Elapid snake envenomation in dogs in New South Wales: a review

Elapid snake envenomation in dogs is a commonly occurring yet poorly described clinical entity. Twelve species of dangerously venomous elapid snakes are found in New South Wales that are capable of causing disease in dogs. Geographical distribution of these species varies, as does their venom composition and systemic envenomation syndromes produced in target species. Elapid venom may be divided into the components of prothrombin activating enzymes, lipases and peptidic neurotoxins. Each species of elapid snake may possess venom components that fit any or all of these classifications. The action of these venom components may result in neurotoxic (pre-synaptic and post-synaptic), haemotoxic (red-cell destruction and coagulation disturbance), cardiovascular, myotoxic and secondary nephrotoxic effects. Marked variability may occur in venom composition between and within snake species, resulting in varying toxicity between species and also potentially unreliable clinical syndromes following envenomation. The existence of certain components consistently within the venom of each snake species allows the broad definition of basic pathological processes and clinicopathological changes resulting from snake species-specific envenomation and these are discussed. Diagnosis of snake envenomation is unreliable if based on clinical signs alone and the use of these signs in conjunction with history, physical examination and laboratory investigation, including snake venom detection kits, is recommended. Treatment of systemic envenomation should be undertaken with initial effective first aid and subsequent administration of snake species-specific antivenom.     

SnakeMap: four years of experience with a national small animal snake envenomation registry

SnakeMap is a national cloud-based, veterinary snakebite registry. It was designed to prospectively collect data of the clinical circumstances and temporospatial information on cases of snake envenomation in dogs and cats. We herein introduce the project and summarise the data from the first 4 years of SnakeMap. The registry is a veterinary community-based online database allowing case entry from veterinary hospitals across Australia. Registry data comprise hospital characteristics, patient characteristics, envenoming snake type, treatment and outcome variables, including time and geolocation of the snake bite. We present summative information on select key variables from the SnakeMap registry (1 July 2015 to 30 June 2019). Twenty-eight hospitals from 6 states/territories entered 624 cases into the registry, including 419 dogs (67%) and 205 cats (33%). Bite time was available in 216 animals of which 90 (42%) were reported to be bitten in the 3 hours between 03:00 pm and 05:59 pm; median bite to presentation interval was 60 (interquartile range [IQR] 30, 211) minutes in dogs and 95 (IQR 41, 238) minutes in cats. Bites occurred in the owner's yard in 356 dogs (85%) and 53 cats (26%). A snake venom detection kit was used in 172 cases (28%) and antivenom was administered in 523 cases (85%). Most animals (n = 534, 88%) survived to discharge (median hospitalisation of 25 [IQR 16, 62] hours). SnakeMap effectively collects relevant clinical data from dogs and cats with presumed snake bite and provides locally specific information on the epidemiology of snake envenomation in small animals.     

Prospective determination of the specificity of a commercial snake venom detection kit in urine samples from dogs and cats

Objective To determine the specificity of a snake venom detection kit in urine samples from dogs and cats presenting to a referral centre for diseases unrelated to snake envenomation. Design Urine was collected from 50 dog and 25 cats presented for investigation and treatment of diseases unrelated to snake envenomation. Urine was collected as a voided sample, by cystocentesis or by catheterisation, and routine urinanalysis was performed. Snake venom testing was performed within 2 h of collection using a commercially available snake venom detection kit, which was observed continuously during the 10-min colour reaction phase for evidence of a visible colour indicating a positive test. Results No false-positive reactions occurred in any sample analysed. Conclusion The snake venom detection kit appears to have 100% specificity for using urine as a test sample.     

