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

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(Fig. 34B). Bacterial streaming can also be seen rnicroscopically in thin sections of infected tissue mounted in water under a cover slip. This bacterial exudate, combined with wilting and related symptoms, distinguishes this wilt from fungous wilts, Underground stems, stolons, and roots of plants with initial foliage symptoms show few advanced symptoms of infection, Grayish brown discoloration, usually evident through the tuber periderm, indicates well-established infection. Tubers from infected plants may or may not show symptoms: cross sections usually show distinct, grayish brown vasculardiscoloration that may extend into the pith or cortex from the xylem tissue, However, certain strains from Portugal and Kenya produce no browning of the vascular ring. When tubers are cut in half and light pressure is applied, grayish white droplets of bacterial slime ooze out of the vascular ring (Fig. 34A). The eves. often at the bud orapical end, become grayish brown, and a sticky exudate may form on them or at the stolon connection (Plate 15). The bacterial ooze mixes with the soil, causing soil particles to adhere to the tuber surface. An infected tuber left in the ground continues to decay; secondary organisms convert it to a slimy mass surrounded by a thin laver of cortex and periderm. Causal Organism Pseutdomonas solanacearum F3. F. Smith is a nonsporeforming, noncapsulate, Gram-negative, nitrate-reducing, ammonia-forming aerobic, rod-shaped bacterium. In liquid media, the wild-type bacterium is usually nonmotile and does Fig. 34. Brown rot: A, bacterial exudate from vascular ring of tuber; B, streaming of bacteria from infected stem in water; C, cells of Pseudomonas solanacearum (electron micrograph) of avirulent type with wavy flagellum; D,virulent form (flagellum is atypical). (A,Courtesy L.W. Nielsen; B,courtesy C.Martin; C and D, courtesy A. Kelman) 30 not form a polar flagellum. Avirulent variants that develop in culture are actively motile (Fig. 34C and D). Starch is not hydrolyzed by this bacterium, and gelatin is liquefied slowly or not at all. . solanacearuniis sensitive to desiccation and is inhibited by relatively low concentrations of salt in broth cultures. Optimal growth of most strains occurs at 30-32' C,although some strains from Colombia grow relatively well at lower temperatures. Strains differing in biochemical characteristics and host range have been described. A strain pathogenic to potatoes is weakly virulent on tobacco but avirulent on banana; the banana strain is avirulent on potato; in contrast, tobacco and tomato strains are usuall \iitnllI potato. Somic strains of P..hnacearinm from Portugal and ..*;iya do not forl the typical lyrosinase reaction in cult ure tiedia. Cultures of . o/tltlcealIII)rlll aintinied io unicratcd liquid ilcdia rapidly lose kirulcnce and \iahilit and shilt tron the Iltuidal (11oni6otilC) \\ill-tvp'C to a\ irulnt. highl\ Motile variants. Colonies of virulent wild-types are irregularly round and are white with pink centers; colonies of avirulent variants aic uiiifolumly round, butyrous, and deep red. Colony characteristics are best observed when cell suspensions are streaked on plates of peptone casamino acid glucose agarcontaining 2,3,5triphenyltetrazolium chloride and examined in obliquely transmitted light after incubation at 32'C for 36-48 hr. Epidemiology In tropical and semitropical regions (southeastern Asia, Central and South America, and parts of Africa and Australia) the pathogen can be borne by tubers; quarantines exist against importation of seed potatoes in sonie areas. Infected seed potatoes are an important factor in the distribution and increasing severity of the disease in tropical countries such as