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

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tissues. Many different kinds of variants can be produced by developing adventitious growths from callouses on tubers where eyes have been removed. Selected References DEARBORN, C. H. 1963. "Stitched end," "giant hill." and fasciated stem of potatoes in Alaska. Am. Potato J. 40:357-360. HOWARD, H. W. 1967. The chimerical nature of a potato wilding. Oxygen Deficit Oxygen requirements of underground parts of the potato during plant development are high. When oxygen concentration is reduced, stolons are abnormal and tuber development is impaired and abnormal. The degree of abnormality depends upon the severity of oxygen deficit, Although soil compaction exerts various stresses upon underground parts of the plant, oxygen deficit may be one of the most important, resulting in delayed plant emergence, moderate to severe yield reductions, and frequently, but not always, abnormal tuber shapes. Oxygen levels within soil, root distribution, and yields are increased by cultural and tillage practices that favor improved soil porosity. Selected References BUSHNELL,J.1956. (;rowd,response from restricting the oxygen at roots of young potato plants. Am. Potato .1.33242-248. GRIMES, D. W., and J.C. BISHOP. 1971. The influence of some soil physical properties on potato yields and grade distribution. Am. Potato J.48:414-422. HARKETT, P. J.. and W. G. BURTON. 1975. The influence of low oxygen tension on tuberization in the potato plant. Potato Res. 18:314-319. SOMMERFELDT, T.G.. and K. W. KNUTSON. 1968. Effects of soil conditions in the field on growth of Russet Burbank potatoes in southesastern Idaho. Am. Iotato .. 45:238-246. (Prepared by W. J. Hooker) Low Temperature Tuber Injury Low temperature tuber injury may range from outright freezing and killing of some or all of the tuber to gradations of .A- B A Adverse Environment Plant Pathol. 16:89-92. HOWARD, H. W. 1969. The chimerical nature of a feathery wilding. Eur. Potato J. 12:67-69. HOWARD, H. W. 1970. Chimaeras. Pages 68-88 in: H. W. Howard, ed. Genetics of the Potato, Solaium tuherosum. Logos Press, Ltd., London. 126 pp. (Prepared by J. Munro) injury (chilling) following prolonged exposure to temperatures slightly above freezing. Tubers may be frozen in the ground before harvest or injured later by low storage temperatures. Tubers of many cultivars freeze at temperatures below - 1.7' C. Freezing results in formation of ice crystals within the tissue, followed by rapid death. Chilling results in eventual death of cells or tissues even though the tissies may not actually have been frozen. Symptoms The line of demarcation between frozen and unfrozen tissue is usually distinct. Upon thawing, tissue may change progressively from dull off-white to pink and red and eventually to brown, gray or black. Frozen tissue promptly breaks down in a soft, evaporates. watery rot or collapses, leaving a chalky residue as the water Low temperature surface injury occurs in diffuse patches as a brownish black metallic discoloration. Such tissue is predisposed to surface mold growth (Fig. 7A). Effects of low temperature storage are primarily inernal. Tuber tissue chilled to near freezing is typically adiffuse smoky gray to black and resembles certain aspects of Pythium leak. Chilling causes formation of reducing sugars in stored tubers, resulting in itsweet flavor when cooked. Development is most rapid at temperatures slightly above freezing (0-2.5oC), progressively less severe from 2.5 to 3.5O C, and usually absent at 3.8-4.4C. Reducing sugars cause brown discoloration in french fries or chips. Tubers stored at low temperatures frequently turn gray to black when boiled. Chilling injury may also take the form of net necrosis, in which phloem tissue isselectively killed because it has greater sensitivity to cold than do the surrounding parenchyma storage cells (Fig. 7B). The necrotic phloem may be scattered throughout the tuber or on the chilled side or be concentrated f-. , / C D Fig. 7. Low temperature injury of tubers: A, surface injury of immature skin in low temperature storage; B, net necrosis resulting from selective killing of phloem tissue; C and D,tissue breakdown in the vascular area. 8
more heavily in the vascular region. Cold-induced net necrosis is very similar in appearance to virus leafroll net necrosis. Following severe injury, blackish patches or blotches may develop near the vascular ring, which may also be partially or completely blackened (Fig. 7C and D). Injury is usually more severe near the stolon end. Internal mahogany browning (Plate 2) is a different low temperature response, in which diffuse brownish red to black discoloration ispresent, usually in the central part ofthe tuber. This disorder grades into blackheart. Shrinkage in affected tissue results in cavities. Blackheart and probably internal mahogany browning result primarily from asphyxiation of internal tuber tissue. Epidemiology Individual tubers from the same lot vary considerably in response to a given temperature. Immature tubers are frequently more severely injured. Biecaiuse of hardening or