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

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<strong>Seed</strong> Infection by Bacteria 187embryos <strong>of</strong> naturally infected as well as artificially inoculated symptomatic fruits(Wall and Santos, 1988; Wall, 1989; Rane and Latin, 1992).Burkholderia glumae, the causal bacterium <strong>of</strong> rice grain rot, enters lemma andpalea through stomata, multiplies in intercellular spaces in the parenchyma, andreaches the surface <strong>of</strong> the endosperm and embryo. The bacterium never invaded theendosperm and embryo (Tabei et al., 1989). The sites <strong>of</strong> occurrence <strong>of</strong> B. glumaein naturally infected and artificially inoculated grains were the same.6.2.3 RATHAYIBACTER AND CLAVIBACTERSeveral phytopathogenic bacteria previously placed in the genus Corynebacteriumhave been transferred to the genera Rathayibacter and Clavibacter (Table 6.1).Rathayibacter tritici, which causes yellow slime disease or yellow ear rot in wheat,has drawn considerable attention (Cheo, 1946; Vasudeva and Hingorani, 1952; Sabet,1954a,b; Gupta and Swarup, 1968). Neergaard (1979) mentioned that Rathayibactertritici (Conynebacterium tritici) and R. rathayi (Conynebacterium rathayi) are probablyvascular pathogens, but none <strong>of</strong> the histopathological investigations conformto this possibility. The bacterium is transmitted by Anguina tritici. Sabet (1954a)determined that infection takes place in the soil, and aerial infection does not occurunder field conditions even in plants infested with the nematode. Using sterilizedand unsterilized soil, sterilized and unsterilized nematode larvae, and nematode galls,Swarup and Singh (1962) observed that the bacterial disease symptoms appearedonly when the nematode galls as such were used for inoculation. They concludedthat possibly the bacterium was carried on the gall surface.Sabet (1954a) found that R. tritici spreads on the surface <strong>of</strong> the affected plantsand only in leaf sheath and terminal internode (ear-stalk); it may invade internally,occupying intercellular spaces. Early spike infection is from the inner surface <strong>of</strong> thesheath. Bacteria spread and fill in all gaps between the organs <strong>of</strong> spikelet, causingdisintegration <strong>of</strong> tissues and results in yellow slime. If the bacterium is sparselydistributed on the leaf sheath, rachis, and parts <strong>of</strong> florets, slight or no disintegration<strong>of</strong> the internal tissues occurs. In such spikes either no grains or distorted ungerminableor germinable grains are formed. The germinable grains may give rise toeither healthy or affected seedlings (Sabet, 1954a).In plants raised from artificially inoculated seeds, Sabet (1954b) observed thatthe bacterium spread on the surface <strong>of</strong> affected plants and caused complete or partialinflorescence infection. In partially affected inflorescence, the stamens were affected,one or more <strong>of</strong> the anther’s four pollen chambers compressed and tissues disintegrated,and slimy mass was seen on the surface. The bacterium either coveredvirtually the whole surface <strong>of</strong> the styles and ovary (carpel) or was restricted to certainareas on the ovary. The infection might reach the ovary cavity, and depending onthe amount <strong>of</strong> slime, the developing ovule was affected. Severe infection preventedpollination and further development <strong>of</strong> grains. However, in less affected florets,grains may develop. The affected grains had mostly bacterial crust in and aroundthe groove. Bacterial cells also occurred between the pericarp and seed coat,endosperm below the groove, and rarely in between the pericarp and embryo.

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