Peru, where latent infections can occur in seed grown at high elevations. Temperature plays an important role in the geographic distribution of the organism, which is rare where mean soil temperaturesare below 15' C. In North America, seed potatoes are grown in the temperate regions where P. solanaearumdoes not occur, and tuber transmission is not a problem. tligh temperatures favor growth of the pathogen in vitro and development of the disease in the field. Recently, however,/: solanacearutn was reported in Sweden and at high altitudes in Costa Rica, Colombia, Peru, and Sri l.anka. Thus, the bacterium can possibly survive and infect potato crops at relatively low temperatures. The disease occurs in soil types ranging from sandy to heavy clay and over a wide range of soil pH. Disease usually develops in localized areas often associated with poor drainage. On newly cleared forest land, bacterial wilt may be severe if a susceptible crop is planted. Other Hosts Important economic hosts of P. solanacearum include tobacco, tomato, pepper, eggplant, peanut, banana, and a number of ornamentals and weeds. Although species in over 33 different plant families may be attacked, most susceptible hosts are in the Solanaceae. Resistance At least three dominant and independent genes control resistance in potato to certain strains of bacterial wilt. Resistance is relatively sensitive to changes in environment; increased temperatures and decreased light intensity enhance susceptibility to wilt. Immunity or high levels of resistance have not been identified in clones of S. ttu/erosum. Colombian clones of S. phure/aJuz. & Buk. with resistance to bacterial wilt have been crossed with haploid lines of S. tuberosuim. Strains of P. solanaceartan differing in virulence have complicated breeding for wilt resistance, but two resistant varieties, Caxamarca and Molinera, have been released in Peru.
Control I) Use disease-free tubers and disinfect the cutting knife. 2) Soil treatment chemicals such as sulfur are not widely accepted because of the low level of control and the high cost. 3) P.solanaceartni survives for extended periods in some soils. In others it may not survive 1-6 months of fallow, 4) Some crop rotation sequences reduce disease severity; they may act indirectly by reducing populations of root-knot nematodes that enhance bacterial wilt disease infection in potato. Selected References fllI)DEN IIAGI-N, I..and A. KELMA\ 1964. tiologicil and physiological aspects of bacteiial v%!t causcd by I.%edO mtontals sola m)ceartom . A nnu. Rev. PhIytopathol. 2:203-231. F ))INS. A. If. 1936. Irowvn rot of Irish potatoes and its control. Fl. Agric. F-xp. Sin. Bull. 299,.44 pp. FII.I)MESSER, .1.,and R. W. (Ill. 1970. Association of root knot with bacterial wilt of potato. Phytopathology 60:1014 (Abstr.). IIAY\WARI). A. C. 1964. Characteristics of Aseudonoas khn'aocarum.I.1. Appl. Itacteriol. 27:265-277. Causal Organism Cor' neacteritm sepedonictn (Spieck. & Kott.) Skapt. & Burkh. I is a (ram-positive nonmotile bacterium. Cells are KIFtM AN.A. 1953. fhe bacterial wil ca used by P'odomonal .vohaa ('varulrm. N.C. Agric. F\p. Sin. fcch. Bull. 99. 194 pp. KIlIMAN. A. 1954. The relationship of pathogenicity in Pveudomo as 'ram stain (Reeds rapid) for bacterial smears: Stains vola'a'curon are Gram to colony appearance on a tetra/olium medium, positive bacterial cells blue and Gram-negative cells pink. Mix Phyt opathologv in equal 44:093- 695. parts: I) crystal or gentian violet 0.251" aqueous KII.MAN. with 2)NaIICO A., and .1. IIRtSCII .KA. 1973. The role of motility and 1.25(7 alqneous. Hood fot 1(lsee and drain. Mix 201i iodine aerotaxis in If in the selective increase of avirulent bacteria in still broth NaOII and dilute 1:10 in watcr. Flood for 10sec and wyash. C l t -resof Pwvd1 Ilotoo Iolata caru mt. . Ge. M cr0 il. acetone Mix I part svashes from and sicar. 