Venomous varmints and other creepy-crawly creatures (Proceedings)


A venomous animal produces a toxin to attack its prey or defend itself. Animal venoms are protein in nature and primarily enzymes.

Venomous varmints could include members of almost ever phylum in the animal kingdom and include: Protozoa - dinoflagellates (shellfish toxicity), Porifera - sponges, Coelenterata - hydroids, Portuguese man-o-war, jellyfish, anemones, coral, Echinodermata - echinoderms, urchins, Mollusca - shellfish, snails, octopus, Annelida - segmented worms, Arthropods - insects, arachnids (Hymenoptera is the winged insects) and Chordata - fishes, amphibians, reptiles, birds, mammals. This discussion will be about insects, spiders, snakes and toads. A venomous animal produces a toxin to attack its prey or defend itself.  Animal venoms are protein in nature and primarily enzymes. They may be characterized as  phosphodiesterases, hyaluronidases, hemolytic, anti-clotting, .peptides, polypeptides and amino acids, neurotoxic, cytotoxic, necrotizing, or proteolytic. Snake bites, spider bites and toxic toads will be discussed in some detail.

Snake bites - Pit viper

An estimated 150,000 dogs and cats are bitten by pit viper in the U.S. each year. Pit vipers belong to the family, Crotalidae, and are distributed into 4 genera. Rattle snakes are in the genera Crotalus and Sistrurus spp., while cotton mouth moccasins and copperheads are in the genus Agkistrodon spp. Snakes can control the amount of venom they inject during a bite, depending upon the snake's perception of the situation. Defensive bites may be nonenvenomating while in offensive bites, they may inject the entire amount of venom. There are estimates that 30% - 50% of pit viper bites are nonenvenomating or considered mild envenomations, which gives the clinician much anxiety when initiating therapy.

The Mojave rattlesnake of the southwestern U.S. produces the most toxic venom of any native snake in North America; slightly more toxic than coral snake venom. The Eastern Diamondback is probably the most dangerous snake due to the combination of the toxicity of the venom and the amount of venom available. The Western Diamondback is not far behind. Additionally, in the Mojave rattlesnake's venom, there is a potent neurotoxin. At least 3 species of rattlesnakes are known to be potent neurotoxins, and there is a possibility of other species containing some neurotoxins.

There are many factors which affect the severity of envenomations. These can be divided into snake factors and host factors. The snake factors affecting the severity of envenomations include:  the species of snake, size of the snake, amount of venom present (length of time since snake has eaten), 30- 50% of bites are dry with no envenomation, the type of bite wound (number of fangs, type of tissue injected), and whether the bite is defensive or offensive.

Host Factors include: age, weight, general condition; ste of bite - head, body, extremity; aount of physical activity following bite; and length of time between bite and treatment. Early in season, venom yield is low giving rise to mild local reactions, whereas late in season, venom yield is high causing severe local reactions. Cats may be more resistant to snake venom that dogs, but cats are more prone to get offensive bites than dogs. Cats also tend to hide after being bit causing a delay to receiving treatment.

The clinical signs of envenomation from a pit viper bite may vary depending upon the situation but the following may be seen: the bite may have up to 6 fang marks due to 1o, 2o, and 3o fangs. OR there may be only 1; marked edema and erythema at the site of the bite. (This may extend over the entire head or a limb and part of the body); pain - swelling is painful to the touch. (There may be painful, stiff locomotion.); excessive thirst; shock - more important in small animals, especially cats; nausea, vomiting, diarrhea in small animals; CNS signs including  incoordination and respiratory paralysis.

Anaphylaxis is rare but the clinician should caution owners about the possible severity of subsequent snake bites although some practitioners feel that subsequent snake bites are less severe due to the development of “immunity.”  Dyspnea may occur especially if bite is on nose or on cervical region. Other signs may include: hemolytic anemia - seen only if the animal lives for a number of hours; tissue slough and local infection, anorexia - animal may be unable to eat because of swelling; blood stained frothy exudate from nose in a head bite and inability to see because eye lids may be swollen shut. Hypovolemic shock is a common finding.


