5. THE PHYLUM PROTOZOA
171
J. D. Andrews’ laboratory a t the Virginia Institute of Marine Science,
the appearance and persistence of M . nelsoni in oysters are not seasonal.
Andrews and Wood (1967) have given a detailed account of the history
and distribution of M . nelsoni in oysters in Virginia.&
Evidences collected thus far appear to indicate that M . nelsoni is
specific for C. virginica and is limited to the mid-Atlantic coast of the
United States. However, histological examination of C. gigas from
Taiwan by U.S. Bureau of Commercial Fisheries personnel and by me
have revealed the presence of multinucleated plasmodia similar to
M . nelsoni. Thus far no mass oyster mortalities have been reported
from Taiwan.
Pathology. Although Minchinia nelsoni is generally believed to be
highly lethal to C. virginica as based on epizootiological evidences,
there is comparatively little histopathological change in parasitized
oysters. When few plasmodia are present, slight lesions in the surrounding connective tissue (Leydig cells) generally occur. Furthermore,
there may be some leucocytes surrounding the plasmodia but their
number is seldom large and definitely does not compare with the more
typical encapsulation phenomenon. When large numbers of plasmodia
occur, relatively large number of Leydig cells may be ruptured. Here
again, leucocytosis and encapsulation are not particularly pronounced.
In addition, Haskin et al. (1965) have reported frequent and extensive
sloughing of the gill, palpal and suprabranchial epithelia during invasion
by M . nelsoni.
Relative to the lethality of this parasite, Haskin et al. (1966) have
reported that epizootic kills begin within 3 weeks after first appearance
of plasmodia in gills. I n lightly infected oysters, however, death may
be delayed.
It is being mentioned at this point that Parley (1965b) has proposed
that histopathological changes in C. virginica can be categorized into
five stages. According to him, initial infections, most commonly
encountered during July through early September, are characterized
by localized infection in the gills. Intracellular plasmodia first appear
in the ctenidal columnar epithelia, each surrounded by a clear zone
which is believed to have resulted from lysis. From these locations,
the plasmodia migrate to the underlying basement membrane where
plasmotomy occurs and thence into the connective tissue and blood
sinuses of the gills. During this initial stage, Parley has reported a
concentration of “ lymphocyte-like cells ” surrounding the parasite.
Each of these cells measures 8 p in diameter and includes a large
nucleus that measures 5 p in diameter.
* See note on p. 389.
171
J. D. Andrews’ laboratory a t the Virginia Institute of Marine Science,
the appearance and persistence of M . nelsoni in oysters are not seasonal.
Andrews and Wood (1967) have given a detailed account of the history
and distribution of M . nelsoni in oysters in Virginia.&
Evidences collected thus far appear to indicate that M . nelsoni is
specific for C. virginica and is limited to the mid-Atlantic coast of the
United States. However, histological examination of C. gigas from
Taiwan by U.S. Bureau of Commercial Fisheries personnel and by me
have revealed the presence of multinucleated plasmodia similar to
M . nelsoni. Thus far no mass oyster mortalities have been reported
from Taiwan.
Pathology. Although Minchinia nelsoni is generally believed to be
highly lethal to C. virginica as based on epizootiological evidences,
there is comparatively little histopathological change in parasitized
oysters. When few plasmodia are present, slight lesions in the surrounding connective tissue (Leydig cells) generally occur. Furthermore,
there may be some leucocytes surrounding the plasmodia but their
number is seldom large and definitely does not compare with the more
typical encapsulation phenomenon. When large numbers of plasmodia
occur, relatively large number of Leydig cells may be ruptured. Here
again, leucocytosis and encapsulation are not particularly pronounced.
In addition, Haskin et al. (1965) have reported frequent and extensive
sloughing of the gill, palpal and suprabranchial epithelia during invasion
by M . nelsoni.
Relative to the lethality of this parasite, Haskin et al. (1966) have
reported that epizootic kills begin within 3 weeks after first appearance
of plasmodia in gills. I n lightly infected oysters, however, death may
be delayed.
It is being mentioned at this point that Parley (1965b) has proposed
that histopathological changes in C. virginica can be categorized into
five stages. According to him, initial infections, most commonly
encountered during July through early September, are characterized
by localized infection in the gills. Intracellular plasmodia first appear
in the ctenidal columnar epithelia, each surrounded by a clear zone
which is believed to have resulted from lysis. From these locations,
the plasmodia migrate to the underlying basement membrane where
plasmotomy occurs and thence into the connective tissue and blood
sinuses of the gills. During this initial stage, Parley has reported a
concentration of “ lymphocyte-like cells ” surrounding the parasite.
Each of these cells measures 8 p in diameter and includes a large
nucleus that measures 5 p in diameter.
* See note on p. 389.