3 parts Flood 957 with ethyl watr. alcohol. I)ilute Rinse basic until 76:177-1818. fuchsin no saturated more color in ethyl alcohol I: 10 in water. Stain not ,\er 2 sec. rinse thoroughlv, LOZANO. and .1.C.. ard I.. S OI lR.,'.. 197). )ifferentiation ofraces of dry. (Front Glick. 1).P.,1). A. Ark, and It. N. Racciot. 1944. Am. Po\'l' by a leaf infiltration technique. Phyto- Potato J. 21:311-314.) ~toloill.I .;/apla~uvarm pathology 60:833-838. NIFI.SFN. I.. W., and F. I. IIAYNES. .Ir. 1957. Control of southern bacterial \kilt. Potato tHandbook Vol. 2. Am.Potato Assoc., New Itrunsssick. N.I. pp. 47-51. NIIlSEN, L. V..and F. I.. IIAYN-S, Ir. 1960. Resistance inSola,,tn t/'troulll tI P''tdowtoIaI .\oNl'anac'rumI..Atn. Potato .1. 37:200- 207. ROIlNSON, R. A. 1968. the concept oIf vertical and hori/ontal resistance as illustrated bv bacterial wilt of potatoes. Phlvopathol. Paper No. Ill Cottntonsn. Mvcol. Inst.. Kew, Surrev. England. 37 ROWE,1. R.. and I.. SEQUI£1RA. 1970. Inheritance of resistance to I.tml"ola(w(1l armin in Soh/11 (l IIrc0. Ph t tIth 61:1499-1501. SfAIP, C. 1965. Die bakteriellc Schleitifliule und ihr Erreger 'oIlIeodImoia .11solancearumi. Zentralb. flakteriol. Parasitenkd. Itfektionskr. Ilyg, Aht. 2 119:166-190. I'ItI, fON,II. I).. and .1.C. LOZANO. 1968. Resistance to bacterial s iltof potatoes in(o1hmbian clones of SI(anui ptureia. Am. Potato .1.45:51-55. (Pr1,epred by A. Kelman) Ring Rot Ring rot, or bacterial ring rot, was first recorded in Germany in 1906 and has since been found in man),other areas. Despite the lack of documentation in a few countries, ring rot has probably occurred wherever potatoes are grown. Through seed certification programs, many countries have successfully eradicated the disease. Symptoms Plant symptoms begin with wilting of leaves and stems after midseason. L.ower leaves, slightly rolled at the margins and pale green. are usually the first to wilt (Plate 16). As wilting progresses, pale yellowish areas develop between veins. Often only one or two stems of an infected hill develop symptoms. Two important diagnostic features are the wilting of stems and leaves and a milky white exudate that can be squeezed from the vascular ring of tubers (Fig. 35) and of stems when crosssectioned at their base. A dwarf-rosette type of symptom has been described in the Russet Burbank cultivar in the western United States (Fig. 36). This disease derives its name from the characteristic internal breakdown in the vascular ring of an infected tuber crosssectioned at the stem end. Squee/ing the tubers, particularly those fror.1 storage, expels creamy, cheeselike ribbons of odorless bacterial ooze, which leaves a distinct separation of tissues adjacent to the ring. Secondary invaders (usually soft rot bacteria) cause further tissue breakdown in advanced disease stages, obscuring ring rot symptoms. Pressure developed by this breakdown can cause external swelling, ragged cracks, and reddish brown discoloration, especially near the eyes (Plate 17). Although typical tuber symptoms are invariably apparent in badly infected lots at harvest, some infected tubers may remain symptomless for man weeks in cold storage. Occasionally, sym ptoms ay n bond ste n d typical internal symptoms may not he apparent at the stem end of the tuber but may be found near the apical or rose end. - • . " 1 " " 4,t " I "ology Fig. 35. Bacterial ring rot: A, surface cracking from Corynebacterium sepedonicum infection; B, cheesy breakdown of tuber vascular tissue. Fig. 36. Dwarf rosette symptom of ring rot. (Courtesy J. R. Letal) 31
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: should be planted on land with at l
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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