The host – pathogen interaction in the wasting disease of eelgrass, Zostera marina

Abstract

A marine epidemic of wasting disease decimated populations of eelgrass, Zostera marina L., in the early 1930s. Labyrinthula, a marine slime mold was the suspected pathogen, although the cause was never clearly determined. Presently, a recurrence of wasting disease of Z. marina was documented in populations along the coasts of North America and Europe. A pathogenic species of Labyrinthula, described as Labyrinthula zosterae Porter et Muehlstein, was identified as the primary microorganism causing the present wasting disease. Of all the microorganisms tested in laboratory disease tests, only L. zosterae caused disease symptoms. Direct microscopic observations revealed that Labyrinthula cells were found most frequently associated with marginal areas of disease symptoms and appeared to move rapidly through the tissue, directly penetrating cell walls. The ectoplasmic network that surrounds Labyrinthula cells appeared to have an important role in the enzymatic degradation of plant cell walls and presumably a role in the destruction of cytoplasmic contents of the plant cells. Direct contact of diseased leaves with healthy leaves was the mechanism of disease spread from plant to plant. Key words: Labyrinthula, Zostera marina, eelgrass wasting disease.

Antifungal defenses of seagrasses from the Indian River Lagoon, Florida

“…The ''eelgrass wasting disease'' epidemic of Zostera marina in the 1930s was the most notorious outbreak resulting in massive destruction of eelgrass beds on both coasts of the Atlantic Ocean (Milne and Milne, 1951;Cottam and Munro, 1954). The marine slime mold Labyrinthula zosterae was the suspected pathogen, but was not clearly identified until a more localized and less severe outbreak developed in the 1990s along the coasts of North America and Europe (Short et al, 1986;Muehlstein, 1992). Outbreaks of disease in seagrass beds of Thalassia testudinum are most often attributed to the protist pathogen Labyrinthula sp.…”

“…Outbreaks of disease in seagrass beds of Thalassia testudinum are most often attributed to the protist pathogen Labyrinthula sp. (Muehlstein, 1992), but have also been caused by fungal pathogen Lindra thalassiae (Porter, 1986). Etiological studies suggest that these organisms are secondary decomposers of senescent or stressed seagrasses, yet there is some evidence to suggest they may be also opportunistically pathogenic (Muehlstein, 1992).…”

“…(Muehlstein, 1992), but have also been caused by fungal pathogen Lindra thalassiae (Porter, 1986). Etiological studies suggest that these organisms are secondary decomposers of senescent or stressed seagrasses, yet there is some evidence to suggest they may be also opportunistically pathogenic (Muehlstein, 1992). Environmental stressors such as low light or high temperatures may compromise the resistance of seagrasses resulting in higher levels of infection.…”

Impact of the wasting disease pathogen, Labyrinthula zosterae, on the photobiology of eelgrass Zostera marina

“…Microscopic examination of necrotic tissues has revealed that the pathogen moves rapidly (175 µm min -1 ) through tissues, penetrating cell walls. The protist appears to initiate enzymatic degradation of the cell wall, followed by destruction of the cytoplasmic contents of the seagrass leaf cell (Muehlstein 1992). The exact mechanism of mortality resulting from Labyrinthula zosterae infection is still not known.…”

Biochemical and Molecular Methods for the Study of Marine Fungi

“…One of the species (Labyrinthula zosterae) is capable of causing the symptoms of the wasting disease of the eelgrass Zostera marina. Enzymes in the ectoplasmic net degrade the plant cell walls and cytoplasmic contents of the plant cells, allowing the labyrinthulid cells to rapidly move through the plant tissue (Muehlstein, 1992). The taxonomy of the labyrinthulids is not welldefined; morphological differences are difficult to discern and molecular techniques may provide the ability to differentiate species (Leipe et al, 1994).…”