Two cases of envenomation of dogs by the highland copperhead snake (Australeps ramsayi)

Geoff Freeth

Summary

Two clinical cases of confirmed envenomation of dogs by the highland copperhead (Australeps ramsayi) are presented. Case 1 showed only mild signs of envenomation and was successfully treated with intravenous fluids and a pressure immobilization bandage without antivenom while case 2 exhibited moderate signs of envenomation and was successfully treated with intravenous fluids, antibiotics and tiger snake antivenom.

Both animals showed hematuria and no evidence of muscle damage. Case 2 exhibited moderate lower motor neuron dysfunction which was not quickly reversed with antivenom administration.

Case 1 showed abnormalities in both extrinsic and intrinsic pathways of the coagulation cascade while the common pathway was normal. Hematuria was the only clinical sign of a coagulation abnormality in both cases.

Identification of the correct species of snake responsible for an envenomation is essential to correct, effective and safe antivenom administration. It is likely that the species of snake involved in envenomations of veterinary patients are frequently incorrectly identified.  

Introduction

This report outlines the clinical manifestations and recovery, with treatment, of two dogs with confirmed envenomation by the highland copperhead snake. Reports of envenomations by copperheads are uncommon in the human literature and largely unreported in the veterinary literature. Information gathered on the effects of the venom of the highland copperhead are generally in an experimental environment, limited to specific aspects of the venom or treatment and likely to have been inaccurate in the identification of the species of snake.

While one survey estimates that there are 6270 snake envenomations presented to veterinary clinics across Australia each year (Mirtschin et al 1998) there are no case reports in the literature involving the highland copperhead.   

There are three species of Australian copperhead. The pigmy copperhead (Australeps labialis), found around the Mount Lofty ranges and Kangaroo island, the lowlands copperhead (A. superba) found in southern Victoria and south eastern Australia, and the highland Copperhead (A ramsayi) found extending from east of Melbourne north to the blue mountains of NSW, the Barrington tops and the New England region (Shea 1999, Weigel 1990, Rawlinson 1991).

Previous studies are likely to have included A.ramsayi in their studies of copperheads due to the recent recognition of Australeps as composed of three separated species. This differentiation was proposed in 1975, and before that the family was recognized as a single species, A. superba, formerly Denisonia superba (Rawlinson 1965). Almost all work found by the author in a literature search in regards to the venom of the Australeps family relates to A. superba  or D. superba, though it is likely that some of the literature prior to 1975 is actually a reference to A. ramsayi (Fairley 1929).  The dearth of information on the highland copperhead led one author to describe A. ramsayi as having suspected lethal toxicity with notably understudied venom (Fry 1999).

Venom from Australian elapid snakes occupy nineteen of the top twenty five most toxic snake venoms in the world with the venom of A.superba  eleventh on the list (Broad et al 1979, Fry 1999). Elapids are the family of front fanged snakes, which include the Indian cobra (Naja naja), of which all Australian venomous snakes belong (Tan and Ponnudurai1990).

The assumption that the species A. ramsayi and A. superba have identical venom is an unsafe one as it has been shown that there is intraspecies variation (Yang et al1991, Fry et al 2003) in venom constituents, so venom constituents must be expected to vary between species. One venom researcher expects that the effects of the venom of A. superba would not vary greatly from A. ramsayi (pers comm. Fry 2004).  

A sample of A. ramsayi venom was found to have an LD₅₀ of 0.6 mg/kg which is comparible to that found by Broad et al (1979) for A. superba of between 0.5 and 0.56 mg/kg in studies on mice. The murine model using a subcutaneous injection with either saline or bovine serum is the model widely adopted for the purposes of ranking the toxicity of snake venom (Broad et al 1979). Sensitivities to venom vary enormously between species envenomated. In general the smaller the animal the greater the proportional resistance to snake venom is seen. An estimate of a certainly lethal dose rate (LD₁₀₀ ) by subcutaneous injection for the copperhead ( D. superba) venom is 0.02 mg/kg for the horse, 0.1 mg/kg for sheep,1.2 mg/kg for cats, 0.7 mg/kg for the rabbit and 1.4 mg/kg for the rat (Kellaway (a)1929). Dogs were not included in this study.

