Venomous snakes of Southwest Asia

Reviews

Venomous Snakes of Southwest Asia MARCO COPPOLA, DO, CPT, MC,* DAVID E. HOGAN, DO, MAJ, MC*t Although no official statistics have been released, unofficial reports from physicians in Southwest Asia indicate a higher number of venomous snake bites than previously expected. Because of the possibility that troops will be stationed in this region for an extended period of time, this article serves as a reference on the type and characteristics of snakes found in the region. A brief description of the common venomous snakes and a general geographic distribution is given. Also discussed is the reported medical implications of envenomation from each animal and the availability of antivenom. THESNAKES The more common and medically important venomous snakes endemic to Southwest Asia are listed in Table 1. The primary genera represented are the Viperidae and Elapidae. In general, vipers cause most of the snakebites. The Elapids, of which the cobra is a member, exist in the area but inflict fewer bites and cause less morbidity. The Elapidae Naja haje, the Egyptian cobra, was sacred in ancient Egypt and was represented on the crown of the Pharaohs. The reptile is found throughout Africa but can also be found in the western part of Saudi Arabia, the eastern part of Jordan, and throughout Yemen (Figure 1). The snake’s head is flat and and it’s neck is capable of wide flaring which forms the characteristic hood. The color may vary from brownish yellow to black. Their length varies from 4 to 8 ft with the average being 5 to 6 ft. These snakes are found close to villages but tend to stay in bushes, rocky areas, and rodent burrows. They prey mostly on reptiles and amphibians but will also eat small mammals and birds. Egyptian cobras are From the Department of Emergency Medicine, *Darnall Army Community Hospital, Fort Hood, TX; and Tthe Division of Emergency Medicine, Department of Medicine, Texas A&M University, College of Medicine, College Station, TX. Manuscript received May 6, 1991; revision accepted December 30, 1991. Opinions or assertions contained herein are the private views of the authors and should not be construed as official or as reflecting the views of the Department of the Army or the Department of Defense. Address reprint requests to Dr Coppola, Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, TX 76544-5063. Key Words: Southwest Asia, venomous snakes. Copyright 0 1992 by W.B. Saunders Company 0735-6757/92/l 003-0013$5.00/O 230

not aggressive snakes and are slow to defend themselves. When disturbed they raise their bodies off the ground and expand their neck; however, they may strike without this aggressive display. The expanded hood is remarkable among snakes and will aid in its recognition. The venom of N haje can be fatal and contains phospholipases, cardiotoxic, and neurotoxic substances.’ Antivenom is available to assist in therapy.‘,* Walterinnesia aegyptia, the desert black snake, is located in northeastern Egypt and throughout Jordan, Israel, Lebanon, Iraq, Kuwait, the southern portion of Syria, northern Saudi Arabia, and western Iran (Figures 2 and 3). Its head is small, flat, and indistinct from the neck, with size varying from 3 to 4 ft. The snake’s scales are glossy which helps distinguish it from the dull scales of the cobra. It inhabits gardens and irrigated areas, but can also be found in rocky hillsides and sandy desert regions with little vegetation. W aegyptia can strike its prey up to 3 ft away. The black snake’s venom, unlike the cobra’s, lacks cardiotoxic properties but is extremely neurotoxic.’ Interestingly there are no published reports of this snake attacking humans. Antivenom exists but has only in vitro studies supporting its use.lm3 The Viperidae Atractaspis microlepidota, the Arabian mole viper, occurs throughout central Africa and Yemen. Atractaspis engaddensis, the oasis mole viper or burrowing asp, is a second species occurring throughout Egypt and western Jordan as well as southern Lebanon and Israel (Figure 4). These snakes are very similar in appearance with small heads, long fangs, tiny round eyes, and a black body. They range in length from 18 to 25 in. They are nocturnal and are found more often in inhabited areas than in the desert. Their flexible neck enables them to bite with only one fang. The venom of A microlepidota causes mostly local irritation and edema. Fever, vomiting, and hematuria are seen in severe cases, and deaths have been reported.* The effects of A engaddensis venom have been described as hemorrhagic, neurotoxic, and cardiotoxic.4 The venom exerts a positive inotropic effect on the human heart. Coronary vasospasm has been reported as the primary cause of death with this snake.5 In mice, the venom has been shown to induce atrioventricular block and subsequent cardiac arrest.6*7 Antivenom for Atractaspis species is not available; however in 1987, Ovadia was able to show that Vipera palaestinae antivenom and ethylenediamine tetraacetic acid individually

