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

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Fig. 30. Calcium deficiency on potato sprouts: A, healthy sprout; B, sprout treated with calcium sulfate; Cand 0, calcium-deficient sprouts. Note necrosis of tips and tendency for lateral branching. (Courtesy P.W. Dyson and J.Digby, and copyright permission of Macaul,y Institute for Soil Research) flecks form in the pith. Tubers may be extremely small. Internal rust spot is more severe on dry soils with low Ca, a tendency towards acidity, and amoderate to low base-exchange capacity. (See also internal heat necrosis and phosphorus deficiency.) Seed tubers in Ca-deficient soil remain hard and produce relatively normal roots. Sprouts become necrotic immediately behind the tip and fail to grow (Fig. 30). In storage, sprouts become necrotic 3-5 mm below the tip due to collapse of outer cortex and inner pith and, later, of vascular tissue. Multiple lateral branches form below the sprout tips, and, with certain cultivars, small tubers known as "little potato" form prematurely before the development of aboveground sprouts. Ca deficiency and internal sprouting show certain relationships. Symptoms are most severe on sandy soils below pH 5.0, where symptoms of Mn or Al toxicity may also be present. Calcium treatment of sprouts reduces incidence of necrosis below the tip. liming the soil above pH 5.2 should be avoided because of potential Tranferof problems ld lave Ca with fom toyoun common levesand scab. romthe Transfer of ('a from old leaves to young leaves and from the top of the plant to the tubers is limited. Ca must therefore be available during the entire growing period, particularly during tuberization. Selected References BRAUN, H., and I). E. WILCKE. 1967. lodenprofile und ihre Beziehungen zum standortbedingten Auftreten der Eisenfleckigkeit bei Kartoffeln. Phytopathol. Z. 59:305-336. DeKOCK, P. C., P. W. DYSON. A. HALL, and F.B.GRABOWSKA. 1975. Metabolic changes associated with calcium deficiency in potato sprouts. Potato Res 18'57-5 I. WALI.ACET.,and E.J.HEWITT. 1948. Effects of calciumdeficiency on potato sets in acid soils. Nature 161:28. Magnesium Mg deficiency is one of the most commonly encountered nutritional problems. Because Mg is highly mobile within the plant, new growth appears essentially normal and symptoms develop on older leaves. A pale, light green color--later, amore definite necrosis begins at the leaf tips and margins and 24 progresses between the veins, becoming most severe toward the center of the leaf. l.eaves are usually thick and brittle and roll upward, with tissue raised between tile veins (Plate 10). Necrotic leaves either hang on the plant or abscise. Roots are stunted, reducing the ability of the plant to absorb Mg. Mg deficiency usually occurs on sandy acid soils that are readily leached. but may occur on heavier soils. High rates of K fertilizer or high K levels in soil accentuate Mg deficiency. Solubility of Mg is increased b. acid-forming fertilizer. Sym ptomis freq uenti'follow leaching after periods of heavy rain. Exchangeable Mg should exceed 50 ppm for mineral soils and higher (100 ppm) for muck soil. Mg may be supplied as MgSO 4 in fertilizer or dolomitic limestone or as a 2'i MgSO 4 foliage spray. Higher concentrations usually may be applied to foliage without injury. Selected References BONI)E, R. 1934. Potato spraying -- lhe value of late applications and magnesium-bordeaux. Am. Potato .1.11:152-156. CH UCKA, J.A., and B.E.BROWN. 1938. Magnesium studies with the potato. Am. Potato .. 38:301-312. SAWYER. R.L.,and S.L.I)AI.t.YN. 1966. Magnesium fertiliation of potatoes on Long Island. Am. Potato J. 43:249-252. Sulfur S deficiency, as reported in several locations in Wisconsin on Planefield loamy sand, is a generai yellowing with a slight upward rolling of leaflets. Symptoms vary from slight to marked chlorosis over the entire plant. Beneficial responses have been obtained with sulfur soil applications or with fei ,;,'izers containing sulfur. Aluminum A Itoxicity causes roots to become short and stubby with few branches. Leaves remain normal in color although plants are small and spindly, with branches rising at acute angles. Potato;, relatively tolerant to Al toxicity. Al solubility is often high in soils below pH 5.0. Soil conditions may be corrected by adding superphosphate fertilizers, increasing soil pli to 5.5 or above with lime, or increasing the organic content of the soil. Selected References BROWN, B.A.. A. H AWKINS, F.. J. RI)BI3NS. A. V. KING.and R.I. MUNSEI.LI. 1950. Causes of very poor growth of crops on a formerly productive soil. Soil Sci. Soc. Am. Proc. 15:240-243. HAWKINS, A.. B.A. BROWN, and E..1. RUIBINS. 