Clin-Path tests should include WBC, PCV, TP, CPK, and thrombocytes. If the urine hemoglobin/myoglobin is 3 -  4+, this indicates a probable snake bite. The area around the bite should be measured with a tape 2 - 3 times around bite site. If rapidly increasing, indicates a  probable snake bite.

Therapy of snake bites is sometimes controversial. First measures to be avoided include: cold packs or sprays, incision and suction, tourniquets,  administration of aspirin or tranquilizers, waiting to see how bad it is before getting medical care, electric shock and heat packs. Dr. Mike Peterson has developed a snakebite severity scoring system which could assist the clinician in making assessments about the patient.(Small Animal Toxicology, 2nd Ed., Peterson and Talcott, 2006)

Snake bite patients should be scored at least every 6 hours. Treatment should consist of aggressive IV fluid therapy, early IV administration of antivenin, monitoring biochemical and hemostatic profiles and the judicious use of antibiotics. Polyvalent Crotalidae Antivenin is available from Butler Shein NLS (Fort Dodge-Wyeth product). The antivenin should be reconstituted gently and then added to crystalloids and warmed. Shaking or overheating destroys the antivenin. Antivenin is very effective in preventing the clotting defects associated with pit viper envenomnation. The antivenin in crystalloids should be given slowly and the patient monitored for allergic reactions.

Normally, the first indication of an allergic reaction is a reddening of the pinna of the ear. If this happens, an antihistamine can be administered, IV and after 10 minutes the antivenin infusion can be re-started. The average dose of antivenin in dogs and cats is 1 - 2 vials. The use of corticosteroids in snake bite is controversial. Many studies have shown that corticosteroids are of no value in snake bites and some have shown that these agents may increase the toxicity of the antivenins. However, many practitioners in the field feel that these agents are extremely beneficial.

CroFabAV (Protherics, Inc, Brentwood, TN) is a new antivenin made from sheep Fab immunoglobulin fragments. In humans receiving this agent, many developed a subsequent coagulopathy. CroFabAV costs approximately $1,000.00 per vial and from 10 to 47 vials are used in human patients. Red Rock Biologics has developed a vaccine for rattlesnake venom against all North American rattlesnake species except the Mojave rattlesnake, and is reported to give some protection against copperhead bites. Interestingly, the manufacturer states that even in immunized dogs, snake bites should be treated as a medical emergency and bitten immunized animals may have to receive antivenin.

Coral snake bites

Coral Snake Bites are rare in veterinary patients and coral snake venom is primarily neurotoxic with little local tissue reaction at the site of envenomation. Pain and numbness may or may not be present. The clinical signs may be delayed for 10 to 18 hours. In dogs, the clinical signs include: acute CNS depression, emesis, excessive salivation, quadriplegia with depressed spinal reflexes in all limbs and respiratory depression. Intravascular hemolysis along with hypotension and ventricular tachycardia may occur. The clinical signs of coral snake envenomation in cats are reported to be acute ascending flaccid paralysis, CNS depression and reduced responses to painful stimuli.

Envenomated animals should be treated as an emergency with respiratory and cardiovascular support and monitoring, including pulse oximetry. Because of the delay in onset of clinical signs, close monitoring is required. As in pit viper bites, coral snake antivenin should be given to envenomated animals and the antivenin should be handled as was described for the pit viper antivenin. The antivenin should be diluted in a warm crystalloid for IV administration.

The recommended dosage of the coral snake antivenin is 1 to 2 vials. More vials may be required depending upon the progression or lack of progression of the syndrome. If antivenin is not available, the affected animals may have to be mechanically ventilated for up to 72 hours. Antibiotics and general supportive care are the main other treatments. Animals bitten by the Sonoran coral snake is empirical as there is no antivenin available.

