that hosts other than potato act as a virus reservoir in the temperate regions. Nonsolanaceous hosts are found in the Amaranthaceae. Tuber Indexing Symptom development in eye sprouts can be used to index for virus infection in postharvest glasshouse tests. The often-used Igel-Lange test (deep blue staining of phloem sieve tubes after 10 rin in Il " aqueous resorcin blue) is based on increased deposits of callose in the phloem (Fig. 73C). Neither method is completely reliable because symptoms are not always produced and because callose, which is not always observed in infected tubers, may also be found in healthy tubers. Electron microscope techniques alone are unreliable because of the low concentration of virus particles in infected plants. In combination with serological techniques, electron microscopy is efficient. The recent application of EI.ISA to detect the virus in tuber and other plant material has resulted in improved indexing techniques. A reliable method, although laborious to perform, involves aphid transmission tests on eye sprouts, using indicator plants such as P..1loridana. A technique in which leaves, stems, and small pieces of tuber are grafted to D.stramonium isnow used on a large scale in seed multiplication work in Brazil. This method is considered to be less time-consuming than that using aphids and P.floridana. Control I) Breeding resistant cultivars has met only limited success. Resistance is determined by many genes with additive effects and can only gradually be built up. Varying levels of resistance are found in some seedlings. Crossing of unrelated resistant parents may result in a higher proportion of resistant offspring than does inbreeding. Resistance isalso found in progenies from S. de'nissun, S. and(igena, S. acaisle, S. chacoense, S. stololnferunn, and S. etuherosuim. 2) Disease-free seed tubers are essential for maximum production. Seed tubers with a low percentage of infection can be produced in areas where sources of virus are limited and aphids appear late in the season. Seed plots should be harvested as early as possible, compatible with reasonable yields, to avoid late season aphid transmission. Dates for lifting may be determined by the number of aphids caught in yellow traps or assessed by other methods. 3) To minimi/e infection, measures such as clonal selection, early planting of virus-free tubers (from seed certification programs), and early lifting and roguing of infected plants and killing or removal of volunteer plants in and around the field can be Lused. 4) Aphids should be controlled by toxic sprays or systemic insecticides. Application of granulated systemic insecticides has been successful in certain cases. Spread cannot be controlled by oil sprays. 5)Tubers may be freed of the virus by heating, e.g., 25 days at 37.50 C. Selected References BACON, 0. G., V. E. BURTON, D. .. McLEAN. R.H. JAMES, W. t). RII.EY, K.G.BAGHIOTT, and M.G.KINSEY. 1976. Control of the green peach aphid and its effect on the incidence of potato leaf roll virus. J. Econ. Entomol. 69:410-414. CHIKO, A. W.. and .1.W. GUTHRIE. 1969. An hypothesis for selection of strains of potato leafroll virus by passage through Phrsalisfloridana.Am. Potato .1.46:155-167. CUIPERIINO. F. I1.. and A. S. COSTA. 1967. l)eterminaciodo virus do enrolamento em hastas velhas de batalal para sementes. Bragantia 26:181-186. l)AVI)SON.l-.M. W. 1973. Assessing resistance to leafroll in potato seedlings. Potato Res. 16:99-108. de BOKX. .1.A. 1967. [he callose test for the detection of leafroll virus I. .,.T. . :. ,.. " - Fig. 73. Potato leafroll virus (PLRV): A, phloem net necrosis of tuber; B, phloem necrosis in petiole (bar represents 10 pm); C, callose at stolon end of infected tuber (Igel-Lange stain); D,PLRV particles, 24 nm in diameter, negatively stained with phosphotungstic acid and (E)precipitated with PLRV antiserum and similarly stained. (C-E. Courtesy D. Peters) 0 69
Page 1 and 2:
, ,. ,o . ; , . o , . r. , -' .L ,
