Serum agglutinins or lectins are reported to be induced in marine moll
uscs by exposure to bacteria and may enhance bacterial clearance from
the host; however, there is a little information on possible relations
hips between lectins and protozoan parasites of molluscs. Two protozoa
ns, Haplosporidium nelsoni and Perkinsus marinus, cause mortality of e
astern oysters, Crassostrea virginica. We tested the hypothesis that i
f hemolymph agglutinins or other hemolymph proteins are important in t
he defense against these parasites, oysters with high ''baseline'' (pr
e-exposure) levels, or oysters that produce these substances after cha
llenge, should have lower parasite burdens and survive longer than ani
mals without these characteristics. In May 1990, individually labelled
oysters were placed in Chesapeake Bay, MD, where they were exposed pr
imarily to P. marinus, and in Delaware Bay, NJ, where they were expose
d to both parasites. Changes in parasite densities, total protein, and
agglutination titers were followed by repeated sampling of hemolymph
from individual animals over a year. Oysters in Delaware Bay were affe
cted initially by H. nelsoni, but mortalities from both parasites redu
ced survival to only 10% by September 1990. In Chesapeake Bay, mortali
ties were attributed to P. marinus only and survival was 36% by May 19
91. There was no correlation between survival time and individual prot
ein concentrations in samples from both locations collected during the
pre-exposure or post-exposure/pre-mortality periods. The high mortali
ty rate in Delaware Bay precluded hemolymph sampling after September 1
990, but continued collections in Chesapeake Bay showed that protein c
oncentrations eventually became inversely correlated with parasite bur
dens and survival time. This happened, however, only after most oyster
s had systemic P. marinus infections and were beginning to die. Agglut
ination titers were not correlated with parasite densities or survival
time. We conclude that the serum agglutinins tested play no role in d
efense against either H. nelsoni or P. marinus, and that differences i
n total protein were related to pathology rather than disease resistan
ce.