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.     

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.     

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 bites recorded by veterinary practices in Australia

Objective To determine the extent of the snake bite problem in domestic animals, its regional significance and the effects of antivenom treatment.
Design A questionnaire was designed seeking information on the number and type of domestic animals referred, whether treated or untreated, type of snakes and management of the bite.
Procedure The survey form was sent to 10% of veterinary surgeons, selected at random throughout Australia.
Results The response of 106 veterinary surgeons revealed that snake bite in domestic animals is frequent, with an estimated 6200 cases reported annually. Bites were more prominent in rural (78%) than urban areas (22%) with brown, tiger and black snakes accounting for 76%, 13% and 6% of cases, respectively. Cats and dogs were the most frequently reported victims. Ninety-one percent of cats and 75% of dogs survived following the administration of antivenom whereas 66% of cats and 31% of dogs survived without antivenom. Overall, in 33% of cases antivenom was not used, and venom detection kits were used in only 1% of cases. A number of drugs were used in various combinations with or without antivenom and intravenous fluids in the treatment of animals with snake bite, but their role in reducing the severity of envenomations was not assessed.
Clinical implications Antivenom significantly improves the chances of survival of domestic animals bitten by snakes.     

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.     

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。     

Snake care and husbandry.

The snake has long been a contradictory species; you either love them or hate them. In the United States, these reptiles are popular pets.There is also a significant amount of energy placed into developing captive breeding programs to produce different color morphs for many species. In some cases, such as the ball pythons (Pythonregius), these color morphs can sell for 20,000 dollars to 30,000 dollars each. In comparison to domestic mammals, snakes are long-lived. It is not uncommon for corn snakes (Elaphe guttata guttata) to live for 15 to 25 years and for ball pythons to live 35 to 45 years. Because of the longevity and value of these animals, more snakes are being presented to the veterinarian to manage medical and surgical problems,as well as for routine medical care. Veterinary personnel working with snakes should familiarize themselves with the specific husbandry and medical requirements of these animals so that they can make informed decisions regarding their management.     

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.     

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.     

Microclimate and Animal Life in the Equatorial Mountains

The venom apparatus in both species of Dendroaspis shows great similarity to that described in other proteroglyphs. There is a posterior bulbous portion or main gland and an anterior narrower portion, the accessory gland, that surrounds the secretory duct. The gland is enclosed in a very tough connective tissue capsule. Fibres from the m. adductor externus superficialis insert on the connective tissue capsule on the dorsal aspect of the venom gland. They serve to compress the gland and expel the venom when the snake strikes. Ventrally, fibres of the m. pterygoideus are also inserted on the investing sheath. This muscle supports the gland ventrally and also appears to play some role in venom ejection. The arrangement of the jaw musculature is similar in both species of Dendroaspis. Since the m. adductor externus superficialis is closely associated with the venom gland it has become highly specialized and exhibits great variation among snakes. This muscle in Dendroaspis differs from that in other proteroglyphs in the extension of its origin in a ventral direction over the postorbital bone to the maxilla. As in other elapids, the m. levator anguli oris is absent in both species of Dendroaspis.     

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.     

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.     

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.     

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.     

Megaoesophagus in adult dogs secondary to Australian tiger snake envenomation

Four cases of megaoesophagus secondary to tiger snake envenomation are reported. History in all cases suggested megaoesophagus was not present prior to snake envenomation. Diagnosis of megaoesophagus was confirmed by thoracic radiography in all cases. One dog died of respiratory failure. The remaining three dogs recovered, with gradual resolution of clinical signs associated with megaoesophagus.     

The diagnosis and management of snakebite in dogs--a southern African perspective

