170
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
this parasite, including the sporulating and spore stages. To test its
specificity, Barrow and Taylor reacted the conjugated antiserum against
fifteen disease-causing entities in C. virginica (Table XIII) and found
it to be highly specific.
The complete life cycle of Minchinia nelsoni remains
unknown. Various postulated life cycle patterns have been advanced
from time to time but until concrete experimental evidence becomes
available, I have chosen not to recognize the majority of these. Experimental studies carried out at several distinguished laboratories, especially
a t the New Jersey Oyster Research Laboratories of Rutgers University
under the directorship of Dr. H. H. Haskin, have indicated that
M . nelsoni cannot be transmitted from oyster to oyster when placed
in the same aquarium or through the transplantation of infected tissues.
Relative to the developmental stages within the oyster, although
plasmotomy and sporulation have been observed, these findings have
been made in histological sections of naturally infected oysters from
areas where other species of Haplosporida are known to occur and
hence cannot be accepted without question. According to the most
popular hypothesis, the development of M . nelsoni within its molluscan
host is similar to that of other members of the genus Minchinia, with
the mature spore produced within the host serving as the infective
stage for others.
Ecology. Continuous surveys conducted by the personnel of various
laboratories along the New Jersey, Delaware, Maryland, and Virginia
coasts have revealed the continuous spread of M . nelsoni in C. virginica
along these shores from 1957 until the present. Its current distribution
is represented by a continuous zone encompassing this region of the
Atlantic coast of North America, extending from Long Island Sound
to Virginia. For some reason, most probably the inability of M . nelsoni
to withstand lower salinities, this parasite will disappear from oysters
maintained in waters with salinities lower than 20%,. Hence in the
past, oysters living in estuaries with low salinities were essentially
free of M . nelsoni; however, as the result of the severe droughts which
affected the mid-Atlantic coasts during 1961-66, there has been a marked
increase in salinity in normally low salinity areas and the spread of
M . nelsoni, as a consequence, has been conspicuous and disastrous t o
the oyster industry in these areas. Temperature, on the other hand,
does not appear to affect the survival of M . neboni in oysters but does
alter the rate of pathological effects, with warm summer temperatures
being most deleterious to parasitized oysters.
According to information from H. H. Haskin’s laboratory and from
Life cycle.
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
this parasite, including the sporulating and spore stages. To test its
specificity, Barrow and Taylor reacted the conjugated antiserum against
fifteen disease-causing entities in C. virginica (Table XIII) and found
it to be highly specific.
The complete life cycle of Minchinia nelsoni remains
unknown. Various postulated life cycle patterns have been advanced
from time to time but until concrete experimental evidence becomes
available, I have chosen not to recognize the majority of these. Experimental studies carried out at several distinguished laboratories, especially
a t the New Jersey Oyster Research Laboratories of Rutgers University
under the directorship of Dr. H. H. Haskin, have indicated that
M . nelsoni cannot be transmitted from oyster to oyster when placed
in the same aquarium or through the transplantation of infected tissues.
Relative to the developmental stages within the oyster, although
plasmotomy and sporulation have been observed, these findings have
been made in histological sections of naturally infected oysters from
areas where other species of Haplosporida are known to occur and
hence cannot be accepted without question. According to the most
popular hypothesis, the development of M . nelsoni within its molluscan
host is similar to that of other members of the genus Minchinia, with
the mature spore produced within the host serving as the infective
stage for others.
Ecology. Continuous surveys conducted by the personnel of various
laboratories along the New Jersey, Delaware, Maryland, and Virginia
coasts have revealed the continuous spread of M . nelsoni in C. virginica
along these shores from 1957 until the present. Its current distribution
is represented by a continuous zone encompassing this region of the
Atlantic coast of North America, extending from Long Island Sound
to Virginia. For some reason, most probably the inability of M . nelsoni
to withstand lower salinities, this parasite will disappear from oysters
maintained in waters with salinities lower than 20%,. Hence in the
past, oysters living in estuaries with low salinities were essentially
free of M . nelsoni; however, as the result of the severe droughts which
affected the mid-Atlantic coasts during 1961-66, there has been a marked
increase in salinity in normally low salinity areas and the spread of
M . nelsoni, as a consequence, has been conspicuous and disastrous t o
the oyster industry in these areas. Temperature, on the other hand,
does not appear to affect the survival of M . neboni in oysters but does
alter the rate of pathological effects, with warm summer temperatures
being most deleterious to parasitized oysters.
According to information from H. H. Haskin’s laboratory and from
Life cycle.