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

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Kennebec potatoes caused by high concentrations of maleic hydrazide. Can. .1.Plant Sci. 50:591-593. STEPHENS, H.J. 1 9 65. The place of herbicides in the potatocrop. Eur. PotatonJ. 8:33-51. (Prepared by W. J. Hooker) Stem-End Browning Stem-end browning describes an internal, brown discoloration of tuber tissue near the stem end or stolon attachment. In its broadest sense, the term is applied to a shallow discoloration with one or more unknown causes. These may include chemical injury, sudden death of the vines, or infection from pathogens, including viruses. Usually it does not show up at harvest but develops during the first one to three months in storage. It is often confined to the 12-mm section at the stolon end of the tuber and is more frequent in smaller tubers. If penetration is deeper, the brown strands are confined to the xylem of the vascular ring. The disorder may b" :onfused with virus leafroll net necrosis (Fig. 28A). However. the latter penetrates deeper into the tuber, and its brown necrotic strands involve the phloem either inside S-. A B "' -z--. -. ,. Fig. 28. A, Stem-end browning; B, virus leafroll net necrosis. (Courtesy Main Life Sciences and Agricultural Experiment Station) Nutrient deficiencies or excesses are frequently difficult to diagnose without analysis of the plant and may beconft sed with other environmental stresses. )eficiency or exce.;s of a particular nutrient may be influenced by its availability, its balant e with other nutrients, soil pH. ion-exchange hivels, and other factors. Because potatoes are grown unjer widely different conditions of altitude, day length, light inensities, soil types, temperatures, and soluble salts, general symptoms described for nutrient disorders are often based upon controlled sand culture trials rather than on field conditions. Potatoes grow well in soils above pH 5.0. In more acid conditions, Ca atd Mg deficiency, phosphate fixation, and ammonium, Mn. and Al toxicity may occur, and leaching of some nutrients (e.g.. Mg) is increased. Conversely, highly calcareous or overlimed soils crL.Ite unfavorable alkaline reactions that reduce availability of Mn, Fe, B, and Zn. General References CHAPMAN, H. D.. ed. 1966. Diagnostic Criteria for Plantsand Soils. University of California. I)ivision of Agricultural Science. 793 pp. 22 Nutrient Imbalance or outside of the xylem. It is more prevalent in larger tubers, and affected tubers always produce leafroll-infected plants. Recently, stem-end browning has been associated with early season leafroll virus infection, in which a limited amount of tissue is affected and the virus does not always establish infection. Thus affected tubers ma: not produce leafrol plants. Stem-end browning may also come from another virus, as yet unidentified. The virus isapparently graff-transmitted and is more prevalent in certain clone lines: its characteristics have not been further clarified. Stem-end browning has noapparent effect on yield, although affected tissue is believed to he sterile. Stem-end browning is distinguished from Fusarium or Verticillium wilts by culture techniques and from Verticillium infection or defoliants by darker color and coarser strands. Other tuber discolorations often confused with stem-end browning include those due to rapid vine killing (by chemicals or flame) or to frost or frost necrosis. Control Cultivars differ in resistance. Avoid excessive applications of phosphorus, potassium, or chlorine in the fertilizer. Selected References FOLSON, D., and A. E. RICH. 1940. Potato tuber net-necrosis and stem-end browning studies in Maine. Phytopathology 30:313-322. MANZER. F. E.. I). C. MERRIAM. and R. Hf. STORCH. 1977. Effects of time of inoculation with PIRV on internal tuber necrosis. Am. Potato J. 54:476 (Abstr.). RICH. A. E.1950. '1hle effect of various defoliants on potato vines and tubers in Washingion. Am. Potato .. 