, pub-6663105814926378, DIRECT, f08c47fec0942fa0 SNAKEBITE IN THE U.S. 4289


Approximately 120 species of snakes inhabit the U.S., with only 21 species being venomous.1 Many venomous snake species are small, produce low potency venom, or have such an insular or restricted range that animal bite exposure is unlikely. The more important species involved in animal envenomation are listed in Table 1. Distribution of these species is illustrated in figures accompanying a description of the snake. Snakes are not spread in a uniform distribution pattern throughout their range. Suitable habitat, availability of adequate prey, and freedom from encroachment by human activities influence where snakes are found. Two species of coral snakes (Elapidae) are native to the U.S. (Table I, Figure 1 ), but they pose little risk to animals because of their small size and secretive behavior. The major dangerous species are pit vipers (Crotalidae),

The eastern diamondback rattlesnake (Crotalus adamanteus) is the largest crotalid in the U.S., with some specimens reaching a length of 213 em (7ft), (Figures 2 and 3).2 Diamondback venom is not highly toxic (1.54 to 2.4 mg/kg, mouse i.v.); but because of the snake's aggressive behavior and large potential injection dose (up to 683 mg dry weight), a bite in a small animal may be fatal. Most of the cases of severe envenomation of animals within its range are caused by the eastern diamondback. The western diamondback rattlesnake (Crotalus atrox) is only slightly smaller than its eastern cousin (Figures 3 and 4). It also has a pugnacious disposition and produces approximately the same amount of venom with a similar toxicity. 2 The Mojave (green) rattlesnake, Crotalus scutulatus (Figure 5), is a small snake [maximum length approximately 123 em (4ft)] that inhabits deserts and mountains from southern California and Arizona into central Mexico (Figure 6). Venom yield varies from 8 to 139 mg dry weight, but the toxicity of Mojave rattlesnake venom (0.14 to 0.21 mg/kg) makes this species the most dangerous snake crotalid in the U.S.2 Together, the nine subspecies of Crotalus viridis inhabit most of the western U.S. (Table 1 and Figures 7 and 8). Subspecies vary in maximum length from 70 em (2ft) to 175 em (5.75 ft). Venom yield in larger snakes may reach 200 mg dry weight, with a toxicity of 1.0 to 3.0 mg/kg. Large snakes may produce moderate to severe envenomation in animals. The timber rattlesnake, Crotalus horridus horridus (Figure 9), and the canebrake rattlesnake, C. horridus atricaudatus, are both large snakes [maximum is estimated that 45,000 people are bitten annually by snakes in the U.S.; of these, approximately 7000 are treated by a physician for envenomation. 1 Statistics for the prevalence of snakebite in animals are unavailable, but it is reasonable to assume that snakebite in animals is more common than in humans. Most incidents of animal snakebite go undetected and untreated. Snakebite occurs in every state except Alaska and Hawaii. Venomous snakes may be active year round in the southern tier of states; but in the northern temperate regions, activity is restricted to late spring, summer, and early fall. Inasmuch as snakes are ectothermic, feeding and resting patterns are determined by ambient temperature. In desert regions, snakes tend to be nocturnal to avoid lethal daytime temperatures. The prairie rattlesnake, Crotalus viridis viridis, inhabits regions from southern Saskatchewan in Canada to northern Chihuahua in Mexico. Its activity patterns vary with the region. Dogs may be bitten when coursing through fields and woods, especially in tall vegetation. If an inquisitive dog sees a snake, it may move within striking distance to investigate. Young, inexperienced dogs are most likely to approach too closely. Rattlesnakes may not rattle before striking. Yard-confined pets have been bitten by snakes returning to newly established residential areas that were previously snake habitat.

