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

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elonging to primitive species grown in the Andes. carry considerable frost tolerance, some to as much as -5°C . Control I) Potato crops seldom justify frost protection such as spray irrigation, mechanical air movement, or smoke application during low temperatures. 2) Proper diagnosis of nonlethal injury is necessary in seed fields. 3)Low temperature tolerance (approaching -6°C) of hybrids involving S. acau'le and other tuber-bearing Solanum species permits potato cultivation at high altitudes and possibly also at extreme latitudes. Selected References CHEN, P. M., M.,I. BURKEand P. IH.LI. 1976. -Thefrost hardinessof several Solanium species in relation to the free,,ing of water, melting point depression, and tissue water content. 3ot. (ia/. (Chicago) 137:313-317. ESTRAI)A, R. N. 1978. Breeding frost-resistant potatoes for the tropical highlands. Pages 333-341 in: It. I'. l.i and A. Sakai. eds. Plant Cold Hardiness nd Freeing Stress. Academic Press. New HOOKER. W... 1968. Suhlethal chilling injury of potato leaves. m. Potato 45:250-254. v. Potao .1 45250-54.potatoes .I, P. H. 1977. Frost killing temperatures of60 tuber-hearing Solaium species. Am. Potato .1.54:452-456. McKAY, R.,and P. F.M. CI.INCH. 1945. Frost injurysitnulating virus disease symptoms on potato foliage. Nature 156:449-450. PAulA. .1.P.. and P. Ht.1.1.1979. Frost-hardiness in relation to leaf anatomy and natural distribution of several Solarum species. Crop. Sci. 19:656-670. (Prepared by W. J. Hooker) Blackheart Blackheart results from inadequate oxygen supply for respiration (asphyxiation) of internal tuber tissue. Internal mahogany browning and internal heat necrosis grade into blackheart in severe instances and thus are, in different environments, symptoms of incipient to acute suboxidation. Blackheart was amajor problem when potatoes were shipped in Symptoms 131ackheart symptoms consist of black to blue-black discoloration in irregular patterns in the central portion of the tuber (Fig. 9). With acute oxygen deficiency, the whole tuber may be discolored. Demarcation at the margins is usually definite, although the black discoloration may diffuse into relatively unaffected tissue. Discolored tissue is frequently firm but on exposure to room temperatures may become soft and inky. Individual tubers vary in their responses to conditions causing blackheart. Blackheart develops when oxygen isexcluded from orunable to reach internal tuber tissue. Longer times are required for blackheart development at lower temperatures. However, blackheart develops more rapidly between 0and 2.5°C than at 51C. At extreme temperatures of 36-40'C or of 0 C or slightly below, blackheart may develop without oxygen exclusion because gas diffusion through the tissues is not sufficiently rapid. Tuber storage in closed bins or in deep piles without adequate aeration may result in blackheart development. Control I) Do not expose tubers to high temperatures no. to prolonged storage near 0C. 2) Provide forced aeration of potatoes in closed bins. Selected References BENNETT, J. P..and E.T. BARTHOLOMEW. 1924. The respiration of potato tubers in relation to the occurrence of blackheart. Calif. Agric. Exp. Sin. Tech. Paper 14.41 pp. STEWART, F. C..and A. i. MIX. 1917. Blackheartand theaeration of 436:321-362. in storage. N.Y. Agric. Exp. Sin., Geneva. tech. Bull. (Prepared by W. J. Hooker) High Temperature Field Injury Stems may be injured at the soil line by high soil temperatures, particularly when plants are small and leaves are not large enough to shade the soil at the base of the plants. Stems typically are girdled and surfaces secondary are organisms tan to white, may although ',ometimes discolor the tissue to a darker brown and, in severe cases, cause follow rotting. Injurycan defoliation also or vine displacement that suddenly lower exposes stems to intense sunlight. This results in a scalded apperance on the exposed side ofthestem or girdling at the soil line (Fig. 10). Tubers exposed may to be sunlight injured as they and lie thereby in the field predisposed after digging to rot in transit or storage without immediate external symptoms except possibly for watery exudates from lenticels. Intense exposure causes sunken scalded areas in a circular pattern. The threshhold of tuber flesh temperature predisposing tissue to soft rot is approximately 430C. Such internal temperatures may exceed Fig. 9. Blackheart at two cross sections of the same tuber. Fig. 10. Scald of stems following exposure to sun. 10
