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

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elatively high at I and 2°C, drops to a low at 5 0 C, is slightly higher at 15 0 C, and then rapidly rises to 25' C and above. The relatively high respiration rates within a few degrees of freezing account for problems of suboxidation such as internal mahogany browning and blackheart. The increase in respiration rates at higher temperatures contributes to internal heat necrosis and also to blackheart. High respiration rates in freshly packaged tubers during transit deplete 02 and release CO, in sufficient quantities to predispose tubers to bacterial soft rot and cause severe losses. Increasing CO. concentration in storage causes increased cell membrane permeability, sucrose content, and decay. Oxygen levels of I% or lower at 14°C or higher temperatures severely impair wound healing reactions, stimulate anaerobic respiration, and increase surface mold growth, severity of decay, and blackheart. At lower temperatures these effects may not be so evident. Selected References BURTON, W. G. 1965. The permeability to oxygen of the periderm of the potato tuber. J. Exp. Bot. 16:16-23. BURTON, W.G,, and M.J. WIGGINTON. 1970. fheeffect ofa film of water up,n the oxygen status of a potato tuber. Potato Res. 13:180-136. LIPTON, W. J. 1967. Some effects of low-oxygen atmospheres on potato tubers. Am. Potato J. 44:292-299. MEINL, Kartoffelknollen. G. 1967. Zur Eur. Bezugsgrbsse der Respirations Potato Intensitait von NIELSEN, J. t.. W. 10:249-256. 1968. Accumulation of respiratory CO2 around potato tubers in relation to bacterial soft rot. Am. Potato J. 45:174-181. WIGGINTON, M.J. 1973. Diffusion of oxygen through lenticels in potato tuber. Potato Res. 16:85-87. WORKMAN, M., E. KERSCHNER, and M. HARRISON. 1976. The effect of storage factors on membrane permeability and sugar content of potatoes and decay by Erwinia carotovora var. atrosepticaand Fusariumroseum var.sa9b34cinum. Am. Potato J. 53:191-204. (Prepared by W. J. Hooker)
Part I. Disease in the Absence of Infectious Pathogens Somatic mutations arc of economic importance in clonally propagated potato because they may modify foliage type, tuber shape, or color of plant parts; delay maturity; and reduce crop yield. Whether yields and tuber shape are affected or not, variations are undesirable because foliage type and growth habits are principal features used to identify cultivars. A change as simple as an excess or loss of foliage vigor will cause doubt as to cultivar identity. Wildings These differ from normal plants by low growth, close bushy habit, numerous thin stems, reduced numbers of leaflets, large rounded terminal leaflets, almost complete absence of flowers, and increased numbers of stolons with numerous small tubers that produce many weak sprouts during storage. Yields are reduced severely by this abnormality. The small tubers may reduce the total weight of the crop by as much as 50%, but :ubers of table stock size are particularly affected and, in quantity, may reduce the weight by as much as 80-90%. Feathery Wildingr Feathery wildings bear no rese "blance to true wildings except that, compared to normal plat they produce more thin stems and many more small tubers. Plants closely resemble the normal, but the top leaflets are small, narrow, and pointed. In some cultivars, tubers have numerous eyes clustered at the apical i' d, producing many small, thin sprouts several weeks earlie? i an normal. Yield reductions from this disease are similar to those from the wilding abnormality. Giant Hill Plants (Plate I) have greater height and stronger, more vigorous vines, with leaflets smaller and often coarser and thicker than those of normal plants. Tubers sprout late and plants are late in maturing, which can result in reduced yields. They have flowers and fruits in profusion and large matted roots and numerous long stolons. When allowed to mature, they produce larger and coarser tubers than do normal plants. Giant hill plants survive late blight for three weeks longer than do normal plants. Because of its late maturity, this variant is most serious in crops of early cultivars. Although giant hill occurs in most commercial cultivars, it can be rogued with ease. However, the current practice of early foliage destruction of certified seed crops, before all giant hill plants are obvious, is probably responsible for their regular appearance in some stocks. Tall Types These are intermediate between giant hill and normal plants, Genetic Abnormalities being a little taller, more vigorous, and two or more weeks later in maturity. Like the giant hill, the tall type is not apparent until full vine growth and may affect up to 3% in certain cultivais. Giant hill and tall types are more frequent in the long days of higher latitudes than in lower latitude short days. Maximum yields are rarely obtained, however, because when the normal crop plants are ready to be harvested, giant hill and tall type plants are still immature. Given sufficient time for full maturity, giant hill plants may actually outyield normal plants. Other Variations Many other abnormal types of plants or plant parts too numerous to detail may occur in commercial crops. Examples are most russet-skinned variants (Fig. 6) and multiple-leaf, dahlia-leaf, raspberry-leaf, coarse-leaf, little-leaf, and stitchedend variants. Nature of Variations Most of the abnormalities described above are periclinal chimaeras caused by genetic changes, usually in the outer layers of tubers or stems. Normal plants may be recovered by excising tuber eyes and permitting growth to develop from the deeper t . a Fig. 6. Russet skin somatic mutation, in a white tuber, initiated near the stolon tip early in tuber enlargement, possibly a chimaera. 7
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: +q I B Fig 4. Natural openings in a
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 and 94:
penetration, and subsequent disease
Page 95 and 96:
have been demonstrated, including t
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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
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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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