Toxic dinoflagellate 'causing' increased mass moralities of oysters

The study of Vibrio diseases has been a prominent aspect of marine microbiology for many years, this can be attributed to their complex ecology and virulence and etiology. The yearly summer mortalities if Crassostrea gigas has been an area of interest for many years thought to be associated with Vibrio splendidus but many other Vibrios can cause the summer mortality. Many studies have commented on the complexity of this disease and can be affected by water temperature and salinity among other environmental factors.

Abi-Khalil et al., 2015 explored the associations between Alexandrium catenella a paralytic shellfish toxin producer (PST), Crassostrea gigas and Vibrio tasmaniensis which is associated with the oyster summer mortalities in this area, to determine in exposure to the PST can lead to an increases susceptibility to the Vibrio.

After observations made in 2014 that a massive juvenile oyster mortality event occurred when the sea water was between 13-17^OC and A. catenella were present in the water column at Thau Lagoon (France). C.gigas juveniles were experimentally infected with V. tasmaniensis strain LGP32, after the oysters were exposed to A. catenella, the juveniles were exposes for 48hours to A. catenella or a non-toxic alga, after 24 h exposure the oysters were injected with a lethal dose of V. tasmaniensis or sterile seawater as a control and monitored for 10 days.

The oysters that were previously exposed to A. canenella had a significantly higher mortality compared to the individuals that were starved or exposed to the non-toxic dinoflagellate. The LD₃₀  (lethal dose 30%) was calculated and for individuals feed with A. catenella reaches the LD₃₀  at day 3, while it occurred at days 7, 6 and 9 for oysters starved, fed with A. tamarense or fed with T. lutea (non-toxic algae) and no mortalities were recorded over the 10 days for individuals injected with sterile sea water.

Once the oysters died the PST levels were determined from their tissues, PSTs were not detected in the oysters which died in day 1 or 2 of the incubation, oysters that died as day 3 or on wards has accumulated enough PSTs for them to be detected in their tissues.

This study was the first of its kind and provided some interesting and surprising results, the authors hypothesis that the PSTs polarize the oyster’s immune response by triggering immune mechanisms that predidopose to bacterial infections, but protect from viral infections. They also comment that the reasons why there was no PSTs in oysters that died on day 1 and 2, it could be due to the selective uptake of toxins in the oyster tissues, metabolic interconversions and elimination of the toxins, but after a few days these mechanisms can be exhausted causing an accumulation of the toxins in the tissue.

This study showed for the first time a direct link between a previous exposure to a PST producer and the mortality induced by a pathogenic microorganism in marine invertebrates, although this paper provides some great first steps in understanding these 3 way pathogenic interactions, there is still more work that is required, and mechanisms need to be established. The Authors conclude with a statement that I wholly agree with that in addition to complex environmental factors explaining mass mortalities of bivalves, feeding on toxic algae should now be considered contributing factor, this again reinforces that after many years of study there is still a lot we need we don’t know about the complex interactions between marine invertebrates and pathogens, and unlike many terrestrial we cannot simply attribute a disease to one pathogen but an array of contributing factors that increase or may decrease the susceptibility of a  disease. 

reviewed paper:

Abi-Khalil, C., Lopez-Joven, C., Abadie, E., Savar, V., Amzil, Z., Laabir, M. and Rolland, J.-L. (2016) ‘Exposure to the Paralytic shellfish toxin producer Alexandrium catenella increases the susceptibility of the oyster Crassostrea gigas to pathogenic Vibrios’, Toxins, 8(1), p. 24. doi: 10.3390/toxins8010024.