Symptoms of the Disease

A wilting and yellowing of the lower leaves, which extends upward until all the leaves appear golden yellow in appearance is the first recognizable symptom of bacterial wilt in ginger. As the disease progresses, the pseudostem becomes water soaked and readily breaks away from the underground rhizome. The vascular tissue of the stem darkens to a black color and symptoms progress very rapidly until the ginger plant collapses (Pegg et al., 1974). Diseased rhizomes are usually darker than healthy ones and have water-soaked areas with pockets of milky exudates. When diseased rhizomes or pseudostems are cut, white milky exudates flows freely from the cut surface (Figure 9.2). High concentrations of bacteria in the vascular tissue deprive the plant of water and nutrients from the soil, which adversely affects plant development and ultimately results in death (Buddenhagen and Kelman, 1964). Infected ginger plants become stunted and chlorotic and the lower leaves dry out gradually before the plant is finally killed. The inner core of the rhizome, including the vascular tissue, is rotten leaving the outer epidermis intact. However, it is not clear whether the rotting is due to the primary pathogen or caused by secondary saprophytic microflora or microfauna.

Figure 9.2 Bacterial ooze from the cut end of the pseudostem of ginger.

In susceptible host plants this pathogen disrupts water transport, alters physiology, and induces a severe, usually total, bacterial wilt (Hayward, 1991). Complete wilt commonly occurs 3 weeks after inoculation. The most notable symptom of the disease is rapid wilting of foliage primarily due to vascular dysfunction (Denny et al., 1990). Intercellular spaces of the root cortex and vascular parenchyma are subsequently colonized and cell walls are disrupted, facilitating spread through the vascular system (Vasse et al., 1995). In xylem vessels, bacterial populations reach very high levels (>1010 cells/cm of stem in tomato), concomitant with wilting and plant death. The bacterium then returns to the soil, living as a saprophytic organism until it infects a new host plant. Studies using artificial inoculation methods and avirulent mutants suggest that the production of copious amounts of extracellular polysaccharide is the key factor in virulence and the major requirement for infection via roots as well as wilting and killing of the host plant.

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