eMedicine Specialties > Emergency Medicine > Environmental
Snake Envenomation, Mohave Rattle
Updated: Jul 24, 2008
Introduction
Background
Envenomation by some rattlesnakes, such as the Mohave rattlesnake (formerly Mojave rattlesnake) (Crotalus scutulatus), may cause a different clinical presentation than that generally encountered after most rattlesnake bites. In addition, other species, such as the Southern Pacific rattlesnake Crotalus oreganus helleri, (formerly Crotalus viridis helleri), may cause signs and symptoms consistent with typical rattlesnake envenomation combined with signs and symptoms similar to Mohave rattlesnake envenomation. (See Snake Envenomations, Rattle for a more complete discussion of typical rattlesnake envenomation.)
Mohave rattlesnakes inhabit desert areas of the southwestern United States and central Mexico. Specimens with type A venom, which cause a different pattern of injury than other rattlesnakes, have been reported in southern California, Nevada, Utah, Arizona, Texas, and New Mexico. Populations with venom B and intergrades of types A and B venom have been found in south-central Arizona, around Phoenix and Tucson.
The Mohave rattlesnake may be difficult to distinguish from the western diamondback rattlesnake (Crotalus atrox), which inhabits an overlapping geographical range. Some Mohave rattlesnakes are greenish, but they may have a similar color as western diamondbacks. In the Mohave rattlesnake, the diamond pattern fades into bands along the caudal third of the back, whereas the diamonds continue to the tail in the western diamondback. The Mohave rattlesnake's white rings encircling the tail are much wider than the narrow black rings, whereas western diamondbacks have much more predominant black rings. The postocular stripe extends posteriorly above the mouth in the Mohave but intersects the corner of the mouth in the western diamondback. In Mohave rattlesnakes, supraocular scales are separated by fewer than 4 scales at their closest point. In western diamondbacks, at least 4 scales (usually >4) separate the supraocular scales.
This is a juvenile Mohave rattlesnake (postmortem). Note that the diamondback pattern fades into bands along the latter part of the snake's dorsum. Photo by Sean Bush, MD.
Other rattlesnakes in the Mohave rattlesnake's range and niche are distinguishable by the absence of a dorsal diamond pattern with light margins, black and white tail rings, facial stripes, or by the same criteria used to distinguish Mohave rattlesnakes from western diamondbacks.
Pathophysiology
Venom A populations of Mohave rattlesnakes possess Mohave toxin, which has been experimentally shown to induce neurotoxic effects. Mohave toxin or a similar toxin has been detected in the venom of other rattlesnake species. This toxin impairs presynaptic acetylcholine release. Mohave toxin may cause severe neurologic effects clinically, although this presentation has been reported only a few times in the literature. Envenomation by several other species of rattlesnakes has been reported to cause serious neurologic signs and symptoms (eg, severe motor weakness, respiratory difficulty).
Venom A Mohave rattlesnakes cause less local injury and less hemorrhagic/proteolytic effects than other rattlesnakes. In contrast, venom B specimens cause local, proteolytic, and hemorrhagic effects typical of other rattlesnakes. Severe rhabdomyolysis with myoglobinuric renal failure has been reported with Mohave rattlesnake envenomation. This article focuses mainly on envenomation by venom A populations of Mohave rattlesnakes.
Mortality/Morbidity
Mohave toxin is one of the most lethal venom components found in US snakes.
- Venom B populations are less lethal than venom A populations.
- At least one death has been attributed to a Mohave rattlesnake in the Annual Report of the American Association of Poison Control Centers, although a number of deaths have been documented.
- Most documented deaths are associated with bites in which the bitten individual was intentionally interacting with the snake and when a delay occurred in seeking medical care.
Sex
Males are bitten more commonly than females.
Age
Young adults are most commonly bitten.
Clinical
History
- In some cases, it may be helpful to know where the bite occurred (geographically) and whether venom A populations are known to occur in the area.
- Pain around the bite site
- Redness around the bite site
- Swelling (which may be less with Venom A Mohave rattlesnakes)
- Nausea, vomiting, or diarrhea
- Difficulty breathing
- Chest pain
- Neurologic symptoms
- Weakness
- Paresthesias
- Syncope, near syncope
Physical
- Fang marks
This is the typical appearance of a southern California Mohave rattlesnake bite site. Photo by Sean Bush, MD.
- Edema and erythema (Generally, local tissue effects are much less pronounced than typically observed after rattlesnake envenomation.)
