Conotoxins are a type of poisonous biological molecule derived from the cone snail (Anderson & Bokor, 2012). The molecule itself is cysteine rich and is known to be used by the cone snail to kill its prey. People are becoming increasingly concerned about this toxin because it has been shown that human exposure to this can be lethal. Although the level of lethality is dependent on the species of cone snail it is derived from, all of the toxins are dangerous. Symptoms of exposure to conotoxins include “aintness, ptosis, poor coordination, absent gag reflex, areflexia, paresthesia’s, urinary retention, diplopia (double vision), blurred vision, speech difficulties, dysphagia, weakness, nausea, generalized numbness, and respiratory arrest (Anderson & Bokor, 2012). Therefore, it is easy to observe when someone has been infected by a conotoxin. However, it is important to consider that many of these symptoms are severe (such as respiratory arrest) and could potentially lead to death.
Conotoxins are becoming increasingly concerning in the homeland security field. There are beliefs that terrorists can take advantage of the toxic properties of this biomolecule and weaponize it by making it into an aerosol. The three toxins that are at risk of terrorist use include α-conotoxins, κ-conotoxins and δ-conotoxins because these are the three most dangerous conotoxins to humans. Furthermore, first responders would not be able to distinguish inhaled α-conotoxins from botulinum; since botulinum inhalation occurs more frequently, people would be offered incorrect treatments and therefore die before the correct diagnosis could be made. It is therefore important to understand the physical differences between the conotoxins and more common toxins like botulinum in terms of mechanism of action in the body and pharmacological structure; first responders will be able to take advantage of this information in case terrorists choose to utilize conotoxins as a weapon and be able to treat the infected patients before their condition is able to worsen.
Firstly, experiments have shown that conotoxins target and influence many of the neurotransmitter surface receptors in the brain, including glutamate, adrenergic, serotonin, and cholinergic and ion channels of sodium, potassium and calcium. The α-conotoxins, the most dangerous form of this toxin to humans, is mainly an antagonize of the nicotinic receptors in the brain. When α-conotoxins bind to the nicotinic receptors, the natural functions of these receptors are inhibited and the body experiences paralysis as a side effect. In order to fight against this toxin, physicians should therefore develop a molecule that is a competitive inhibitor of this molecule; if the natural molecule is delivered to the site and binds, normal function of the nicotinic receptor will be able to resume even in the presence of α-conotoxins. This occurs because there are more natural signals than α-conotoxins; in the majority of situations, the natural molecule will preferentially bind. Although it would be difficult to test this theory in humans, it would be advantageous to see if this method prevents paralysis in laboratory animals. Then, if conotoxins were ever truly used by terrorists, we would have an excellent idea as how to prevent death of the victims.
Even though there is a potential threat of use of conotoxins as a biological weapon, it is important to note that collecting a significant enough amount of this chemical for an attack would be difficult. A lot of conotoxins are needed to infect a victim through air or food, so the terrorists would need to find ways to gather it and reproduce it, which requires a lot of funding. Furthermore, the United States Department of Health and Human Service requires an intense monitoring process for those who handle the toxin in doses more than 100 mg. Although it is unlikely that conotoxins will be used by terrorists, we must consider this possibility and develop therapy for treatment just in case.
Anderson PD, Bokor G. (2012). Conotoxins: Potential Weapons from the Sea. J Bioterr Biodef 3:120 doi:10.4172/2157-2526.1000120