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

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Epidemiology In the United Kingdom, higher than average soil temperatures (20-24' C) during crop growth keep '. e.vi gi var. /iolait inoculum levels low. However, wet soil conditions, night frosts, or low day temperatures (less than 12' C) around harvest time and low storage temperatures (2-00C) following lifting, grading, or handling all increase gangrene incidence. laty in Is II haulm destruction of seed crops or in harvest of both seed aind market crops encourage soilo inthe a inoculum otat bsece hot. buildup i 'xgiw in the soil. ar.periderm In field soils intle absence of a potato host, n .isoua var. li,\a[ usually becomes undetectable by present isolation or baiting techniqles after 1s moths. whereas !'e.iguu var. i,,U is (letectable in most soils. Otier losts 1'.vx.iua var. exi,u occurs oil various parts ofa wide range ofiplants. I.e.xIi,ua var./0 'eaia occurs mostly on potato but has occasionally been found on weed species growing in potato lields. Control I)Avoid highly susceptible cultivars, damage to the tuber skin, and exposure to low temperattires, especially after damage. 2) Burn vines and harvest tubers as soon as practical. Hold tubers at 18-20' C for one week to permit wound healing. 3) Disinfect tubers with organic mercury dips (where permitted), by fumigation with 2-aninobutane, or by mist sprays of thiabendatole within three weeks of harvest. Selected References BOI'REMA. G. II. 1976. the Phonia species studied in culture by I)r. R. W. G. )ennis. Itr.Mycol. Soc. Trans. 67:289-319. BOYI) A. E.W. 1972. Poiato storage diseases. Rev. Plant Pathol. 51:297-321. LOGAN, C.. R. It. COPEIANI), and G. I..ITE. 1975. Potato gangrene control by ilt ra low volurme sprays of thia bendaole. Ann. AppI. Biol. 81):199-20)4. AB (Prepared by C. Logan) t 4• Fusarium Dry Rots Fusarium dry rots are found on potatoes worldwide. Symptoms After This disease about one affects month tubers of storage, in storage tuber and lesions planted at seed wounds tubers. are visible as small brown areas. Infection slowly enlarges, and visibeam over the rowareaion lesion sinks and s wrinkles. lowlyoenires sometimies in nd concentric rings, as the dead tissues dr' out Wig. 64). Fungus pustules containing mycelia and spores may emerge from the dead periderm. Rotted tubers shrivel and become mummified (Plate 46). Internal necrotic areas are shades of brown from fawn to dark chocolate. with the advancing margin faint for lighter shade!, and distinct for darker shades. Older dead tissues assume it variety ofcolors, develop .:'v.ities lined with mycelia and spores, and are dry and punky in texture (Pltte 47). When relative humidity in storage is saturated or approaching saturation, I:ruiniaspp. are frequently secondary Fig. 64. Fusarium dry rot wound infection from storage. Note periderm wrinkling over rotted tissue and internal cavity. (Courtesy L. W. Nielsen) Fig. 65. A,Fusarium seed piece decay after two weeks at 13'C, showing pits on cut surfaces and mycelium growing in pits. B, Periderm removed from surfaces exposes rot from several infections. Comparative plant growth from healthy seed piece (C)and Fusarium decayed seed pieces (D and E). (Courtesy L. W. Nielsen) 58 .
invaders through the IFusarium lesions and rapidly rot the reinainder of the tuber. Suspended bacteria and juices exuded from the soft rot endanger surrounding tubers. Whole-tuber seed becomes infected through wounds during storage or preparation for planting. The cut surfaces of large seed tubers are major infection courts. In stored seed tubers, brown to black flecks appear on the cut surface in about one week and depressions or pits form in two weeks (Fig. 65A and B). Mycelia often grow on the depressed surfaces, and undet humid conditions, depressions may become slimy and black from bacterial growth. Soft rotting bacteria may also invade through the IFttsarium lesions and accelerate decay. With numerous cut-surfacc infections, lesions coalesce: the seed piece rots from the surface inward: and buds (eyes) are destroved as decay progresses. In the field, the shriveling of infected seed tubeis and pitting of infected pieces may not he evident. The surface over the lesions is brown, and the underlying necrotic tissues have fewer cavities. Necrotic tissue may attract soil insects and larvae such as the seed-corn maggot, which is avector of Erwiniaspecies. In wet soils, these species often enter as secondary pathogens. Fusarin spp. alone or in conjunction with Erwinia spp. partially or completely destroy the seed piece, resulting in extreme variability in plant size and manl, missing plants (Fig. 651) and E). Often single ;prots emerge: these are small, grow slowly, produce few marketable tubers, and have a high incidence of blackleg. Causal Organisms 1usariun solani (Mart.) App. & Wr. emend Snyd. & Hans. 'Coeruleum and 1.ro'seum (l.k.) Snyd. & Hans. 'Sambucinum' are most frequently implicated in seed piece decay. In sonic regions one species is dominant over the other, nut both are often associated with a seed stock. I. solani is most frequently encountered and is the more aggressive pathogen. Both grow and are maintained ott potato-dextrose agar, and the acidified medium facilitates their isolation when bacteria are present. F roseu'um grows more rapidly, forming athin, white mycelial mat and abundant pink to salmon spores. The slower growing . soani forms a denser, white mycelial mat that exhibits a purple pigment with age (Plate 48). F.slthnisporulates in culture more sparsely than does I-'. rosetun (Fig. 66). The optimum temperature for growth in culture is 20-25°C and for infection, 10-20" . 