Histopathology of Seed-Borne Infections - Applied Research Center ...

Recommendations

Info

Seed Infection by Bacteria 173bBbACFIGURE 6.3 SEM photomicrographs of stigma of flowers colonized by Erwinia amylovora.A, Stigma of pear flower pistil with bacterial cells present on the stigmatic surface. B,Enlargement of bacterial cells on stigmatic surface of pear flower pistil. C, Mass of bacterialcells on stigmatic surface of apple flower. (Abbreviations: b, bacteria; sti, stigma.) (FromThompson, S.V. 1986. Phytopathology 76: 476–482. With permission.)that most of the flowers that were experimentally pollinated by contaminated pollendeveloped infected nuts. Ivanoff (1933) also reported that maize pollen may beinfected or contaminated by Pantoea stewartii subsp. stewartii (Erwinia stewartii),and this may cause infection of maize florets through the stigma; however, nohistopathological studies of these two systems have been made.Wounds or openings caused by any injury, whether mechanical or by insects ornematodes, form easy passages for entry of bacteria (Zaumeyer, 1932; Skoric, 1927;Thiers and Blank, 1951; Nelson and Dickey, 1970). Artificial inoculations (Figure6.2E, F) pricking the plant surface also demonstrate this (Kelman, 1953; Offutt andBaldridge, 1956; Dickey and Nelson, 1970; Getz, Fulbright, and Stephens, 1983).Ralstonia solanacearum enters through insect wounds and lenticels in peanut plants(Miller and Harvey, 1932). Azegami, Tabei, and Fukuda (1988) observed that duringseedling growth, ruptures occur in the surfaces of coleoptile and roots at the pointsof emergence of leaves or secondary roots. B. plantari enters through such woundsas well as stomata. Vakili (1967) has shown the importance of wounds in bacterialspot disease of tomato caused by X. vesicatoria.Available information on the role of plant–parasitic nematodes in the initiationof bacterial diseases was summarized by Pitcher in 1963. According to Pitcher, allnematodes puncture plant cells and can act as inoculants, but the micropuncturemade by a nematode stylet is not the type of wound most likely to favor the entryof bacteria. The endoparasitic nematodes, which enter the host bodily and, perhaps,cause local necrosis, seem better suited for entry and establishment of bacteria.Anguina tritici for Rathayibacter tritici in wheat and Aphelenchoides ritzema-bosi
174 Histopathology of Seed-Borne Infectionsfor Rhodococcus facians (Corynebacterium fascians) in strawberry and cauliflowerare reported to be essential as vectors of these pathogens (Hunger, 1901; Carne,1926; Vasudeva and Hingorani, 1952; Crosse and Pitcher, 1952; Pitcher and Crosse,1958).6.1.2 SPREAD IN PLANT AND COURSE OF ENTRY INTO OVARYAND FRUIT AND OVULE AND SEEDAfter entering the plant tissue, the bacteria multiply in a substomatal cavity(Figure 6.1A, C, E) or space beneath the site of entry. Within the host, the bacteriafollow two courses for further spread: they invade xylem elements and move verticallyafter coming in contact with vascular elements and they multiply and spreadin intercellular spaces (Figure 6.1B, D). The latter course usually results in arestricted spread. Vascular bacteria can move over long distances, and they can alsospread laterally after dissolving the walls of the vessels (Smith, 1911; Yu, 1933;Pine, Grogan, and Hewitt, 1955) or after escaping through openings (pits) in thewalls of vessel elements (Ivanoff, 1933; Wolf and Nelson, 1969). Nelson and Dickey(1966) have also suggested lateral movement of bacteria through plasmodesmatalconnections in the pit membranes of vessels. Association of bacteria with phloemis observed, but it probably plays no significant role in their spread (Pine, Grogan,and Hewitt, 1955).Several seed infecting bacteria are systemic vascular pathogens (Zaumeyer,1930; Pine, Grogan, and Hewitt, 1955; Cormack and Moffat, 1956; Mukerjee andSingh, 1983; Du Plessis, 1990). Pine, Grogan, and Hewitt (1955) have given adetailed account of the spread of C. m. subsp. michiganensis, a bacterial cankerpathogen, in young tomato plants and provided evidence of longitudinal and lateralmovement of the organism in xylem elements (Figure 6.4A to D). Bacterial pocketswere formed in phloem and pith, but they gave no indication of vertical movement.During earlier studies, C. m. subsp. michiganensis was described primarily as aphloem parasite (Smith, 1914, 1920). However, Zaumeyer (1930) has also observedinvasion of xylem elements in leaf (Figure 6.1F) and stem (Figure 6.1G) by X. a.pv. phaseoli, and its subsequent spread throughout the organism. X. oryzae pv. oryzaehas a similar course in