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

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shows PSTV nucleic acid produced by all strains of PSTV as a band additional to those in healthy plants. Epidemiology Transmission is largely mechanical. principally by man himself and to a lesser extent by chewing insects. Eidence that sucking insects are involved is inconclusie. This is one of the few potato diseases transmitted readily by pollen and true seed. Other Hosts About two to three weeks after inoculation of L'copersicon esculentut with severe strains, new leallets show marked rugosity, epinasty. and down-curling (Fig. 951)). Internodes become shorter, forming a rosette or bunch\- top. Later veinal necrosis can become very severe. With mild strains, syvmptorns are slight epinasty and stunting. Bunchy top is increased in continuous light of 1,000 FC or more. Mild strains temporarily cross-protect against later inoculation with severe strains, and the reaction calr be used to demonstrate the presence of mild strains in otherwise syrnpton less plants. Scopolia sinensis responds with dark brown, necrotic local lesions in two or three weeks and later with systemic necrosis (Fig. 95C). Severe strains cause symptoms earlier than do mild strains. Optimrium conditions are rnanganese-rich soil nutrition. 18-23'C' incubation in not over 300-400 FC of light. preinoculation shading, and inoculuri in 0.05,1f K 2 H P04, pH 9.0, buffer. Certain insecticides severely impair local lesion formation. Many plant species belonging to most genera of the Solanaceac are syiptomlessly infected. PSTV also infects members oftbe Amaranthaceae, Boraginaceae, Campanulaceae, Caryophyllaceae. Compositac, Convolvulaceae. Dipsaceae, Sapindaceae. Scrophulariaceae, and Valeriaceac. Control I) Use seed tubers known to be free from PSTV, such as government-inspected certified seed. 2) Avoid mechanical transmission by planting whole, rather than cut, seed, and avoid leaf contact by equipment in field operations. 3) Decontaminate knives and other equipment by dipping them itt or \\aishin tlttu \\ilhi odium h.tpocltlorite 11 ).25I ol calciiih l\hpochloritc 11.1 ,1. 4) Roguing of diseased plants in seed fields is ineffective because of indistinct plant symptoms. 5) Plant seed fields with whole (uncut) tubers and wide spacing for large tubers or by the tuber unit method: the latter aids in disease identification but introduces the danger of transmission during cutting. Selected References )IENER. 1. 0.. and A IIAI)II)I. 1977. Viroids. Comp. Virol. 11:285-337. DIENER. T. 0.. and W. I3. RAYMER. 1971. Potato spindle tuber 'virus.- No. 66 in: I)escriptions of Plant Viruses. Coin on . Mycol. Inst.. Assoc. Appl. 13iol.. Vey. Surrey. England. FERNOX\. K. H. 1967. Toinaitoas a test plant fordeteciing mild strains ol potato spindle tuber \irus. Phytopathology 57:1347-1352. McCI,.'AN. A. P. I). 1948. Bunchv-top disease of the tornliat: Additional host plants, and the transmission oi the \irus through the seed of infected plants. S. Afr. Dep. Agric. Sci. Bull. 256. 28 pp. MORRIS. 1. I.. and N. S. WRI(ilII. 1975. l)etection on polyacrylarinide gel of a diagnostic iucleic acid Ironi tissue inIected with potato spindle tuber siroid. /\il. Potato .1. 52:57-63. SINGH. R. P. 1973. Experimental host range of the polato spindle tuber "virus. An. Potato .. 48:262-267. SINGI. R. P.. R. E. FINNI E.and R. If. HAGNAII.. 1971. lossesdue to the potato spindleItuber \irus. Ani. Potato .1.48:262-267. YANG. T. C., arnd W. .1.1100K ER. 1977. Albinism of potato spindle tuber viroid-inlected Ruitgers totmato in continuous light. Amn. Potato .1.54:519-530. 90 (Piepared by R. '. Singh and K. H. Fernow) Sugar Beet Curly Top Virus Curly top. caused by the sugar beet curly top virus (BCIV), mvssol thlrough the pota to plant and isapparently uotnc littemp onc Current season syrptoms consist of dwarfing. yellow,ing. elongation, and upward rolling of tie midrib of terminal leaflets, leaflets near the gro\ing point ha\e marginal yellowing, elongation. cupping, rolling. twisting. bulging, and roughness ( Fig. 96). lu her-pcrpet uated sv nptorns are extremely \ariaible. Tubers from infected plants may produce healthy appearing plants. sproits delayed in emiergence or failing to emerge, (r sprouts having extremely short shoots \with unmottled lea\es ranging from dark to light green and yellow. The green dwarf symptom consists of shoots dela" ed in emergence with leaves failing to unfold completely aInd remaining stiff and erect. As stenis elongate, they stav stiff and erect, with the growing point pinched together. Symptorsare remarkab!y similar to certain svmptoris of the mvcoplasma vellows disease and therefore ma\ ha\e escaped identification. Transmission in nature is ,,y the leafhopper. Circul~ir (Neoliturus) tenelu.s, in which the virus is circulati\e. Selected References BENNI: . C. W. 1971. The curly top disease (i stigarber and other plants. Monogr. 7.Am. Phytoparhol. Soc.. St. Paul, MN. 8t pp. GARDNER. W. S. 1954. Curly top of the potato in tIah and its possible relationship to hayvwire." Plant l)is. Rep. 38:323-325. GII))NGS N. .1. 1954. !ioie studies of curl\ rop on potaloes. Plhytopatlology 44:125-128. STOKER, G. I... and 0. S. CAN)NON. 1962. Ctirrent-season arnd tuber-perpetuated s.ni ptonis o! portaro cirly it)p. Plant I)is. Rep. 46:176-180. (Prepared by W. .I. Hooker) Fig. 96. Sugar beet curly top virus, showing leaf rolling and dwarfing, (Courtesy N.J. Giddings, from Bennett, C. W., 1971)