Extradural haematoma secondary to brown snake (Pseudonaja species) envenomation

A 4-year-old Siberian Husky dog was treated with brown snake antivenom by his regular veterinarian after a witnessed episode of brown snake envenomation. The dog was discharged 5 hours post presentation despite an ongoing coagulopathy. The dog was presented to the emergency centre 2 hours later because the owner believed the dog to be in pain. Initial examination revealed an ambulatory but neurologically normal patient with thoracolumbar pain and laboratory evidence of a coagulopathy. Despite correction of the coagulopathy, the signs progressed to bilateral hind limb paresis after approximately 3 hours of hospitalisation, and continued to deteriorate over the next 56 hours to loss of deep pain perception in the right hind limb. Computed tomography imaging identified the presence of an extradural haematoma which was subsequently removed via a hemilaminectomy. Surgical decompression was successful in treating the spinal compression and the dog recovered with minimal complications. To our knowledge this is the first report of extradural haematoma secondary to coagulopathy induced by brown snake envenomation.     

Coral Snake (Micrurus Fulvius Fulvius) Envenomation In Five Dogs: Present And Earlier Findings

The purpose of this study is to report on five cases of coral snake envenomation in the dog to substantiate earlier findings in four dogs reported previously, and to describe any additional clinical features that have not yet been noted. The combined results from both studies allow for a more accurate projection of the frequency of certain clinical signs. Both groups showed signs of lethargy, lower motor neuron weakness (8 of 9 dogs) and varying hematologic changes with hemolysis and hemoglobinuria occurring most commonly (7 of 9 dogs). Cardiac dysrhythmias were recorded infrequently (2 of 9 dogs). Not reported previously was the presence of a subtle bite wound located on the upper or lower lip of three dogs in the present series. An unexpected finding in this second series was the occurrence of an anaphylactoid reaction in one dog presumably attributed to the antivenin. Close examination of the lip might reveal the site of envenomation (as found in 4 of 9 dogs from both studies). Treatment with coral snake antivenin should be given as early as possible and followed by close observation for signs of anaphylaxis. The results of this study substantiate earlier findings and provide for a larger data base for further reference.     

Snake envenomation in dogs in New South Wales

OBJECTIVE: To obtain baseline data on the prevalence of elapid snake envenomation in dogs presented to veterinary practices in New South Wales and to assess attitudes of veterinarians to this clinical entity. PROCEDURE: A mailed questionnaire, sent to all veterinary clinics within New South Wales, was utilised to collect epidemiological information regarding elapid snake envenomation in dogs. RESULTS: A response rate of 68% was obtained and a yearly prevalence of snake envenomation in dogs across New South Wales veterinary clinics was estimated as 0.31%. The most common species reported to be responsible for envenomation within NSW was the Red Bellied Black snake (Pseudechis porphyriacus) followed by the Brown snake (Pseudonaja textilis) and then Tiger snake (Notechis scutatus). The reported envenomation syndromes caused by these common snake species were perceived to be similar for Brown and Tiger snakes but differed for Red Bellied Black snakes. Diagnosis of snake envenomation was based predominantly on the recognition of clinical signs. Specific diagnostic tests, such as venom detection kits, were used infrequently. The most common treatment was reported to be a combination of intravenous fluid therapy and antivenom, and monitoring of response to this treatment was usually through assessment of clinical signs. Survival after antivenom administration was reported to be highest for Red Bellied Black snake species. Survival was perceived to be associated with time between envenomation and presentation to the veterinary clinic and with antivenom administration. CONCLUSIONS: Current attitudes and perceptions of veterinarians have been defined. Diagnosis of species-specific snake envenomation is shown to be made on the basis of clinical signs which are, however, reported as similar for each species. Clearer definition of these envenomation syndromes and identification of accessible diagnostic testing procedures are needed.     