Aggressive dogs may attack a snake and be bitten, as it is not possible for a dog to jump away from a rattlesnake strike. Even the legendary mongoose is incapable of successfully attacking a crotalid. A mongoose may kill a cobra because of the cobra's striking behavior, see page 115, Chapter 13, but a crotalid strike is much too fast to dodge. It is estimated that several hundred horses are bitten each year.3.4 Horses may be bitten on the head or neck while grazing in tall grass. Limb bites occur while walking in tall vegetation or along trails in the wilderness. Inquisitive foals and yearlings frequently experience bites on the nose . Occasionally, a horse may accidentally step on a resting crotalid, but given any kind of warning, the snake tends to move away. Llamas and alpacas are naturally inquisitive and even adults may approach strange animals in their environment. Venomous snakes are essentially nonexistent in the native habitats of South American camelids; thus, there has been no evolutionary selective pressure to avoid snakes. Nose and face bites are the most common. Crotalid snakes and non-prey sympatric wild animal species generally coexist without harm, but accidental encounters resulting in bites must surely occur. Captive wild animals have been bitten when snakes entered their enclosures. Crotalid venoms tend to be more complex than those of elapid snakes. 2 Rattlesnake venoms contain a high percentage of non-neurotoxic proteins (90% of the dry weight of rattlesnake venom is protein),5 with proteolytic enzymes, hemorrhagic toxins, and myotoxins predominating. Neurotoxins predominate in coral snake venom. Two new neurotoxins (crotoxin and Mojave toxin) have been isolated from the neotropical rattlesnake, Crotalus durissus, and the Mojave rattlesnake. The venoms of these snakes produce syndromes (described later) differing from the syndrome of typical crotalid envenomation. It is of interest to note that the concentration of Mojave toxin isolated from venom of the Mojave rattlesnake varies markedly from north to south within the snake's distributional range. Snakes in the southern aspects of the range (Mexico) have a much more potent venom.5
All pit vipers are venomous, but smaller species or those that produce less potent venom may cause minimal clinical signs. Envenomation may be classified as mild, with swelling, pain, and erythema occurring only at the bite site within an hour of the bite; moderate, if swelling progresses beyond the bite site and there is pain, local hemorrhage, and, possibly, subsequent tissue necrosis; or severe, if systemic manifestations develop. All degrees of envenomation occur from crotalid bites, depending on the injected dose of venom (size of snake, single or multiple bites, and aggressiveness of snake), potency of the venom, type of bite inflicted (single or double fang, scratch, or subcutaneous or deep injection), and the species of animal bitten. The larger the snake and the smaller the victim, the more the likelihood of severe envenomation.
l. Human Crotalid Envenomation 1•6•7
Usually, one or two fang marks are evident, with a distance between fang marks of 0.5 to 4.0 em. Swelling may enhance the distance and subsequent estimation of the size of the snake. Most victims experience a burning pain sensation immediately following the bite, followed within a few minutes by swelling (pitting edema) that progresses to involve an entire limb within 6 to 8 h. Discoloration from subcutaneous hemorrhage appears initially at the bite site, and may progress proximally up the limb. If severe envenomation is untreated, or if treatment is delayed, marked edema with bullae formation or hemorrhagic blebs will develop in 6 to 36 h. Neurologic signs are minimal in most crotalid bites; but if paresthesia of the scalp, face, and lips or a metallic taste in the mouth occur, severe envenomation is indicated. 1 Other signs of envenomation include weakness, faintness, nausea, and vomiting. Crotalid venom contains a hemotoxin that damages endothelium, allowing hemorrhage to occur both externally and internally at any body site (epistaxis, melena, hematuria, cutaneous petechiae, and ecchymoses).' The ultimate effects of severe, untreated envenomation are hypovolemic shock, pulmonary edema, and renal failure. Human envenomation by the Mojave (green) rattlesnake produces a different syndrome. Little or no immediate pain or swelling may be associated with the bite; but within a few hours, signs of neural dysfunction appear, including diplopia, hoarseness, inability to swallow, and dyspnea associated with progressive respiratory paralysis. 1 Russell6 felt that neural dysfunction may be a reflection of cerebral hypoxemia associated with severe anemia. However, more recently, a neurotoxin (Mojave toxin) has been identified in Mojave rattlesnake venom.5 Terminal convulsions may result from the effects of Mojave toxin or simply reflect agonal struggling.6 This snake accounts for the majority of fatal human snakebites in California. The syndrome associated with this snakebite has not been reported in animals, but probably occurs in dogs under the same circumstances as for human bites. Bites of humans from other pit vipers (water moccasin, copperhead, pygmy rattlesnake, and massasauga) usually fit into the mild to moderate crotalid envenomation category.

