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

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Seed Infection by Bacteria 191in the intestinal tract of corn flea beetle (Chaetocnema pullicaria). Robert (1955)found that 10 to 70% of the beetles emerging from hibernation carried the bacterialwilt organism, and up to 75% of the beetles feeding on corn in midsummer may actas carriers.Vegetative cells of bacteria are not subject to dormancy; still, many are tolerantto desiccation and survive relatively long periods under dry conditions as mentionedin the preceding paragraphs. Do these bacteria have any means of protection in theseed? They occur in varied conditions in seeds as contaminants of the seed surfacein the form of loose cells or embedded in the bacterial slime or ooze, in seed tissuesin intercellular spaces, including the vascular elements (xylem). They may occur inseed galls along with the nematode, e.g., R. tritici or exclusively, R. rathayi. R.rathayi cells are closely packed in a regular fashion along the wall of the gall andalso within the gall (Bird, Stynes, and Thompson, 1980). Bird, Stynes, and Thompson(1980) regard this as an anhydrobiotic state, although they have not carried outstudies on the survival of the bacterium. Chand (1967) observed that R. triticisurvived in soil debris under laboratory conditions for about 7 months only, whereasMathur and Ahmad (1964) had reported that the bacterium remained viable for atleast 5 years in the gall of A. tritici.Bacterial ooze or slime has been considered protective to bacterial cells (Rosen,1929, 1938; Hildebrand, 1939). Erwinia amylovora is believed to be very susceptibleto desiccation, but survives a long time in dry exudate (Rosen, 1929, 1938). Hildebrand(1939) recovered virulent bacterial cells of E. amylovora from dry exudateafter 15 and 25 months, but the organism survived only 13 days in moist exudate.Leach et al. (1957) found an appreciable number of viable X. a. pv. phaseoli cellsin exudate for as long as 1325 days under different conditions.Bacteria present in seed tissues may have better chances of survival than thosepresent on the seed surface. However, environmental conditions, inherent seed factors(structural features), and the inherent characteristics of the pathogen affectsurvival as well as transmission. Schuster and Coyne (1974) have reviewed theliterature on this aspect. It may, however, be indicated that complete information onthe above aspects is not available even for one disease.6.4 CONCLUDING REMARKSGood information is available on initial penetration, multiplication, and spread ofbacteria in plant tissues and penetration of ovule and seed (Zaumeyer, 1930, 1932;Skoric, 1927; Cook, Larson, and Walker, 1952; Wiles and Walker, 1951; Pine,Grogan, and Hewitt, 1955; Getz, Fulbright, and Stephens, 1983; Mukerjee and Singh,1983; Tabei, 1967; Tabei et al., 1988, 1989; Azegami, Tabei, and Fukuda, 1988;Fukuda, Azegami, and Tabei, 1990). There is, however, very little experimentalevidence on penetration and association or establishment of bacterial infection inseeds during the postharvest period. The former may become systemic with longdistance movement through tracheids and vessels or it may be localized, multiplyingand spreading in the intercellular spaces. The course of short distance systemicinfection as shown by Kritzman and Zutra (1983) needs support from histologicalstudies.
192 Histopathology of Seed-Borne InfectionsPresence of C. m. subsp. tessellarius in sieve element of wheat needs confirmationbecause earlier observations by Smith (1914, 1920) on C. m. subsp. michiganensisthat described the bacterium as primarily a phloem parasite have provederroneous (Pine, Grogan, and Hewitt, 1955). In their excellent review on histopathologyof plants infected with vascular bacterial pathogens, Nelson and Dickey (1970)have clearly shown that primary infection of tissues by such pathogens is in thexylem elements, and subsequently the infection may spread to surrounding tissues,mostly in the parenchyma cells.Studies on the location of bacteria are meager and mostly inconclusive. Recentobservations by Sharma, Agarwal, and Singh (1992) on seed infection of rapeseedand mustard and X. c. pv. campestris and by Sharma et al. (2001) on X. a. pv. cajani(X. c. pv. cajani) in pigeon pea seeds have clearly demonstrated that affected seedsvary in the degree of the severity of infection, and the location and effects on seedtissues are directly correlated with it. The spread of infection varies in asymptomaticand symptomatic seeds. Severely infected seeds carry infection in all seed tissues.Similar detailed accounts are needed for full insight into the location of bacteria inseeds in other cases.REFERENCESAgrios, G.N. 1988. Plant Pathology, 3rd ed. Academic Press, San Diego.Ark, P.A. 1944. Pollen as a source of walnut bacterial blight infection. Phytopathology 34:330–334.Azegami, K., Tabei, H., and Fukuda, T. 1988. Entrance into rice grains of Pseudomonasplantarii, the causal agent of seedling blight of rice. Ann. Phytopathol. Soc. Japan54: 633–636.Basu, P.K. and Wallen, U.R. 1966. Influence of temperature on the viability, virulence, andphysiologic characteristics of Xanthomonas phaseoli. Can. J. Bot. 44: 1239–1245.Biddle, J.A., McGee, D.C., and Braun, E.J. 1990. Seed transmission of Clavibacternebraskense in corn. Plant Dis. 74: 908–911.Bird, A.F., Stynes, B.A., and Thomson, W.W. 1980. A comparison of nematode and bacteriacolonizedgalls induced by Anguina agrostis in Lolium rigidum. Phytopathology 70:1104–1109.Brinkerhoff, L.A. and Hunter, R.E. 1963. Internally infected seed as a source of inoculumfor the primary cycle of bacterial blight of cotton. Phytopathology 53: 1397–1401.Bryan, M.K. 1930. Studies on bacterial canker of tomato. J. Agric. Res. 41: 825–851.Burkholder, W.H. 1921. The bacterial blight of the bean: a systemic disease. Phytopathology11: 61–69.Burkholder, W.H. 1930. The bacterial disease of the bean. A comparative study. New York(Cornell) Agric. Exp. Sta. Mem. 127, 93 pp.Carne, W.M. 1926. Earcockle (Tylenchus tritici) and a bacterial disease (Pseudomonas tritici)of wheat. J. Dept. Agric. Western Australia 3 (Ser. 2): 508–512.Chand, J.N. 1967. Longevity of Corynebacterium tritici (Hutchinson) Burk. causing ‘tundu’disease of wheat in Haryana. Sci. and Cult. 33: 539.Cheo, C.C. 1946. A note on the relation of nematodes (Tylenchus tritici) to the developmentof the bacterial disease of wheat caused by Bacterium tritici. Ann. Appl. Biol. 33:446–449.
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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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100 Histopathology of Seed-Borne In
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