COPPOLA

TABLE 1. Southwest

AND

HOGAN

Venomous Asia Scientific

W VENOMOUS

Snakes

Name

Elapidae Naja haje Walterinnesia aegyptia Viperidae Atractaspis engaddensis A microlepidota Bitis arietans Cerastes cerastes C vipera Echis carinatus E coloratus Pseodocerastes persicus Vipera lebetina V xanthina

Endemic

SNAKES

to the

OF SOUTHWEST

Middle

Common

East

and

Name

Egyptian cobra desert black snake

Cerastes vipera, the homless desert viper, is a second species and can be found in north Africa, Israel, southern Lebanon, and unofficially in Saudi Arabia. The C vipera is similar to C cerustes but lacks supraorbital horns. It ranges in size from 13 to 22 in. This snake is also nocturnal, spending the day buried in the sand near vegetation. The venom has mild hemorrhagic toxicity. Antivenom is available

burrowing asp Arabian mole viper puff adder horned desert viper hornless desert viper carpet viper saw scaled viper Persian horned viper levantine viper near East viper

neutralize the in vitro hemorrhagic activity of Arructaspis venom.4 Bitis arietans, the puff adder, is found in Yemen and the southwestern portion of the Arabian peninsula as well as throughout Africa (Figures 5 and 6). This snake has been described as “. . . the greatest killer of Man”.’ It’s head is very distinct and the eyes are vertically elliptical. A diagonal light-colored band is located from the posterior aspect of the eye to the corner of the mouth. The snake’s color may vary from yellow to brown or black. Alternating dark and light chevrons on the back are unique and help to differentiate this snake from others. Average length may range from 3 to 5 ft. They are nocturnal and usually inhabit grasslands. They are not found in rain forests or in true deserts. A slow-moving snake, B arietans remains still when approached. The venom is extremely toxic and the average-sized puff adder carries enough venom to kill four to five men. Studies have shown that Bitis species venom contains the protein bitistatin which inhibits platelet aggregation and prolongs bleeding time in human and canine models.’ Further studies on Bitis venom revealed a kinin-releasing enzyme capable of hydrolyzing insulin and fibrinogen.’ Extensive tissue damage, bleeding, and death within 24 hours characterize the clinical effects of Bitis venom.” Antivenom is available.’ Cerastes cerastes gasperettii, the horned desert viper, can be found in north Africa and throughout Jordan, Israel, Saudi Arabia, southern Lebanon, the western parts of Iraq and Kuwait, and possibly throughout Syria and Yemen (Figures 7 and 8). The head is flattened and distinct from the neck, and the pupils are vertically elliptical. They escape their predators by sinking into the sand. This is accomplished through the use of lateral scales which have serrated angled keels capable of removing sand from under the animal and placing it over them. Upright spines or supraorbital horns serve to keep the eyes free of sand. The snake’s color is yellow to light brown with dark rows on the dorsum. It ranges in size from 20 to 25 in. They can be found in arid places, near rocks, or in rodent burrows. It is nocturnal and travels using a side-winding motion. The bite of C cerastes is painful but usually not serious and is rarely fatal.’ The venom induces platelet aggregation and contains both coagulant and anticoagulant components.1“‘3 Antivenom is available.

231

ASIA

2.11-13

Echis carinatus, the carpet viper, is located in Africa and India and throughout Saudi Arabia, Yemen, the United Arab Emirates, Iran, Kuwait, and southern Iraq (Figures 9 and 10). A second species, Echis coloratus, the saw-scaled viper, can be found in eastern Egypt, the southern part of Lebanon, and throughout Jordan, Israel, and the Arabian Peninsula (Figure 9). The head of both snakes is broad and distinct from the neck with a white arrowlike marking of four points: three directed posteriorly and one anteriorly. The pupils are vertically elliptical. Their color is tan to olive brown with white spots undulating laterally on the back. Both snakes attain a length from 15 to 32 in. Echis species are nocturnal in the summer and diurnal in the winter. They find shelter in almost anything from rodent burrows to rock fissures. When threatened, their bodies characteristically inflate and coil into tight “figure of eights.” Serrated scales rasp against each other and produce the sound of a saw cutting wood. Loud hissing and a savage strike follow this display. Both snakes possess a toxic venom responsible for many fatalities. Transient hemostatic failure, including disseminated intravascular coagulation, prolonged clotting time, hypofibrinogenemia, and increased fibrin split products, is the hallmark of Echis species envenomation.‘4*‘5 It is reported that hemostatic failure with E coloratus is less severe than with E carinatus. Envenomation by E coloratus is usually self-limited with full recovery expected.ls Untreated, E carinatus envenomation is associated with a 7% to 15% mortality rate.’ Echis venom contains echistatin, a powerful inhibitor of platelet aggregation, similar in action to bitistatin.‘” In 1988, Kamiguti and colleagues reported that the venom of E carinatus from Saudi Arabia was a poor activator of prothrombin and contained calcium-dependent Factor X activator,