2. Dog Crotalid Envenomation 9?14
Snakebite of a dog is seldom witnessed; therefore, signs have usually progressed to those of moderate envenomation before the animal is seen by a veterinarian. Schaer9 described the collective syndrome in a study of a series of eastern diamondback rattlesnake bites in dogs. Dogs were usually depressed and tachypneic upon presentation. Blood was frequently oozing from fang marks on the face, limbs, or body. Significant edema of the head (Figure 14) or limbs and hemorrhage were consistent findings (epistaxis, gingival and labial petechia and ecchymoses, and subcutaneous petechia on the ventral abdomen). Additional signs of moderate envenomation included sinus tachycardia, laryngeal edema, and chemosis. 10 •11 Systemic signs of severe envenomation also included shock, ventricular premature contractions, anuria, hemolysis, ventricular fibrillation, hemorrhagic diathesis (prolonged clotting time and disseminated intravascular coagulation), periorbital cellulitis, panophthalmitis, fibrinolysis, tissue necrosis and sloughing, (Figure 15), and, ultimately, death. All dogs that died had hemorrhagic diathesis or hemolysis. Mansfield11 reported similar signs in a series of snake envenomation in dogs, but also observed vomition, diarrhea, hypotension, anorexia, excessive salivation, tremors, coma, pulmonary edema, oliguria or anuria, paralysis, and convulsions.

3. Horse Crotalid Envenomation
In horses bitten on the nose, head, neck, or limb, pitting edema occurs at the bite site and progresses to include the entire head or limb. The author's experience has been with bites from the northern Pacific rattlesnake, Crotalus viridis oreganus, which is a relatively small snake that usually produces only mild to moderate envenomation. In bites of the nose or head, edematous swelling of the nose (Figures 16 and 17) and nasal mucosa may be accompanied by blood-tinged fluid oozing from one or both nostrils.3A The eyelids swell (chemosis) and excessive lacrimal secretions may be tinged with blood. The entire head, including the lips and ears, may become edematous. The pitting edema is not hot to the touch. progresses up the limb to include contiguous areas of the trunk (Figures 18 and 19). Tissue necrosis has been rare in the author's experience, but it has been reported in areas of the country where diamondback rattlesnakes are found. Dyspnea is a vital sign that must be monitored carefully. The horse is an obligate nasal breather because of an elongated soft palate. Swelling of the nostrils or nasal mucosa occludes the air passageways and may cause suffocation if not observed and treated. Pharyngeal swelling from a neck bite may obstruct air flow at that level. Death from snakebite is rare in horses unless there is hemorrhage into a vital organ or if head bites go untreated and the horse suffocates.

4. Llama Crotalid Envenomation
Signs of snakebite in llamas are similar to the syndrome observed in horses (Figures 20 and 21). 15 Llamas are also obligate nasal breathers and bites on the nose may be fatal within 2 h if a tracheostomy tube is not placed. No tissue necrosis or systemic signs have been observed with envenomation by northern Pacific rattlesnakes , but bites from large diamondback rattlesnakes may cause necrosis if envenomation is severe.