Venoms from Australian snakes can be divided into those with procoagulant activity, such as found in tiger, brown and taipan venom, and those with non-procoagulant activity which includes death adder venom, which shows little anticoagulant activity, and A. superba venom which exhibits anticoagulant activity (Chester and Crawford 1980, Tan and Ponnudurai1990). Non-procoagulant venoms generally exhibit low protease, low phosphodiesterase, low to high acetylcholinesterase and moderate 5- nucleotidase activities (Tan and Ponnudurai1990).

The anticoagulant activities of copperhead venom were first identified in 1929 (Kellaway (b)1929) since then there have been a number of attempts to identify the anti-platelet and anti-coagulant active substances in the venom (Subburaju and Kini 1997, Singh et al 1999, Yuan et al 1993).

Between 1982 and 1992 humans treated with antivenom for snake envenomation had a survival rate of 99.3% (White 1998). A recent survey of veterinary patients indicated that overall 91% of cats recovered from snakebite that had received antivenom compared to only 75 % of dogs (Best 1998). Clearly veterinary patients are at greater risk than their human counterparts of death despite treatment with antivenom. Possible reasons for this may be the lack of use of snake venom detection kits (SVDKs)for proper snake identification, lack recovery and identification of the  snake responsible, a greater time period between the bite and receiving medical attention, the cost and availability of therapy (such as long term ventilatory support) and inappropriate or inability to apply, first aid.

Case 1

A 2 year old, entire male, Blue cattle dog (23kg) was found with a dead snake and veterinary attention was sought within 2 hours after he developed a left forelimb lameness, hypersalivation, lethargy and tachypnea. The snake was retrieved and identified as a highland copperhead on morphological characteristics (Shea 1998).

On presentation the dog had a grade 3 lameness of its left foreleg with an area of mild swelling on the cranial aspect of the midshaft of the left radius. The area was licked constantly by the dog and was very painful when palpated. A bite wound was not found.

On examination the dog was panting and agitated, with a marked hypersalivation. The rectal temperature was 39.5^○C. Heart rate was 168 beats per minute (bpm) and a slightly elevated systolic blood pressure of 188mmHg. Mucous membranes were bright red and the capillary refill time was less than 1 second. No evidence of hemorrhages were seen on examination of the mucous membranes. The dog had normal proprioception, muscle tone, spinal reflexes, dilated pupils which were rapidly responsive to light, possibly indicating catecholamine release rather than nerve dysfunction, and all other cranial nerve responses were normal. Replacement intravenous fluids were given, in the form of Hartmans solution, at the greater than maintenance rate of 100ml/hour over the first three hours because circulatory derangements were anticipated. Intravenous fluids were reduced after three hours to 60 ml/hour and continued at this rate for 14 hours.

The left foreleg was bandaged with a constrictive bandage of vetwrap with a hexalite splint. The bandage was commenced proximal to the presumed bite site and above the elbow joint and firmly applied in a distal direction, over the bite and down to include the paw. The leg was splinted with hexalite which was then applied in a double layer from proximal to the elbow to the paw along the caudal aspect of the leg and a second layer of vetwrap applied, firmly, in a proximal direction to end above the elbow. An Elizabethan collar was placed on the dog as he became agitated and attempted to traumatize the bandage possibly due to the effect of the bandage on the notably painful suspected bite area.

