Chapter 16 Biology of Zostera
371
(Nienhuis, 1978; Baldwin and Lovvorn, 1994b; Portig et al., 1994; Schutten et al., 1994; Fox, 1996;
Vermaat and Verhagen, 1996).
The importance of Z. marina to estuarine and
coastal productivity was highlighted in the 1930s,
when a large-scale die-off of Z. marina occurred on
both sides of the Atlantic due to wasting disease
(Rasmussen, 1977). The disease resulted in the loss
of over 90% of the North Atlantic Z. marina population, and this loss had a catastrophic effect on estuarine productivity including the disappearance of the
scallop (Argopecten irradians) fishery and drastic reduction in brant geese (Branta bernicla) populations
(Milne and Milne, 1951).
In addition to functions as nursery and feeding
ground, Zostera beds enhance the local productivity
of an area through increased epibenthic and benthic
production, providing substrate for epiphytes and
enhancing benthic invertebrate production (Fredette
et al., 1990). Zostera beds act as a filter of estuarine
water, trapping and binding sediments (Rasmussen,
1977; Fonseca et al., 1983; Fonseca and Fisher, 1986;
Fonseca, 1992; Heiss et al., 2000) and dampening
wave and current energy (Grizzle et al., 1996; Koch
and Verduin, 2001). These plants also take up and
bind contaminants (Lyngby and Brix, 1982; Fran¸ cois
et al., 1989; Ward, 1989; Hoven et al., 1999). Zostera
beds produce and release O 2 to the water, create and
export organic material, and facilitate the accumulation of organic matter in the sediments (Costanza
et al., 1997). Zostera is important in the nutrient cycling of the coastal ocean, increasing decomposition
in the sediments, accelerating nutrient regeneration,
and regulating nutrient cycles (Short, 1987; Hansen
et al., 2000).
B. Disease
“Wasting disease” dramatically reduced eelgrass,
Z. marina, populations in the 1930s along the Atlantic Coast of North America and Europe by 90%
(Muehlstein, 1989). At the time, speculations about
the causative agents of the wasting disease were numerous, and included pathogenic microorganisms,
salinity, temperature, irradiance, drought, and oil
pollution (Renn, 1934; Stevens, 1936; Short et al.,
1988; Muehlstein, 1989). Recently, it was shown that
the eelgrass wasting disease symptoms are caused by
the infection of a marine slime mould-like protist,
Labyrinthula zosterae Porter and Muehlstein (Short
et al., 1987; Muehlstein et al., 1991) which has been
reported in several species of Zostera (Short et al.,
1987, 1993b). It has been stated that Labyrinthula
is a secondary decomposer of senescent leaves (den
Hartog, 1987; den Hartog et al., 1996). Now however, Ralph and Short (2002) have demonstrated that
L. zosterae rapidly invades the healthy green tissue
around black disease spots, impairing photosynthesis, and is a primary pathogen causing the wasting
disease infection.
Wasting disease continues to affect Z. marina beds
in North America and Europe with variable degrees
of loss, though none to date as catastrophic as the
epidemic of the 1930s (Short et al., 1986, 1988,
1993a; den Hartog, 1994). Wasting disease infection spreads through a population by direct leaf-toleaf contact with an infected plant or by contact with
drifting detached leaves. The symptoms of wasting disease are black-brown dots or streaks on the
leaves, which expand to form patches, larger blackened spots, and longer streaks (Short et al., 1988;
Muehlstein, 1989). The characteristic wasting disease spots result from enzymatic browning of L.
zosterae infection (Vergeer et al., 1995). The area
of green healthy-looking tissue around the spots is
already infected with the pathogen, such that the extent of the disease infection (Burdick et al., 1993)
is much greater than is visually evident (Ralph and
Short, 2002). Microscopic examination of necrotic
tissues has revealed rapid movement of the pathogen
through tissues, penetrating internal cell walls. The
“slime track” of Labyrinthula precedes the organism, initiating enzymatic degradation of eelgrass
cells and destroying the cell cytoplasm (Muehlstein,
1992). The mechanism of mortality resulting from L.
zosterae infection appears to be reduced photosynthetic activity (Fig. 7; Ralph and Short, 2002) that
creates a negative carbon balance.
Many investigators have suggested that Labyrinthula infection in Z. marina is linked to already
stressed eelgrass (Young, 1943; Tutin, 1938; Rasmussen, 1977), and it is believed healthy tissue can
generally resist infection by the ubiquitous marine
pathogen (Vergeer and den Hartog, 1994). However, using Koch’s postulates, Labyrinthula has been
demonstrated to be the etiological agent of the wasting disease (Short et al., 1987), and subsequent studies have demonstrated that the infectious L. zosterae
is a host-specific pathogen transferred by direct contact of plants (Short et al., 1987; Muehlstein et al.,
1988, 1991). It is clear that salinity plays a role in
regulating disease activity (Burdick et al., 1993); the
371
(Nienhuis, 1978; Baldwin and Lovvorn, 1994b; Portig et al., 1994; Schutten et al., 1994; Fox, 1996;
Vermaat and Verhagen, 1996).
