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

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Therefore, control can concomitantly diminish incidence of mop-top. Other Hosts The fungus infects and completes its life cycle on other tuberbearing Solt/um spp. and on roots of nontuber-bearing S. nigrm L. and Nicotianarustica L. Other hosts that are infected without formation of resting spores include dicotyledons, monocotyledons, and a gymnosperm. Control 1) No completely adequate measures have been developed. Resistant cultivars are recommended, but no immune varieties are known, r ot 2) Crop rotations of three to 10 ,ears have been recommended, depending on climate and soil conditions. 3) Plant disease-free seed. 4) Crop in porous and well-drained soils, and avoid planting on hmnd known to be contaminated. 5) )o not use manure from animals fed infected tubers. 6) Fertilizers and other chemical soil treatment.s are generally not effective. Sulphur has given beneficial result!, bilt its use is limited because soil may be made too acid for optimum potato growth. 7) Soaking infected seed tubers in solutions of formaldehyde or mercuric chloride reduces seedborne inoculum. Selected Reference C(OOPER..1. I.,R.A.C..(ON.S, and B.I). HARRISON. 1976. Field and glasshouse experiments on the control of potato mop-top virus. Ann. Appl. Biol. 83:215-231). I IMS. I..I.. and I. F. PR lI('F.1975..lgo .lUhtrrranca.No. 477 in: Descriptions of Pathogenic Fungi and Bacteria. Commonw. Mycol. Inst.. Kew. Surrey, England. 2 pp. KAR .IN(..I.S. 1968. 1)nwderyv Scab of I')ot itoL5eand Crook Root of Watercress. Pages 180-192 in: .1.S.Karling, ed. The Plasmodiophorales. Ilafner Pub. Co., New York and London. KOILIE, A. P. 1954. A contribution to the knowledge of Spongospora .tllerra'a (Wallr.) L.angerh.., the cause of powdery scab of polatoes. lijdschr. Ilantcn/icktcn 60:1 05. KOIE. A. P.. and A. .. GIEIINK. 1963. The significance of the Moosporangial stag-_-in the life cycle of the Plasmodiophorales. Neth. .. Plant Pathol. 69:258-262. WENZI., If. 1)75. l)ie Bekiimpfung des Kartoffelschorfes durch Kulturmassnahmen. Z. Pflanzenkr. Pflanienschut7 82:410-440. (Prepared by C. H. Lawrence and A. R. McKenzie) Wart Wart has been recorded in Africa. Asia, Europe, and North and South America. In certain areas, disease spread has been contained through strict quarantine. Symptoms Warty outgrowths or tumorous galls, pea-sized to the size ofa man's fist, develop at the base of the stem. Aboveground galls are green to brown, becoming black at maturity and later decaying. Occasionally galls form on the upper stem, leaf, or Ilow~r. Belowground galls appearat stem bases, stolon tips, and tuber eyes (Plate 24). Tubers may be disfigured or completely replaced by galls (Plate 25). Subterranean galls are white to brown, becoming black through decay. Roots are not known to be attacked. Causal Organism .Sivfchittrimu endlohioticuint (Schilb.) Pere. does not produce hyphae but enters the host epidermis as a zoospore, swells to a prosorus, and develops into a sorus. Haploid sori form inside the cells, each sorus containing 1-9 sporangia. Resting or winter sporangia are golden brown, spheroidal, measuring 35-80pm in diameter. The thick sporangium wall is prominently ridged, 36 generally with three ridges confluent at two sides of the sporangium. Zoospores measure 1.5-2.2 /m in diameter, are pear-shaped, and are motile by a single posterior flagellum. The fungus exists in a number of physiologic races, making evaluation of resistance difficult. Zomsore reochesebd " Zo-,or penclrot1- Ecess,ve Grmlnoling potolocell celld ion p r O s o 0uS . .. . - zoo,e n cell / enlargement Sorus of ,... P ro 7 'Germmuhmg -es '-" 0zoSI,e emtCts ,,ln9 se tube, Sporongurm Molure Zyqole ,reoflanq siy3mPsckonrl ,ellc S pututo tuber "Zgoe '.,lmrooot mq Zoospores Fig. 40. Disease cycle of black wart caused by Synchytrium endobioticum. (Reprinted, by special permission, from Plant Pathology, 2nd ed., by G. N.Agrios. c,1978 The Academic Press, New York) . A . • W 0 0 N . n . Fig. 41. Synchytrium endobioticum winter sporangia (A, resting; B, germinating) range in diameter from 35 to 80 pm. (A,Courtesy M. E. Hampson; B, courtesy F. Frey) "
Histopathology Sort of sporangia develop in epidermal cells of meristematic tissues of growing points, buds, stolon tips, or young leaf primordia. Invaded and surrounding cells enlarge. Rapid cell division following infection from either zygotes or haploid zoospores causes an increase in meristematic tissue, providing additional infection courts. The gall is a malformed branch system largely composed of thin-walled parenchyma. In nearimmune cultivars, the warts remain superficial and scablike, whereas, in resistant cultivars, tilezoospore dies soon after invasion by necrotic abortion (hypersensitive reaction) of the infected tissute. Disease Cycle From the initial infection, summer sporangia form as membranous sacs, producing motile zoospores (Fig. 40). Zoospores encyst and penetrate epidermal cells of susceptible tissue approximately 2 hr after formation. After a developmental period, ioospores are released outside tileplant. These may reinfect surrounding meristematic tissue in a secondary cycle, or they may conjugate fortning a zygote that reinfects several cells deep, giving rise to the resting or winter sporangium (Fig. 41). Resting sporangia are released from galls through decay of host tissue. The fungus can survive in soil as resting sporangia for as long as 38 years, even through adverse conditions. Spread of inoculum is through soil-infested tubers, implements, containers, etc. Resting