A venom detection test was indicated and performed due to the lack of other signs such as neurological dysfunction, commonly associated with snake envenomation. The test was performed using urine from the dog taken 3 hours after the bite, with the tiger snake antigen well showing a positive reaction. Tiger snake antivenom treatment was recommended and rejected by the owners on the basis of cost. Blood and urine samples were collected for hematology, biochemistry profile, clotting profile and urinalysis (tables 1,2 and 3) and the dog was given cage rest.

The laboratory tests revealed a stress leukogram with a mild left shift, a low bicarbonate with an increased anion gap, albumin was markedly increased with a normal protein level. It was assumed the low bicarbonate was due to a respiratory acidosis induced by the tachypnea and the anion gap came as a consequence of this. A prolonged prothrombin time (PT), activated partial thromboplastin time (APTT), normal thrombin time (TT) with a decreased fibrinogen level points toward defect of coagulation located in both extrinsic and intrinsic pathways with a normal common pathway. A buccal mucosal bleeding time was performed and was within normal range at 2 .5 minutes indicating normal platelet function.

On urinalysis there was a moderate hematuria.

At fourteen hours after presentation he had chewed the intravenous drip line some distance from the catheter site and this bled profusely from the intravenous catheter and remaining attached drip line, possibly due to the anticoagulant effects of the envenomation. The intravenous catheter was removed and intravenous fluids discontinued because the dog was hydrated. At this time he was tachycardic with a heart rate of 198 bpm, mucous membranes were abnormally bright red, capillary refill time (CRT) less than one second with no hemorrhages noted. He was neurologically normal with constricted pupils rapidly responsive to light.

Eighteen hours after the bite urinalysis showed that a more severe hematuria had developed. The plasma bicarbonate and its effect of the anion gap was similar to the previous sample, there was a spurious hypoglycemia (due to delay in processing a lithium heparin sample) and mild elevations in triglycerides and GGT. At eighteen hours the clotting profile was normal with an increased fibrinogen, in contrast to the sample take at three hours post bite. The hyperalbulminemia seen in the three hours sample had been maintained despite fluid therapy and the stress leukogram was still present. 

The dog was confined to a hospital cage, normal food and water was given and the bandage and splint were kept in place for a further 48 hours (62 hour post bite). A coagulation profile was performed 42 hours after the bite (Table 7).  At this time the dog was clinically normal with no evidence of hemorrhage, neurological deficit or discomfort in the leg. The bandage was gradually removed over three hours with an intravenous catheter maintained in place and resuscitative equipment on standby. The bandage was removed by cutting the bandage approximately 5 cm from its proximal border every 30-60 minutes until the bite site was reached. At this time the remaining bandage was removed. The dog was monitored in hospital for the next 24 hours and no abnormalities were noted. The suspected bite site was not painful or swollen and not able to be identified.

The dog was sent home with instructions to rest and made an uneventful recovery.

Case 2
An eight year old entire male kelpie cross (18 kg) presented with a 12 hour history of sudden onset of progressive lethargy and ataxia. The owner had noted that the dog was passing blood coloured urine.

On examination the dog was ataxic having difficulty standing or walking unassisted for more than a few seconds. There were mild proprioception deficits in both hind legs and with normal proprioception in the fore legs. Patella, cranial tibial and biceps brachi spinal reflexes were all moderately hypo-reflexic. Muscle tone was moderately reduced and there was no discomfort on muscle palpation. The pupils were bilaterally dilated and the papillary light reflex was sluggish..

The mucous membranes were bright pink with a capillary refill of less than one second. There was no evidence of hemorrhage on the mucous membranes or elsewhere. Heart rate was 98 beats per minute and respiration rate 44 breaths per minute. No other abnormalities were noted on clinical exam. The rectal temperature was 38.5^○C.

The catheterized urinalysis results are shown in table 8 and reveal a mild hematuria. Consequently a blood sample was taken and processed on the in house IDEX machine (table 9). They show a hematuria and proteinuria in concentrated urine and a mild hyperglycemia.