Leban

ASwiaj n

‘\-v

FIGURE

1. Distribution

of Naja haje.

232

AMERICAN

JOURNAL

OF EMERGENCY

MEDICINE

n Volume

10, Number

3

n May

1992

Iran

Saudi

Saudi

Arabia

Arabia

ti.A.E

Oman

FIGURE 2. Distribution of Walterinnesia aegyptia.

FIGURE 4. Distribution of A (light shading).

microlepidota

(dark shading)

and

A

engaddensis

unlike venom of E carinatus from India, Iran, and Oman.” Many investigators have recommended the use of antivenom for both E carinatus and E coloratus envenomation.2.‘4“7 The main effect of E carinatus venom is increased vascular permeability and damage to the vascular endothelium. Ecchymosis and bleeding are commonly seen with Echis envenomation. Bleeding most commonly occurs from the gums but may also develop in the brain, lungs, kidneys, and gastrointestinal and urinary tracts. Bleeding may start from 1 to 36 hours after envenomation, even in antivenom-treated patients. The demonstration of noncoagulating blood is the single most important diagnostic test in E carinatus envenomation. The use of the clot quality test as described by Reid in

1963 may help to conserve antivenom.” The test should be repeated every 6 hours after the first antivenom dose until clotting is reestablished. Following this the test should be repeated daily for 3 days to ensure coagulability and that no further venom has been absorbed from the bite site. Pseudocerastes persicus, the Persian horned viper, is found in southern Lebanon, Jordan, Iran, Israel, western Iraq, Kuwait, northern Saudi Arabia, and possibly throughout Syria, Oman, and the United Arab Emirates (Figure 1I). Its head is broad and distinct from the neck with vertically elliptical pupils and dorsolateral nostrils. Like C cerastes, P persicus possessessupraorbital horns. However, the horn of Ppersicus is composed of several small scales, in contrast to the single upright spine or “horn” of C cerastes. Their color is pale or bluish gray, with a dark band on the side of the head. The maximum length is recorded at 35 in with the average length being 22 to 28 in. The snake can be found in rodent burrows and amongst rocks. The P persicus is a nocturnal snake and hisses loudly when disturbed. Although not particularly savage, it should be considered a dangerous species. The venom of the subspecies P persicus fieldii pro-

Iran

FIGURE 3. Walterinnesia Snakes of the World.‘)

aegyptia.

(Adapted from Poisonous

FIGURE 5. Distribution of Bitis

arietans.

COPPOLA

FIGURE World.‘)

AND

HOGAN

m VENOMOUS

SNAKES

OF SOUTHWEST

ASIA

233

6. Bitis arietans. (Adapted from Living Snakes of the

duces very little local tissue damage, but is highly neurotoxic. Hematologic effects are not seen with the venom of this species. Antivenom is available.” Vipera lebetina, the Levantine viper, is found throughout Syria, Lebanon, Iraq, Kuwait, Iran, Jordan, northern Israel, and Saudi Arabia and possibly Jordan (Figure 12). Its head is triangular with vertically elliptical pupils and a long slender neck. Its dorsal color is light gray or khaki with dark rectangular spots. The snake can attain a maximum length of 5 ft. The V lebetina is nocturnal and can be found in rocky desert areas. It is sluggish and appears to be unaware of stimuli during the day. At night the animal may strike quickly and savagely. It is an important cause of snake bite in the Middle East. Its venom is extremely potent and has been known to kill humans as well as camels.* Antivenom is available. Vipera xanthina, the Near-East viper, is found throughout Syria, Jordan, Israel, Lebanon, and the northern part of Iran (Figure 12). Its pupils are vertically elliptical and there is a very conspicuous dark V-shaped mark pointing anteriorly on the head. The snake’s color is yellow to brown with a dark wavy stripe broken into several segments. The maximum length is 4 ft. It is also nocturnal, spending most of the day