Snake bite: coral snakes

North American coral snakes are distinctively colored beginning with a black snout and an alternating pattern of black, yellow, and red. They have fixed front fangs and a poorly developed system for venom delivery, requiring a chewing action to inject the venom. The severity of a coral snake bite is related to the volume of venom injected and the size of the victim. The length of the snake correlates positively with the snakes venom yield. Coral snake venom is primarily neurotoxic with little local tissue reaction or pain at the bite site. The net effect of the neurotoxins is a curare like syndrome. In canine victims there have been reports of marked hemolysis with severe anemia and hemoglobinuria. The onset of clinical signs may be delayed for as much as 10 to 18 hours. The victim begins to have alterations in mental status and develops generalized weakness and muscle fasciculations. Progression to paralysis of the limbs and respiratory muscles then follows. The best flied response to coral snake envenomation is rapid transport to a veterinary medical facility capable of 24 hour critical care and assisted ventilation. First aid treatment advocated in Australia for Elapid bites is the immediate use of a compression bandage. The victim should be hospitalized for a minimum of 48 hours for continuous monitoring. The only definitive treatment for coral snake envenomation is the administration of antivenin (M. fulvius). Once clinical signs of coral snake envenomation become manifest they progress with alarming rapidity and are difficult to reverse. If antivenin is not available or if its administration is delayed, supportive care includes respiratory support. Assisted mechanical ventilation can be used but may have to be employed for up to 48 to 72 hours.     

Snake bite: pit vipers

Pit vipers are the largest group of venomous snakes in the United States and are involved in an estimated 150,000 bites annually of dogs and cats. The severity of any pit viper bite is related to the volume and toxicity of the venom injected as well as the location of the bite, which may influence the rate of venom uptake. The toxicity of rattlesnake venom varies widely. It is possible for pit vipers' venom to be strictly neurotoxic with virtually no local signs of envenomation. Venom consists of 90% water and has a minimum of 10 enzymes and 3 to 12 nonenzymatic proteins and peptides in any individual snake. The onset of clinical signs after envenomation may be delayed for several hours. The presence of fang marks does not indicate that envenomation has occurred, only that a bite has taken place. Systemic clinical manifestations encompass a wide variety of problems including pain, weakness, dizziness, nausea, severe hypotension, and thrombocytopenia. The victim's clotting abnormalities largely depend upon the species of snake involved. Venom induced thrombocytopenia occurs in approximately 30% of envenomations. Many first aid measures have been advocated for pit viper bite victims, none has been shown to prevent morbidity or mortality. Current recommendations for first aid in the field are to keep the victim calm, keep the bite site below heart level if possible, and transport the victim to a veterinary medical facility for primary medical intervention. The patient should be hospitalized and monitored closely for a minimum of 8 hours for the onset of signs of envenomation. The only proven specific therapy against pit viper envenomation is the administration of antivenin. The dosage of antivenin needed is calculated relative to the amount of venom injected, the body mass of the victim, and the bite site. The average dosage in dogs and cats is 1 to 2 vials of antivenin.     

Retrospective study of snake envenomation in 155 dogs from the Onderstepoort area of South Africa

A retrospective study was undertaken to evaluate the incidence, signalment, haematological and biochemical changes, therapy, and outcome of dogs presented to the Outpatients section of the Onderstepoort Veterinary Academic Hospital for confirmed snake envenomation. Three hundred and seventy-six records of dogs presented for snake envenomation from 1998 to 2002 were reviewed and 155 were selected on the basis of there being a positively identified snake. The 2 most commonly encountered snake envenomations in dogs were puff-adders (Bitis arietans) and snouted cobras (Naja annulifera annulifera). The majority of cases (56%) occurred in the autumn (March to May), with most being bitten by puff-adders. Dogs were 3 to 168 months old with a median of 36 months. No sex predilection was identified. Ten per cent of cases died because of the snake envenomation. Fifty-seven per cent and 43% of snakebites were puff-adders and cobras, respectively. There was no difference in mortality between the 2 groups of snakes. Of the cobras 60% were the snouted cobra, 14% Mozambique spitting cobra, and 24% rhinkals. Swelling in the area of the bite, usually the face and forequarters, was the primary clinical abnormality. Significant haematological findings were leukocytosis (median 17.3 x 10(9)/l; range 0.4-44), neutrophilia (median 13.6 x 10(9)/l; range 0.3-39.9), band neutrophilia (median 0.4 x 10(9)/l; range 0-5.32), and thrombocytopaenia (median 124 x 10(9)/l; range 3-555). Dogs envenomated by a puff-adder and Mozambique spitting cobra had a greater degree of thrombocytopaenia: median of 68 and 66, respectively, versus 243 for the cobra group. The most commonly used treatments were intravenous fluids, antibiotics and glucocorticoids. Thirty-eight dogs were treated with polyvalent antiserum: 9 for puff-adder envenomation and 29 for cobra envenomation. Only 2 of the dogs that received antisera died, both of them of cobra envenomation. The study concluded that snake envenomation in dogs is associated with high morbidity but moderate mortality rate and that the most significant haematological abnormality is thrombocytopaenia.     

