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Parasite Evasion of Host: Perkinsus marinus/Eastern Oyster as a Model
Interaction
G. Burresonwww.disease-watch.com/.../ CD/index/images/pm.jpg
Christina Panko
Introduction
Disease induction:
www.nwfsc.noaa.gov/.../ ec/ecotox/immuno2.jpg
Pathogen: protozoan parasite Perkinsus marinus
Host: eastern oyster, Crassostrea virginica
Environmental factors: temperature and salinity
History
Late 1940’s (Mackin, Owen and Collier)
Discovered and recorded in Louisianna oysters
Early 1950’s (Mackin)Characterized and termed “Dermo” disease
(Dermocysidium marinun)
1952 (Ray)Developed a culture technique to quantify disease
1980’s (Cheng) Oyster hemocyte research began
1990 (Vasta) Continuous in vitro culture
1995-present (Volety, Anderson, Ahmed, Schott, Vasta)
Parasite/hemocyte interaction research
Pathogen
80% infection of oysters in the Gulf of Mexico and along the U.S. Atlantic coast
Favorable environmental conditions are temp >20◦C and salinity >15ppt
Depletes host energy resources causing decreased growth and reproduction and increased mortality
Rapidly proliferates and spreads via hemolymph (oyster blood) through tissues causing deterioration and organ failure
www.jaxshells.org/ guide.htm
S. Bowerwww.disease-watch.com/.../ CD/index/images/pm.jpg
www.vims.edu/env/research/ shellfish/gallery.html
Host
Innate immune system, both humoral and cell-mediated
Humoral=lectins, lysozyme, and uncharacterized hemolymph proteins
Cell-mediated=hemocytes (main effector cells)
Hemocytes function in wound repair, shell repair, internal defense mechanisms, excretion, and nutrient digestion and transport
Phagocytosis is the main effector function of hemocytes
P. marinus/hemocyte Recognition and Eventual Phagocytosis
Conjugate cell surface receptors mediate pathogen entry into the hemocyte
Hemocytes have both membrane-bound and soluble lectins with specificity for galactose residues
Coincidentally, P. marinus has cell-surface ligands composed of galactose
Lectin recognition of non-self induces binding between the conjugate receptors on hemocytes and P. marinus. Once bound, signal transduction occurs and the hemocyte receives signals to activate a cellular response (i.e. phagocytosis)
Soluble lectins in the circulating hemolymph may enhance cell surface receptor
recognition through opsonization (flag to mark particles as foreign and facilitate their recognition and phagocytic removal)
P. marinus Engulfed by a Hemocyte
S. Bower www.disease-watch.com/.../ CD/index/images/pm.jpg
Contrary to other protozoan parasites, P. marinus adapted a mechanism to
gain entry into hemocytes by specifically presenting cell surface ligands
that are rapidly recognized by the hemocyte cell surface lectins
When hemocytes phagocytose P. marinus, it facilitates rapid intracellular
proliferation
P. marinus Secreted/Excreted
Scavenging Enzymes
P. marinus subverts an array of intracellular toxic ROI’s through an
“offensive response” before a host defensive challenge
Enzymes: 1. Superoxide dismutase (SOD)--catalyzes the oxidation and
reduction of superoxide to oxygen and hydrogen
peroxide
2. Ascorbate dependent peroxidase (APX)—may
potentially convert hydrogen peroxide to water
3. Protein phosphatases (PP)—may destabilize
NADPH oxidase(remove phosphate group)
Collectively the P. marinus SODs, APXs, and PPs may
provide an advantage for the parasite to evade the host
Significance
1. Design more insightful therapeutic targets
2. Apply therapies in aquaculture to rebuild commercial output and potentially restore wild populations
3. Serve as a model of intracellular parasite evasion of host that parallels human intracellular parasites (i.e. Malaria parasite)