5. Sheep and Other Livestock
Clinical signs are usually restricted to localized swelling of the head (Figures 22 and 23) or limbs. 16?21

6. Wild Animals
Accidental envenomation of wild animals other than prey species must surely occur, but diagnosis is rarely made.22 Envenomation by the prairie rattlesnake occurred in eight captive Rocky Mountain elk, Cervus elaphus nelsoni, maintained in a herd in an enclosure in Colorado.23 Clinical signs included painful swelling (restricted to the face, muzzle, and submandibular space), inspiratory dyspnea, epistaxis, frothy, blood-tinged nasal discharge, epiphora, anorexia, and depression. Fang marks were observed in only two of the elk. One elk was bitten on two separate occasions. A privately owned ocelot (Felis pardalis) was bitten on a paw by a northern Pacific rattlesnake that wandered into its cage. Signs were minimal, including swelling, erythema, and pain that was restricted to the bite site

1. Signs of Elapid Snakebite (Coral Snake) in Humans Coral snakes must grasp a segment of anatomy, usually a digit, that is small enough to be surrounded by the open mouth and grasped while chewing. Pain and swelling at the bite site are usually minimal. Signs of neural dysfunction may begin within 90 min or be delayed for several hours. Signs include  numbness and weakness of the affected limb, apprehension, drowsiness to unconsciousness, muscle fasciculation, tremors of the tongue, dysphagia, increased  salivation, nausea, and vomiting.6•8 Other signs reported include headache, photophobia, colic, miosis, dyspnea, convulsions, and paralysis. In fatal bites, death usually results from paralysis of the respiratory musculature or cardiac failure.
2. Coral Snake Envenomation in Pets Coral snakebite may occur in pets, but no descriptions of the clinical syndrome have been published. The dog has been used as an experimental subject for the study of coral snake venom. Signs reported from these studies indicate a syndrome similar to that of the human victim, with signs of muscular weakness, paresis, paralysis, dyspnea, dysphagia, muscle fasciculation, and cardiac failure.

A history of bite exposure is confirmatory, but seldom available. Season of the year, prevalence of venomous snakes, and experience with previous snakebite cases are heavily relied upon. Evaluation of clinical signs is paramount.
The toxic effects of crotalid snake venoms produce changes that are reflected in hematologic and biochemical values. Laboratory determinations may be used for initial evaluation of the case as well as for monitoring progress of therapy. The following laboratory analyses should be conducted in moderate to severe envenomation cases. Common abnormalities are a reduction in erythrocyte numbers and hemoglobin concentration along with hypofibrinogenemia and thrombocytopenia. Clotting mechanisms are inhibited, resulting in prolonged prothrombin, thrombin, and clotting times. Serum enzyme levels may be elevated, with tissue necrosis. Excessive protein, glucose, and blood or hemoglobin are commonly observed in urine.

1. Serology
Recently, serologic tests (ELISA and immunodiffusion) have been used to identify snake venom antigens or antibodies.23 Blood or serum oozing from a fang mark have been tested. In countries where numerous species of snakes are found, it is important to identify the snake so that specific antivenin may be administered. This is not of great consequence in crotalid bites in the U.S.
2. Differential Diagnosis
Small Pets: head trauma (contusion or cranial fractures), migrating grass awns, insect bites, and foreign body penetration must be considered. Horse: snakebite is only one of several factors to consider in head swelling of a horse. Trauma and pharyngeal abscesses may obstruct venous drainage of the head. Purpura hemorrhagica (a toxic reaction to bacterial infection) produces similar swelling, but with considerable ecchymoses. Multiple stings from bees or wasps may also cause head swelling.
For general management of crotalid snakebite in animals, refer to Chapter 14. Antivenin for crotalid bites in the U.S. is Wyeth's or Fort Dodge's Antivenin (crotalidae) polyvalent (Table 3 in Chapter 14). A. HUMAN
Treatment for human crotalid snakebite in the U.S. is described in Chapter
B. DOG9,11-14,29,30
Severely envenomated dogs should be observed frequently. Periodic evaluation of blood pressure and an electrocardiogram is important during the course of therapy. If hemorrhage is already present when the patient is first examined, blood should be collected for cross-matching, in anticipation of the necessity for blood transfusion. Cross-matching cannot be performed once antivenin therapy begins. 1 Administration of antivenin may be crucial to saving the life of a pet envenomated by a large eastern or western diamondback rattlesnake. The cost of therapy should be discussed with the client before administering antivenin because each vial costs from $130.00 to $150.00. The quantity of antivenin required for a dog is the same as for a human child or adult. The critical factor is the amount of venom injected that must be neutralized. Veterinarians practicing in areas inhabited by the diamondback rattlesnakes may administer five or more vials of antivenin. The effectiveness of corticosteroid therapy is controversial, but corticosteroids are not contraindicated. Broad-spectrum antibiotics should be administered. It is not necessary to administer tetanus antitoxin or toxoid, as dogs are quite resistant to tetanus. 11 Numerous other medications and forms of therapy for dogs have been reported in the literature (see Chapter 14). There are no reports of true anaphylactoid reactions to antivenin nor development of serum sickness in dogs.9 Dogs do develop allergic reactions such as erythema of the pinnae that  is responsive to benadryl administration.*

