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Y. Bruchim1
1Senior Lecturer of Veterinary Medicie,
The Hebrew University of Jerusalem, Jerusalem, Israel
Snakebites are a common problem in human and veterinary medicine. Vipers are member of the family Viperidae, a group of snakes found all over the world, except in Madagascar and Australia.
The viper family includes 223 species of venomous snakes that are divided into 2 main subfamilies: pit vipers (subfamily Crotalinae), true vipers (subfamily Viperinae). Vipers are characterized by a pair of long, hollow, venom- injecting fangs. They feed on small animals and hunt by striking and envenomating their prey. Pit vipers are the largest group of venomous snakes with 151 species and are responsible for ~150,000 envenomations of dogs
and cats in the United States annually 1. The other major subfamily, the true vipers, includes 66 species, and is
also known as pitless vipers. They are distinguished by their lack of the heat-sensing pit organs that characterize the pit vipers. Among them, Vipera berus is found from Western Europe and Great Britain to the Far East 2. Vipera palaestinae (VP) is the most common venomous snake in the Middle East. It is responsible for most envenomations in humans and domestic animals in Israel 3. The snake is endemic to Israel, can be found in all country parts except the desert, and has adapted to life in agricultural and suburban areas. Envenomations were reported in people, dogs, cats, horses and a ram 3,4.
The viper’s venom contains about 30 components, 16 of which were identified, with the most important ones being proteases, hemorrhagins (metaloproteinases), amino
acid esterases, phospholipase-A2, phospholipase-B
and neurotoxins 5. The hemorrhagins activity leads
to endothelial cell damage, causing high vascular permeability, bleeding and fluid extravasations into inflamed tissues. Phospholipase-A2 is considered the most important component in many snake venoms. It
has both pro-coagulant and anti-coagulant activities as reflected by inhibition of the protrombinase, inhibition and activation of platelet aggregation, and activation
of Factor V and plasminogen 5. The amount of venom injected in a single bite increases with increased ambient temperatures, and may reach as much as one gram (dry weight); nevertheless, bites may contain no venom at all 6.
Most of canine Vp envenomations in Israel occur between May and October and between 14:00 – 22:00, and parallel the viper’s seasonal and diurnal activity. This pattern, however, may also result from increased seasonal and diurnal dog activity 4.
The onset of clinical signs following envenomation may be delayed for several hours. This phenomenon is highlighted by the fact that 40% of all severe envenomations in humans are graded as mild to non clinical signs upon admission. In addition, 20% of the bites were dry envenomations (venom free) with an additional 25% classified as mild envenomations 1. The severity of the envenomation is influenced by species and victim factors such as the bite location, victim body mass, post-bite excitability, the species and snake
size, its age and motivation and the degree of venom regeneration since last bite 1.
Risk factors for mortality in dogs included envenomation during the first summer months and low body
weight (<15kg), envenomations in the limbs and identification of the snake’s bite as well as shock and bleeding tendencies 3,4. In a recent study describing envenomation of 18 cats in Israel, variables associated with mortality included lower body weight, lower body temperature and haematocrit at arrival and 12-24 hours later, and lower total plasma proteins 12-24 hours post presentation.
Most canine VP envenomations are in the head and neck area (80%) and less frequently in the limbs (20%)
3,4. In a study on dogs with Vp envenomation, skin marks consistent of snakebite were identified in only 51% of
the dogs 4. The most common local signs in canine snakebite include swelling, edema and hematoma
which are attributed mostly to venom hemorrhaging activity. Acute lameness with pain may appear when
limb envenomations occur 3. Reported systemic signs include anaphylactic, hemorrhagic or neurogenic shock, tachypnea, tachycardia, local lymphadenomegaly and cardiac arrhythmias 3. To date, no specific cardiotoxin has been identified in the viper’s venom, although myocardial necrosis as a rare complication was reported in dogs and horses following VP envenomation 7. Cardiac injury in VP envenomed dogs as was reflected by increased serum cardiac troponin T and I (biomarkers of myocardial damage) 8,9. In the study, serum cardiac troponins concentration were increased in 65% of the dogs envenomed by Vp. Dogs with increased cardiac troponin were found to have a significantly higher occurrence of arrhythmias (58% vs. 19%)8.
The most common hematological findings in Viper envenomation include hemoconcentration, leucocytosis and thrombocytopenia and nucleated red blood cells
in the peripheral circulation. Drastic drop of total solids
in the first 24 h after envenomation is very common, as well as mild elongation of prothrombin (PT) and activated partial thromboplastin (aPTT) times and decrease in anthitrombin activity. The most common biochemical abnormalities observed include increased activities of muscle enzymes: lactate dehydrogenase, creatine kinase and aspartate aminotransferase. Additional abnormalities
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