Oesophageal compliance in naturally occurring canine megaoesophagus

SUMMARY The passive blomechanical property of oesophageal compliance (OC) was measured in 8 naturally occurring cases of canine megaoesophagus, 8 matched control and 7 vagotomised control dogs. Of the 8 dogs with megaoesophagus, 6 had congenital Idiopathic megaoesophagus and 2 had secondary megaoesophagus attributable to generalised skeletal muscle disease. Stepwise distension of the whole oesophagus was employed for measurement of OC at the 4.0 and 8.0 mL/kg Injected volume steps within the control volume range (0 to 12.0 mL/kg). At both Injected volume steps OC was higher In megaoesophagus dogs than in either matched control or vagotomised control dogs (P / 0.01 In both cases), and no significant difference was observed In OC between matched control and vagotomised control dogs. No correlation was demonstrated between OC and the estimated duration of clinical signs of dogs with megaoesophagus. These findings suggest that In most cases of canine megaoesophagus the viscoelastic properties of the oesophageal wall are significantly altered, that In such cases the disorder is unlikely to be purely dynamic and that processes other than the duration of oesophageal dilatation are responsible for the alteration in oesophageal wall blomechanical properties. The relevance of these findings to current concepts on pathophysiological mechanisms underlying the evolution and resolution of various forms of canine megaoesophagus Is discussed.     

Myotoxicity and nephrotoxicity of common tiger snake (Notechis scutatus) venom in the dog

SUMMARY The myotoxicity and neurotoxicity of common tiger snake (Notechis scutatus) venom are major factors in the pathogenesis of envenomation in the dog. Histological examination of the tissues of experimentally envenomed dogs has demonstrated the importance of muscle damage in affecting the clinical syndrome of tiger snake envenomation. Within one hour of injection of the venom into dogs, there was selective involvement of some muscles. Cardiac and smooth muscles were not significantly affected. The severity of myofibre damage was influenced by the amount of venom injected. Immobilisation under general anaesthesia resulted in significant protection against the myotoxic effects of high doses of venom. Lesions in the kidneys of experimentally envenomed dogs were acute tubular necrosis and the variable presence of a small amount of proteinaceous material in tubules. These lesions, which were similar to those in cases of natural snake bite, were indicative of a direct nephrotoxic effect, which could be complicated by the effects of myoglobinuria. These findings emphasise the need for supportive treatment aimed at maintenance of renal function in the treatment of dogs suffering from tiger snake envenomation.     

Four cases of snake envenomation responsive to death adder antivenom

Death adder envenomation is rare in humans and there is only one brief report previously in dogs. This paper details three cases of canine common death adder (Acanthophis antarcticus) envenomation and one case of bardick (Echiopsis curta) envenomation which were responsive to death adder antivenom. The available literature on death adder envenomations is also reviewed. The main clinical sign in the four dogs was severe lower motor neuron paralysis. There was no clinical evidence of coagulopathy or myopathy. Use of a snake venom detection kit was essential for selection of appropriate antivenom. Death adder and bardick envenomation in dogs potentially has a good prognosis if sufficient antivenom is administered and intensive supportive care is available.     