Initially the presumption was, given the history and clinical signs, the dog had been bitten by a common brown snake. Treatment was commenced using 1000IU brown snake antivenom given intravenously in 500ml Hartmans solution and pre-medicated with 0.2 mg adrenaline subcutaneously immediately prior to administration. Intravenous saline was given at 150 ml/ hour  then maintained on Hartmans at 45 ml/hour and the dog was observed continuously and examined half hourly. The dog was given cage rest, during which he remained sternally recumbant, started on 300mg cephalexin subcutaneously twice daily for possible aspiration pneumonia and given nil per os. A bite wound was not found.

The dog showed no change in clinical signs, particularly the neurological signs, over the next 3 hours during which time the owners retrieved a dead snake from their property which was identified as a highland copperhead on morphological examination (Shea 1998).

Three thousand units of tiger snake antivenom were administered intravenously in 500 ml Hartmans solution at 150 ml/ hour and once finished intravenous fluids were continued as before. The dog’s neurological status remained stable for the next 18 hours when some muscle tone and strength returned with spinal reflexes remaining mildly hyporeflexic. The pupillary light reflex at 18 hours after presentation was normal with pupils of appropriate size. The dog continued to produce dark brown/red urine over this period.

A urine dipstick and microscopy analysis performed 28 hours after presentation (table 10) on a voided urine sample, it showed an ongoing hematuria.

Near normal neurological function returned over 48 hours with some remaining muscle weakness and the dog was offered oral water 32 hour after presentation and food 48hours after presentation. Cephalexin tablets replaced subcutaneous injection at this time and continued for 4 days. The dog was clinically normal 56 hours after presentation and was discharged, with instructions to rest, monitor water intake and note any signs of bleeding.

On examination a week after initial presentation the dog was clinically normal.

Discussion

The quantity of venom injected in case 1 is likely to have been sub-lethal, which if using an excepted mouse LD₅₀ of 0.5 mg/kg  for A.superba(Broad et al 1978) means that there was likely to be less than 11.5 mg of venom injected into the dog by the snake. The period between the bite and presentation of case 2 was more difficult to assess and so more difficult to extrapolate the possible outcome without therapy. Neurological signs develop up to some hours after the hematological effects in bites by the common brown snake (Henderson et al 1993, Sutherland and Tibballs 2002).

A.superba have an average fang length of 3.3 mm with a maximum of 4.5 mm (Sutherland and Tibballs1983) and this short fang length may mean that the hair coat of dogs and cats offers some protection. Copperhead snakes are relatively docile and considerable provocation is required before they will bite (Sutherland and Tibballs 1983, Weigel 1990). The cases presented were likely to have been bitten when the dogs were in the process of killing the snake. Defensive bites by brown snakes (Pseudonaja texalis) are known to only lead to envenomation 30% of the time whereas defensive bites by the coastal taipan (Oxyuranus spp) almost always lead to envenomation (pers comm. CSL 2004).

One study states that venom from A. superba exhibited high acetylcholinesterase activity and acted as an anticoagulant (Tan and Ponnudurai1990). Yuan et al (1993) found a PLA₂ of 15,000 Da which inhibited platelet aggregation. Subburaju and Kini (1997) found two proteins with PLA₂ activity, superbin I and superbin II, with molecular weights of 13252 Da and 13212-13235 Da respectively, which had an enzymatic inhibition of platelet aggregation and a weakly anticoagulant activity. Singh et al (1999) found four phospholipase A₂ enzymes, superbins a,b,c, and d, all of which are basic, with molecular weights between 13140 and 13236 Da and with a range of platelet aggregation inhibitory activities (Singh et al 1999). Inhibitors of platelet aggregation are sought after in the prevention and treatment of vascular diseases and regulation of tumour growth in human medicine (Kini and Evans 1990).There was no evidence of platelet dysfunction in either case presented.

