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

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ATuber Fig. 19. Blackspot internal bruising. (Courtesy S.L.Sinden and R. W.Goth) days before harvest tend to predispose to bruising injury, Hecause oftuber hydration differences, tubers with high specific gravity are usually more susceptible to bruising than are tubers with low specific gravity from the same lot. Susceptibility can increase du ring storage because of physiological aging and dehydration, Mature tubers are more susceptible than immature tubers, altdi the stolon end is more susceptible than tile apical end. " emperature of' tile tubers at the time of bruising influences ses erit v. lit bers br tirsed at 20-.30 C*are less aIf ected b lilac kspot than are those brui:--d at temperatures below 10°C. Because of differences in both mechanical strength and solids content, cultivars differ significantlv in susceptibility to bruising and blackspot de elopient. Tubers harvested from soils deficient in potassium tend to be i1re susceptible to Ilrisinug arid blackspot deelopnerit. I.o\ potiassium content ill tubers is associated with high phenolic content and low tuber hydration. High phenolic content and active oxidase systems in damaged cells result in abundant produ ction of melanin. Nitrogen fertili/ation. ethylene concentrations, and soil carbon dioxide lesels Itrse been reptorted to affect blackspot susceptibility in some growing areas. The specific effect of any oi ens ironimental factor on susceptibility of tubers to blackspot depends on the cultivar, the cultural conditions, and tile interaction with other environmental factors. Control I) Reduction of bruising is most important for control of blackspot. Use Cltiplllclll Ion harvesting. trainsporting. grading, and handling tubers that is well designed and carefully adjusted to minimize impact forces. 2) Use sound cultural management practices, including adequate I pIOAPST. potash fertilization, especially on heavy soiils that are likely to be deficient in potassium. Irrigate ars long as vines are green. 3) Warm tubers in storage to 200 C before grading and other handling operations. Using sprout inhibitors and adding 16 moisture to the storage atmosphere will help prevent dehydration and bruise damage in tubers taken out of storage. 4) Use resistant cultivars. Selected References ")WI .lI, . It. B..(. I. SI \1.1 KNI- II I R.IE. V cl)( l.l. aid .1..1. )PAVI-K. Effects of soil potash treatnent aid storage temperature on blaekspot bruise development iii tihers off our Sohonuor ruhr'routot ctiltixars. Amf Potato .1.54:137 146. KUNKEI., R.. M. I.. WEAVER, and N. M. lIOISVAI). 1970. Blackspot of Russet Burbank potatoes and the carbon dioxide content of soil and tubers. Am. Potato .1.47:105-fl 7, SCIII PIERS. P. A. 1971. Measurement of black spot susceptibility of potatoes. Am. Potato .1.48:7 1-81. SMft III0. I''X. Internal black spot olpotatoes. Pages 303-307 in: O. Smith. cd. Potatoes: PIrductior. Storing. Processing. A\i Publishing (o.. Iic.. Westport. C 1.642 pp. IIM M, II.. M.YAMAGI ('III. l).I.llt'(illl!S. arf M. I. WEAVER. 1976. Influence of ethylene oil black spor of potato tubers. Am. Potato .1.53:49-56. (Prepared by S. L. Sinden and R. W. Goth) Greening and Sunscald When tubers are exposed for some time to light in the field or after harvest, chlorophyll forms in the leucoplasts and tuber tissue turns green. Stiln green. somieties less correctly called siriscald, develops in tubers not covered by soil in the field and therefore exposed to intense sunlight. Green tissue may extend 2 cm or more into the tuber and is often accompanied by purple pigmentation. Such tissue is high in solanine, bitter in flavor, and believed to be toxic to hurnaits when ingested. The processes of greening and solanine production are independent. Affected tubers are not marketable. and losses may be high. Srnnscald iniur\ de\clops in tubers exposed ftrintenrise sunlight as restricted areas with ahiost-white skin. often covering a sunken necrotic area. (See high temperature field i ni ry.) Certain potato cultivars have atendency to set tubers near the soil surface. Throwing soil toward tie planats during ct,ltivatiens often effectively covers tubers and redces greening. However. tubers may be exposed later by soil erosion or by cracks formed is soil dries or tubers enlarge. Ordinarily, severely greened tubers ire not predisposed to rot unless sunlight and heat have been intense. Table stock potatoes should be stored in the (lark. Fluorescent or natural lighting in market displays causes superficial and, occasionally, deeper lavers of the tuber to turn green. Color is persistent it.is not removed by placing tubers in the dark. Greening develops more rapidly at room temperature than in cold storage. Potato cultivars show differences in intensity of greening and the depth to which it develops. Tuber rinses with surfactants. used experimentally, show promise of reducing the intensity of greening. Selected References AKEIFY. R. V., i. V. C. ItOUGII.ANI, and A. E. SIIARK. 1962. Genetic differences in potato-tuber greening. Am. Potato .1. 39:419-417. G I1.1.. 1).D.. and . M. ISENItER(. 1960. Chlorophyll and solanine content and distribution in foul varieties of potato tuber. Proc. Am. Soc. Ilorlic. Sci. 75:545-556. I'. A.. I. PRICE. arid F.R.FORSY III. 1978. Controlling post storage greening it table stock potatoes with ethoxylated mono-and diglyceride surfactants and i,adjuvant. Am.Potato J. 55:35-42. (Prepared by W. .1.Hooker)
