Parasite immune system evasion -- assigned article 9 Sept 2014 Kenneth Bixgorin

a. The parasite studied was the tapeworm Schistocephalus solidus. The mechanism postulated was a
switch in surface sugar antigen between host stages. A copepod (crustacean) eats the coracidium.
Then, the procercoid larva penetrates the gut. A fish eats the copepod, and the parasite grows as a
plerocercoid, and, finally, a bird eats the fish.

b. The authors investigated by mixing tapeworm procercoid and plerocercoid forms with lectins
(membrane-type glycoproteins), specific to different sugars, and tagged them with different
fluorescent dyes. The results were found via epifluorescent microscopy using different filters for each
dyed lectin, and hence, for each sugar type. Procercoids (from copepods) bound galactose and NAc
galactosamine, and procercoids (from fish) bound sialic acid and NAc glucosamine. This result was
fitting, as sialic acid covers all vertebrate cells, and it is these residues that the parasite evades.
Additionally, the procercoid contains galactose on the surface layer and NAc glucosamine in the
interior, fitting the expectation that during metamorphosis, the parasite loses its outer surface layer,
exposing the interior sugars.

c. Further questions involve researching the relationship between sugar composition and fitness. A
high sialic acid content in fish plerocercoids correlates with poor infectivity (innate immunity) but large
body size, related to large numbers of eggs (adaptive immunity suppression. Also, the authors wished
to study the procercoid's oncosphere but were unable to remove the outer layer of the coracidia.

d. The mechanism discussed in the article is listed in our textbook's tables as antigen variation (here
between developmental stages) and molecular mimicry (using sialic acid).