4. ANALYSIS OF FACTORS INVOLVED I N SYMBIOSIS
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cysts, C. emasculans produces the most profound pathological changes.
This is because the relative larger sporocysts are little or non-motile
and thus form “ blocking layers ” in the proximal portion of the hepatopancreas. These “ blocking layers ” prevent the flow of nutrients
towards the cells at the distal end and at the same time prevent waste
products from being conducted to the host’s nephridium. For these
reasons, according to W. J. Rees, not only are the hepatopancreatic
cells in the immediate vicinity of the sporocysts lysed or atrophied,
but the entire organ distad to the “ blocking layer ” becomes atrophied.
In the case of C. ubiquita, the small sporocysts cause little damage.
Even in fairly heavily infected snails, only local cytological changes,
similar to those reported by F. G. Rees (1934), occur. Again, W. J.
Rees has postulated that infected snails probably would recover from
their infections.
The active sporocysts of C. littorinae migrate throughout the intertubular spaces in the host’s hepatopancreas, and are relatively evenly
distributed. Damage to the host’s cells is rather severe. Again this
investigator believed that such is primarily due to physiological
pressures resulting from excess wastes and starvation.
Although the studies of F. G. and W. J. Rees are exceedingly
interesting and serve as baselines for future research, direct modern
biochemical evidences of the toxicity of the parasites’ excreta on host
cells, as well as direct evidences for the uptake of the hosts’ nutritions,
should be attempted to confirm their interpretations.
Cooley (1958, 1962) has given a brief account of the histopathology
in the southern oyster drill, Thais haemastoma, parasitized by the rediae
of Parorchis acanthus. This trematode, in its adult stage, parasitizes
marine birds, primarily gulls and terns, and utilizes a number of
marine gastropods, including Urosalpinx cinerea, Thais lapillus, T.
haemastoma, Littorina planaxis, L. pintado, Melogena sp. and Cerithium
sp., as the intermediate host. Hopkins (1957b) had stated earlier that
Parorchis acanthus larvae will castrate Thais haemastoma. Cooley
has been able to confirm this. In addition, he has reported extensive
destruction of the snail’s digestive gland, which he believed to be the
result of ingestion by rediae. Approximately 70-90% of the hepatopancreas is destroyed. Of the remaining tubules, most, if not all, are
mechanically compressed so that their lumina are obliterated. Cooley
has also reported the presence of basophilic cytoplasmic inclusions in
large “ triangular cells ” of the hepatopancreas of parasitized T.
haemastoma, the significance of which is not understood. He has also
reported the grouping of amoeboid cells, believed to be phagocytes,
around some of the rediae in the hepatopancreas. Relative to damage
111
cysts, C. emasculans produces the most profound pathological changes.
This is because the relative larger sporocysts are little or non-motile
and thus form “ blocking layers ” in the proximal portion of the hepatopancreas. These “ blocking layers ” prevent the flow of nutrients
towards the cells at the distal end and at the same time prevent waste
products from being conducted to the host’s nephridium. For these
reasons, according to W. J. Rees, not only are the hepatopancreatic
cells in the immediate vicinity of the sporocysts lysed or atrophied,
but the entire organ distad to the “ blocking layer ” becomes atrophied.
In the case of C. ubiquita, the small sporocysts cause little damage.
Even in fairly heavily infected snails, only local cytological changes,
similar to those reported by F. G. Rees (1934), occur. Again, W. J.
Rees has postulated that infected snails probably would recover from
their infections.
The active sporocysts of C. littorinae migrate throughout the intertubular spaces in the host’s hepatopancreas, and are relatively evenly
distributed. Damage to the host’s cells is rather severe. Again this
investigator believed that such is primarily due to physiological
pressures resulting from excess wastes and starvation.
Although the studies of F. G. and W. J. Rees are exceedingly
interesting and serve as baselines for future research, direct modern
biochemical evidences of the toxicity of the parasites’ excreta on host
cells, as well as direct evidences for the uptake of the hosts’ nutritions,
should be attempted to confirm their interpretations.
Cooley (1958, 1962) has given a brief account of the histopathology
in the southern oyster drill, Thais haemastoma, parasitized by the rediae
of Parorchis acanthus. This trematode, in its adult stage, parasitizes
marine birds, primarily gulls and terns, and utilizes a number of
marine gastropods, including Urosalpinx cinerea, Thais lapillus, T.
haemastoma, Littorina planaxis, L. pintado, Melogena sp. and Cerithium
sp., as the intermediate host. Hopkins (1957b) had stated earlier that
Parorchis acanthus larvae will castrate Thais haemastoma. Cooley
has been able to confirm this. In addition, he has reported extensive
destruction of the snail’s digestive gland, which he believed to be the
result of ingestion by rediae. Approximately 70-90% of the hepatopancreas is destroyed. Of the remaining tubules, most, if not all, are
mechanically compressed so that their lumina are obliterated. Cooley
has also reported the presence of basophilic cytoplasmic inclusions in
large “ triangular cells ” of the hepatopancreas of parasitized T.
haemastoma, the significance of which is not understood. He has also
reported the grouping of amoeboid cells, believed to be phagocytes,
around some of the rediae in the hepatopancreas. Relative to damage