104
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
9. Cells are altered from the columnar to the squamous type, especially
hepatopancreatic cells.
10. Displacement of hepatopancreatic tubules occurs.
11. Abnormal mitosis in the form of multipolar spindle fibers may occur.
12. Veins in the intertubular spaces in the hepatopancreas may be
13. Changes in the carbohydrate, lipid, and protein compositions of cells
ruptured.
occur (discussed under Section 11, A, 3).
Apparently the amount of damage inflicted by trematode larvae is in
most instances directly proportional with the number of parasites
present (Kikuth and Gonnert, 1948) and is also correlated with the type
of larva present. Cheng (1962), for example, has pointed out that
rediae, because of their capacity to actively ingest host cells, inflict
comparatively more damage than do sporocysts. Similarly, Brown
(1926) has shown that echinostomes, which possess a redial stage or
stages, cause more damage than certain other species. Brown has also
pointed out that stylet-bearing cercariae cause more damage.
Little is known about the lethality caused by trematode-induced
pathology. F. G. Rees (1931) has expressed the opinion that in spite of
the damage done to the hepatopancreas, the vitality of the mollusc
does not appear to be greatly reduced. Similarly Kendall(1964) considers
that infected molluscs “ suffer ” only moderately, at least during the
initial stages of infection, Faust and Hoffman (1934) are also of the
opinion that negligible damage occurs during the initial stages of
infection since the first generation larvae are generally very few;
however, they believe that as the result of asexual multiplication and
rapid cercarial development, the tunica propria of the host’s hepatopancreas may become ruptured, which commonly leads to death.
Working with Australorbis glabratus infected with Schistosoma mansoni,
Schreiber and Schubert (1949) went as far as to quote a ‘‘ half-life ”
for infected snails and have suggested that the frequent stimuli to shed
cercariae is most probably what shortens the life-span. Similarly Pan
(1965) has indicated that the high mortality of parasitized snails
coincides with the heavy emergence of cercariae and the appearance of
severe generalized tissue reactions.
It is generally agreed that parasitized molluscs are more prone to
die if they are maintained under adverse conditions. Kendall(l964) has
suggested that parasitized snails exposed to stress, e.g. excessive
heat, have shorter life-spans. Olivier et ul. (1953) have reported that
S. mansoni-infected A. glabrutus are less able to withstand long periods
under anaerobic conditions than uninfected ones. At least some of the
infected snails included much less polysaccharides than uninfected ones.
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
9. Cells are altered from the columnar to the squamous type, especially
hepatopancreatic cells.
10. Displacement of hepatopancreatic tubules occurs.
11. Abnormal mitosis in the form of multipolar spindle fibers may occur.
12. Veins in the intertubular spaces in the hepatopancreas may be
13. Changes in the carbohydrate, lipid, and protein compositions of cells
ruptured.
occur (discussed under Section 11, A, 3).
Apparently the amount of damage inflicted by trematode larvae is in
most instances directly proportional with the number of parasites
present (Kikuth and Gonnert, 1948) and is also correlated with the type
of larva present. Cheng (1962), for example, has pointed out that
rediae, because of their capacity to actively ingest host cells, inflict
comparatively more damage than do sporocysts. Similarly, Brown
(1926) has shown that echinostomes, which possess a redial stage or
stages, cause more damage than certain other species. Brown has also
pointed out that stylet-bearing cercariae cause more damage.
Little is known about the lethality caused by trematode-induced
pathology. F. G. Rees (1931) has expressed the opinion that in spite of
the damage done to the hepatopancreas, the vitality of the mollusc
does not appear to be greatly reduced. Similarly Kendall(1964) considers
that infected molluscs “ suffer ” only moderately, at least during the
initial stages of infection, Faust and Hoffman (1934) are also of the
opinion that negligible damage occurs during the initial stages of
infection since the first generation larvae are generally very few;
however, they believe that as the result of asexual multiplication and
rapid cercarial development, the tunica propria of the host’s hepatopancreas may become ruptured, which commonly leads to death.
Working with Australorbis glabratus infected with Schistosoma mansoni,
Schreiber and Schubert (1949) went as far as to quote a ‘‘ half-life ”
for infected snails and have suggested that the frequent stimuli to shed
cercariae is most probably what shortens the life-span. Similarly Pan
(1965) has indicated that the high mortality of parasitized snails
coincides with the heavy emergence of cercariae and the appearance of
severe generalized tissue reactions.
It is generally agreed that parasitized molluscs are more prone to
die if they are maintained under adverse conditions. Kendall(l964) has
suggested that parasitized snails exposed to stress, e.g. excessive
heat, have shorter life-spans. Olivier et ul. (1953) have reported that
S. mansoni-infected A. glabrutus are less able to withstand long periods
under anaerobic conditions than uninfected ones. At least some of the
infected snails included much less polysaccharides than uninfected ones.