116
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
Sudds (1960) and others, it is recalled, have found that incompatible
parasites are commonly encapsulated in molluscs but need not be,
although the non-encapsulated parasites do not develop normally and
eventually die. Thus James’s finding suggests a third type of manifestation of resistance, where the parasites do not elicit encapsulation
or die from abnormal development but develop in less numbers.
Considerably more investigations of this nature must be forthcoming
before any conclusions may be drawn. However, the findings of Sudds,
Heyneman and James suggest the presence of some innate humoral
factor(s) which is responsible for at least partial host-specificity.
Another interesting aspect of James’s study is that he does not
agree with W. J. Rees (1936a) that the size of the germinal sacs,
especially sporocysts, influences the degree of damage inflicted. In fact,
he has pointed out that the small sporocysts of C. ubiquita and C.
roscovita cause more damage than the larger germinal sacs of C. parvatrema homoeotecnum and C. lebouri. He does agree that the occurrence
of rediae, rather than sporocysts, especially if they possess strong
pharynges, would contribute to mechanical ingestion of hepatopancreatic cells.
At this point it is of interest to comment on whether larval trematodes could cause the death of their molluscan hosts. Prom the
observations of James (1965) and others, it would appear that lethality
is dependent upon (1) the number of parasites present, (2) the rate of
development and proliferation of the parasite as correlated with the
host’s life-span, hence a specific phenomenon, and consequently (3)
the amount of damage inflicted. Even then, some still unknown factor
appears to be involved since Cheng and Snyder (1962a), engaged in
similar studies, have stated: “ . . . the survival of Helisoma trivolvis
does not appear to be impaired by Glypthelmins pennsylvaniensis even
in instances of extremely dense infections where only a few isolated
liver tubules were retained.” Yet during an earlier study, Cheng and
James (1960) have reported that the bivalve Xphaerium striatinurn is
killed when heavily infected with Crepidostomum cornutum rediae.
Similarly Hopkins (1957a) and others have claimed that Bucephalus
cucuZus will not kill Crassostrea virginica, its oyster host, but Millar
(1963) has reported that an undetermined species of bucephalid
trematode will kill oysters. Again, Cheng and Burton’s (1965b) study
on the histopathology of C. virginica parasitized by Bucephalus sp.
has failed to incriminate this trematode as a lethal agent. It is thus
evident that critically controlled laboratory studies, involving known
numbers of parasites and knowledge of their rate of proliferation,
controlled nutritional and ambient factors, chemical knowledge of
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
Sudds (1960) and others, it is recalled, have found that incompatible
parasites are commonly encapsulated in molluscs but need not be,
although the non-encapsulated parasites do not develop normally and
eventually die. Thus James’s finding suggests a third type of manifestation of resistance, where the parasites do not elicit encapsulation
or die from abnormal development but develop in less numbers.
Considerably more investigations of this nature must be forthcoming
before any conclusions may be drawn. However, the findings of Sudds,
Heyneman and James suggest the presence of some innate humoral
factor(s) which is responsible for at least partial host-specificity.
Another interesting aspect of James’s study is that he does not
agree with W. J. Rees (1936a) that the size of the germinal sacs,
especially sporocysts, influences the degree of damage inflicted. In fact,
he has pointed out that the small sporocysts of C. ubiquita and C.
roscovita cause more damage than the larger germinal sacs of C. parvatrema homoeotecnum and C. lebouri. He does agree that the occurrence
of rediae, rather than sporocysts, especially if they possess strong
pharynges, would contribute to mechanical ingestion of hepatopancreatic cells.
At this point it is of interest to comment on whether larval trematodes could cause the death of their molluscan hosts. Prom the
observations of James (1965) and others, it would appear that lethality
is dependent upon (1) the number of parasites present, (2) the rate of
development and proliferation of the parasite as correlated with the
host’s life-span, hence a specific phenomenon, and consequently (3)
the amount of damage inflicted. Even then, some still unknown factor
appears to be involved since Cheng and Snyder (1962a), engaged in
similar studies, have stated: “ . . . the survival of Helisoma trivolvis
does not appear to be impaired by Glypthelmins pennsylvaniensis even
in instances of extremely dense infections where only a few isolated
liver tubules were retained.” Yet during an earlier study, Cheng and
James (1960) have reported that the bivalve Xphaerium striatinurn is
killed when heavily infected with Crepidostomum cornutum rediae.
Similarly Hopkins (1957a) and others have claimed that Bucephalus
cucuZus will not kill Crassostrea virginica, its oyster host, but Millar
(1963) has reported that an undetermined species of bucephalid
trematode will kill oysters. Again, Cheng and Burton’s (1965b) study
on the histopathology of C. virginica parasitized by Bucephalus sp.
has failed to incriminate this trematode as a lethal agent. It is thus
evident that critically controlled laboratory studies, involving known
numbers of parasites and knowledge of their rate of proliferation,
controlled nutritional and ambient factors, chemical knowledge of