A recent retrospective analysis of 542 envenoming snakebites in southern Croatia (total population, ∼500,000) reported a mean annual incidence of bites of approximately 5 per 100,000. The most common signs and symptoms were coagulopathy, extensive swelling and edema, ecchymosis, and regional lymphadenitis, but clinical signs and symptoms of neurotoxicity such as ptosis, ophthalmoplegia, dysphagia, dysphonia, and neuromuscular weakness occurred in as many as 16% of the cases (2, 3)
(1) The venom of the Southeastern France population of
V. a. aspis seems to be PREDOMINANTLY neurotoxic
(in contrast to that of the “normal” aspis elsewhere) - or so they say in the 2002 paper, or somewhere.
(2) The venom of
V. a. ammodytes is predominantly haemotoxic, as illustrated by the statistics showing ONLY 16%
of the patients showing any symptoms of neurotoxic envenomation. They said “as many as” instead of my “only”,
but that is a usual way to stress a fact that was (at that time) rather new and surprising, rather than claiming that 0.16 is a big number as such. Actually, the team from the Split hospital in their 2006 paper used neither “as many
as” nor “only”, they just wrote down the statistics of their clinical observations. So, 16% = 0.16, that's it.
And that's what I had in mind when I said that the
V. ammodytes venom is only MILDLY neurotoxic for humans.
(Also, if I got it right, this neurotoxic component of the
V. ammodytes venom doesn't kill, and is treated as a rather
minor accompanying problem that soon goes away.)
So, why would the neurotoxic component of the venom of
V. ammodytes be more pronounced/efficient in a
hybrid like the "neurotoxic
V. a. aspis" than in its "pure, original form"? (Of course I know life is complicated, I know genetics is complicated, but still, commonsensically...?)