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<< Bites and Stings Snakes, Spiders, and Scorpions in the United States

Part III. Scorpions: Epidemiology, Etiology, And Pathophysiology

Epidemiology

Centruroides exilicauda is found throughout Arizona and other adjacent areas in the Southwestern United States. Parts of Texas, northern Mexico, and small areas of California also have C. exilicauda populations. Scorpion envenomations are a relatively common occurrence in the southwestern United States. In 2005, the American Association of Poison Control Centers reported 14,521 nationwide reports of scorpion envenomations, with 4074 occurrences in patients less than 19 years of age. Twenty patients were considered to have "major" or life-threatening outcomes, but no deaths were reported.5,88,89

Etiology

Centruroides exilicauda (previously known as Centruroides sculpturatus) or bark scorpion is the only scorpion in the United States of medical importance with venom potent enough to produce a potentially life threatening illness. It ranges in size from 13 - 75 mm, depending on maturity. Centruroides exilicauda has slender pincers which are about six times as long as the broadest part of the arthropod. It also has a small tubercle located at the base of the stinging apparatus and the proximal tail segment is rectangular rather than square-shaped. Its five segmented tail contains a bulbous end segment called the telson that contains the venom apparatus which stings rather than bites. The venom apparatus contains a pair of venom glands and a stinger. Centruroides exilicauda is unique in that it is a climbing species and never burrows. As the common name "bark scorpion" describes, this scorpion prefers to live in or near trees. They are not aggressive and usually only sting when handled or threatened. Centruroides exilicauda sting by grasping the victim's flesh with their pincers and repeatedly thrusting their tail over their bodies into their victim.6,31,88,90

Pathophysiology

Centruoides exilicauda venom contains two groups of neurotoxins which are heat stable low molecular weight proteins that bind to sodium channels. One group, termed "stabilizers," causes incomplete sodium channel inactivation, resulting in a prolongation of the action potential. A second group induces a slowly developing inward sodium current after membrane repolarization which results in sodium channel activation and cell membrane depolarization. These toxins prolong the action potential and enhance membrane depolarization by producing inward sodium currents at more negative membrane potentials, causing repetitive firing of neuronal axons. This results in over-stimulation of sympathetic and parasympathetic nervous systems, resulting in excessive acetylcholine and catecholamine release. Ultimately, catecholamine induced myocarditis, dysrhythmias, myocardial ischemia, and myocardial infarction may occur.31,88,91

As in the case of the black widow spider venom, there are no local cytotoxins so there is usually no erythema, swelling, or blanching at the site of the sting. Peripheral motor neuron and cranial nerve manifestations may appear in small children, including uncontrolled jerking movements of the extremities, peripheral muscle and tongue fasciculation, roving eye movements, and facial twitching. Severely  affected infants may be misdiagnosed as experiencing seizures and respiratory distress.6,88

Symptoms develop rapidly after envenomation, peak after several hours, and may persist for one to two days.92


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Last Modified: 06/27/2017
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