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PACIFIC SCIENCE, Vol. XXII, April 1968 
germinal sacs. The current belief that these 
stored fatty acids are not utilized in energy 
production while within the mollusc’s hepato- 
pancreas stems from von Brand’s (1951) be- 
lief that this environment is essentially anaero- 
bic and hence is not conducive to lipid metabo- 
lism. The non-occurrence of aerobic metabolism 
in sporocysts and in rediae appears to be con- 
firmed by the electron microscopic studies of 
Bils and Martin (1966), which revealed the 
absence of mitochondria in sporocyst and redial 
walls. On the other hand, mitochondria have 
been demonstrated in the wall of Parorchis 
acanthus rediae (Rees, 1966), and in the walls 
of Philophthalmus gralli rediae (Cheng and 
Hamamoto, unpublished data). 
Cheng and Snyder (1962^, h\ 1963), by 
employing histochemistry, arrived at the conclu- 
sion that glucose and fatty acids are taken up 
by sporocysts through their body walls. Electron 
microscope studies by Bils and Martin (1966) 
tend to corroborate this with the finding of con- 
spicuous microvilli along the outer surfaces of 
sporocysts. In the case of rediae, Cheng (1962, 
1963c) found that the ingestion of the host’s 
cells is the primary method of nutrient acquisi- 
tion, although some absorption may occur 
through the body wall also. This, again, appears 
to be corroborated by the finding of microvilli 
on redial walls by Bils and Martin (1966), 
Rees (1966), and Cheng and Hamamoto 
(unpubl.). For a detailed account of nutrient 
acquisition and contents of intramolluscan larval 
trematodes, see the reviews by Cheng (1963^, 
1967). 
Relative to the relationship between nutri- 
tion and compatibility and incompatibility, it 
may be asked whether the introduction of 
germinal sacs to some site within its natural 
molluscan host, or into a foreign host, where 
the physico-chemical nature of the host-parasite 
interphase prevents the uptake of nutrients could 
cause the parasite to fail to become established. 
For example, could the destruction of heavily 
encapsulated germinal sacs in incompatible hosts 
actually represent, at least in part, death due 
to starvation? 
It is known that the rate of cercarial develop- 
ment is dependent upon the amount of food 
assimilated by the snail host and upon the num- 
ber of larvae competing for the available nutri- 
ents in the snail, among other factors (Kendall, 
1949). It would follow that, even if the host- 
parasite interphase is favorable for nutritional 
uptake but nutrients are not sufficiently available 
as the result of a poorly nourished host or be- 
cause of competition between a large number 
of germinal sacs, normal development could not 
occur — and this would constitute incompatibility. 
Lethality to Host 
Surprisingly little information is available 
pertaining to the lethality of trematode larvae 
to molluscs. Some investigators (Rees, 1931; 
Kendall, 1964; and James, 1965) have sug- 
gested that during certain mollusc-trematode 
associations death of the host does not occur. 
Yet Schreiber and Schubert (1949) and Pan 
(1965), both working with B. glabrata para- 
sitized with S. mansoni, have shown that a 
high incidence of mortality does occur. In fact, 
Schreiber and Schubert went as far as to quote 
a "half life” for parasitized snails. These known 
mortalities, however, cannot be considered to 
reflect incompatibility, since the parasites do 
develop normally and death, as Faust and Hoff- 
man (1934), Schreiber and Schubert (1949), 
and Pan (1965) have pointed out, has resulted 
from the rapid multiplication of larvae and 
mass emergence of cercariae. From the available 
information, it would appear that the death of 
molluscs resulting from invasion by "patho- 
genic” trematodes is extremely rare. No in- 
disputable examples have yet been reported, al- 
though Kendall (1950) has shown that Fas- 
ciola hepatica does inflict conspicuous deleteri- 
ous effects on Lymnaea stagnalis , L. palustris , 
and L. glabra , but not on L. auricularia. The 
fact that mass mortality seldom occurs could be 
interpreted to mean that the defense mechanisms 
of molluscs are highly efficient. 
It appears appropriate at this point to interject 
the following comment. Death of molluscs due 
to a pathogenic trematode infers extremely se- 
vere pathogenicity, a topic which has been 
reviewed recently (Cheng, 1967). Yet, despite 
known instances of drastic histopathological 
alterations in parasitized molluscs caused by 
trematode larvae, few proven cases of rapid and 
virulent deaths are known. This should serve as 
a warning to shellfisheries biologists and mol- 
luscan pathologists, who have been known to 