Cases of snakebite envenomation are frequently presented to veterinary practitioners in southern Africa. Despite this, no published guidelines exist on how this medical emergency should be managed. Southern African snake venoms can be classified into 3 main types based on the main mechanism of venom action and clinical presentation. A polyvalent antivenom is manufactured in South Africa and contains antibodies against the most important southern African snake venoms. The cytotoxic venoms are represented mainly by the puff-adder (Bitis arietans), Mozambique spitting cobra (Naja mossabica), black-necked spitting cobra (Naja nigricollis) (in the Western Cape and Namibia) and the stiletto snake (Atractaspis bibronii). These venoms may cause dramatic local swelling, high morbidity and low mortality and infrequently require the use of antivenom for survival (the only cytotoxic venoms used to prepare the antivenom are the puff-adder and Mozambique spitting cobra). The neurotoxic venoms (represented chiefly by the non-spitting cobras and mambas) cause high mortality due to rapid onset of paresis and require antivenom and mechanical ventilatory support which is life-saving. The boomslang (Dispholidus typus) and the vine snake (coagulopathic venom) rarely bite humans but dogs may be bitten more frequently. These venoms cause a consumption coagulopathy and successful treatment of boomslang bites requires the use of snake species-specific monovalent antivenom. There is no antivenom available for treating vine snake (Thelotornis capensis), berg adder (Bitis atropos), night adder (Causus spp.), stiletto snake and other lesser adder bites. There are some important differences between the way snakebites are managed in humans and dogs.     

The hematology of lead poisoning in man and animals

The hematologic abnormalities are used to aid in diagnosis and understanding of the pathophysiologic mechanisms of lead poisoning. Erythrocyte shape abnormalities, basophilic stippling, porphyrin abnormalities and normoblastosis have been associated with lead ingestion in many species. This paper reviews literature on these aspects of hematology of lead poisoning in both man and domestic animals.     

Black widow spider envenomation

Black widow spiders are found throughout the continental United States and north into the southern Canadian provinces. Male black widow spiders are of little medical importance. Female black widow spiders can be 20 times larger than males. The female can be identified by the hourglass pattern, red or orange in color, on the ventral aspect of her shiny, globose black abdomen. Black widow spiders control the amount of venom they inject; an estimated 15% of bites to humans are non-envenomating. Cats are very sensitive to the venom and deaths are common. Dogs have severe clinical signs but are considered more resistant than cats. A single bite is capable of delivering a lethal dose of venom to companion animals. There are several toxic components consisting of five or six biologically active proteins. These include a potent mammalian neurotoxin called alpha-latrotoxin, which induces neurotransmitter release from nerve terminals. Acetylcholine, noradrenalin, dopamine, glutamate, and enkephalin systems are all susceptible to the toxin. Onset of clinical signs usually occurs during the first 8 hours post envenomation. The condition is extremely painful in moderate to severe envenomations. Abdominal rigidity without tenderness is a hallmark sign of Latrodectus envenomation. In cats, paralytic signs may occur early and are particularly marked. Hypertension is a significant threat. First aid is of no value in the treatment. The primary treatment for black widow spider envenomation is the administration of specific antivenin, which provides the most permanent and quickest relief of the envenomation syndrome, usually within 30 minutes of infusion. The prognosis of Latrodectus envenomation is uncertain of several days, and complete recovery may take weeks.     

Neuroanatomical phenotyping in the mouse: the dopaminergic system

Voluntary movement in animals is modulated by a number of subcortical systems. One of these resides in the basal nuclei and their associated projections and utilizes dopamine as a neurotransmitter. Apart from regulating movement, the dopaminergic axis is also involved in the control of goal-oriented behavior, cognition, and mood. Disorders of this system result in common human neurologic disorders such as Parkinson's and Huntington's diseases, as well contributing to a host of behavioral conditions, such as schizophrenia, attention deficit hyperactivity disorder, and addiction. Many individual mouse models of human dopaminergic dysfunction have been described in varying degrees of detail. However, when evaluating this region of the brain, the veterinary pathologist is confronted by a paucity of information summarizing the comparative aspects of the anatomy, physiology, and pathology of the central dopaminergic system. In this review, a systematic approach to anatomic phenotyping of the central dopaminergic system in the mouse is described and illustrated using tyrosine hydroxylase immunohistochemistry. Differences between murine neuroanatomy and comparable regions of the nonhuman primate brain are highlighted. Although the mouse is the focus of this review, conditions in domestic animals characterized by lesions within the basal nuclei and its projections are also briefly described. Murine behavioral and motor tests that accompany abnormalities of specific anatomic regions of the dopaminergic axis are summarized. Finally, we review mouse models of Parkinson's and Huntington's diseases, as well as those genetically altered mice that elucidate aspects of dopamine metabolism and receptor function.