27:87-92. RICH, A. F. 1951. Phlocm necrosis of Irish potatoes in Washington. Wash. Agric. Exp. Sin. Bull. 528. ROSS, A. F. 1946. Susceptibility of Green Mountain and Irish Cobbler commercial strains to stem-end browning. Am. Potato J. 23:219-234. ROSS. A. F. 1946. Studies on the cause of stem-end browning in Green Mountain potatoes. Phytopathology 36:925-936. ROSS, A. F., J. A. CHUCKA, and A. HAWKINS. 1947. The effect of fertilizer practice including the use of minor elements on stem-end browning, net necrosis, and spread of leafroll virus in the Green Mountain variety of potato. Maine Agric. Exp. Sin. Bull. 447:96-142. (Prepared by A. E. Rich) HOUGHIAND. G. V. C. 1964. Nutrient deficiencies in the potato. In: Sprague. II. B.. ed. 1964. Ilunger Signs in Crops. 3rd ed. David McKay Co., Inc.. New York. 461 pp. WAlLACE. T. 1961. The I)iagnosis of Mineral )eficiencies in Plants by Visual Symptoms, a Colour Atlas and Guide, 3rd ed. Chemical Publishing Co.. Inc.. New York. 125 pp. with 312 color plates. Nitrogen Adequate N in the presence of sufficient P and K stimulates apical and lateral meristems and thus increases leaf development. Adequate N should be available during rapid plant growth and tuberization. N requirements increase rapidly with plant growth, as N is translocated from lower to upper leaves and much of it eventually to the tubers. Deficient plants are generally chlorotic, slow growing, erect, and have small, erect, pale green leaves (Plate 8). Lower leaves are most severely affected. Veins stay green somewhat longer than does interveinal tissue. The extent ofdeficiency determines
sevritof stnting, chiorosis. loss of' lower leaves, and vied reduction, Speckle leaf'. brown to black spots about I mm in diameter that may coalesce on lower leaves of some early cultivars. is particularly severe ollos ing heavy rainfall or irrigation and is alleviated by nitrogen side dress. When N toxicity occrs.iCiclds arc reduced: root de\ehlptiicnt C' is poor: and lea\es may roll upward or be deforned as "mouse ear.- N toxicity can result from the forn of N available to the plant. Alnmonil illd or nitrites formed Iromii urea and dianmroniuni phosphates are toxic. Incertain soil conditions, principally \,er acid soils. conversion of amlnoniuni nitrogen to nitrate nitrogen is i paired. In nutritional leafroll, nitrate nitrogen is insufficient to balance ainotherwise normal amount Fig. 29. Potassium deficiency symptoms on tubers. ot annioniur Note corky nitrogen a\ailable to tie plant, sunken areas at stolon end. (Courtesy W. M.Laughlin) Surf'ace applications of urea. esrecially when banded tihigh rates. can cause damage from ammonia \olatiliiation. 1Burning of leaves and stem lesions de\elopi ng near urea pellets are due to green spots (approximately I mm in diameter) appear between am monia \olatili/ation and not to an osmotic or salt effect, veins of larger leaflets, resembling mild mosiac. When K is in relatively short supply, older leaves first become bronzed, then Selected References necrotic (Plate 9). and senesce early. Leaflet margins from the middle to the top of the plant roll NIItN(iIR.I upward. l.eaflets are small, 1). R. IOt'll)l Nand E. I). JONES. 1978. Potato cupped, crowded together, ield crinkled, reductions and associated bronzed on \%ith the certain upper fertiliier mixtures. Am. surface. The overall bronzed Ilotarn effect .I. 55:227-234. of the foliage is predominant, leaves frequently VI ;OSL have dark I. I... brown and specks R. W.('IIASE. on the atfected by fr tier and ,sater manuagement. 1973. Speckle leaf A m. of Potato potato as .I. lower S m surface, t m which a' may d v. coalesce rr and i cause l 'i'' marginal necrosis. . ' 50:311-314. Phosphorus Symptoms bright weather may develop rapidly following within four days during cloudy, sunny, rainy periods. Necrosis is severe and may superficially resemble early blight. Stalks may be slender with short internodes. When K is acutely deficient, P1is essential early in plant growth and later in tuberization. Early season deficiency retards growth of terminals, and plants are small, spindly, and somewhat rigid. l.eaflets fail to expand nornially. are crinkled or