FIGURE 8. Cerastes cerastes. (Adapted from Living Snakes of the World.?

in crevices, burrows, and clumps of vegetation. The animal is frequently found near human settlements. The subspecies V xanthina palaestinae is the leading cause of snakebites in Israel and the surrounding area with a 5% mortality rate.‘** The venom has been shown to possess hemorrhagins, neurotoxins, and phospholipases. The antivenom available has both antihemorrhagic and antineurotoxic effects. l9 DISCUSSION The snakes of medical importance found in the region are primarily members of the Viperidae and Elapidae genera. The medical implications of snake envenomation is not unlike that in the United States, except for a higher frequency of neurotoxic effects. The Vipera are a varied group with 11 species recognized throughout the world. The Vipera of southwest Asia, with the exception of Atractaspis species, have the usual characteristics of venomous snakes; a broad head, vertically elliptical pupils, narrow neck, and cylindrical body. The venom of the Vipera species has both hemorrhagic and neurotoxic

Saudi Arabia

FIGURE 7. Distribution of C c gasperettii and C vipera (dark shading).

gasperettii

(light shading) and C c

FIGURE 9. Distribution of E carinatus (light shading), E coloratus (dark shading), and E carinatus and E coloratus (medium shading).

234

AMERICAN

JOURNAL

OF EMERGENCY

MEDICINE

l Volume

10, Number

3

n May 1992

FIGURE 10. Echis carinatus. (Adapted from Living Snakes ofthe World.*)

activity. The effects of Vipera envenomation are variable depending on the species. For example, Pseudocerastes species are mainly neurotoxic, while the venom of Echis is mainly hemorrhagic. In general, immediate onset of pain and swelling following a snake bite should be considered due to Viperidae. ’ The Elapids of the region are primarily cobras with only two species being recognized as common to southwest Asia, N naje and W aegyptia. Cobras usually expand their neckhoods in a warning gesture to encroaching creatures. Venom effects from these creatures are primarily neurotoxic and cardiotoxic. In contrast to the Viperidae, pain and swelling within 10 minutes of the bite is more characteristic of Elapidae strikes. i Snake venom is a complex mixture of substances; enzymes, ions, biogenic-amines, lipids, amino acids, and proteins. Most snake venoms have 10 to 25 major fractions with toxic properties. These properties vary with the species, season, and physiologic response of the animal to their environment .*’ Hyaluronidase can be found in many venoms, acting as a spreading factor. Proteases digest tissue and phospholipases hydrolyze lipids, disrupt neurotransmission, and cause hemolysis. *i The major effects of snake venom can be broken down into local tissue destruction, hemotoxicity, cardiotoxicity, and neurotoxicity. Local tissue destruction is generally due to tissue digestion by proteases, hyaluronidase, and myotoxins.** Even with the use of antivenom these effects can become signifi-

FIGURE 11. Distribution of Pseudocerasres persicus.

