Role of nitric oxide in the defenses of Crassostrea virginica to experimental infection with the protozoan parasite Perkinsus marinus

2007 ◽  
Vol 31 (10) ◽  
pp. 968-977 ◽  
Author(s):  
Luisa Villamil ◽  
Javier Gómez-León ◽  
Marta Gómez-Chiarri
1995 ◽  
Vol 47 (1-2) ◽  
pp. 121-126 ◽  
Author(s):  
Patricia Petray ◽  
Esmeralda Castaños-Velez ◽  
Saul Grinstein ◽  
Anders Örn ◽  
Martín E. Rottenberg

Author(s):  
M.E. White ◽  
E.N. Powell ◽  
E.A. Wilson ◽  
S.M. Ray

Perkinsus marinus, a protozoan parasite of oysters, is an important cause of oyster mortality in the Gulf of Mexico and along the south-eastern coast of the United States (Hofstetter, 1977; Quick & Mackin, 1971). Infections are patchily distributed on many reefs, often with uninfected oysters adjacent to infected oysters. The primary mechanism of transmission from one oyster to another is through the water (Ray, 1954; Mackin, 1962; Andrews, 1965). Because dilution rapidly reduces the number of infective elements below the dosage required to initiate new infections (Andrews, 1979), transmission is most efficient over very short distances and declines rapidly within a few metres of the source.


PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5046 ◽  
Author(s):  
Jennafer C. Malek ◽  
James E. Byers

Background Changes in climate are predicted to influence parasite and pathogen infection patterns in terrestrial and marine environments. Increases in temperature in particular may greatly alter biological processes, such as host-parasite interactions. For example, parasites could differentially benefit from increased reproduction and transmission or hosts could benefit from elevated immune responses that may mediate or even eliminate infections. In the southeastern United States, the Eastern oyster, Crassostrea virginica, is infected by the lethal protozoan parasite, Perkinsus marinus. Under field conditions, intertidal (air-exposed) oysters have been found to have significantly higher P. marinus infection intensity and marginally higher infection prevalence than subtidal (submerged) oysters. During summer, air temperatures are much warmer than water and this exposure of intertidal oysters to higher temperatures is a suggested mechanism for increased infection intensity. Methods We simulated intertidal exposure using controlled laboratory experiments to determine how host traits (survival and immune response) and parasite infection intensity will respond to elevated air temperature ranging from 27 °C to 53 °C during emersion at low tide. In Georgia, where our work was conducted, the average summer water temperature is 29 °C and the average maximum high air temperature in July is 33 °C (though oysters have been shown to survive at much higher air temperatures). Results Host survival declined as temperature increased, with a definitive drop-off between 39–43 °C. Negative effects of air temperature on host immune response (phagocytic activity) were detectable only at extremely high temperatures (47–50 °C) when hosts were suffering acute mortality. Parasite infection intensity peaked at 35 °C. Discussion Our results suggest that an increase in average summer air temperature to 35 °C or higher could affect oyster survival directly through temperature-related impacts in the short-term and indirectly through increased P. marinus infection intensity over the long-term.


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