rice (Mukerjee and Singh, 1983).The systemic vascular infection often enters the reproductive shoot and causesovary and fruit infection (Zaumeyer, 1930; Cormack and Moffatt, 1956; Mukerjeeand Singh, 1983; Du Plessis, 1990). Zaumeyer (1930) traced the passage of X. a.pv. phaseoli from plant to pods in beans and noted that the bacteria in the xylemvessels of the stem travels up and through the vascular elements of the pedicel andpasses into the vascular supply of the pod. Mukerjee and Singh (1983) observedthat X. o. pv. oryzae reaches the rice husk through vessels of the infected rachilla.Skoric (1927) reported that Pseudomonas syringae pv. pisi is largely a parenchymainvader and only occasionally may enter the vessels under field conditions.The bacterium penetrates pods through wounds and spreads in intercellular spaces,forming abundant slime on the inner side of the pod. After artificial inoculation byP. s. pv. lachrymans of the stem 1.5 m from the fruit, Kritzman and Zutra (1983)observed systemic invasion of the cucumber fruits. No histopathological studies were
Page 2 and 3:
Histopathology ofSeed-Borne Infecti
Page 4:
PrefaceThe book deals with only one
Page 8 and 9:
The AuthorsDalbir Singh, Ph.D., for
Page 10 and 11:
ContentsChapter 1 Introduction ....
Page 12 and 13:
4.3.2 Routes for Infection from Ova
Page 14:
8.4 Survival in Seed ..............
Page 17 and 18:
2 Histopathology of Seed-Borne Infe
Page 19 and 20:
4 Histopathology of Seed-Borne Infe
Page 22 and 23:
2Reproductive Structuresand Seed Fo
Page 24 and 25:
Reproductive Structures and Seed Fo
Page 26:
Page 29 and 30:
14 Histopathology of Seed-Borne Inf
Page 31 and 32:
Page 33 and 34:
Page 35 and 36:
Page 37 and 38:
Page 39 and 40:
Page 41 and 42:
Page 43 and 44:
Page 45 and 46:
Page 47 and 48:
Page 49 and 50:
Page 51 and 52:
Page 53 and 54:
Page 56 and 57:
Page 58 and 59:
Page 60 and 61:
Page 62 and 63:
3Structure of SeedsThe seed habit i
Page 64 and 65:
Structure of Seeds 49(1971) of usin
Page 66 and 67:
Structure of Seeds 51is found in as
Page 68 and 69:
Structure of Seeds 53dry seed of Ly
Page 70 and 71:
Structure of Seeds 553.3.2 SEED COA
Page 72 and 73:
Structure of Seeds 57Endosperm: One
Page 74 and 75:
Structure of Seeds 59scendembepsmuA
Page 76 and 77:
Structure of Seeds 61Endosperm: Sca
Page 78 and 79:
Structure of Seeds 63Chalaza simple
Page 80 and 81:
Structure of Seeds 65stystypmerA Bc
Page 82 and 83:
Structure of Seeds 67epsent endCADB
Page 84 and 85:
Structure of Seeds 69perhscendembpe
Page 86 and 87:
Structure of Seeds 71eposgepi′epo
Page 88 and 89:
Structure of Seeds 73(Zea and Sorgh
Page 90 and 91:
Structure of Seeds 75Baker, D.M. an
Page 92 and 93:
Structure of Seeds 77Maheshwari Dev
Page 94:
Structure of Seeds 79Vries, M.A. de
Page 97 and 98:
Page 99 and 100:
Page 101 and 102:
Page 103 and 104:
Page 105 and 106:
Page 107 and 108:
Page 109 and 110:
Page 111 and 112:
Page 113 and 114:
Page 115 and 116:
100 Histopathology of Seed-Borne In
Page 117 and 118:
Page 119 and 120:
Page 121 and 122:
Page 123 and 124:
Page 125 and 126:
Page 127 and 128:
Page 129 and 130:
Page 131 and 132:
Page 133 and 134:
Page 135 and 136:
Page 137 and 138: 122 Histopathology of Seed-Borne In
Page 163 and 164: TABLE 5.6Location of Mycelium of St
Page 187: 172 Histopathology of Seed-Borne In
Page 214 and 215: 7Seed Infection by VirusesViruses a
Page 216 and 217: Seed Infection by Viruses 201TABLE
Page 220 and 221: Seed Infection by Viruses 205Unlike
Page 222 and 223: Seed Infection by Viruses 2073. The
Page 224 and 225: Seed Infection by Viruses 209Wilcox
Page 228 and 229: Seed Infection by Viruses 213floret
Page 230 and 231: Seed Infection by Viruses 215ptowvv
Page 232 and 233: Seed Infection by Viruses 2177.4.2
Page 234 and 235: Seed Infection by Viruses 219seed(s
Page 236 and 237: Seed Infection by Viruses 221AMV fo
Page 238 and 239:
Seed Infection by Viruses 223REFERE
Page 240 and 241:
Seed Infection by Viruses 225Hunter
Page 242:
Seed Infection by Viruses 227Wolf,
Page 245 and 246:
Page 247 and 248:
Page 249 and 250:
Page 251 and 252:
Page 253 and 254:
Page 255 and 256:
Page 257 and 258:
Page 259 and 260:
Page 261 and 262:
Page 263 and 264:
Page 265 and 266:
Page 267 and 268:
Page 269 and 270:
Page 271 and 272:
Page 273 and 274:
Page 275 and 276:
Page 277 and 278:
Page 279 and 280:
Page 281 and 282:
Page 283 and 284:
Page 285 and 286:
Page 287 and 288:
Page 289 and 290:
Page 291 and 292:
Page 293 and 294:
Page 295 and 296:
Page 297:
show all

Histopathology of Seed-Borne Infections - Applied Research Center ...

Create successful ePaper yourself

Delete template?

Save as template?