FIGURE 12. Distribution of V lebetina (dark shading)and V lebetina and V xanthina (light shading). cant. If sufftcient tissue destruction occurs, compartment syndromes may develop requiring surgical intervention. Compartment pressures should be monitored. Envenomation from B arietans usually results in the most extensive local tissue destruction of the snakes within the region.” The hematologic effects of venom are multiple. Activity of the venom on red blood cell and platelet membranes can result in hemolysis and thrombocytopenia. Other factors interfere with and activate portions of the coagulation cascade, resulting in hemorrhage and disseminated intravascular coagulation.23 Thrombin-like enzymes found in many venoms act to deplete fibrin and increase fibrin-split products. This results in inhibition of clot-stabilizing factors which enhance anticoagulation in vivo.24 Neurotoxic effects of venom often results from inhibition of acetylcholine release presynaptically. Neurologic abnormalities occur commonly after Naju, Wulterinnesia, Pseudocerastes, and Vipera species envenomations. Motor disturbances such as weakness, fasciculations, paresthesias, and paralysis result from neurotoxin B affecting the myoneural junction. *’ Dysphagia, p sy chosis, and seizures are the result of neurotoxin A affecting the central nervous system. Recent studies have shown that treatment with anticholinesterases may be of some benefit for cobra envenomation.26 As with neurotoxic envenomations in the United States from coral snakes, it may be wise to consider antivenom therapy for clearly envenonated patients even prior to neurotoxic symptomatology. The cardiovascular effects of venom are also multifactoral. Vascular endothelial injury results in changes in peripheral vascular resistance, leading to increased cardiac workload .*’ Fluid extravasation and third spacing of fluid may result in hypotension requiring high volumes of crystalloid infusion (200 to 700 mL/h) to maintain filling pressure.** Vasoactive mediators such as serotonin, bradykinin, and histamine are released by direct stimulation by the venom on mast cells. This multiplies the stress on an already overworked cardiovascular system. Myocardial ischemia and direct myocardial necrosis have been demonstrated with some venoms.29*30Envenomation by A engaddensis has been reported to cause coronary vasospasm, atrioventricular blocks, and cardiac arrest resulting in death.’ The prehospital treatment of snake envenomation involves calming the patient, keeping the extremity in neutral position, and applying a light lymphatic constriction band

COPPOLA AND HOGAN n VENOMOUS TABLE 2.

Antivenoms

and Their Country of Manufacture

Snake Name Elapidae Naje haje Wakerinnesia

Antivenomt

Country (Manufacturer)* France (Pasteur Vaccins)

aegyptia

Viperidae Atractaspis microlepidota# Atractaspis engaddensis# Bitis arietans Cerastes cerastes* Cerastes vipera* Echis carinatus Echis coloratus

Pseudocerastes Vipera lebetina Vipera palaestinae Vipera xanthina

235

SNAKES OF SOUTHWEST ASIA

persicus

Pasteur Antirept Pasteur lpser Afrique Behring Central Africa Polyvalent (in vitro studies only)

Germany (Behringwerke AG) South Africa (South Africa Institute) no antivenom no antivenom France (Pasteur Vaccins) Germany (Behringwerke Algeria (Institute Pasteur France (Pasteur Vaccins) Germany (Behringwerke France (Pasteur Vaccins) Germany (Behringwerke France (Pasteur Vaccins)

AG) d’Algeria) AG) AG)

Germany (Behringwerke AG) France (Pasteur Vaccins) Israel (Rogoff Institute) South Africa (South Africa Institute for Medical Research) Iran (Razi Medicine Company) France (Pasteur Vaccins) Algeria (Institute Pasteur d’Algeria) France (Pasteur Vaccins) Germany (Behringwerke AG) France (Pasteur Vaccins) Israel (Rogoff Institute) Germany (Behringwerke AG) Iran (Razi Medicine

Company)

available available Pasteur Antirept Pasteur lpser Afrique Behring Central Africa Antiviperin Pasteur Antirept Behring Near and Middle East Pasteur Antirept Behring North and West Africa Pasteur Antirept Pasteur lpser Afrique Behring Near and Middle East Pasteur Antirept Israel E colorata South Africa Echis carinatus Iran Persica Iran Polyvalent Pasteur Antirept Algeria Antiviperin Pasteur Antirept Behring Europe Pasteur Antirept Israel Vipera palaestinae Behring Europe Behring Near and Middle East Iran Polyvalent

See Table 3 for manufacturers’ addresses. t Antivenoms are listed in order of decreasing potency. + May use V. palaestinae antivenom and EDTA. Data from Antivenom index 7989 to 1990.32 l

proximal to the bite. Other modes of prehospital treatment such as electrical shock, incision and suction, ice, elevation, and tight tourniquet application have been recommended. However these modalities are generally considered to be detrimental. Hospital therapy of snake envenomation involves local wound care, careful observation, baseline laboratory studies, and the proper use of antivenom. Much controversy exists in the United States regarding the use of antivenom. Because antivenom is derived from horse serum, patients may be skin tested prior to its administration. Skin testing serves to make the physician aware that the patient may have a severe reaction to horse serum. A positive test should not generally deter the administration of antivenom, but rather should indicate the need for pretreatment for allergic reaction. Skin testing should not be done unless antivenin is going to be administered, as it can sensitize the patient to further administration of horse serum products. Antivenom is administered intravenously with careful observation.31 Anaphylaxis can still occur despite negative skin testing. Exact details of the complications of antivenom administration are beyond the scope of this paper.

