122
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
found that the mean shell diameter of parasitized adolescent snails is
larger than that of non-parasitized snails during the f i s t few weeks
after infection but parasitized snails eventually become stunted.
Similarly, Menzel and Hopkins (1955a,b) basing their conclusion on
the growth rate of a single specimen of Crassostrea virginica, have
suggested that parasitic castration by Bucephalus cuculus causes
unusually fast growth during the first year of its life, followed by a lag
slightly behind that of uninfected oysters. Eventually it fails to gain
in length or height during the last two months of the experiment.
Although gigantism in the form of weight gain has been reported in
a number of parasitized hosts, including sheep infected with Fasciola
hepatica (Neumann, 1905), lambs infected with trichostrongylid
nematodes (Whitlock, 1949), Australorbis glabratus infected with
Schistosoma mansoni (Chernin, 1960 ; Pan, 1962), rats infected with
Trypanosoma lewisi (Lincicome and Shepperson, 1961 ; Lincicome et al.,
1960, 1963 ; Lincicome, 1963), and mice (Mus domesticus), deer mice
(Peromyscus sp.) and hamsters (Cricetus sp.) experimentally inoculated
with the plerocercoid (spargana) larvae of Spirometra mansonoides
(Mueller, 1962, 1963, 1965a,b), the exact causes of the increased growth
in all these hosts remain uncertain except that in the instances of
parasitic obesity in rodents caused by S. mansonoides spargana, Mueller
( 1965a) has hypothesized that some worm-produced hormone may leak
out into the host system and in some manner influence the host. Even
in the detailed studies by Rothschild, the explanation offered, i.e.
parasitic castration, leaves a great deal to be desired since this
presumes the existence of a hormonal system in molluscs comparable
to that in birds and mammals where caponization or castration is
known t o bring about increased growth. It has only been in recent
years that gonadal hormones have been demonstrated in gastropods
(Abeloos, 1943 ; Laviolette, 1954, 1956) but their influence on growth
has not yet been conclusively determined (Charniaux-Cotton and
Kleinholz, 1964). Even less is known about the gonadal hormones of
pelecypods.
Recently, Zischke and Zischke (1965), in a preliminary note, have
reported that observations on the growth of experimentally infected
snails, specifically Stagnicola palustris infected with Echinostoma
revolutum, indicate that the infected ones grew more slowly during the
60 days post-infection than the uninfected control snails, and Cheng
et al. (1966) have found no significant differences in the shell and soft
tissue weights of Nitrocris dilatatus parasitized by Prosthodendrium
(Acanthatrium) anaplocami. Thus it would appear that gigantism in
trematode-infected snails is not a consistent phenomenon.
MARINE MOLLUSCS AS HOSTS FOR SYMBIOSES
found that the mean shell diameter of parasitized adolescent snails is
larger than that of non-parasitized snails during the f i s t few weeks
after infection but parasitized snails eventually become stunted.
Similarly, Menzel and Hopkins (1955a,b) basing their conclusion on
the growth rate of a single specimen of Crassostrea virginica, have
suggested that parasitic castration by Bucephalus cuculus causes
unusually fast growth during the first year of its life, followed by a lag
slightly behind that of uninfected oysters. Eventually it fails to gain
in length or height during the last two months of the experiment.
Although gigantism in the form of weight gain has been reported in
a number of parasitized hosts, including sheep infected with Fasciola
hepatica (Neumann, 1905), lambs infected with trichostrongylid
nematodes (Whitlock, 1949), Australorbis glabratus infected with
Schistosoma mansoni (Chernin, 1960 ; Pan, 1962), rats infected with
Trypanosoma lewisi (Lincicome and Shepperson, 1961 ; Lincicome et al.,
1960, 1963 ; Lincicome, 1963), and mice (Mus domesticus), deer mice
(Peromyscus sp.) and hamsters (Cricetus sp.) experimentally inoculated
with the plerocercoid (spargana) larvae of Spirometra mansonoides
(Mueller, 1962, 1963, 1965a,b), the exact causes of the increased growth
in all these hosts remain uncertain except that in the instances of
parasitic obesity in rodents caused by S. mansonoides spargana, Mueller
( 1965a) has hypothesized that some worm-produced hormone may leak
out into the host system and in some manner influence the host. Even
in the detailed studies by Rothschild, the explanation offered, i.e.
parasitic castration, leaves a great deal to be desired since this
presumes the existence of a hormonal system in molluscs comparable
to that in birds and mammals where caponization or castration is
known t o bring about increased growth. It has only been in recent
years that gonadal hormones have been demonstrated in gastropods
(Abeloos, 1943 ; Laviolette, 1954, 1956) but their influence on growth
has not yet been conclusively determined (Charniaux-Cotton and
Kleinholz, 1964). Even less is known about the gonadal hormones of
pelecypods.
Recently, Zischke and Zischke (1965), in a preliminary note, have
reported that observations on the growth of experimentally infected
snails, specifically Stagnicola palustris infected with Echinostoma
revolutum, indicate that the infected ones grew more slowly during the
60 days post-infection than the uninfected control snails, and Cheng
et al. (1966) have found no significant differences in the shell and soft
tissue weights of Nitrocris dilatatus parasitized by Prosthodendrium
(Acanthatrium) anaplocami. Thus it would appear that gigantism in
trematode-infected snails is not a consistent phenomenon.