Presentation Abstract
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.
Session Title
Session S-01E: Eelgrass Wasting Disease
Conference Track
Habitat
Conference Name
Salish Sea Ecosystem Conference (2014 : Seattle, Wash.)
Document Type
Event
Start Date
30-4-2014 10:30 AM
End Date
30-4-2014 12:00 PM
Location
Room 613-614
Genre/Form
conference proceedings; presentations (communicative events)
Contributing Repository
Digital content made available by University Archives, Heritage Resources, Western Libraries, Western Washington University.
Subjects – Topical (LCSH)
Zostera marina--Diseases and pests
Geographic Coverage
Salish Sea (B.C. and Wash.)
Rights
This resource is displayed for educational purposes only and may be subject to U.S. and international copyright laws. For more information about rights or obtaining copies of this resource, please contact University Archives, Heritage Resources, Western Libraries, Western Washington University, Bellingham, WA 98225-9103, USA (360-650-7534; heritage.resources@wwu.edu) and refer to the collection name and identifier. Any materials cited must be attributed to the Salish Sea Ecosystem Conference Records, University Archives, Heritage Resources, Western Libraries, Western Washington University.
Type
Text
Language
English
Format
application/pdf
Included in
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.