Page 3 and 4:
Compendium of Potato Diseases W. J.
Page 5 and 6:
In memory ofimy respected colleague
Page 7 and 8:
Acknowledgments Planning Committee
Page 9 and 10:
Introduction 1 Potato Disease 1 The
Page 11 and 12:
A potato disease is an interaction
Page 13 and 14:
Fig. 1.A, Lower portion of young po
Page 15 and 16:
+q I B Fig 4. Natural openings in a
Page 17 and 18:
Part I. Disease in the Absence of I
Page 19 and 20:
more heavily in the vascular region
Page 21 and 22:
the air temperature when tubers are
Page 23 and 24:
iiO A B 'D C Fiq. 14 Second growth:
Page 25 and 26:
identifying tissue bruised by black
Page 27 and 28:
Internal Sprouting multiple sprouts
Page 29 and 30:
conditions permits normal leaf deve
Page 31 and 32:
Epidemiology Oxidant injury is pres
Page 33 and 34:
sevritof stnting, chiorosis. loss o
Page 35 and 36:
Selected Reference brown to bronze
Page 37 and 38:
Part II. Disease in the Presence of
Page 39 and 40:
should be planted on land with at l
Page 41 and 42:
Control I) Use disease-free tubers
Page 43 and 44: FOI-SO M. D, and I. A. FRIEDMAN. )9
Page 45 and 46: Fungi Powdery Scab liberating powde
Page 47 and 48: Histopathology Sort of sporangia de
Page 49 and 50: any time but generally occurs late
Page 51 and 52: '40 ff .. . '1 f . ."L', . '1 .,. "
Page 53 and 54: A \, 2) Powdery mildew is rarely a
Page 55 and 56: R., Inst.. Kew. Surrey. ngland. 609
Page 57 and 58: TORRES, H.. E. R. FRENCH, and I.. W
Page 59 and 60: d AC D A 0 Fig 53 Gray mold. A, Bot
Page 61 and 62: strands of pigmented hyphae. Sclero
Page 63 and 64: tuber malformation. Roots are also
Page 65 and 66: 1. Giant-hill plants, taller than n
Page 67 and 68: 13. Bacterial soft rot. Erwinia car
Page 69 and 70: 24. Wart. Synchytrium endobioticum
Page 71 and 72: 34. Pleospora herbarum (Stemphylium
Page 73 and 74: 44. Charcoal rot. Macrophomina phas
Page 75 and 76: 55. Leafroll virus. Current season
Page 77 and 78: 67. Mop-top virus. Primary tuber 68
Page 79 and 80: 77. Aster yellows mycoplasma sympto
Page 81 and 82: Symptoms Small, localized, light br
Page 83 and 84: obovoid, and 14-30 X 5-10 pm. Pycni
Page 85 and 86: invaders through the IFusarium lesi
Page 87 and 88: necrosis extending into the tuber t
Page 89 and 90: do not survive drying. Both species
Page 91 and 92: cauisal. Tesis Magister Scientiae e
Page 93: penetration, and subsequent disease
Page 97 and 98: In P..floridana,strains of PVY" and
Page 99 and 100: infects certain comnie,-cial stocks
Page 101 and 102: cytoplasm of infected potato cells
Page 103 and 104: WETTER, C. 1971. Potato virus S. No
Page 105 and 106: 3) Resistance has not been identifi
Page 107 and 108: nm), which do code for coat protein
Page 109 and 110: Symptoms AMV may induce Other predo
Page 111 and 112: Disease Cycle I)escriptions of Plan
Page 113 and 114: Selected References KASSANIS, B. 19
Page 115 and 116: Control 1)Avoid locations in wkhich
Page 117 and 118: The "yellows" types of disease, cha
Page 119 and 120: modifying cultural practices and by
Page 121 and 122: immature females in the white or ye
Page 123 and 124: l.aboratory, Control. and Quarantin
Page 125 and 126: They attack many major crops in the
Page 127 and 128: infested areas of North America sev
Page 129 and 130: antennal tb l tuberce u antenna eye
Page 131 and 132: carbon tetrachloride, applied at th
Page 133 and 134: Diagnostic Microbial Structures Scl
Page 135 and 136: Surface and or interior Shades of g
Page 137 and 138: Equivalent Names of Potato Diseases
Page 139 and 140: Common Name Causal Factor Other Nam
Page 141 and 142: Common Name Causal Factor Other Nam
Page 143 and 144: coalesce-union of similar structure
Page 145 and 146:
many days following removal of the
Page 147 and 148:
Index Abrasions, tuber surfaces. 14
Page 149:
Irost tolerance in. 9 aniligena. 68
show all

Compendium of Potato Diseases - (PDF, 101 mb) - USAID

You also want an ePaper? Increase the reach of your titles

Delete template?

Save as template?