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

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Seed Infection by Nematodes 2318.2 HISTOPATHOLOGYOf the genera that cause internal infection of seeds, Ditylenchus, Aphelenchoides,and Pratylenchus are soil- as well as seed-borne. They are facultative endoparasitesand produce most stages in soil. Usually the preadult stage (fourth stage) is infective.Other stages, except egg and first-stage larvae, are also known to cause infection.Anguina shows more marked adaptation to parasitism. They are obligate parasitesand normally complete their development only after invading the inflorescence, but,rarely, galls containing adults may be formed on leaves. Second-stage larvae thatremain in seed galls are released in soil. These become associated with the hostseedlings on which they feed ectoparasitically until they invade the floral parts.8.2.1 ANGUINA TRITICI (STEINBUCK) CHITWOOD(EAR COCKLE DISEASE)The ear cockle disease of wheat caused by Anguina tritici was the first plantnematode disease that was discovered. It was observed by Needham, a Dutch clergyman,in 1743. The nematode is known to infect bread wheat in most wheatgrowingcountries of the world (Southey, 1972). It also infects emmer wheat (Triticumdicoccum), spelt wheat (Triticum spelta), rye (Secale cereale), oat (Avenasativa), and certain grasses. The nematode produces seed galls, which are the majorsource of inoculum.8.2.1.1 Disease Cycle (Figure 8.1)The galls contain second-stage infective quiscent larvae. On sowing, the galls, alongwith healthy seed, reach the soil. The galls absorb moisture, and the larvae becomeactive and are released. They move in a thin film of water and reach different partsof the seedling, including roots and parts of seed, aerial parts (shoot), and spacesbetween coleoptile and leaf and between those of the leaf bases. The nematodes thatbecome lodged in seed tissues are of little consequence in disease development, butthose that reach aerial parts are then carried up with the growing seedling. The larvaefeed ectoparasitically, affect growth, and cause various symptoms in plant parts.After the plant enters the reproductive phase, the larvae in large numbers lie aroundthe differentiating florets in the spike enclosed by the boot leaf. Subsequently, theyenter the primordia of floral structures at the early stages of development. Theinfected structures (stamen and/or carpel) develop into galls, which are green initiallyand turn brown-black at maturity.After becoming endoparasitic, the second-stage larvae molt and differentiateinto adult males and females. The nematode is amphimictic. The females lay eggsinside the galls. The eggs undergo embryogenesis and produce second-stage larvaein the green galls. These larvae remain in quiescent form in dried galls. The totallife period is between 106 to 113 days (Swarup, Dasgupta, and Koshy, 1989). Onlyone generation is completed in a crop season.
232 Histopathology of Seed-Borne Infectionsinfectedear headnormalear headcarpellategallstaminate multiplegall gallcompoundgallwheat seedcontaminatedamphimicticreproductionegg (2nd generation)1stgeneration1st generation2nd stagejuvenile (2nd generation)entrythroughbrushendgerminationof seedunsuccessfulestablishmentof infection rupturedcoleorhizaradicleemergenceof juvenilesbrushendembryoendentry throughpoint ofradicle towardembryo throughrupturedcoleorhizajuvenilesbasalswellingcrinklingtwistingof leaversprostratetilleringjuveniles reachplumule growingpointboot stagesymptomFIGURE 8.1 Life cycle of Anguina tritici in wheat. (Adapted and redrawn after Swarup, G.,Sethi, C.L., and Gokte, N. 1993. In Seed-Borne Diseases and Seed Health Testing of Wheat.Mathur, S.B. and Cunfer, B.M., Eds. Danish Government Institute of Seed Pathology forDeveloping Countries, Copenhagen. Denmark.)8.2.1.2 Origin of GallsAter macroscopic studies, Marcinowski (1910) concluded that galls could arise fromundifferentiated as well as differentiated tissues of spikelets. Byars (1920) agreed
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Histopathology ofSeed-Borne Infecti
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PrefaceThe book deals with only one
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The AuthorsDalbir Singh, Ph.D., for
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ContentsChapter 1 Introduction ....
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4.3.2 Routes for Infection from Ova
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8.4 Survival in Seed ..............
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2 Histopathology of Seed-Borne Infe
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4 Histopathology of Seed-Borne Infe
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2Reproductive Structuresand Seed Fo
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Reproductive Structures and Seed Fo
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14 Histopathology of Seed-Borne Inf
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3Structure of SeedsThe seed habit i
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Structure of Seeds 49(1971) of usin
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Structure of Seeds 51is found in as
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Structure of Seeds 53dry seed of Ly
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Structure of Seeds 553.3.2 SEED COA
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Structure of Seeds 57Endosperm: One
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Structure of Seeds 59scendembepsmuA
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Structure of Seeds 61Endosperm: Sca
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Structure of Seeds 63Chalaza simple
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Structure of Seeds 65stystypmerA Bc
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Structure of Seeds 67epsent endCADB
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Structure of Seeds 69perhscendembpe
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Structure of Seeds 71eposgepi′epo
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Structure of Seeds 73(Zea and Sorgh
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Structure of Seeds 75Baker, D.M. an
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Structure of Seeds 77Maheshwari Dev
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Structure of Seeds 79Vries, M.A. de
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TABLE 5.6Location of Mycelium of St
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Page 214 and 215: 7Seed Infection by VirusesViruses a
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Page 222 and 223: Seed Infection by Viruses 2073. The
Page 224 and 225: Seed Infection by Viruses 209Wilcox
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Page 232 and 233: Seed Infection by Viruses 2177.4.2
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Page 238 and 239: Seed Infection by Viruses 223REFERE
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