Anuric renal failure in a dog after red-bellied black snake (Pseudechis porphyriacus) envenomation

A case of Red-bellied Black snake envenomation resulting in intravascular haemolytic anaemia, rhabdomyolysis and anuric renal failure is described in the dog. A 12-year-old female desexed Golden Retriever was presented with a 15 hour history of profuse salivation, progressive lethargy, obtundence, inappetence and collapse. Significant findings on clinical examination were pallor, icterus, tachypnoea and dyspnoea with increased respiratory sounds and crackles in all lung fields. Generalised abdominal and muscular pain was apparent and dark red-brown urine was present around the perineal region. A diagnosis of Red-bellied Black snake (Pseudechis porphyriacus) envenomation was made and the dog was treated with intravenous fluid therapy, Tiger/Brown snake antivenom, packed red cell transfusions and Intermittent Positive Pressure Ventilation. Continued clinical deterioration occurred and a diagnosis of acute renal failure secondary to myohaemoglobinuric pigmenturia was made 12 hours after admission. Intensive treatment was attempted with diuresis and volume expansion. Oliguria and subsequent anuria ensued and the dog was euthanased due to a grave prognosis and lack of clinical response to treatment. Necropsy examination revealed muscular necrosis, accumulation of fluid in the thoracic and peritoneal cavities, and marked renal tubular necrosis with intraluminal occlusion secondary to pigmentary casts.     

Snake envenomation in cats and its detection by rapid immunoassay

Objective To determine the usefulness of a snake venom detection kit (SVDK) in the management of envenomed cats.
Design A clinical study.  

Animals

Twenty-two cats were investigated.
Procedure Cats injected subcutaneously with approximately 0.25 or 1.0 lethal dose (LD) of tiger snake venom or 1 or 4 LD of brown snake venom were observed for clinical symptoms of envenomation at intervals over the ensuring 24 to 48 hours(h). Blood and urine samples were taken at regular intervals and assayed in a quantitative laboratory assay for snake venoms. Selected samples were assayed in parallel in a rapid, semi-quantitative SVDK.
Results The studies showed that it was important to estimate the elapsed time from envenomation to presentation. If this time was less than 8 h, blood was the most appropriate sample and a negative result should exclude serious envenomation. If the elapsed time exceeded 8 h, it was essential that urine be sampled. Venom levels in urine were high at 8 h and approached the level of test sensitivity over 24 to 48 h; however by this time clinical signs were obvious in endangered cats.  

Conclusions

Careful use of the SVDK is a valuable aid in the management of a potentially envenomed cat.     

Clinicopathologic abnormalities associated with snake envenomation in domestic animals

Envenomation of domestic animals by snakes occurs frequently in certain geographic areas. However, reports describing clinical signs, clinicopathologic abnormalities, therapeutic approaches, and outcomes are sparse. This review summarizes various snake families, venom types associated with harmful snakes, and the significant hematologic, hemostatic, and biochemical abnormalities associated with envenomation. Hematologic abnormalities include RBC membrane abnormalities, hemolysis, hemoconcentration, leukogram changes, and platelet abnormalities, specifically thrombocytopenia. Coagulopathies associated with snake envenomation are well described in human medicine, and many studies have demonstrated properties of venoms that lead to both procoagulation and anticoagulation. As expected, similar abnormalities have been described in domestic animals. Biochemical abnormalities are associated with the effects of venom on tissues such as liver, skeletal and cardiac muscle, vascular endothelium, and kidney as well as effects on protein components and cholesterol. This comprehensive review of clinicopathologic abnormalities associated with envenomation and their relationships to characterized venom constituents should be useful both in the diagnosis and management of envenomation and should serve as a foundation for future research in this field.     

Intramyocardial haematoma causing right ventricular outflow obstruction after brown snake (Pseudonaja species) envenomation in a dog