Internal Sprouting multiple sprouts also cause internal sprouting. Sprouts that develop during storage may become ingrown by penetrating into the tuber. Internal sprouts frequently are in eyes with tightly clustered multiple "rosette" sprouts, which may be unbranched or. more frequently, nranched (Fig. 20). Sprouts may penctratCtile tuber directly above. or sprouts from an eye on the bottom of the tuber may grow up through the same tuber. Sprouts from tubers ssith deep eyes may penetrate into tile side of the eve depression. The disorder has been kno\n for oser a century. It is more frequent in old tubers and in those stored at 12-15 ° C. Pressure on tubers within the storage pile restricts sprout growth and induces sprout penetration of tuber tissue. In old tubers, sprouts often tuberi/e within the parent tuber, splitting it open. Internal sprouting was recently associated with sprout inhibitors used in concentrations below those required for complete sprout inhibition. Concentrations that completely inhibit all external sprouts also inhibit internal sprouts, but insufficient concentrations actually stimulate internal sprouts. Isopropyl-nm-chlorocarbanilate (CI PC) stimulates internal sprouting to agreaterextent than does pressure on tubers under a deep pile. Other chemicals stimulating tightly clustered, r t " Fig. 20. Internal sprouting, showing rosette of sprouts on the underside, small tubers on internal sprouts, and necrosis under or at the sprout apices. The last resembles calcium deficiency. (Courtesy E. E.Ewing) r -'"Coiling Fig. 21. Secondary tubers formed directly on sprouts from physiologically old tubers. Necrosis at or slightly below the sprout apex is common on the external sprouts of tubers containing internal sprouts, and apicies of internal sprouts become similarly necrotic when they emerge from the tuber. (See Ca deficiency.) Selected References EWING. E. E...1. W. LAYER. .1.C. IIOHN, and 1). J. I.ISK. 1968. Effects of chemical sprout inhibitors and storage conditions on WIEN, internal II.C.and sprouting 0. SMITH. in potatoes. 1969. Am. Influenceof Potato .1.45:56-71. sprout tip necrosisand rosette sprout formation on internal sprouting of potatoes. Am. Potato .1.46:29-37. (Prepared by W. J. Hooker) Secondary Tubers Tubers sprout either in storage or in the field, producing tiew tubers directly without forming a normal plant. Secondary tubers form on sprouts from physiologically old tubers after completion of the rest period when carbohydrate reserves are low (Fig. 21). The disorder is associated with warm (200C) storage followed by low temperature after planting or by transfer of sprouted tubers from warm to cold storage. Even at low temperatures, however, physiologically overmature tubers held past normal usage form secondary tubers. Usually the problem is of minor importance, although poor field stands with missing hills result. (See also calcium deficiency.) Selected References BURTON, W.G.1972. The response of the potato plant and tuber to temperature. Pages 217 -223 in: A. R. Rees. K. F. Cockshull. I). W. Hand, and R. G. [lurd. cos. Crop Processes in Controlled Environinents. Academic Press. Ness York. 391. pp. DAVIDSON, T. M. 1958. t)ormancy in the potato tuber and the effects of storage conditions on initial sprouting and on subsequent sprout growth. Am. Potato J. 35:451-465. VAN SCHREVEN, I). A. 1956. On the physiology of tuber formation in potatoes. 1. Premature tuber formation. Plant Soil 8:49-55. (Prepared by W..1. Hooker) Coiled Sprout The disease has been reported primarily from the British Isles, where up to 26% of plants in certain fields are affected, but it probably exists elsewhere. Symptoms Underground sprouts lose their normal negative geotropic habit and coil. sometimes rather tightly, with the curved portion of the stem often swollen and sometimes fasciated or split (Fig. 22). Light brown lesions with transverse or longitudinal cracks may be present on the stem inside the coil. Delay in emergence of coiled sprouts results in uneven stands. Affected plants may produce more stems than normal, and tubers may form unusually early and mature slowly. Causal Factors is believed to be the result of overmature seed, soils resistant to sprout penetration and emergence, or infection by a fungus. Verticillium nuhilunt Pethybridge has been isolated from affected stems. This pathogen has caused superficial browning and russeting of some stem bases, accompanied by shallow cortical invasion underlaid by suberin. In some instances, inoculation with the pathogen has caused coiled sprout, but IVnubihmn is not the sole cause of the disease. Low soil temperatures. presprouting in light, long sprouts at 17
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: identifying tissue bruised by black
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
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obovoid, and 14-30 X 5-10 pm. Pycni
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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
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penetration, and subsequent disease
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have been demonstrated, including t
Page 97 and 98:
In P..floridana,strains of PVY" and
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infects certain comnie,-cial stocks
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cytoplasm of infected potato cells
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WETTER, C. 1971. Potato virus S. No
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3) Resistance has not been identifi
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nm), which do code for coat protein
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Symptoms AMV may induce Other predo
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Disease Cycle I)escriptions of Plan
Page 113 and 114:
Selected References KASSANIS, B. 19
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Control 1)Avoid locations in wkhich
Page 117 and 118:
The "yellows" types of disease, cha
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modifying cultural practices and by
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immature females in the white or ye
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l.aboratory, Control. and Quarantin
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They attack many major crops in the
Page 127 and 128:
infested areas of North America sev
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antennal tb l tuberce u antenna eye
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carbon tetrachloride, applied at th
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Diagnostic Microbial Structures Scl
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Surface and or interior Shades of g
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Equivalent Names of Potato Diseases
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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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Compendium of Potato Diseases - (PDF, 101 mb) - USAID

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