The importance of Z. marina to estuarine and
coastal productivity was highlighted in the 1930s,
when a large-scale die-off of Z. marina occurred on
both sides of the Atlantic due to wasting disease
(Rasmussen, 1977). The disease resulted in the loss
of over 90% of the North Atlantic Z. marina population, and this loss had a catastrophic effect on estuarine productivity including the disappearance of the
scallop (Argopecten irradians) fishery and drastic reduction in brant geese (Branta bernicla) populations
(Milne and Milne, 1951).
In addition to functions as nursery and feeding
ground, Zostera beds enhance the local productivity
of an area through increased epibenthic and benthic
production, providing substrate for epiphytes and
enhancing benthic invertebrate production (Fredette
et al., 1990). Zostera beds act as a filter of estuarine
water, trapping and binding sediments (Rasmussen,
1977; Fonseca et al., 1983; Fonseca and Fisher, 1986;
Fonseca, 1992; Heiss et al., 2000) and dampening
wave and current energy (Grizzle et al., 1996; Koch
and Verduin, 2001). These plants also take up and
bind contaminants (Lyngby and Brix, 1982; Fran¸ cois
et al., 1989; Ward, 1989; Hoven et al., 1999). Zostera
beds produce and release O 2 to the water, create and
export organic material, and facilitate the accumulation of organic matter in the sediments (Costanza
et al., 1997). Zostera is important in the nutrient cycling of the coastal ocean, increasing decomposition
in the sediments, accelerating nutrient regeneration,
and regulating nutrient cycles (Short, 1987; Hansen
et al., 2000).
B. Disease
“Wasting disease” dramatically reduced eelgrass,
Z. marina, populations in the 1930s along the Atlantic Coast of North America and Europe by 90%
(Muehlstein, 1989). At the time, speculations about
the causative agents of the wasting disease were numerous, and included pathogenic microorganisms,
salinity, temperature, irradiance, drought, and oil
pollution (Renn, 1934; Stevens, 1936; Short et al.,
1988; Muehlstein, 1989). Recently, it was shown that
the eelgrass wasting disease symptoms are caused by
the infection of a marine slime mould-like protist,
Labyrinthula zosterae Porter and Muehlstein (Short
et al., 1987; Muehlstein et al., 1991) which has been
reported in several species of Zostera (Short et al.,
1987, 1993b). It has been stated that Labyrinthula
is a secondary decomposer of senescent leaves (den
Hartog, 1987; den Hartog et al., 1996). Now however, Ralph and Short (2002) have demonstrated that
L. zosterae rapidly invades the healthy green tissue
around black disease spots, impairing photosynthesis, and is a primary pathogen causing the wasting
disease infection.
Wasting disease continues to affect Z. marina beds
in North America and Europe with variable degrees
of loss, though none to date as catastrophic as the
epidemic of the 1930s (Short et al., 1986, 1988,
1993a; den Hartog, 1994). Wasting disease infection spreads through a population by direct leaf-toleaf contact with an infected plant or by contact with
drifting detached leaves. The symptoms of wasting disease are black-brown dots or streaks on the
leaves, which expand to form patches, larger blackened spots, and longer streaks (Short et al., 1988;
Muehlstein, 1989). The characteristic wasting disease spots result from enzymatic browning of L.
zosterae infection (Vergeer et al., 1995). The area
of green healthy-looking tissue around the spots is
already infected with the pathogen, such that the extent of the disease infection (Burdick et al., 1993)
is much greater than is visually evident (Ralph and
Short, 2002). Microscopic examination of necrotic
tissues has revealed rapid movement of the pathogen
through tissues, penetrating internal cell walls. The
“slime track” of Labyrinthula precedes the organism, initiating enzymatic degradation of eelgrass
cells and destroying the cell cytoplasm (Muehlstein,
1992). The mechanism of mortality resulting from L.
zosterae infection appears to be reduced photosynthetic activity (Fig. 7; Ralph and Short, 2002) that
creates a negative carbon balance.
Many investigators have suggested that Labyrinthula infection in Z. marina is linked to already
stressed eelgrass (Young, 1943; Tutin, 1938; Rasmussen, 1977), and it is believed healthy tissue can
generally resist infection by the ubiquitous marine
pathogen (Vergeer and den Hartog, 1994). However, using Koch’s postulates, Labyrinthula has been
demonstrated to be the etiological agent of the wasting disease (Short et al., 1987), and subsequent studies have demonstrated that the infectious L. zosterae
is a host-specific pathogen transferred by direct contact of plants (Short et al., 1987; Muehlstein et al.,
1988, 1991). It is clear that salinity plays a role in
regulating disease activity (Burdick et al., 1993); the