Sutherland et al (1981) found a significant prolongation of APTT in a monkey after injection of A. superba venom and also found that monkeys which received pressure immobilization of the injection site showed significantly less coagulation disturbances after release of the bandage than when no first aid was applied, suggesting that some deactivation of the factor responsible in the venom may have occurred while the venom was contained in the tissues close to the bite site.

The weak anticoagulant activity of A.superba venom is expressed through the extrinsic tenase complex rather than through the prothrombinase complex and hence fail to inhibit thrombin times (Subburaja  and Kini 1997).

This is reflected in the coagulation studies in case 1 where there were defects of both the extrinsic and intrinsic pathways but not of the common pathway of coagulation and there was normal platelet function on the basis of the buccal mucosal bleeding time. Though the measured fibrinogen was low the thrombin time is normal and so the level of fibrinogen is adequate for function of the common pathway. In contrast, procoagulant venoms simulate thrombin causing a consumption and exhaustion of coagulation factors and thus cause a paradoxical hypercoagulation and hemorrhage (Johnstone et al 2002, Ouyang et al 1992, Kini and Evans 1990, Williams et al1994). 

Unlike both cases presented in which hematuria was a consistent and prolonged feature, Kellaway (1929a) found that no red cells were found in the urine of two horses that died of copperhead snake bite. (Kellaway 1929a). 

Neurotoxins are the most important component of all Australian elapid venoms (Best 1998) and act pre and post synaptically to produce neuromuscular blockade and lower motor neuron paralysis.

The polypeptide toxins found in snake venom include the post-synaptic acting neurotoxins. The post-synaptic neurotoxins in Australian snake venoms have a high affinity to skeletal nicotinic acetylcholine receptors (Fry 1999), tend to be of low molecular weight and are fast acting and quickly reversed with administration of antivenom (Best 1998). Pre synaptic neurotoxins generally have phospholipase A₂ activity, are larger molecular weight proteins, act by blocking the release of or reducing the amount of acetylcholine available for release and are slower to respond to antivenom (Best 1998, Fry 1999).

Kellaway (1929a) described A. superba venom as “rapidly neurotoxic…and is mainly on the lower motor neurons”. This is a trait it shares with most Australian venomous snakes (Sutherland and Tibballs 1983, Best 1998). Sutherland (1981) described a profound muscle weakness 97 minutes after a monkey was injected with sub-lethal dose (0.15mg/kg) of A. superba venom.  Sutherland and Tibballs (1983) described four post-synaptic neurotoxins in A. superba venom and they exhibited no cardiac toxicity.

Antibodies against notexin, the main neurotoxin from Tiger snake venom, react with a component of Australeps venom and this component is found in double the quantity in A. superba venom compared to A. ramsayi venom (Sutherland and Tibballs 1983). Australeps is the only genus of snake to have levels of this activity other than Tiger snakes. Notexin is a presynaptic neurotoxin and calcium dependent myotoxin with phospholipase A₂ activity (Best 1998, Yang et al 1991).  

Haemolysins and myolysins are generally not notable in Australian terrestrial snake venoms, however studies on A.superba has shown it has considerable activity for both. The cases presented show that these are likely to be clinically unimportant in the mildly or moderately envenomated animal.

A phospholipase A₂ with molecular weight between 13,400 and 14,200 was isolated from A.superba venom and tested in mice for its ability to produce myoglobinuria (Mebs and Samejima 1981). The enzymes produced myoglobinuria when injected subcutaneously into mice at between 0.5 and 5.0 mg/kg and possess low lethality with a LD₅₀ in the range of 4.3 and 7.7 mg/kg. The mechanism involved in the myonecrosis was not elucidated. In both clinical cases presented, there was no evidence of muscle damage as measured by the creatine kinase (CK) levels. However, Sutherland et al (1981) found a four fold increase in plasma CK levels (compared to controls) in monkeys after injection with sublethal doses of A. superba venom. This may be a difference between the effects of A.superba and A. ramsayi envenomation.

