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

More documents

Recommendations

Info

S. ~active Epidemiology Overwintering is by sclerotia on thc surface of tubers or in plant debris in the field. T he pathogen does not appear to bean soil inhabitant, but it may survive in soil for long periods. C. atrameniariumn, generally regarded as a low grade pathogen ,,I " k ._ 'i.+ i,!temperatures, that attacks under conditions of stress, commonly acts in comrelative bination importance with one or difficult more additional to determine. pathogens, Black dot making is most its frequently associated with light sandy soils, low nitrogen, high and poor soil drainage. tl Because C. atranwntariumis elusive and lack ofrecognition is frequent, very little work on disease control has been done. Other Hosts AIn additional to potato, the fungus occurs on tomato and other plants in the Solanaceae (eggplant, pepper, tomato), on weed hosts such as Physalis peruiviana, and, with inoculum increase, on lDandra .stranonium. a common weed. Control I) Clean seed, crop rotation, adequate fertility, and good irrigation management are commonly recommended. 2) No known potato cultivar offers resistance. SSelected References ~~DA V I S, . R., and M. N. 1-1OWA RD.1976. Presece cof Colh'totri(-hum atramentariumn in Idaho and relation to Verticillium wilt (V'erticillium dahliae). Am. Potato J. 53:397-398. DICKSON, B. T. 1926. The "black dot" disease of potato. Phytopathology 16:23-41. HARRISON, D. E.1963. Black dot disease of potato. J. Agric. Victoria 61:573-576. McINTYRE, G.A.,and C. RUSANOWSKI. 1975. Scanning electron microscope observations of the development of sporophores of Colletotricu/n atramentarium(B. etBr.) Taub. on infected potato periderm. Am. Potato J. 52:269-275. STEVENSON, W. R., R.J. GREEN, and G.B. BERGESON. 1976. Occurrence and control of potato black dot root rot in Indiana. Plant Dis. Rep. 60:248-251. THIRtJMALACHAR, M. J. 1967. Pathogenicity of Colleotrichun atranwntarium on some potato varieties. Am. Potato J.44:241-244. (Prepared by J. R. Davis) .-.+/i , '. , . . " .Charcoal Rot - " .The fungus is worldwide but economically important only in warra regions where soil temperatures exceed 281C. T , Symptoms Under hot conditions, the pathogen can attack potato stems '" , and cause a sudden wilt and yellowing. Stem infection is not usually important. More important is tuber attack, which may occur before harvest and in storage, causing loss of the entire crop. Early symptoms develop around the eyes, near lenticels (particularly those that have enlarged), and frequently at the stolon attachment. The skin appears unaffected at first, with underlying tissue, usually that within I cm of the surface, becoming slightly water-soaked and light gray. Cavities filled with black mycelium and sclerotia form later. Rapidly invaded tubers, when cut, exhibit semiwatery, flabby breakdown, with color changing from yellowish (Plate 44) to pinkish to brown and finally to black. Wet rot may later develop from secondary invaders. 9Causal Organism D The pathogen isMacropltoninaphaseoli (Maubl.) Ashby Fig. 62. Black dot: A, on potato root; B, portion of typical (syn. Al.phase'olina(Tassi)Goid., Sc h'rotiumbataticolaTaub.). Colletotrichum atramentarium colony growing on nutrient Na- Sclerotia within roots, stems, leaves, or fruits are black, smooth, polygalacturonic acid medium; C, cross section of acervulus hard, and 0.1-1 mm in diameter. They are smaller in culture. showing setae and conidia arising from acervulus; D, spores Pycnidia, dark brown on leaves and stems, are 100-200 pm in approximately 3.8 x 17.5 um. (Courtesy J. R. Davis) diameter. Single-celled conidia are hyaline, ellipsoid to 56
obovoid, and 14-30 X 5-10 pm. Pycnidia production in culture is rare except on propylenc oxide sterilized leaf tissue in agar. Epidemiology The fungus maiatains itself saprophytically on unthrifty or senescent plant partsand survives unfavorable periodsas microsclerotia. Pycnidiospores are relatively short-lived. Tubers are infected through wounds, eyes, enlarged lenticels, and the stolon. Tubers are predisposed to infection at temperatures of 320 C or higher. Rot development is restricted at low temperatures, slow at 20-25'C, and most rapid at 36'C and above. No secondary spread is apparent during storage, but infected tubers rot in warm storage. Rot stops in refrigerated storage, but when tubers are returned to warm temperature, the rot continues. Thus, seed from cold storage should be warmed before being planted so that infected tubers may be removed. Most commercial cultivars are equally susceptible. Resistance exists in certain Solanum chacoense clones, in some of its hybrids, and in hybrids of the series Commersoniana. Other Hosts The fungus has been found on underground parts of an extremely wide range of plants, both cultivated and wild. Control I) Harvest early, before soil temperatures become high. 2) Avoid bruising and wounding of tubers in harvest and postharvest handling. 