1:.roseum 'Avenaceum' also causes adry rot of potatoes, but less frequently than the other species do. Histopathology Fusariumn spp. cannot infect intact tuber periderni or lenticels. Cuts and periderm-breaking wounds incident to harvesting, storage, grading, and transport are the major infection courts. Wounds from insect and rodent feeding and frost are sometimes infected. The Fusaria can also invade surface lesions of powdery scab, late blight, mop top virus, and possibly other di:,eases. Hlyphae are at first intercellular becoming intracellular in dead cells. In spreading lesions, hyphae may be sparse in intercellular spaces, with host cells :',owing little reaction to the fungus. Toward the center of the lesion, less intercelluar starch spaces is by present, suberin audnt deposited abe inhostcellwalsaandnt nfetoh and the myceliuni. usually abundant, may be confined to the intercellular spaces. In susceptible tissue, starch hydrolysis and suberin deposition are lacking. Small lesions restricted near the site of infection may be underlaid by a continuous layer of wound meristem cells with suberin deposition. With other isolates, hyphae kill and penetrate cells within two cells of normal-appearing tissue. Details of the reaction depend on the pathogen, the resistance of the tuber, and the part of the lesion examined. Disease Cycle Fusariumspp. can survive for several years in field soil, but the primary inoculum is generally borne on seed tuber surfaces. Surfaceborne propagules contaminate containers and equipment used in handling or storing potatoes and enter wounds incident to handling seed tubers. Infected seed tubersand pieces decayand infest the soil that adheres to the surfaces of harvested tubers. Epidemiology Tubers of potato cultivars differ in susceptibility to F. solani and F roseum, but none tested was immune to either pathogen. Certain cultivars are tolerant to both. Tubers are tolerant to infection when harvested. Susceptibility increases during storage and ,:aches its maximumin early spring about planting time. Wound healing can reduce infection. Deposition ofsuberin in the cell walls does not prevent infection, but wound periderm does. Wound periderm forms in three to four days at approximately 21°C with adequate aeration and humidity but more slowly at lower temperatures. At 15'C, near optimum for infection, a period of approximately eight days is required to form periderm; wound healing is not effective at this cr lower temperatures. Dry rot develops most rapidlyin high relative humidityand at 15-20' C. Relative humidities about 70% do not alter rot development, but lower iiumidities retard infection and disease development. Disease development continues at the coldest temperatures safe for potatoes. If the soil temperature and moisture are suitable for rapid sprout growth and emergence, seed tuber or piece decay after planting maybeoflittle consequence. Conditioning seed tubers from cold storage at 20-25' C for one week before cutting pieces reduces decay and accelerates sprout growth. Holding contaminated cut seed several days or weeks before planting or planting in soils too cold or dry for prompt sprout emergence and plant growth will accentuate losses. Excessively wet soils after planting increase secondary infection by Erwinia spp. Other Hosts F. solani isolates from Colocasia corms can infect potato tubers. Generally, tuber-rotting Fusaria do not infect other plants or plant organs. Resistance Differences in resistance exist among potato cultivars. Relative ranking of resistance isinfluenced by the Fusarium sp. used for inoculation. Seed lots infected with potato virus X are relatively more resistant than those free from the virus when harvested within three weeks of top kill. Control 1ontrm I) For storage and seed purposes, harvest tubers from dead vine 2) Use all precautions with machinery and equipment to 171V' I, . __ V.. " ,,00 , .)'. . - Fig. 66. Fusarium solani from culture with many macroconidia and a single microconidium in center. (x950) (Courtesy P. E. Nelson) 59
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, ,. ,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
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Fig. 1.A, Lower portion of young po
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+q I B Fig 4. Natural openings in a
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Part I. Disease in the Absence of I
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more heavily in the vascular region
Page 21 and 22:
the air temperature when tubers are
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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
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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: obovoid, and 14-30 X 5-10 pm. Pycni
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
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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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