acclinmatizatior, tubers that have been drop stored in temperature at low temperatures are less than injured by a sudden are those stored at higher temperatures. .ow temperatures fra few hours or temperaturesjust below free/ing for a short freeingfor time tme call an shrt lower owerintrnalquaityshoten internal quality, shorten storage life, and impair storge suitability ifeuitailiy andimpir of' o the thetubr tuber for fr processing prcesing without leaving visible evidence. Tu,bers may be supercooled to approximately -3.0 C. and even to -6.5' C for a,few hours, without ice crystal formation and, if gradually warmed, do not havc evident injury. However, jolting or jarring supercooled tubers will cause intracellular ice crystals to form and cells to die. Storage at low temperatures, even in the absence of symptoms, impairs the tuber's ability to form wound barriers when returned to favorable temperatures. Injured seed tubers with or without symptoms sprout poorly and may fail to produce plants because of secondary seed piece rots. Alternating temperatures during the storage season avoids chilling injury and its associated problems. Tubers held alternately for three weeks at 0' C and one week at 16' C had a lowered content of reducing sugars (as well as of total sugars), reduced respiration rates, and no low temperature injury, whereas at constant O°C tuber injuries became progressively more severe after eight weeks in storage. Control I) Field-frosted tubers should not be moved into storage if at all possible. 2) Hold storage temperatures at 3.5-4.51C, which is sufficiently high to prevent low temperature injury. 3) Maintaia adequate air movement in stored potatoes to dry frost-injured tubers and provide adequate oxygen for respiration. 4) Tubers injured by low temperatures or suboxidation should not be used for seed. 5) Certain cultivars are more prone to mahogany browning than are others. Varietal differences with respect to other aspects of low temperature injury are not so pronounced. Selected References CUNNINGHAM. H1.IL.. M. V. ZAEH RINGER, G. BRAUSEN. and W. C. SPARKS. 1976. Internal quality' of Russet Burbank potatoes following chilling. Am. Potato .1.53:177-187. tR USCH KA, II. W.. W. I.. SM I If..r., and .1. E. BAKER. 1969. Reducing chilling injury of potatoes by intermittent warming. Am. Potato .1.46:38-53. .JONES. .. R., M. MII.L.ER. and 1. BAILEY. 1910. Frost necrosis of potato tubers. Wis. Agric. Exp. Sin. Res. Bull. 46. 46 pp. LINK. G. K. K.. and G. 1B.RAMSEY. 1932. Market diseases of fruits and vegetables. Potatoes. U.S. Dept. Agric. Misc. Publ. 98. 62 pp. RICHARDSON. L.T.,and W. R. PiIII.I.IPS. 1949. I.ow temperature breakdown of potatoes in storage. Sci. Agric. 29:149-166. (Prepared by W. J. Hooker) Low Temperature Foliage Injury Certain symptoms of nonlethal low temperature foliage injury may be confused with virus symptoms or herbicide damage. Lethal freezing of leaves and stems isreadily identified. Symptoms Frozen leaves rapidly wilt, collapse. and when thawed, become water-soaked. They turn black when damp and brown when dried. Less severe low temperature injury, usually occurring in the early to middle part of the growing season, often produces a buff to light brown or yellow discoloration on the top of the plant and particularly at the bases of young leaflets. Temperatures at or near 0' C selectively injure leaf and stem primordia and possiblycell organelles. Symptoms ofthis injury become evident after leaflet expansion as unilateral leaflet development, irregular distortion of leaflets, or grayish transverse banding accompanied by restricted lateral expansion (Fig. 8). Chlorosis in diffused areas, in spots, or in portions of veins nay be seen and mottle patterns may be present with or without leaf Necrotic distortion specks following may develop nonlethal on young low leaves temperatures following (Plate -0.3° 3). C wet Nertcsckmadvlooiyunlaesflwng-.0 bulb temperatures. Injury of this type appears after leaves from damaged primordia have expanded. Normal growth may precede and should follow these low-temperature effects, but symptoms on injured parts persist. Epidemiology Low temperature injury is usually most severe in low-lying areas of fields. At high elevations and latitudes, freezing may occur at any time in the growing season. Because leaf surfaces are frequently well hydrated and often wet with dew, wet bulb temperatures should be more reliable than dry bulb temperatures in determining critical temperatures for leaf injury. Plants on which some leaves have been frozen recover from injury slowly, suggesting more damage than that of the tissue actually destroyed. Growth retardation may be due to resorption of tissue degradation products. Solarim acauk,, its derivatives, and approximately 10 more wild potato species, as well as several cultivated clones Fig. 8. Leaf deformation following low temperature injury of leaf primordia. 9
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: Part I. Disease in the Absence of I
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 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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