cup-shaped (Plate 8), darker than normal. lusterless, and may be scorched at the margins. L.ower leaves may drop. ILeaflets are not bronzed, leaf petioles are More erect than normal. Maturity may be delayed. Roots and stolons are reduced inboth number and length. lhibers lack external syniptoms. but internal rusty' brown necrotic flecks or spots are scattered throughout the flesh in sometimes radial patterns. (See also internal heat necrosis and calcium deficiency.) l)eficicncy occurs on a \wide range of' soil types: calcareous Soils. pear or rmuck. light soils with low initial P content, and heavy soils in sshich P is lixed. Muclh of the P is translocated frorn vines to tubers, and the crop rerioves a considerable ariount if ' froi the soil. Banding of P lateral to the seed piece decreases P)fixation and improves P uptake over that from broadcast application. little can be done to alleviate P- deficiency symptoms during the growing season, although foliage a pplicatiorns with neutral ammonium phosphate or polyphosphate p herevplea are archeful. hielpf'ul, h , e ln ie Where P levels are vry ig. especially in alkaline soils, the uptake and or utilization of' Zn or Fe may be reduced. the growing point is affected and general dieback develops. Plants become short and squatty with shiortened internodes. They' appear droopy because of downward leaf curling. Roots are poorly developed and stolons ate short. Tuber size and yield are reduced. Necrotic, brown, sunken lesions develop at stolon ends of tubers of plants with necrotic foliage. Later, the affected tissue dries out, Iortiiing a hollow spot. 2mm or more in diameter. surrounded by corky tissue (Fig. 29). K deficiency predisposes to black spot. During early storage, K-deficient tubers frequently develop brown to black enzymatic discoloration (f raw cut surfaces on exposure to air. Discoloration is frequently more severe at the stolon end of the tuber. Tuber flesh also becomes dark after cooking. K deficiency is most common on light, easily leached, sand, muck, or peat soils. Exchangeable K should exceed 200 kg/ ha (178 l b A) in the upper 20 cm of soil. Selected References BAER UG,R., and R. EN(E. 1974. Influence of potassium supply and s:orage conditions on the discoloration of raw and cooked potato tubers of cv. Pimpernell. Potato Res. 17:271-282. FONG, K. It. and A. I.RICl-. 1969. Growing potato plants by the L.AUGHl.IN, ater culture W. technique. M. 1966. Am.Potato Effect of soil .1.46:269-272. applications of potassium, nagnesium sulfate and niagnesi unl sulfate spray on potato yield. composition and nutrient uptake. Am. Potato J. 43:403-411. Selected References L.AUGH I.IN, W. M., and C. I. )EARIBORN. 1960. Correction of leaf necrosis ofpotatoes Nitlh foliar and soil applications of potassium. IIA-Rt'(i. R.. and K. SI ENIIERG. 1971. Influence of placement method and vater supply on the uptake of phosphorus by earl' poratoes. Potato Res. 14:282-291. llt)t'(ilI NI). . '. U. 1960. [he influence of phosphorus on the gros, rh and physiology of the potato plant. Am. Potato .1. 37:127-138. Am.Potato .1.37:1-12. MUL.) R, . G . 1949. Mineral nutrition in relation to the biocliemistry and phvsiology of potatoes. Plant and Soil 2:59-121. Calcium Potassium Ca-deficient plants are spindly, with small, upward rolling, crinkled leaflets having chlorotic margins that later become necrotic (Plate 9). In severe deficiency, leaves are wrinkled and K is essential ftornormal growth and is highly mobile within stem tips cease to funitii. giving a rosette appearance. Root tIre plant. meristems cease to grew. Early appearance of unusually dark green, bluish green, or Tubers on Ca-deficient plantsdevelop diffuse brown necrosis glossy foliage is a dependable symptom of K deficiency. I.ight in the vascular ring near stolor attachnments, and later similar 23
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: Epidemiology Oxidant injury is pres
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 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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