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

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Disease Cycle P. er t/lro.sptica is soilhorne and endemic in many soils, Zoospores, sporangia, or oospores may serve as inoculum, but oospores are probably the significant propagule in pathogen dissemination and survival in soil. Plants of all ages are susceptible, but the disease is most frequently observed in mature plants approaching harvest, Epidemiology Disease develops in soils approaching saturation from poor drainage or excessive precipitation or irrigation. l.arge amounts ofdecomposing plant residues in soil enhance waterabsorption, retention, and disease incidence In wet soil, the disease develops overa wide range oftemperatures but is most severe between 20 and 30' C. Other Hosts Although I'. erth'irosepti'ahas been reported as a pathogen only on potatoes and tulips, it has been recovered from the roots of 17 nonsolanaceous plants, including wheat and rye. Control I) Plant seed tubers in soils with good drainage, 2) Avoid excessive irrigation late in the growing season. Selected References GOSS. R. W. 1949. i Inyk rot of poaioes caused by Hll.1i.tfora £'rtroWIi- 1thN . Neh. Agric. T Fxp. Sin. Re. Bull. 160. 27 ROWE, E.C.. and A.F.SCHlMIlTlHlNNlER. 1977. Potato pink rot in Ohio caused hy /'htropilthora ertihro. i/c'T 1(In I'. rrptogea. plant Dis. Rep. 61:80t7-81t0. STAMPS, 1).J. 1978. 'hoitop/hihoraerrth-.7pti(a. No. 593 in: t)escriptions of IPaihogenic hungi and Bacteria. C'mmonw. Mycol. Inst.. Kew. Surrey, l-ngland. 2 pp. VARGAS, I.. A.. and .. W. NIELSEN. 1972. I'hvtoph/hora rithro.T'apOtt. ini'Peru: Its identilication and pathogenesis. Am. WAtI.R IOUSE. . 1963. Key to the species of I'hthra Ie WarS. No. 92 in: M'co. Kipers ommo,,. Mycol. Inst.. Kew. Surre ' Eingland. 22 pp. (Prepared by R. C. Rowe and L. W. Nielsen) Late Blight Late blight is probably the single most important disease of potatoes worldwide. It is destructive wherever potatoes are grown without fungicides, except in hot, dry, irrigated areas. The Irish potato famine" of the 1840s was caused by PIeqopititorainfisians, the fungus that causes late blight. Immense quantities of fungicides are applied to potatoes throughout the world for protection against P. inf'sian. Symptoms moisture, Leaf lesions light are intensity, highly and variable, host cultivar. depending Initial on smptomsare temperature, typically small, pale to dark green, irregularly shaped spots. Under favorable environmental conditions they rapidly grow to large, brown to purplish black, necrotic lesions that -ay kill entire leaflets and spread via petioles to the stem, ev, .itually killing the entire plant. A pale green to yel!ow halo is often present outside the area of leaf necrosis (Plate 28). Under moist conditions, a white downy mildew of sporangia and sporangiophores appears at the edge of lesions, mostly on the underside of the leaves (Plate 29). In the field, plants severely affected with late blight give offa distinctive odor. This odor actually results from rapid breakdown of potato leaf tissue and also follows chemical vine killing, frosts, etc. Positive identification of late blight requires confirmation of sporangia and sporangiophores either on lesions in the field 40 under moist conditions or on leaf or tuber lesions incubated in a moist chamber. On susceptible cultivars, exteriors of infected tubers show irregular, small to large, slightly depressed areas of brown to purplish skin (Plate 30). A tan-brown, dry granular rot characteristically extends into the tuber approximately 1.5 cm, the depth varying according to length of time after infection, cultivar, and temperature. The boundary between diseased and healthy tissue is not clearly defined; delicate, brown, peglike extensions penetrate to variable depths. Under cool, dry storage conditions, tuber lesions develop slowly and may become slightly sunken after several months. Secondary organisms (bacteria and fungi) often follow infection by '. it/i,stans, resulting in partial or complete breakdown of tubers and complicating diagnosis. Causal Organism Phytoplithora infi 'sans(Mont.) de lary has sporangia (conidia) that are hyaline, lemon-shaped, thin-walled, and 21-38 X 12-23 mm in size. Each has an apical papillum (Fig. 45C). Sporangia of P. infestan.s are borne on the tip of a sporangiophore branch (Fig. 45A); as it elongates, the sporangiophore swells slightly and turns the attached sporangium to the side. The sporangiopore is thus characterized by periodic swellings (Fig. 4513) at points where sporangia were produced. Sporangia may germinate by means of a germ tube (Fig. 45E), but most commonly they form about eight biciliate zoospores (Fig. 45D) that swim freely in waterand encyst on solid surfaces. i'ncysted zoospores can germinate by germ tubes that enter thhotvalfsomabtualyanpreoiu isomd the host via leaf stomata, but usuallyanappressoriumisformed and penetration hyphae enter directly through the cuticle. Once inside the plant, the nonseptate mycelium is intercellular and intracellular by means of haustoria (Fig. 45G) that extend into cells. Sexual reproduction resultsin oospores(Fig. 45F) formed by the union of oogonia and antheridia. Oospores within oogonia are 24 -46 pm in diameter and germinate via a germ tube with a terminal sporangium, which, in turn, either liberates zoospores or forms another germ tube. Disease Cycle Oospores in nature have been found only in Mexico, where both mating types (A 1 and A.) occur. Leaves touching the soil are often infected first, suggesting that oospores probably playa role in the survival of P.itnrestarisunder adverse conditions. In tropical areas where the crop is grown all year, overwintering of R itirestars is not an important consideration. However, where distinct seasons occur, P. ittf'stans overwinters as on mycelium farms or in near unharvested commercial tubers, storages, tubers or dumped tubers in stored cull piles saved for seed. After plant emergence, the fungus and invades a few of the growing sprouts and sporulates under moist conditions, producing primary inoculum. Once primary infection has occured, further spread of P. inl.san. takes place by airborne or waterborne sporangia (Fig. 46). of Tubers succulent on tissue cull piles that frequently are easily infected sprout and by form . it/.Vllns dense masses frotm diseased tubers. spores Spoi ulation within the foliage mass produces pr digious numbers f sp res to infect nearby fields. Epidemiology Tubers, particularly those inadequately covered by soil, may be infected in the field by spores that have been washed from infected leaves into the soil by rain or irrigation. Rapid tuber growth frequently causes soil to crack, exposing tubers to infection. Tuber infection may also occur during wet harvest conditions via contact between ttibers and sporangia on vines or via airborne sporangia. Little, if any, spread of P itiA,stans occurs under optimum conditions in storage. Field infection is most successful under cool, moist conditions. lowever, infections take place over a range of environmental conditions, and high temperature strains of the
'40 ff .. . '1 f . ."L', . '1 .,. " . .. ;, B C .. :-,I -, .141 Fig. 45. Late blight. Phytophthora Infostans: A, sporangiophore; B, sporangiophore branch showing swellings at successive sites of sporangium formation; C, sporangia, germinating by zoospores (D) and germ tube (E=);F, oospore with antheridium; G, haustoria within tuber cells Bar in A represents 50 pm. hars in D. E. and G represent 10 pm. (F. Courtesy of Plant Pathology Section, West Virginia University) 41
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: any time but generally occurs late
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
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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