Patency of the respiratory tract is the primary concern. If the bite is witnessed and the snake identified as venomous, a short segment of garden hose may be placed in a nostril to maintain patency before swelling obstructs the nares.3.4 Such a tube may be sutured in place by a veterinarian. A more satisfactory method is placement of a tracheostomy tube, see page 132. Supplemental oxygen may be insufflated through a tracheostomy tube via a small tube from a tank of oxygen. Broad-spectrum antibiotics should be administered along with tetanus antitoxin, or toxoid if vaccination is current. Horses that become hyperexcited may be quieted with xylazine hydrochloride (0.2 to 0.4 mg/kg) or acepromazine maleate (0.03 to 0.08 mg/kg). As both of these drugs cause lowering of the blood pressure, it is important to monitor the heart for a few minutes after administration. Antivenin usage should be considered in envenomation of a foal or severe envenomation of an adult. However, economic factors may preclude this form of therapy.

Placement of a nasal tube may also be considered as first aid in observed bites of the llama or alpaca, but the space is much more narrow than in the horse and a correspondingly smaller tube is required. The smaller tube may not provide sufficient air flow. Tracheostomy, intravenous fluids to maintain hy-through the nostrils in 48 to 72 h) have been the author's primary method of therapy. When the swelling begins to recede, periodically occlude the tracheostomy tube to determine if the animal can breathe through the nostrils. The value of these animals warrants a discussion with the owner on the merits of antivenin therapy. If the bite or signs are observed and the animal is taken to a veterinary clinic within 2 h of the bite, the administration of antivenin may obviate the need to perform tracheostomy. Later administration of antivenin may shorten the course of envenomation. The author found no mention in the literature of the effects of venom on a fetus of any animal. The epitheliochorial type of placentation of came lids may inhibit transfer of large-molecule toxins to the fetus, but this has not been determined experimentally. Surely, if severe hemolysis occurs from the effects of the venom, hypoxic death of the fetus may ensue. If a pregnant llama is bitten, antivenin therapy may minimize the possibility of fetal death caused by envenomation.

Coral snakes tend to bite and hold on; thus, pets may be observed with the snake still attached. In such cases, the pet should be transported immediately to a veterinary hospital and antivenin therapy begun at once. If therapy is delayed several hours until systemic signs develop, antivenin may be unable to reverse the effects of the neurotoxic venom. A specific antivenin, Wyeth's Antivenin (Micrurus fulvius), is available for the eastern and Texas coral snakes, but, unfortunately, there is no protection against bites of the Sonoran coral snake, Micruroides euryxanthus. If dyspnea indicates respiratory paralysis, positive pressure respiratory assistance may be necessary for hours to days. Other supportive and symptomatic therapy should also be given.

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