Elsevier

Physiological Plant Pathology

Volume 11, Issue 3, November 1977, Pages 333-336, IN31-IN39, 337-342

Ultrastructural histopathology of tomato plants infected with Corynebacterium michiganense

https://doi.org/10.1016/0048-4059(77)90076-5Get rights and content

Abstract

Spread of Corynebacterium michiganense in tomato plants is restricted initially to the xylem vessels; the phloem elements remaining bacterium-free until advanced stages of pathogenesis. Where vessels abut, the adjoining primary walls may swell, shred and completely degrade; however, where an invaded or non-invaded parenchyma cell adjoins an invaded vessel initially only the primary wall of the vessel undergoes these changes, the wall of the parenchyma cell remaining apparently unaffected.

At advanced stages of pathogenesis the secondary thickening may also become degraded, even in the absence of bacterial cells, indicating that the incitant relies for its pathogenicity on an active enzyme complement, particularly extracellular cellulases and, possibly, hemicellulases.

The bacteria eventually pass from the disrupted vessels into the intercellular spaces of the adjacent xylem parenchyma. The cementing substances between these cells are degraded causing the cells to separate, plasmolyse and collapse. The bacteria migrate through the disrupted ground tissue and eventually enter the phloem elements which are rapidly destroyed.

It would seem that wilting of the host is due to degradation of the conducting tissue by bacterial enzyme action rather than to the action of a toxin produced by the pathogen or to the accumulation of plugging substances in the vessels.

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