3) Field irrigation may be useful to prevent excessive soil temperature. 4) Do not leave tubers in soil after plants have matured. 5) Do not harvest during periods in which soil temperatures exceed 28' C. 6) Do not store tubers at high temperatures, 7) Do not use seed originating from areas where the disease is frequent. Selected References IIJARGAVA, S. N. 1965. Studies on charcoal rot of potato. Phvtopathol. Z. 53:35-44. GOTII, R. W., and S.A. OSTAZESKI. 1965. Sporulation of Macroplominaiphaseolionpropylene oxide-sterilized leaf tissues. Phytopathology 55:1156. IOI.LIDAY, P., and E. PUNITIIAI.INGAM. 1970. ,tfacrophonina phaseolina. No. 275 in: Descriptions of Pathogenic Fungi and Bacteria. Cornnionw. Mycol. Inst., Kew, Surrey, England. 2 pp. I1tSlKARNATIIi. 1976. Potato in Sub-Tropics. Orient L.ongman, SAIIAI, ).eB. DJI, and K. D. PAIIARIA. 197t). Reaction of sonic wild and cultivated potato varieties to charcoal rot. Am. potato J.47:427-429. TIIIRUMAI.ACIIAR, M.J. 1955. Incidence of charcoal rot of potato in Bihar (India) in relation to cultural conditions. Phytopathology 45:91-93. von AMANN. Ni. 1960. Untersuchungen Uber einen sklerotienhildenden Pil an Kartoffeln. vermutlich Sclerottiuo hataticola (Taub.), synonyn Macrophotina phaseoli tMaubl.) Ashby. Z. Plianienkr. Pflanzenschutz 67:655-662. (Prepared by L. J. Turkensteen and W. J. Hooker) Gangrene The pathogen Phoma exigua var.foveata was first described in 1940 and is now prevalent in most northern European countries and parts of Australia. P. e'xigua var. exiguaoccurs in most European countries, Russia, the United States, Canada, and Australasia. Symptoms Small dark depressions develop in the tuber skin, usually at wounds, eyes, or lenticels, and may enlarge to form "thumbmark" or larger, irregularly shaped, sharp-edged lesions, the surface area of which isoften unrelated to rot depth. Internally, diseased tissue is well defined. Rots caused by Phoma exigua var..ioveata are usually extensive and dark brown or purplish (Plate 45), with variously shaped cavities; those caused by P. evigta var. cxiguaaresmaller, become restricted, and are usually black with small cavities. Pycnidia may form singly or in clusters on lesions or in the mycelium that lines cavities. Infrequently, lesions may be only of skin thickness, becoming extensive, dark, and irregularly shaped; this condition is termed skin necrosis. Causal Organism Either of two varieties of Phoma exigua Desm. may cause gangrene. rheprincipalcauseis P. t'xiguavar./o'eata(Foister) Boerema (syn. P. foveata Foister; P. solanicola f. foveata (Foister) Malcolmson; P. exigua Desm. f. sp.foveata (Foister) Malcoimson & Gray). The more ubiquitous but weaker parasite is P. exigua Desm. var. exigua (syn. P. solanicola Prillieux & Delacroix; P tuherosa Melhus, Rosenbaum, and Schultz; P. exigua Desm. f. sp. exigua Malcolmson and Gray). The two fungi have similar morphological characteristics. Pycnidia are usually globoid (90-200 pm) and dark brown to black. Initially subepidermal, they become erumpent and extrude hyaline, nonseptate, cylindrical pycnidiospores (4-5 X 2-3 pm). In culture on 2% malt agar, P. exigua var.foveata (having nonzonate colonies) is readily distinguished from P. exigua var. exigua (having zonate colonies) (Fig. 63) by its production of anthraquinone pigments that turn red within seconds on exposure to ammonia vapor. Disease Cycle Infected orcont;ninated seed tubers produce diseased stems, in which infection remains latent during the growing season unless the stems become moribund. Pycnidia appear in sporadic groups, usually associated with nodes, as stems begin to senesce either naturally or through chemical desiccation. Raindrops wash pycnidiospores into the soil and spread inoculum to neighboring plants. Rots in mother tubers usually continue active in the soil, produce pycnidia, and constitute another important source of inoculum for tubers at harvest. Before harvest, tuber infection may occur through eyes and proliferated lenticels, usually when soil moisture is high. Most gangrene, however, develops after harvest through damage to the tuber skin. Wounding introduces infection from contaminated soil on the tuber surface or stimulates development of the fungus already latent in the periderm. Wound infection may occur at lifting, grading, or at any time during handling. A B Fig. 63. Gangrene. Distinguishing characteristics: A, Phoma exigua var. exigua, zonate culture; B, Phoma exigua var. foveata, nonzonate culture, on malt agar. (Courtesy C. Logan; photographs by G. Little) 57
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 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: Symptoms Small, localized, light br
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
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
show all

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

Create successful ePaper yourself

Delete template?

Save as template?