The phycomycete fungus, Ostracoblabe implexa, is responsible for severe shell damage in European oysters (O. edulis), known as maladie de la charnière ('hinge disease'), maladie du pied ('foot disease' erroneously), shell disease and Dutch shell disease (Fig. 20.15). Less severe infections occur in C. gigas,
Fig. 20.15. (Opposite) (a) Conchiolin warts in the shell of Ostrea edulis infected by the fungus Ostracoblabe implexa ('shell disease'). Note lesions at the adductor muscle attachment point of the shell. Photograph courtesy of M.F. Li. (b) Advanced destruction of the nacre layer of the shell of Ostrea edulisdue to infection by the fungus Ostracoblabe implexa. Photograph courtesy of M.F. Li.
Saccostrea cucullata in India, and C. angulata and Cardium edule (Korringa, 1951; Cole and Waugh, 1956; Quayle, 1969; Li et al., 1983; Alderman, 1986; Raghukumar and Lande, 1988) in Europe. Infections first appear as raised white spots, with translucent centres, which coalesce into conchiolin warts on the inner shell surface. In O. edulis, surface irritation results in heavier conchiolin deposition than in other infected bivalves (Alderman, 1982). The protein-rich conchiolin accelerates proliferation of the fungus and thickening of the shell margin and hinge ('maladie de la charnière') or adductor-muscle attachment surface ('maladie du pied). Fungal growth is restricted to warm water temperatures (> 20°C), so severe infections are more common in shallow water. Proliferation of O. implexa over a period of several weeks can lead to shell destruction and the death of the oyster. Microscopic examination of decalcified shell reveals a dense mycelial network of hyphae 1.5-2.5 mm in diameter. Small oval dilatations (chlamydospores) occur at irregular intervals (40-100 mm) along the hyphae, and septa only appear in dying mycelia (Alderman, 1982) (Fig. 20.16). Mantle tissues in direct contact with affected shell may become metaplastic, but are not infected by the fungus. In Atlantic Canada, bivalve species growing beside infected European oysters show no evidence of infection (Li et al, 1983).
The oomycete fungus, Sirolpidium zoophthorum, is well documented as the cause of larval mycosis in hatchery-reared American oysters (C. virginica) and hard-shell clams (M. mercenaria) (Davis et al., 1954; Vishniac, 1955; Johnson and Sparrow, 1961). Veliger and postmetamorphic larvae up to 0.4 mm in length are particularly susceptible and can suffer over 90% mortality within 48 h. Sirolpidium zoophthorum is easily cultured on nutrient agar, producing a branched, septate thallus (10-15 mm in diameter), which thickens to 82 mm in diameter at maturity. Swollen terminal cells produce sporangia. These produce discharge tubes (up to 142 mm in length and 5 mm in diameter), through which biflagellate zoospores (2 mm x 5 mm) are released (Vishniac, 1955).
Another fungus affecting oyster-hatchery production was described as 'digestive-tract impaction'. Pacific oyster (C. gigas) larvae which failed to complete metamorphosis within 12 days of hatching showed over 90% mortality (Leibovitz et al., 1978; Elston, 1980a). The infection was characterized by erosion of the mantle and velar epithelia and occlusion of the stomach by thick-walled spheres. The intestine was dilated or ruptured. The spheres were tentatively identified as a Dermocystidium-like fungus, a phycomycete fungus or a Hyalochlorella colourless alga. No further outbreaks have been reported since the original description from four hatcheries in Washington State in the late 1970s.
A disease of wild and cultured quahaugs (hard-shell clam) M. mercenaria in the Gulf of St Lawrence, Canada, was originally described as an Olpidium-like, chytrid (phycomycete) fungus (Drinnan and Henderson, 1963). Whyte et al. (1994) have since found thraustochytrid-like ultrastructural characteristics; thus the fungal-like agent has been designated 'quahaug parasite X' (QPX) until its taxonomic affinity can be clearly determined. QPX was first observed in dead and dying quahaugs transferred from Prince Edward Island (PEI) to New
Brunswick in the 1960s (Drinnan and Henderson, 1963). No further mortalities were reported until the early 1990s, when mass mortalities (> 90%) of 1- and 2-year-old hatchery-held quahaugs were attributed to the same organism (Whyte et al., 1994).
QPX infects the gills, palps and connective tissue of the digestive gland, gonad and mantle and elicits strong haemocyte infiltration in response to parasite proliferation. Developmental stages range from dense spherical bodies (5-12 |mm in diameter), resembling cysts, to large endosporulating stages (> 100 |mm in diameter), containing daughter cells at various stages of development (Fig. 20.17). Cell walls range from membraneous to thick, translucent cysts and most stages are associated with varying degrees of tissue lysis (Whyte et al., 1994), which appears to be linked to ectoplasmic-like extrusions from the cell wall. Various stages of development may also be found extracellularly, along with debris and haemocytes from lysed lesions. Other bivalve species (C. virginica, A. irradians and M. edulis) held in close proximity to infected quahaugs showed no evidence of QPX transmission.
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