attain a length of 1 cm, are housed within the radular sheath. The act of envenomation is performed by the
release of a radular tooth from the sheath into the pharynx, where it is "charged" with venom from the venom
duct and then transferred to the extensible proboscis. This appendage, which may extend in some species as
far back as the spire of the shell, grasps the venom-impregnated and barbed tooth and thrusts it into the flesh
of the victim. The venom is composed of biologically active peptides (to date, more than 100 "conotoxins"
have been identified) of 13 to 35 amino acids in length. Smaller peptides are probably strategic from an
evolutionary perspective because of the speed of diffusion through a poisoned fish. The venom targets are
neuromuscular transmission and ion channels. At the same site as tetrodotoxin and saxitoxin,
µ-conotoxins
bind and modify muscle sodium channels. Voltage-dependent calcium uptake at the presynaptic cleft and
cholinergic transmission in avian and mammalian neuromuscular junctions are inhibited by
-conotoxins like
that from Conus geographus. These omega-conotoxins bind to neuronal (N-type) rather than the cardiac (L-
type) calcium channels, which prevents the calcium influx necessary for neurotransmitter release. Ziconatide
is a conotoxin under investigation at the time of this writing as a potent analgesic intended for human
application directly to the spinal cord and to prevent cell death in the brain after head trauma and ischemic
events. The
-conotoxins block the nicotinic acetylcholine receptor.
A sleeper peptide in C. geographus
venom causes test animals to enter a deep sleeplike state. If the observation that certain contoxins target N-
methyl-D-aspartate (NMDA) receptors can be translated into an effective drug, this may lead to another
approach to the treatment of epilepsy. Serotonin is present in venom from the cone snail C. imperialis, which
is a worm feeder. In the act of envenomation, milky venom from the venom duct is transformed into a clear
product, which may indicate conversion from an ineffective to effective toxin.
Clinical Aspects. Most stings occur on the fingers and hand, as the unknowledgeable fossicker
incorrectly handles a hazardous specimen. Mild stings are puncture wounds that resemble bee or wasp stings,
with associated burning or sharp stinging sensation. The initial pain is followed by localized ischemia,
cyanosis, and numbness in the area surrounding the wound. Numbness may occur without preceding pain, or
in a rare case, the envenomation may be without any specific dermal sensation. More serious envenomations
induce paresthesias at the wound site, which rapidly encompass the limb and then become perioral prior to
generalized. Partial paralysis transitions to generalized muscular paralysis causing diaphragmatic dysfunction
and respiratory failure; bronchospastic respiratory distress is not commonly seen. Coma has been observed,
and death is attributed to diaphragmatic paralysis or cardiac failure. Other symptoms include dysphagia,
syncope, weakness, failing coordination, areflexia, aphonia, dysarthria, diplopia, ptosis, absent gag reflex,
blurred vision, and pruritus. The bite of C. geographus may be rapidly toxic, with progression to cerebral
edema, coma, respiratory arrest, and cardiac failure within a few hours, perhaps even one hour. While mild
stings may cause symptoms of nausea, blurred vision, malaise, and weakness for only a few hours, a severe
envenomation may induce symptoms that require 2 to 3 weeks to achieve total resolution. C. textile and C.
marmoreus have been reported to kill humans. A fatality has been attributed to C. gloria-maris, but this has
not yet been confirmed.
77
Treatment. No antivenom is available for a cone shell envenomation. Numerous
therapies have been recommended, including the pressure-immobilization technique, application of a
proximal lymphatic-venous occlusive bandage, incision and suction, soaking in nonscalding hot water to
tolerance (upper limit 113
o
F or 45
o
C) until pain is relieved, injection of a local anesthetic (lidocaine 1% to
2% without epinephrine), and local excision. The pressure-immobilization technique makes sense and should
be applied.
Cardiovascular
and
respiratory
support are the usual priorities after a severe envenomation. The
wound should be inspected for the presence of a foreign body (radula). Edrophonium (10 mg intravenously in
an adult) has been suggested as empirical therapy for paralysis. A rational approach would be to administer an
edrophonium (Tensilon) test to determine effectiveness. The clinician should choose a weak muscle group for
which strength can be objectively measured, then inject edrophonium 2 mg IV. If there is improvement, this is
followed by edrophonium 8 mg IV. Adverse reactions to edrophonium (anticholinesterase inhibitor) include
salivation, nausea, diarrhea, and muscle fasciculations. These can be ameliorated with atropine 0.6 mg IV.
Cone shells should be handled only when wearing proper gloves; if the proboscis protrudes, the cone should
be dropped. If the animal must be carried, it should always be lifted by the large posterior end of the shell,