- Tenderness surrounding bite site
- Tachycardia
- Hypotension/shock
- Myokymia (muscle movement, fasciculations)
- Neurologic effects
- Cranial nerve palsies
- Ptosis
- Diplopia
- Dysphagia
- Dysphonia
- Motor weakness (severe, generalized)
- Respiratory paralysis
- Lethargy
Causes
A large percentage of bites occur when the snake is handled, kept as a pet, or abused. These bites are considered intentionally interactive.
More on Snake Envenomation, Mohave Rattle |
 Overview: Snake Envenomation, Mohave Rattle |
| Differential Diagnoses & Workup: Snake Envenomation, Mohave Rattle |
| Treatment & Medication: Snake Envenomation, Mohave Rattle |
| Follow-up: Snake Envenomation, Mohave Rattle |
| Multimedia: Snake Envenomation, Mohave Rattle |
| References |
| Next Page » |
References
Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila). Dec 2007;45(8):815-917. [Medline].
Bush SP. Snakebite suction devices don't remove venom: they just suck. Ann Emerg Med. Feb 2004;43(2):187-8. [Medline].
Bush SP, Cardwell MD. Mojave rattlesnake (Crotalus scutulatus scutulatus) identification. Wilderness Environ Med. Spring 1999;10(1):6-9. [Medline].
Bush SP, Green SM, Laack TA, Hayes WK, Cardwell MD, Tanen DA. Pressure immobilization delays mortality and increases intracompartmental pressure after artificial intramuscular rattlesnake envenomation in a porcine model. Ann Emerg Med. Dec 2004;44(6):599-604. [Medline].
Bush SP, Green SM, Moynihan JA, Hayes WK, Cardwell MD. Crotalidae polyvalent immune Fab (ovine) antivenom is efficacious for envenomations by Southern Pacific rattlesnakes (Crotalus helleri). Ann Emerg Med. Dec 2002;40(6):619-24. [Medline].
Bush SP, Hegewald KG, Green SM, Cardwell MD, Hayes WK. Effects of a negative pressure venom extraction device (Extractor) on local tissue injury after artificial rattlesnake envenomation in a porcine model. Wilderness Environ Med. Fall 2000;11(3):180-8. [Medline].
Bush SP, Jansen PW. Severe rattlesnake envenomation with anaphylaxis and rhabdomyolysis. Ann Emerg Med. Jun 1995;25(6):845-8. [Medline].
Bush SP, Jansen PW. Severe rattlesnake envenomation with anaphylaxis and rhabdomyolysis. Ann Emerg Med. Jun 1995;25(6):845-8. [Medline].
Carroll RR, Hall EL, Kitchens CS. Canebrake rattlesnake envenomation. Ann Emerg Med. Jul 1997;30(1):45-8. [Medline].
Clark RF, Williams SR, Nordt SP, Boyer-Hassen LV. Successful treatment of crotalid-induced neurotoxicity with a new polyspecific crotalid Fab antivenom. Ann Emerg Med. Jul 1997;30(1):54-7. [Medline].
Farstad D, Thomas T, Chow T, Bush S, Stiegler P. Mojave rattlesnake envenomation in southern California: a review of suspected cases. Wilderness Environ Med. May 1997;8(2):89-93. [Medline].
French WJ, Hayes WK, Bush SP, Cardwell MD, Bader JO, Rael ED. Mojave toxin in venom of Crotalus helleri (Southern Pacific Rattlesnake): molecular and geographic characterization. Toxicon. Dec 1 2004;44(7):781-91. [Medline].
Glenn JL, Straight RC. Intergradation of two different venom populations of the Mojave rattlesnake (Crotalus scutulatus scutulatus) in Arizona. Toxicon. 1989;27(4):411-8. [Medline].
Hardy DL. Envenomation by the Mojave rattlesnake (Crotalus scutulatus scutulatus) in southern Arizona, U.S.A. Toxicon. 1983;21(1):111-8. [Medline].
Hardy DL. Fatal rattlesnake envenomation in Arizona: 1969-1984. J Toxicol Clin Toxicol. 1986;24(1):1-10. [Medline].
Jansen PW, Perkin RM, Van Stralen D. Mojave rattlesnake envenomation: prolonged neurotoxicity and rhabdomyolysis. Ann Emerg Med. Mar 1992;21(3):322-5. [Medline].
Wingert WA, Chan L. Rattlesnake bites in southern California and rationale for recommended treatment. West J Med. Jan 1988;148(1):37-44. [Medline].
Further Reading
Keywords
Mohave rattlesnake, Mojave rattlesnake bite, rattle snake envenomation, rattlesnake bite, Crotalus scutulatus, Mojave rattlesnake, snake envenomation, venom A, venom B, lethal venom, antivenom