SUMMARY This report provides a brief description of the venomous snakes encountered in Southwest Asia, as well as a brief review of the clinical implications of envenomation from each animal. Specific therapy for snake envenomation in the United States is somewhat controversial, and it is no less controversial with animals from this region. The most logical approach probably combines medical management with antivenom when available, and surgical intervention when clearly indicated due to elevated compartment pressure or massive tissue necrosis. Antivenom is available for all species except W aegyptia (in vitro only) and Atracfaspis species I-3 Antivenom for V palaestinae may be used for Atracr&is envenomation4 (Tables 2 and 3). This report is dedicated to the seven residents (Howell Davis, DO; David Dwyer, MD; James Ellis, DO; Doug Groshong, DO; Terry Hinkson, DO; Jerry Karr, DO; Kenneth Locke, DO) and four staff physicians (John Lorette, DO; Ronald Moscati, MD; Dennis Plante, MD; Tim Welter, MD) from the emergency medicine residency program at Darnall Army Community Hospital, Fort Hood, TX, who served with distinction in the Second Armored Division and First Cavalry Division during Operations Desert

AMERICAN

236

TABLE 3.

Antivenom

Manufacturers

and

JOURNAL

Addresses

Pasteur Vaccins 3, Avenue Pasteur BP 10, 92430 Marnes, La Coquette Paris, France Phone: 011 33 1 4741 7922 Behringwerke AG Behring Biologicals Postfach 1140 3550 Marburg Germany Phone: 011 49 6421

394131

South Africa Institute for Medical PO Box 1036 Johannesburg 2000 Republic of South Africa Phone: 011 27 11 725 0511

Research

Institute Pasteur d’Algeria Rue Du Doctuer Laveran Alger, Algeria Phone: 011 213 2 672 344 Rogoff Institute Beilinson Hospital Tel-Aviv University Tel-Aviv, Israel Phone: 011 972 3 937 6741 Razi Medicine Company B.P. Box 11365-1558 Tehran, Iran Phone: 011 96 21 926 367 Data

from

Antivenom

Index

1989

to 7990.32

Shield and Desert Storm. They were among the first to take the skills of emergency medicine to the battlefield. Special thanks is directed to AT&T for verifying the addresses and phone numbers found in Table 3, and to the staff of the Arizona Poison Control Center in Tucson for assistance in obtaining many of the references.

REFERENCES 1. Dowling HG, Minton SA, Russel FE: Poisonous Snakes of the World. Washington, DC, United States Government Printing Office, 1966 2. Mehrtens JM: Living Snakes of the World. New York, NY, Sterling, 1967 3. Lee CY, Chen YM: Chromatographic separation of the venom of Egyptian Black Snake (Walterinnesia aegyptia) and pharmacological characterization of its components. Toxicon 1976;14:275-281 4. Ovadia M: Isolation and characterization of a hemorrhagic factor from the venom of the snake Atractaspis engaddensis (Atractaspididae). Toxicon 1967;25(6):621-630 5. Lee SY, Lee CY, Chen YM, et al: Coronary vasospasm as the primary cause of death due to the venom of the burrowing asp, Atractaspis engaddensis. Toxicon 1986;24(3):285-291 6. Wollberg Z, Shabo-Shina R, lntrator N, et al: A novel cardiotoxic polypeptide from the venom of Atractaspis engaddensis (burrowing asp): Cardiac effects in mice and isolated rat and human heart preparations. Toxicon 1966;26(6):525-534 7. Weiser E, Wolberg Z, Kochva E, et al: Cardiotoxic effects of the venom of the burrowing asp, Atractaspis engaddensis (Atractaspididae, Ophidia). Toxicon 1984;22(5):767-774