A 15-month-old, male neutered Staffordshire Bull Terrier cross was presented to its referring veterinarian collapsed and agonal. He was immediately intubated, manually ventilated, and treatment commenced for presumptive snake envenomation with two vials of Tiger/Multi-Brown Snake Antivenom (minimum 7000 units/vial). The dog was transferred to a referral hospital intubated. Additional diagnostics performed following arrival at the referral hospital included a urine snake venom detection kit test, which was positive for brown snake immunotype. Three additional vials of Tiger/Multi-Brown Snake Antivenom (minimum 7000 units/vial) were administered until the dog was extubated and able to stand. Venom-induced consumptive coagulopathy (VICC) was diagnosed based on prolonged clotting times and scleral haemorrhage. Paroxysms of right ventricular outflow tract (RVOT) origin ventricular arrhythmias were treated with lignocaine and sotalol. Four days after presentation, a new-grade IV/VI systolic heart murmur was auscultated, prompting an echocardiogram. An anechoic and compartmentalised mass measuring 43 mm × 19 mm was visualized within the right ventricular wall at the RVOT, immediately adjacent to the pulmonic valve. The mass was causing a RVOT obstruction. Its appearance was suggestive of an intramyocardial haematoma, most likely secondary to VICC. The dog remained cardiovascularly stable, and treatment consisted of supportive care. Recheck echocardiograms at 2 and 7 weeks after discharge revealed progressive improvement of the intramyocardial mass and resolution of the associated heart murmur. Although intramyocardial haematomas are rare, it should be considered as a differential in dogs that develop a newly diagnosed heart murmur and/or cardiac arrhythmia following brown snake envenomation.     

Spontaneous laryngeal paralysis in four white-coated German shepherd dogs

Four cases of spontaneous laryngeal paralysis in juvenile white-coated German shepherd dogs are described. The presenting signs were typical for laryngeal paralysis, with stridor present in all four cases. Laryngoscopy revealed bilateral laryngeal paralysis in three cases, and unilateral paralysis in one. Concurrent megaoesophagus was also identified in one dog. All dogs underwent surgical treatment for laryngeal paralysis. Euthanasia was performed in one case due to intractable regurgitation and aspiration pneumonia. A possible association with white coat colour is discussed.     

ULTRASOUND-GUIDED PERCUTANEOUS LIVER BIOPSY IN SNAKES

Percutaneous ultrasound-guided liver biopsies were conducted in 15 snakes using 18-gauge automatic biopsy devices. The liver samples collected ranged in size from 1.16 ± 0.40 mm to 8.3 ± 0.55 mm. Upon histologic examination, all biopsy samples were of diagnostic quality. Anesthesia with complete immobilization of the snake was necessary to allow proper selection of the target site and limit complications associated with biopsy collection. Percutaneous ultrasound-guided liver biopsy is a rapid, minimally invasive method for collecting liver tissue in snakes.     

蛇毒神经毒素研究进展

我国的蛇类资源丰富,从理论意义和长远的经济效益考虑,蛇毒的研究是一个很有价值的方向。近年来,随着蛇毒神经毒素结构的确定、理化性质和药理性质的测定及蛇毒神经毒素的临床应用,其在镇痛功能方面表现出的维持时间长、效价高、无耐受性和无成瘾性等特点而倍受关注。蛇毒具有广泛的生物学活性,论文就蛇毒组分中近年来研究较为深入的神经毒素的结构、理化性质、药理作用及其应用等方面进行了综述。     

Observations on blood coagulation after snakebite in dogs and cats

Blood samples from 13 cases of snakebite, 6 in dogs and 7 in cats, were tested for activated partial thromboplastin time (APTT), prothrombin time (PT) and fibrin/fibrinogen degradation products (FDP). Four cases were tested for fibrinogen concentration. Based on the results of a commercially available ELISA test, 9 cases were caused by tiger snakes (Notechis scutatus) and 1 case by a brown snake (Pseudonaja textilis). Three other cases had clinical signs and increased creatine phosphokinase values which suggested tiger snake envenomation. Although the period post-envenomation varied, results indicated a marked prolongation of the APTT and PT in 5 of 6 dogs. Three of these 5 dogs also had increased FDP values and 3 (of 3 examined) were hypofibrinogenaemic. Clinical manifestations of this coagulopathy were: haematoma formation after venepuncture (3 cases), gingival petechiae (1 case) and hyphaema (1 case). In contrast, there was minimal or no prolongation of the APTT and PT values, and no increase in FDP, in all 7 cats. Furthermore, no cat exhibited clinical signs of a coagulopathy.