Paralyzing people, but what about the shellfish?
So
we know the economic implications of paralytic shellfish poisoning
(PSP) caused by harmful algal blooms (HABs) as well as the effects in
human health (i.e. paralysis) but what effects does the toxin have on
one of it's phycotoxin vectors, the Pacific oyster?
Mello
et al., (2013) set out to
compare the effects of a saxitoxin (STX) producing algae, Alexandrium
minutum and
the STX itself on in
vitro
haemocytes of Crassostrea
gigas.
Haemocytes are the primary component of molluscan immunity so any
changes in their behaviour could have catastrophic effects on whole
populations. In
vitro
also provides a much more controlled environment with less
inter-individual variability then using whole organisms, especially
where pooled haemolymph samples are used as was in this case. A.
minutum
and STX both caused significant reductions in phagocytic ability of
haemocytes though only A.
minutum
alone caused swelling of haemocytes. This is indicative of the oyster
mounting an immune response with the cells increasing in size ready
for phagocytosis, however there seems to be a mechanism relating to
the algae and toxin that reduces their ability to do this.
Furthermore both treatments had negative impacts on the oxidative
burst, a mechanism by which the haemocytes produces reactive oxygen
species (ROS) to damage invading pathogens. This was most pronounced
in the STX only treatment with between 72 and 80% reductions. As well
a looking at functional biomarkers the authors used the quantitative
polymerase reaction (qPCR) to determine expression of immune and
stress related genes was modulated. Of the genes studied, four
showed some level of up or down regulation relating to STX and one
was up-regulated by the presence of A.
minutum. This
gene was an interleukin (IL-17),
which are usually related to inflammation, so this could signify the
preparation of an immune response in relation to algal infection. In
contrast, the STX treatment caused a reduction in expression of
IL-17.
STX seems to inhibit the interleukin's production and the difference
is likely due to differences in the bioavailability of the toxin
between treatments, as A.
minutum cultures
generally have a low extracellular toxin level until they are 30 days
old (6 days old in this experiment). However the mechanism for
reduction is unclear. The heat shock protein (HSP) gene HSP70
was
up-regulated by STX implying that the toxin has a denaturing affect
as this HSP is a chaperone that acts against misfolded proteins.
Similarly defensin, an antimicrobial peptide (AMP), has increased
expression under STX treatment. AMPs are poorly understood relating
to xenobiotics but it could be due to the oyster recognising STX as a
pathogenic product and preparing for infection, this is however wild
speculation on my part and would need to be studied further. The only
other change in expression was relating to biotransformation. The
down regulation of CYP356A1
by
STX could leave oysters vulnerable to other harmful chemicals though
further research into the synergistic effects would need to be
carried out.
So
from this research it appears that the immune system of the Pacific
oyster is indeed compromised by STX and Alexandrium.
The implication of this is potential infection by other pathogens
which would be devastating for fisheries already impacted by HABs.
However the immune response is very complicated and just looking at
11 genes is not enough. There are many isoforms of CYPs and HSPs in
oysters and these may be activated/deactivated as part of the
response. Ideally transcriptome wide expression would be carried out
for the two treatments and then all differences could be observed.
This is unlikely at the current price but if HABs continue to
increase in frequency it might be an avenue worth investigating in
the future.
Mello,
D. F., Silva, P. M. da, Barracco, M. A., Soudant, P., & Hégaret,
H. (2013). Effects of the dinoflagellate Alexandrium minutum and its
toxin (saxitoxin) on the functional activity and gene expression of
Crassostrea gigas hemocytes. Harmful Algae, 26, 45–51.
I always wondered what effects these toxins must have on the algae bloom feeding shellfish; this study sounds very interesting. As you mentioned, the immune response is dramatically restricted by the toxin if introduce directly, but it still appears that the bivalve is able to cope. Since the dinoflagellates are ingested by the oysters, it could be possible that the animals may have associated gut bacteria that can degrade the toxin/dinoflagellates of some kind and or may be aid the host by the eliminating other pathogenic bacteria/viruses that could harm the oysters even more. Do you know where the authors have introduced the stx to the oysters in this study? May be the response of the host is more extreme depending on the tissues where they are introduced to?
ReplyDeleteThe STX was added to pools of haemolymph maintained in vitro i.e. in a test tube or similar vessel. I did think that perhaps in the time it takes to produce significant levels of toxin (similar to that which has the negative effect) the oysters may have already rid themselves of the dino's or maybe are constantly removing the alga meaning an effective STX concentration is never reached.
ReplyDeleteBy suppressing bivalve immune systems, could harmful dinoflagellates be setting the scene for pathogens such as Vibrio vulnificus to persist in these molluscs, increasing the chance of other types of shellfish poisoning?
ReplyDeleteSeems a reasonable assumption, depending on the parameters that are suppressed. On this case where phagocytosis is reduced this applies to any invading pathogen so the build up of other species could well follow though interspecific competition between pathogens would have to be considered, perhaps the saxitoxin would have some effect on, for example Vibrio vulnificans. Either way you would hope that the presence of STX would be detected and the stock removed from the supply chain before consumption so hopefully no pathogens would reach the consumer. You'd hope.
ReplyDelete