4. ANALYSIS O F FACTORS INVOLVED I N SYMBIOSIS
131
of copepods are present or if prolonged parasitization occurs, the cilia
become depressed or lost and the cells are reduced to low cuboidal or
squamous types. Furthermore, the mucosa may become completely
eroded and, in one instance, an appendage of a copepod has been
observed to protrude into the underlying connective tissue. Although
the cause and effect process has not been demonstrated, Sparks did
report that the cellular metaplasia described above is particularly
conspicuous in ( ( gapers ”, i.e. dead oysters. It is of interest to note
that no increase of leucocytes has been found in any of the parasitized
oysters, even when the parasites perforate the gut. The significance of
this remains unclear, although in this connection it is of interest to note
that both Pillars (1921) and Griffiths and O’Rouke (1950) have
reported that inflammatory lesions are absent during the initial stages
of “ scaly-leg ” infections of fowls caused by the mite Knemidokoptes
mutans and, similarly, Yunker and Ishak (1957) have reported that
there is an absence of any inflammatory reaction in budgerigars,
Melopsitta undulatus, parasitized by Knemidokoptes pilae after the
initial perforation of the skin. It is believed that the arthropod exoskeleton may have served as an antigenically neutral shield that does
not elicit host cellular response (see Cheng, 1964b). Sparks did report
that beneath the areas of epithelial metaplasia there appears to be a
trend towards fibrosis of the underlying connective tissue, with the
cells becoming more densely packed and containing less cytoplasm.
Sparks has stated : ‘‘ This condition suggests an attempt by the organism to protect the underlying tissue by encapsulation of the copepod,
and may be a cellular aspect of resistance to a Iarge mass of foreign
material as suggested by Stauber (1961).” It has also been found that
Mytilicola orientalis, while occupying a large portion of the intestinal
lumen, will cause the distension of the gut and in one instance extrinsically occluded a nearby blood vessel.
Prom what is known about parasites which penetrate the gut wall of
molluscs, it is not surprising that cellular reaction does not occur in the
intestinal epithelium. Cheng (1966a) has shown this to be true when the
coracidium of Tylocephalum penetrates the gut wall of Crassostrea
virginica. The lack of cellular reaction even after the wall is completely perforated, as stated, may be explained by the antigenically
inert property of arthropodan cuticles. This hypothesis is in need of
further testing.
A third species of Mytilicola, M . porrecta, has been described by
Humes (1954b) in several species of marine pelecypods. Pathological
changes associated with it, if any, remain unstudied. The same is true
of a number of other copepods parasitic in molluscs.
131
of copepods are present or if prolonged parasitization occurs, the cilia
become depressed or lost and the cells are reduced to low cuboidal or
squamous types. Furthermore, the mucosa may become completely
eroded and, in one instance, an appendage of a copepod has been
observed to protrude into the underlying connective tissue. Although
the cause and effect process has not been demonstrated, Sparks did
report that the cellular metaplasia described above is particularly
conspicuous in ( ( gapers ”, i.e. dead oysters. It is of interest to note
that no increase of leucocytes has been found in any of the parasitized
oysters, even when the parasites perforate the gut. The significance of
this remains unclear, although in this connection it is of interest to note
that both Pillars (1921) and Griffiths and O’Rouke (1950) have
reported that inflammatory lesions are absent during the initial stages
of “ scaly-leg ” infections of fowls caused by the mite Knemidokoptes
mutans and, similarly, Yunker and Ishak (1957) have reported that
there is an absence of any inflammatory reaction in budgerigars,
Melopsitta undulatus, parasitized by Knemidokoptes pilae after the
initial perforation of the skin. It is believed that the arthropod exoskeleton may have served as an antigenically neutral shield that does
not elicit host cellular response (see Cheng, 1964b). Sparks did report
that beneath the areas of epithelial metaplasia there appears to be a
trend towards fibrosis of the underlying connective tissue, with the
cells becoming more densely packed and containing less cytoplasm.
Sparks has stated : ‘‘ This condition suggests an attempt by the organism to protect the underlying tissue by encapsulation of the copepod,
and may be a cellular aspect of resistance to a Iarge mass of foreign
material as suggested by Stauber (1961).” It has also been found that
Mytilicola orientalis, while occupying a large portion of the intestinal
lumen, will cause the distension of the gut and in one instance extrinsically occluded a nearby blood vessel.
Prom what is known about parasites which penetrate the gut wall of
molluscs, it is not surprising that cellular reaction does not occur in the
intestinal epithelium. Cheng (1966a) has shown this to be true when the
coracidium of Tylocephalum penetrates the gut wall of Crassostrea
virginica. The lack of cellular reaction even after the wall is completely perforated, as stated, may be explained by the antigenically
inert property of arthropodan cuticles. This hypothesis is in need of
further testing.
A third species of Mytilicola, M . porrecta, has been described by
Humes (1954b) in several species of marine pelecypods. Pathological
changes associated with it, if any, remain unstudied. The same is true
of a number of other copepods parasitic in molluscs.