Abstract Title

Session S-01E: Eelgrass Wasting Disease

Keywords

Habitat

Start Date

30-4-2014 10:30 AM

End Date

30-4-2014 12:00 PM

Description

During the 1930s, ‘wasting disease’ decimated eelgrass, Zostera marina L., meadows along the Atlantic Coast of North America and Europe with over 90% loss. Outbreaks of wasting disease were also documented in the Pacific Northwest and New Zealand. Wasting disease continues to affect eelgrass meadows with variable degrees of loss, though none as catastrophic as the 1930s. Speculations concerning the causative agent of the 1930s wasting disease included microorganisms, oil pollution, drought, or changes in salinity, temperature, or irradiance. In 1987, it was shown using Koch’s postulates that the eelgrass wasting disease is caused by infection with a marine slime-mold-like protist, Labyrinthula zosterae, a host-specific pathogen. Wasting disease infection spreads either through direct contact with an infected growing plant or drifting detached plant parts. The initial symptoms are black-brown areas on the leaves, which, as the infection develops, coalesce to form patches, larger blackened spots and streaks; ultimately, the plant dies. The photosynthetic efficiency of green leaves is reduced by half at the margins of the necrotic region, and above these blackened spots photosynthetic activity is diminished. Microscopic examination of necrotic leaves reveals that the pathogen moves rapidly (175 μm min–1) through tissues, penetrating cell walls. The protist initiates enzymatic degradation of the cell wall and destruction of the cytoplasm, creating the black spots. Labyrinthula activity slows at salinities less than 20 to 25. Elevated temperature and low light were implicated in the 1930s epidemic. Recent studies show that elevated temperature and prolonged low light levels create metabolic stress which increases plant susceptibility to the disease while high phenolic levels in eelgrass reduce susceptibility. The reports of unexplained eelgrass die-off in Californian estuaries, as well as observations of blackened leaf tissue along the west coast, prompt the need for scientific investigation of wasting disease across the region.

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Apr 30th, 10:30 AM Apr 30th, 12:00 PM

Eelgrass Wasting Disease: an Overview

Room 613-614

During the 1930s, ‘wasting disease’ decimated eelgrass, Zostera marina L., meadows along the Atlantic Coast of North America and Europe with over 90% loss. Outbreaks of wasting disease were also documented in the Pacific Northwest and New Zealand. Wasting disease continues to affect eelgrass meadows with variable degrees of loss, though none as catastrophic as the 1930s. Speculations concerning the causative agent of the 1930s wasting disease included microorganisms, oil pollution, drought, or changes in salinity, temperature, or irradiance. In 1987, it was shown using Koch’s postulates that the eelgrass wasting disease is caused by infection with a marine slime-mold-like protist, Labyrinthula zosterae, a host-specific pathogen. Wasting disease infection spreads either through direct contact with an infected growing plant or drifting detached plant parts. The initial symptoms are black-brown areas on the leaves, which, as the infection develops, coalesce to form patches, larger blackened spots and streaks; ultimately, the plant dies. The photosynthetic efficiency of green leaves is reduced by half at the margins of the necrotic region, and above these blackened spots photosynthetic activity is diminished. Microscopic examination of necrotic leaves reveals that the pathogen moves rapidly (175 μm min–1) through tissues, penetrating cell walls. The protist initiates enzymatic degradation of the cell wall and destruction of the cytoplasm, creating the black spots. Labyrinthula activity slows at salinities less than 20 to 25. Elevated temperature and low light were implicated in the 1930s epidemic. Recent studies show that elevated temperature and prolonged low light levels create metabolic stress which increases plant susceptibility to the disease while high phenolic levels in eelgrass reduce susceptibility. The reports of unexplained eelgrass die-off in Californian estuaries, as well as observations of blackened leaf tissue along the west coast, prompt the need for scientific investigation of wasting disease across the region.