1951. Extreme case of soi toxicity to potatoes on a forme rlyproductive soil. Am. Potato .1.28:563-577. Boron In plants with B deficiency, growing points die; lateral buds become active: internodes are shortened: leaves thicken and roll upward: and tileplant assumes aI bushy appearance. Starch accumulation in leaves is pronounced and may resemble virus leafroll. Roots are short, thick, and stunted. Tubers are small. showing surface cracking particularly at the stolon end and localized brown areas under the skin near the stolon end or brown vascular discoloration. Some sandy soils, peat soils, and overlimed, acid, upland, podzolized soils are inherently low in B or apparently fix B so that it becomes unavailable to plants. Applications of B should be made cautiously because B is toxic to potatoes in relatively small amounts and deficiency is rare.
Selected Reference brown to bronze areas, later becoming necrotic, may develop on leaves near the middle of the plant and later involve all leaves. MIIGI.EY. A. R., and 1). F. I)IINKII. 1940. Ihe cause and nature Brownish spots may develop on petioles and stems. of oserliming injury. VI Agric. Exp. Stin. Bull. 460. 22 pp. Zn deficieney in recently developed land. alkaline soils, or soils with excessivcly high1P results in severe stunting, leaf Zinc malformation, and indistinct bron/ing or yellowi ng around leaf margins. The "fern leaf" sympton (Fig. 31 ) is present when the youngest leaves are cupped upwards and rolled, becoming thick, Zn deficiency causes stunting of plants and upward rolling of brittle and puckered from expansion of intercostal tissue and young. chlorotic leaves suggestive of early virus leafroll apparent lack of expansion of leaf margins. Severely affected symptoms, with terminal leaves being somewhat vertical. Gray plants die early. Foliage applications of ZnC I : or ZnS0 4 alleviate deficiency symptoms. In some cases without recogni/able Zn deficiency. yield increases have been obtained when Zn salts were applied to foliage as fungicides or used as soil treatments. Excessive liming or application of 1)enhlnces symptoms of Zn deficiency. Speckle bottom (small to large necrotic spotting and chlorosis of basal leaves, which progress upward) has responded to applications of zinc. In laboratory studies, Zn toxicity develops as general stunting, with a slight chlorosis at tips and margins of upper leaves and purple coloration on the undersides of lower leaves. Selected References HOAWN, I.. C., and (i. lECGE'. 1963. Zinc deficiency of the Russet Burbank potato. Soil Sci. 95:137-141. CIPAR. M.S., D. E. ItUN IR. W. W. WE1IR. R. MII.1.ER.and P. PORIER. 1974. Soil fumigation and /inc stattus of soils in relationship to potato speckle-hottom disease de\elopment and control. Potato Res. 17:30'/-319. HOYMAN. W. G. 1948. Potato-lungicide experiments in 1948. N.D. Agric. Exp. Stn. IBimonthly Bull. 11:32-35. Fig. 31. "Fern leaf" symptom of zinc deficiency. (Courtesy L. C. I.ANGII.E, A. I.. and R. I. IATlEESE, Jr. 1974. Influence of inc Bowan and G. E. Leggett) concentration in nutrient solution on growth and elemental content • | .., ' 4l' Fig. 32. Manganese toxicity: A, early symptoms on stems; later symptoms of manganese toxicity within (B) and on (C) stems. (A, Courtesy H. W. Gausman; B and C, courtesy K. C. Darger) 25
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: sevritof stnting, chiorosis. loss o
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 and 94:
penetration, and subsequent disease
Page 95 and 96:
have been demonstrated, including t
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
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