the air temperature when tubers are in the soil within 2.5 cm of the surface, remain on the ground after digging, or are held in bags in the sun. (See also tuber greening.) Selected References NII'IS|-N. I.. WV. 1954. [he susceptibility of"seven potato varieties to bruising and bacterial soft rot. Phytopathology 44:30-35. (Prepared by W. .1.Hooker) Internal Heat Necrosis Considerable confusion exists both in symptom description and in terminologv for the causal factors of internal necrosis of tubers. The underlying cause of necrosis is believed to be suboxidation of rapidly respiring internal tissues during active tuber growth and high temperatures. (See also phosphorus deficiency, vello\k d\\art. mop-top, and stem mottle.) In recent literature, the name Eiserifleckigkeit refers specifically to internal heat necrosis, whercas l'ropfenbildtung and Spraing are used for stem mottle virus infections, Symptoms Syniplonis do not develop in vines. Affected tubers usually do not sho%%external syniptoims. Necrosis may be severe toward the center of larger tubers, appearing as light tal, dark yellowish to reddish bro, n. or rust-colored Ifccks that become, in extreme cases, dark brown or even black (Fig. II). 1n usually severe s. mptonis may be identical to blacklicart. Necrotic flecks are ustallyv clustered off-center in the pith towards the apical end. Necrotic flecks are firtii, do niot break do%%n or predispose to rot, and remain firm after cooking. Cortical tissues are seldom aft ected. .\ relat ionship exists bctx\ en Iisenfleckigkeit atid acid soils that ate Io\ iti calcium. (See also calciun deficiency.) losses can be se\ere because of buyer discrimination against internal discoloration. .\ sonlew\hal similar disorder. present in Israel, produces necrotic spots in the coritx near the vascular ring and maproduce interior cavities. I)amage is visible from the tuber sirft:ce. with h!:ckening of the eves at the apical end, sunken surface spots. and a silvery sheen. No true rot develops, but many affected tubers fail to sprout. Symptoms are believed to develop intstorage following high field temperature before har\est. Ifistopathology Suberin develops in walls of affected pith parenchyma cells. Cell walls first become dark at the corners. Protoplasm becomes granular and aggregates. Walls ofadjacent cells also darken and finally collapse at the corners. l.ayers of peridermlike cells may develop outside the necrotic tissue and may isolate it. Internal pressure from periderm formation may cause the collapse of necrotic cells, but cell lysogeny has not been observed. Starch grains are generally absent in affected cells. Epidemiology Internal necrosis becomes progressively more severe during the growing season and is most severe during hot, dry years in light soils of sand. gravel, muck, or peat. Lack of adequate soil moisture may be as influential as high temperature in predisposing to internal necrosis. Disease is most severe in tubers near the soil surface and progressively less frequent and severe with increasing tuber depth. Straw mulch reduces soil temperature and sexeritv of disease. Ini areas where the disease was formerly severe, maintenance of good vine coverage of the soil through adequate irrigation and good cultural practices has almost eliminated the problem. Discoloration does not increase and ma' decrease in storage if affected tubers are not predisposed to storage rots. Transmission through affected seed tubers has not been observed, although spindly sprouts have been reported from tubers exposed to 30-40°C. Control I) Cultivars differ in tolerance and sensitivity. 2) Maintain vine growth adequate to shade the ground through the use of appropriate cultural practices (good fertility, Fig. 12. Second growth: A, dumbbell; B, pointed end; C, protruding eyes that later form knobs. Stoton end ineach case is Fig. 11. Internal heat necro'sis, at left. A rr.. V, 11
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: more heavily in the vascular region
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
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carbon tetrachloride, applied at th
Page 133 and 134:
Diagnostic Microbial Structures Scl
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Surface and or interior Shades of g
Page 137 and 138:
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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