Human envenomation by the aquatic snail genus Conus is an infrequent but potentially fatal injury amongst divers and shell collectors in the Indian and Pacific Oceans. As with other causes of neurotoxic envenomation such as Elapid snakebites, the onset of paralysis may be rapid. Death occurring within 1 h of injury has been reported. Prompt diagnosis and resuscitation, including airway protection and respiratory support, if necessary, may be lifesaving. We describe a non-fatal case of envenomation due to Conus geographus treated at Honiara Central Hospital, Solomon Islands. A 24-year-old male nurse was admitted with a 12-h history of progressive generalised weakness and poor coordination. The previous night, while collecting seashells, he had suddenly felt a mild stinging sensation in his right hand. His systemic symptoms began about 30 min after this local injury. On examination he had a small puncture wound on the middle finger of his right hand, without erythema or swelling. He was dysarthric, had bilateral ptosis, and an absent gag reflex. All peripheral muscle groups were weak, and his coordination was impaired without cerebellar features. His peak expiratory flow rate was 290 L/min (predicted 600 L/min). The remainder of his physical examination was normal. The shell responsible for the injury was recovered by his relatives (figure). He was admitted for observation and a portable pulse oximeter was used to monitor the adequacy of his ventilation. His oxygen saturation remained above 95% on room air. 12 h after admission he developed acute urinary retention for which he required catheterisation. Although weak, he could walk unaided after 48 h. He was discharged after 72 h at which time his physical examination was normal. When reviewed at medical outpatients a month later he had no complaints. Recorded stings by cone shells are rare. Before 1980, 16 fatalities had been recorded, 12 of which were due to C geographus. It is estimated that one quarter of all stings from this species may prove fatal. Two other species, C textile and C marmoreus, have also been reported to kill human beings, although the plausibility of these reports has been questioned on the basis of venom studies on dissected shells. Nocturnally active, carnivorous cone shells are widely distributed in tropical and subtropical waters. They are often found in shallow waters under rocks, along reefs and crawling on sand. Most human stings occur when a collector attempts to clean a freshly-caught shell, or to place it in his or her pocket. The venom is injected into the shell’s natural prey or its human victim through a harpoon-like tooth or radula. The active components, conotoxins, are predominantly polypeptides of less than 30 aminoacids. Their paralytic actions include postsynaptic blockade of the acetylcholine receptor, as well as inhibition of motor endplate depolarisation by sodium-ion channel blockade. Presynaptically, other conotoxins inhibit acetylcholine release by blockade of voltage-gated calcium ion channels. Non-paralytic toxins also exist but their actions, if any, are unknown. Despite efforts to develop an antivenom, there is no specific treatment for cone-shell poisoning and management is essentially supportive. Paralysis, when it occurs, is generally reversible within 24 h, so mechanical ventilation may be justifiable in even the most basic health-care settings. A survey of health workers at our National Referral Hospital revealed little knowledge of this condition. Our patient was a registered nurse who had lived by the sea all his life and supplemented his income by collecting shells, yet he was unaware of the dangers involved. The most likely explanation for such widespread lack of awareness is the rarity of serious envenomation. However, mild cases may go unrecognised or unreported, and fatalities may be misattributed to drowning.`
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Oct 12, 2001
Boris Wittekindt + 6
Open Access