on my thumb, so I pulled my hand away as fast as I could
- sheer reflex. When I finished the job I had a look at my
thumb; it had been sliced longitudinally with one fang,
not too deep but the cut was bleeding profusely. Being
younger and still silly, I decided to ignore it and
continued to look for another taipan. No signs of
envenomation whatsoever. I was lucky; it couldn’t be
considered a dry bite, because it wasn’t a bite at all.
Why did taipans evolve such long fangs and large venom
glands capable of producing copious amounts of super-
potent venom? The species’ main diet consists of large
avian and mammalian prey including rats, bandicoots,
possibly Giant White-tailed Rats (Uromys
caudimaculatus), etc., which are capable of inflicting
serious injuries to the snake intent on predating upon
them. Their long fangs enable taipans to inject copious
volumes of powerful venom deep into the tissues without
having to hold onto the prey item. This thereby reduces
the risk of retaliation and possible injury.
In broad terms, the taipan produces neurotoxic venom.
The key toxin, called taipoxin, affects the nervous
system, causing respiratory paralysis and subsequent
death in humans. However, there’s more to it than that.
Taipoxin is not what kills the taipan’s prey; rodents don’t
die from the neurotoxocity but instead succumb to rapid
pulmonary thrombosis. The blood in their veins and
arteries clots so quickly that they drop dead within
seconds, before the neurotoxin kicks in. Tests on
laboratory mice showed that when they were injected
with massive doses of taipoxin alone, they took much
longer to die. The cause of rapid death in mice injected
with a high dose of taipan venom is very likely due to the
thrombotic effect of the prothrombin activator. It is
somewhat puzzling that a venom that has a high
concentration of one of the most potent neurotoxic
components yet described in any snake species relies
upon an alternative mechanism (intravascular
coagulation) to dispatch prey, based in particular on the
action of procoagulants present in relatively low levels.
Taipan venom works very differently when injected into
us humans, as it’s not the procoagulant but the
neurotoxin that is the killer. So, how is this possible? It’s
simply a matter of size. Humans have a much greater
body mass than rodents, and this negates the effects of
the procoagulant. Instead of our blood turning into curd,
all of our clotting factors become used up, and it runs like
water! Because our blood will no longer clot, we wind up
with a double whammy – irreversible neurotoxicity plus
bleeding.
When the Australian continent was joined with New
Guinea by land bridge during the Pleistocene, significant
exchange of fauna occurred. Amongst the reptilian
emigrants to New Guinea were taipans. Previously
described as a subspecies (Oxyuranus scutellatus canii),
the New Guinea taipan is morphologically slightly
different from the Australian version, having an orange
dorsal stripe and a generally darker body. As a result of
recent reclassification, the subspecific status has been
rejected and both forms now comprise a single species,
Oxyuranus scutellatus. However, when it comes to
venom, there is an interesting twist. The New Guinea
taipan’s venom is six times more potent than that of its
Above: sequence of photos depicting the author catching
a Coastal Taipan in Julatten, Far North Queensland.
Images courtesy Michael Cermak.