Spider bites

Latrodectus mactans (Black Widow)  and other “Widow” spiders contain a labile toxinwhich appear to be most toxic in fall and lowest in spring. The venom contains 5-6 active proteins, some of which induce increase Ca++ permeability causing a massive release of both nor-epinephrine and acetylcholine and other neurotransmitters. Exercise slows clinical signs.


The clinical signs seen in dogs include regional numbness, abdominal rigidity without tenderness, and muscular fasiculations. There is generally pain around the bite but it is seldom fatal to dogs. Cats are extremely susceptible to Black Widow spider bites. Paralytic signs often develop rapidly and severe pain is manifested by loud vocalizations and howling. Excessive salivation may occur along with vomiting and diarrhea.. Tremors and ataxia often precede the complete paralysis. The cause of death is respiratory collapse. (On a side note, horses and camels are extremely sensitive to black widow venom.)

Treatment of black widow bites includes hospitalization for at least 48 hours. A specific antivenin®( Merck) is available and it should be diluted in a warm crystalloid.. The diluted antivenin often gives relief w/in 15 min.. As with all intoxications, the envenomnated patient should be closely monitored for shock and may require IPPV. Methocarbamol-(Robaxin®) or diazepam may be used if antivenin is not available. Administration of calcium gluconate by is no longer recommended.

Brown recluse spider

Loxosceles reclusa  (Brown Recluse Spider) (Fiddle-back spider)  was first recognized in 1950's as a cause of toxicity and they may live in homes, on the floor or behind furniture. Pets may be bitten by trapped spiders in the bedding. Dogs are very susceptible to the venom. The clinical signs associated with a brown recluse spider bite will be a non-painful or mildly painful bite that goes undetected until the dermonecrotic lesion is detected.  The envonmation produces a wound that won't heal for months. In 8 to 15 hours, the area may become edematous and black.

Necrosis develops at bite w/in 72 hours and While systemic signs may be seen in humans, these signs are uncommon in dogs with the exception of a hemolytic anemia followed by hemoglobinuria and possible renal effects. Treatment of brown recluse spider bites is primarily symptomatic with good wound treatment. Dapsone -  (Avlosulfon®) (sulfonamide for treating Leprosy) -  1 mg/kg, TID for 10 days - blocks complement and PMN infiltration) has been used experimentally. Oxygen at 2 atmospheres, 15 min, BID for 3 days has shown some efficacy. Dexamethasone sub Q at wound site was advocated. If systemic signs appear, the animal should be aggressively treated. Surgical excision is no longer recommended.

Amphibians (toads)

The toxic species of toads in North America include Bufo alvarius (Colorado River Toad) (West Texas, California) and Bufo marinus  (Marine Toad) (Florida, Hawaii). Most toads, toxic and non-toxic, secrete substances in skin glands that are repulsive to animals that mouth them, particularly dogs and induce profound salivation. Puppies usually do not make the mistake twice. The parotid glands (skin glands behind the eye) of the Bufo toads secrete a complex venom with an action similar to cardiac glycosides. Bufadienolides make up the primary component of the secretions but many other biologically active compounds may be present.

Mouthing a toad by a dog can result in clinical signs within a few minutes with profuse salivation, pawing at the mouth and bright red mucous membranes,  which owners describe as foaming at the mouth. The animals may become ataxic and prostrated with some opisthotonic posture. These may progress to convulsions and death in as little as 15 minutes. Clinically the animals will have cardiac arrhythmias (bradycardia to tachycardia with PVCs) pulmonary edema and hypertension.

Treatment should consist of washing the mouth with flowing water and this may be done by the owners prior to transportation. Because of the severity of the neurologic signs, the animals must  be treated for the convulsions before instituting therapy of the cardiac condition. Initially, diazepam may be used but the animal may require treatment with pentobarbital to control the convulsions. The subsequent treatment regimen is as for cardiac glycoside overdosage and includes: Atropine to control salivation and control the bradycardia or propranolol (beta blocker) to control arrhythmias. Oral potassium chloride may be necessary as the animal has been losing potassium ions.

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