The "yellows" types of disease, characteristic of mycoplasma infections that have been studied in some detail possess rather broad host ranges. Some have been reported to infect potato in the field or have been transmitted to potato experimentally. Unfortunately, disease symptoms in the potato itself are hardly of diagnostic value except to distinguish two large groups of agents, those causing the aster yellows and the witches' broom types of disease. Mycoplasma-like organisms (M 1.0). formerly considered viruses with somewhat unusual characteristics, were first demonstrated in plants in 1967 by electron microscopy. Actual proof that MI1.0 cause disease in potato is needed by Koch's postulates, although the presence of MLO in plant tissue constitutes the best evidence so far available. More accurate methods of differentiating between these pathogens are urgently needed, particularly because potato is a relatively incompatible host. None of these diseases is contact-transmissible. Grafting is often used for experimental transmission. All of the pathogens rely on leaflioppers for transmission and dispersal, and their occurrence and distribution is determined by lealfiopper activity. Variations in symptomatology, host range, or vector relations of different source materials of each disease suggest that strains of these pathogens occur. Symptoms and M I. may be suppressed by antibiotics of the A7 Mycoplasmas tetracycline group. and individual plants may be cured by heat therapy. Aster Yellows and Stolbur Aster yellows and its allied diseases occur worldwide. Stolbur is found in Europe, tomato big bud in Australia, purple top roll in the Indian peninsula of Asia, and parastolbur and metastolbur in Europe. In the western hemisphere, aster yellows has been variously called purple top wilt, yellow top, bunch top. purp!e dwarf, apical leafroll. haywire, latebreaking virus, blue stem, and moron. Symptoms Upper leaflets roll and develop purple or yellow pigmentation (Plate 77). Aerial tubers are common, and occasionally some proliferation of axillary buds occurs (Plate 78). Often only a single stem in a hill isaffected. Plants are often stunted and may die prematurely(Fig. 97A and B). Under field conditions, lower stems frequently develop cortical necrosis, shredding of tissue, and vascular discoloration. At harvest, an affected hill usually has some normally mature and some immature tubers. In stolbur, flaccid (gummy) tubers Fig. 97. Aster yellows mycoplasma in potato: A, primary symptoms; B,advanced wilting of stolbur in left stem with stem at right unaffected; C, aster yellows mycoplasma in infected tissue of aster (electron microscope photograph, bar represents 1pm. (A and C, Courtesy N. S. Wright; B,courtesy V. Valenta) 44; 91
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, ,. ,o . ; , . o , . r. , -' .L ,
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Compendium of Potato Diseases W. J.
Page 5 and 6:
In memory ofimy respected colleague
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Acknowledgments Planning Committee
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Introduction 1 Potato Disease 1 The
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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
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the air temperature when tubers are
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iiO A B 'D C Fiq. 14 Second growth:
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identifying tissue bruised by black
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Internal Sprouting multiple sprouts
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conditions permits normal leaf deve
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Epidemiology Oxidant injury is pres
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sevritof stnting, chiorosis. loss o
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Selected Reference brown to bronze
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Part II. Disease in the Presence of
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should be planted on land with at l
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Control I) Use disease-free tubers
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FOI-SO M. D, and I. A. FRIEDMAN. )9
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Fungi Powdery Scab liberating powde
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Histopathology Sort of sporangia de
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any time but generally occurs late
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'40 ff .. . '1 f . ."L', . '1 .,. "
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A \, 2) Powdery mildew is rarely a
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R., Inst.. Kew. Surrey. ngland. 609
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TORRES, H.. E. R. FRENCH, and I.. W
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d AC D A 0 Fig 53 Gray mold. A, Bot
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strands of pigmented hyphae. Sclero
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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: Control 1)Avoid locations in wkhich
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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Compendium of Potato Diseases - (PDF, 101 mb) - USAID

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