OF EMERGENCY

MEDICINE

n Volume

10, Number

3

n May

1992

8. Shebuski RJ, Ramjit DR, Bencen GH, et al: Characterization and platelet inhibitory activity of bitistatin, a potent arginine-glycine-aspartic acid-containing peptide from the venom of the viper Bitis arietans. J Biol Chem 1969;264(36):21550-21556 9. Sekoguchi S, Nikai T, Suzuki Y, et al: Kinin-releasing enzyme from the venom of Bitis arietans (puff adder). Biochim giophys Acta 1986;884(3):502-509 10. Puah RNH. Theakston RDG: A clinical studv of vioer bite poisoning. Ann ?rop Med Parasitol 1987;81(2):13&149 ’ 11. Soslar G, el-Asmar MF, Parker J: Cerastes cerastes (Egyptian sand viper) venom induced platelet aggregation as compared to other agonists. Biochem Biophys Res Commun 1968; 150(3):909-916 12. Daoud E, Tu AT, el-Asmar MF: Mechanism of the anticoagulant, Cerastase F-4, isolated from Cerastes cerastes (Egyptian sand viper) venom. Thromb Res 1986;41(6):791-799 13. el-Asmar MF, Shaban E, Hagag M, et al: Coagulant component in Cerasles cerastes (Egyptian sand viper) venom. Toxicon 1986;49(11-12):1037-1044 14. Merchant MR, Khanna UB, Almeida AF, et al: Clinicopathological study of acute renal failure following viperine snake bite. J Assoc Physicians India 1989;37(7):430-433 15. Gilon D, Oded S, Jochanan B: Treatment of envenomation by Echis coloratus (Mid-East Saw Scaled Viper): A decision tree. Toxicon 1989;27(10):1105-1112 16. Gan ZR, Gould RJ, Jacobs JW, et al: Echistatin. A potent platelet aggregation inhibitor from the venom of the viper, Echis carinatus. J Biol Chem 1988;263(36):19627-19832 17. Kamiguti AS, Theakston RD, Tomy SC: An investigation of the coagulant activity of the venom of the saw-scaled viper (Echis cafinatus) from Saudi Arabia. Ann Trop Med Parasitol1988;82(5):503-509 18. Shabo-Shina R, Bdolah A: Interactions of the neurotoxic complex from the venom of the false horned viper (Pseudocerastes fieldii) with rat striatal synaptosomes. Toxicon 1987;25(3): 253-266 19. Moroz C, De Vries A, Goldblum N: Preparation of an antivenin against Vipera palaestinae venom with high antineurotoxic potency. Toxicon 1966;4:205-208 20. Gregory UM, Russel FE, Brewer JR, et al: Seasonal variation in rattlesnake venom proteins. Proc West Pharmacol Sot 1984;27:233-236 21. Fraenkel-Conrat H: Snake venom neurotoxins related to phospholipase A2. J Toxicol Rev 1962-1983;1:205-221 22. Harris JB: Toxic constituents of animal venoms and poisons. I. Incidence of poisoning, clinical and experimental studies and reptile venoms. Adverse Drug React Acute Poisoning Rev 1982;1:65-92 23. Schmater AH, Claypool W, Colman RW: Crotalocytins: Recognition and purification of a timber rattlesnake platelet aggregsing protein. Blood 1980;56:1013-1019 24. Ellenhorn MJ. Barceloux DG: Medical Toxicoloav. Diaanosis and Treatment of Human Poisoning. New YGrrk, NY, Elsevier, 1988, pp 1111-1131 25. Podgorny G: Reptile bites. In Tintinalli JE, Krome RL, Ruiz E (eds): Emergency Medicine, A Comprehensive Study Guide (ed 2). New York, NY, McGraw-Hill, 1966, pp 768-773 26. Watt G, Theakson R, Hayes C, et al: Positive response to edrophonium in patients with neurotoxic envenomation by cobras. New Engl J Med 1986;62(2):266-291 27. Wingert WA: Poisoning by animal venoms. Top Emerg Med 1980:2(3):89-l 18 26. Curry SG, Kunkel DB: Death from a rattlesnake bite. Am J Emerg Med 1985;3:227-235 29. Bonilla CA, Fiero MK, Novak J: Serum enzyme activities following administration of purified basic proteins from rattlesnake venoms. Chem Biol Interact 1971;4:1-10 30. Abel JH, Nelson AW, Bonila CA: Crotalus adamanteus basic protein toxin: Electron microscopic evaluation of myocardial damage. Toxicon 1973;11:59-62 31. Otten EJ: Antivenin therapy in the emergency department. Am J Emerg Med 1983;1:83-93 32. Antivenom Index 1989 to 1990. American Association of Zoologic Parks and Aquaria and American Association of Poison Control Centers, 1989