The hemolysis seen experimentally with A.superba venom is likely to be mediated by a phospholipase B and when this component was isolated it was strongly hemolytic for washed rabbit erythrocytes (Doery and Pearson 1964, Bernheimer et al 1986). A.superba and the red-bellied black snake (Pseudechis porphyriacus) have the highest activities of phospholipase B activity of the Australian terrestrial snakes (Bernheimer et al 1986).  Both Doery an Pearson (1964) and Bernheimer et al (1986) considered A.superba and A.ramsayi to be the same species in their studies. There was no evidence of hemolysis in either case.  

The venom of A.superba produces a drop in blood pressure across a range of animals (Kellaway 1936). More recent research in rabbits indicates that may be produced by reducing the constrictor responses to norephinephrine and histamine in rabbit ear arteries (Carroll 1979). This action was not time dependent, unlike the effect copperhead venom had on isolated, driven left atrium, where it produced an increase in beat amplitude which peaked 15-20 minutes after it had been exposed (Carroll 1979). Only case 1 had systolic blood pressure taken on one occasion and it was hypertensive rather than hypotensive and both cases exhibited tachycardia and bright pink mucous membranes. In contrast case reports on brown snake bites in humans describe wild and unexplained swings in blood pressure which is thought to be due to the coagulant effects causing disseminated intravascular coagulation (Henderson et al 1993, Johnstone et al 2002).   

There were some consistencies between the cases, namely,

1)      no evidence of muscle damage as measured by CK levels

2)      both had hematuria with no urinary casts were noted and there was no other evidence of renal damage

3)      there was no evidence of significant liver damage

4)      platelets numbers were within normal limits, there was no anemia despite evidence of increased bleeding times and blood loss in the urine and there was no evidence of gross hemorrhage from any area other than in the urine.

5)      both cases presented with bright pink gums perhaps showing capillary dilation.

The first case showed no evidence of neuro-toxin activity despite evidence of definitely having been bitten ( local pain, prolonged bleeding times and positive identification on the snake venom detection kit). The second case, in contrast, presented due to lower motor neuron inhibition and discoloured urine, perhaps due to a greater time difference between the occurrence of the bite and the presentation and the volume of venom injected. Case 2 also had evidence of a gross change in the colour of the urine, which was not tested for myoglobin though there was no evidence of muscle damage. Case 1 showed a marked hypersalivation not seen with case 2. Nausea is commonly reported in the human literature and this may have been a reflection of this. The low bicarbonate level seen in case 1 likely reflects the tachypnea which in turn may have been as a result of the pain associated with the bite.

While fibrinogen was low initially with case 1 the thrombin time indicates that there was no coagulation dysfunction because of it. This contrasts with the procoagulation venoms such as Tiger snake or Brown snake where there is a defibrination coagulopathy due to consumption of factors (Williams et al 1994). The PT is independent of platelet function and is a measure of the extrinsic cascade.

The current recommendations made for human patients for the treatment of snakebite firstly involves correct first aid through the use of pressure immobilization bandage and splint or local pressure where a bandage is unable to be applied, such as with a bite to the head or torso. Snake venom generally spreads through the lymphatic circulation (Sutherland et al1981) and the correct use of pressure immobilisation will virtually stop the movement of venom into the systemic circulation (Sutherland et al 1981, Stewart 2003).

