Compatibility in Trematodes and Molluscs — Cheng 
151 
the parasites. On the other hand, the extensive 
capsules which surround parasites in unnatural 
hosts usually result in destruction of the para- 
sites. The chemical basis for this destruction 
remains undetermined; nevertheless, it may be 
generalized that encapsulation by leucocytes 
and/or fibers resulting in death is by far the 
most effective form of innate defense mech- 
anism in molluscs against incompatible trema- 
tode larvae. 
Although supposedly innate humoral factors 
in molluscs have been reported by various work- 
ers (see the review by Cheng, 1967), their ef- 
fectiveness as defense mechanisms against 
invading trematode larvae is unknown or un- 
certain. Recently, however, Heyneman (1966) 
has successfully demonstrated in transplantation 
studies that the inability of Echino stoma malay- 
anum to become established in Lymnaea ru- 
biginosa and of E. audyi in Indoplanorbis 
exustus is due to "physiological rejection within 
snail tissues distinct from the factors responsible 
for failure of miracidia to attach to or penetrate 
the body wall of the nonadapted host.’’ Al- 
though it would be tempting to interpret Heyne- 
man’s findings to indicate the occurrence of an 
innate humoral factor, the destruction of E. 
malayanum and E. audyi larvae could very well 
have resulted from encapsulation. Unfortu- 
nately, follow-up histological studies which 
would confirm this conclusion are not available. 
Two other examples of possible occurrence of 
innate humoral immunity which prevents the 
establishment of larval trematodes have been 
reported. Benex and Lamy (1959) showed that 
tissue extracts from the planorbid snail Planor- 
bis c omens will immobilize S. mansoni mira- 
cidia, and these French workers suggest that 
species of snails which are refractory to S. man- 
soni infection may possess "immune-like" im- 
mobilizing substances. Sudds (I960) has shown 
that when Trichobilharzia elvae miracidia pene- 
trate two abnormal hosts, Bulimnaea megasoma 
and Fossaria abrussa, the parasites die and begin 
to degenerate within 1.5-6 days, without any 
indication of a host tissue reaction. Again, it 
would be tempting to interpret these findings as 
indications of the presence of innate humoral 
immunity but, under the conditions of the ex- 
periments, other possible explanations cannot 
be completely ruled out. 
Occasionally suggestions have appeared in 
the literature (Sogandares-Bernal, 1965) that 
snails at different ages present different degrees 
of susceptibility to infection by trematode larvae. 
Most, if not all, of these reports have resulted 
from either field studies (where the ages of 
snails have been estimated by their sizes) or 
qualitative assays of infectivity. Whether such 
age-correlated resistance is due to some innate 
humoral factor or even to a cellular factor re- 
mains unknown. 
The only evidence of acquired cellular im- 
munity I have been able to find is that presented 
by Barbosa and Coelho (1956). They dem- 
onstrated that, although Biomphalaria glabrata 
previously "cured" of Schistosoma mansoni in- 
fection can be reinfected, some tissue reaction 
involving leucocytes and fibrous elements is 
evoked in reinfected snails, a phenomenon not 
found in initial infections. This finding could 
mean that some type of incomplete acquired im- 
munity exists in B. glabrata after the initial in- 
fection and is manifested during reinfection as 
cellular response. 
The belief held by some workers that ac- 
quired humoral immunity can occur in molluscs 
stems primarily from the reports of Winfield 
(1932) and Nolf and Cort (1933). These in- 
vestigators reported that the presence of Coty- 
lurus flabelliformis sporocysts in varieties of 
Lymnaea stagnalis prevents almost all of the 
cercariae of this trematode from successfully 
penetrating and encysting as metacercariae. 
Later, Cort et al. (1945) repeated these studies 
and reported that the same phenomenon occurs 
in Stagnicola emarginata angulata parasitized by 
C. flabelliformis sporocysts. They noted that the 
few cercariae which did succeed in penetrating 
were inhibited from developing into meta- 
cercariae unless they entered sporocysts and were 
thus presumably protected from the host’s anti- 
bodies. On the basis of these reports, Culbert- 
son (1941) concluded that ". . . it is clear that 
snails acquire an immunity after infection by 
trematodes. ..." Several later authors, especially 
Michelson (1963) and Cheng (1967), have 
cautioned that this generalization is unwarranted 
since, as of this date, the ability of molluscs to 
produce antibodies has not been conclusively 
demonstrated. 
The results of two other studies suggest the 
