I do not know whether anyone has done detailed, quantitative research to prove that its toxin gives Cb a significant ecological advantage, but in principle it is not unreasonable to suspect that it does. Cb survives in anaerobic conditions, such as in soil, compost, or rotting carcases, and if its poison causes something to die there, it has some nice, concentrated food to grow in. What is more, if any creature eats a victim, it is likely to become a victim as well, adding to the feast, and very likely establishing a new Cb colony somewhere not too close.

Not everything that swallows Cb will die from it; for example, many small invertebrates, such as grubs, will accumulate the toxin in their bodies. This even can pass in its concentrated form into the bodies of larger, predatory grubs, and when birds and some kinds of fish join the food chain, they get a hefty slug of the toxin. In a dam near our home there are practically annual bird deaths. Revealingly, they are mainly among the birds that eat plankton and small grubs; only occasionally does a larger bird succumb. The clearest example is that Egyptian geese rearing a clutch begin very well, but then the clutch is likely to thin out; the parents do fine, but babies suddenly go paralytic and die.

Why so? Because the adults and adolescents are practically herbivorous, but the youngsters need protein-rich small fry to tide them over their early growth period; you can watch them filtering out the surface water layers.

Occasionally we also find a dying plover adolescent, and I even have had to kill a paralysed ibis that probably had eaten the wrong earthworms or something.

This is commonplace among water-body conservation sites, and one of the main counter-measures is to remove as many carcases as possible as soon as possible. That suggests that the carcases are indeed sources of Cb growth.

Sorry I can't be more definitive, but I hope you find that usefully indicative.