sporangia germinate erratically, producing zoospores. Epidemiology The fungus is most active where susceptible tissue is present in growing sprouts, stolons. buds, and eyes. Water is required for germination of winter and summer sporangia and for zoospore distribution. Cool summers with average temperature of 18' C or less, winters of approximately I60days of 5'C or less, and an annual precipitation of 70 cm are necessary for disease development, and disease is limited to such environments. Soil reaction is of less importance, with disease occurring in soil with pH from 3.9 to 9.5. Temperatures of' 12-24'C favor infection. S. endobioticum is reported to serve as vector for potato virus X. Other Hosts Potato isthe principal [lost, although S.enelohioticn has been experimentally transferred to a number of the Solanaceae. Roots and leaves are attacked, with resting sporangia developing sparsely. Tomato cultivars are particularly susceptible Plants other than potato are not believed to be of importance in specie the disease s show cycle. resistance Some to a South var iahle American extent. wild potato Control I) Worldwide control of spread is being attempted through quarantine legislation, 2) Resistant cultivars have been developed in Europe and North America. 3) No chemical control is known that is not also injurious to soil and crops. 4) [ie herbicide dinoseb ( 2 -sec-butyl-4,6-dinitrophenol) reduces infection to some extent. Selected References BRAUN. II. 1959. Rassenhildung der Kartoffelkrebs (Si'nch'triun 'ndoioticun).Kartoffelhau 10:234-237. CURTIS, K. M. 1921. The life-history and cytology of Sinchyitrium endoioticuni (Schilb.) Per., the cause of wart disease in potato. Philos. Trans. R. Soc. London Ser. 1 210:409-478. I1AM ISON, M. C.. and K. ;. PROII)FOOTl. 1974. Potato wart disease, its introduction to North America, distribution and control problems in Newfoundland. [AO Plant Prot. Bull. 22:53-64. KARIING, .1.S. 1964. Svnchytrium. Academic Press. New York. 470 PP. NOBLE, M., and M. D.GI.YNNE. 1970. Wart )isease of Potatoes. FAO Plant Prot. Bull. 18:125-135. (Prepared by M. C. Hampson) Skin Spot The disease is common in northern Europe and also occurs in North America and Australasia. Symptoms Following infection, roots, stolons, and stems belowground develop discrete, light brown lesions that enlarge, darken, and crack transversely. Cortical tissues may become detached. !n storage, purplish-black, slightly raised spots up to 2 mm in diameter form on tubers singly or in groups, either at random over the surface or aggregated arourd eyes, stolon scars, or damaged skin (Fig. 42A). Sometimes larger necrotic areas form over the tuber surface. Brown lesions may occur on sprouts of tubers stored in humid conditions (Fig. 42B). Irregular stands and delayed plant emergence frequently follow severe infection of seed tubers. Causal Organism Po/y sc*talum pustulans (Owen & Wakef.) M. B. Ellis (syn. Oospora pustulans Owen & Wakef.) has erect, branched conidiophores up to 140pm long, the lower part pale brown and sometimes swollen at the base (Fig. 42C). Conidia are dry, cylindrical, mostly unicellular but occasionally l-septate, measuring 6-18 X 2-3 pm. They develop in chains that fragment readily. In culture, colonies are gray and powdery. Sclerotia up to I mm in diamneter may form in aging cultures. Histopathology Conidia germinate and infect tubers through lenticels, eyes, and skin abrasions. The fungus penetrates tuber tissue to a depth of about 12 cells and within two weeks is checked by formation of a cork cambium; after two months, infected tissues degenerate and spots become visible. If formation of a cambium is delayed or prevented, e.g., by treatment with certain sprout inhibitors, the fungus can penetrate deeper into tuber tissue, subsequently causing larger spots to develop. Toward the end of the growing season, sclerotia form within cells of decaying cortical tissues of stems and tubers. Disease Cycle First infections originate from inoculum on seed tubers. Brown lesions develop initially on stems near the attachment to the h seed e dt tuber b and r f n later a e a i nodes. o es Stolons t h s are a e often ot n first f rti infected at the apex, f c e and the fungus infects buds and bud scales of tuber eyes as they form. Further irfection of underground parts before harvest and of tubers during harvest and in storage originates from conidia produced abundantly on infected tissues. Infected tubers usually appear symptomless when harvested; skin spots and necrotic buds in eyes develop about two months later and increase in storage. Epidemiology The disease, spev,du(&iciI cool wet seasons and is more severe in crops grown on heavy clay loam than in those grown on sandy or organic soils. Skin spot is common in crops lifted moist and stored cool (40 C), and conidia produced on the spots spread infection in storage. Cultivars with thick tuber skin develop few skin spots. Cultivars susceptible to skin infection are usually also susceptible at tuber eyes. Most inoculum originates from infected seed tubers, but sclerotia of P. pustulans in decaying stems can remain viable in soil for at least eight years. Other Hosts Skin spot develops only on potatoes, but brown lesions can develop on roots of other Solanaceae (Solanum spp., lcopersicon escuilentuni, Nicotiana spp., and Datura spp.). 37
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: Fungi Powdery Scab liberating powde
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
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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