In humans, the use of pressure immobilization is a measure which is used until it can be taken off once the patient is in an environment where antivenom and intensive medical support is available. For the antivenom to be effective it must come into contact with the venom and this necessitates removal of the bandage so that the venom can get into the systemic circulation and exposure to antivenom. Also local tissue damage due to the venom and the bandage is possible with its prolonged application (Sutherland and Tibballs1983). There is some evidence that the components which are responsible for coagulation defects may be inactivated in the tissues but there is no evidence that there is any neurotoxin inactivation and so delayed removal of pressure immobilization bandages is unnecessary (Sutherland 1981). Local tissue damage with most Australian snake venoms is minimal, with the possible exception of the Mulga snake, and so accurate identification of a bite site in a veterinary case is often difficult if not impossible as occurred with both these cases.  The pain around the bitten area in case 1 indicates that copperhead bites are painful in the early stages and hence pressure immobilization and pain relief may be applicable. There was evidence with case 1 of coagulation deficits without evidence of neurological deficits at any stage, perhaps further indicating that the bite contained a sub lethal volume and that the anticoagulant effects occur at lower venom doses and before than the effects of neurotoxin are seen. This mirrors the situation seen with the Pseudonaja textalis bites where the coagulation effects of the venom are often first seen before the envenomation progresses to produce neurological deficits (Henderson et al 1993, Johnstone et al 2002).  It is possible that there was some inactivation of the neurotoxic components of the venom in case 1 or that the bandage was unable to completely stop the venom entering the systemic circulation and was excreted slowly having little clinical effect. No coagulation studies were done on release of the pressure bandage and though there was no clinical evidence of a coagulopathy. 

Snake bites seen in veterinary practices are largely treated by the use of appropriate antivenom (Mirtchin et al 1998). The choice of the correct antivenom is important, though some cross protection occurs, it is generally very moderate. For example, the brown snake antivenom given to case 2 would only neutralize approximately 3% of copperhead venom (Sutherland and Tibballs 2002). Neutralisation of copperhead venom by Tiger snake antivenom is approximately 32% (Sutherland and Tibballs 2002) and hence is the recommended antivenom.

The dose of antivenom needed is dependent on the quantity of venom injected in the bite and species of snake. The current recommendation for copperhead snake bite is 3000-5000 units of Tiger snake antivenom (White 2001). Some studies with human Brown snake envenomations indicate that the acute procoagulant effects may require a greater quantity of antivenom than previously thought (Johnstone et al 2002, Henderson et al 1993). The dose should be dependent on the clinical response, with the vials containing enough antivenom to neutralize the average venom yield on milking a particular species of snake. However, the second case presented with clinical signs (flaccid paresis) indicating antivenom therapy was required (Best 1998). 

Dilution of the antivenom in 4-10 times its volume and administration over 20 minutes intravenously is recommended to decrease the incidence of anaphylactic reactions (Best 1998). The volume used in case 2 was greater than this because it was felt the patient was not of critical status to warrant more rapid administration. Acute reactions come about due to the anticomplement activity of antivenom (Arunanthy and Hertzberg 1998, White 1998). The possibility of anaphylactic reaction has led to the manufacturer and some researchers (Sutherland 1992, Best 1998) to use subcutaneous adrenaline (10 ug/kg SC) and antihistamine premedication in human and veterinary cases. Others say that the use of premedication is controversial with the possibility that it may be hazardous and so do not recommend pre-medication prior to administration of anti-venom (White 1998).

Reactions to antivenom are more likely, both delayed and anaphylactic, if large loads of antivenom are given (Sutherland 1992, Arunanthy and Hertzberg 1998, White 2001) so the appropriate antivenom for the snake involved is recommended thus reducing the antigenic load, rather than the polyvalent, larger volume, antivenoms available. This necessitates correct identification of the snake involved. 

Correct identification of a species of snake by lay people is unlikely (Shea 1999). Identification of the snake species is more difficult in a veterinary situation, in that the snake is often not seen and identified and the bite site is generally not identified (Shea 1999, Best 1998). Case 2 was initially diagnosed as a brown snake bite on clinical signs and incorrectly treated with brown snake antivenom which increased the chances of antivenom induced reactions and also was likely to be of little use. Both cases would likely have been misdiagnosed without recovery and identification of the snake involved.   

The use of snake venom detection kits (SVDK) (CSL limited 45 Poplar Road, Parkville, Victoria 3052) in human medicine, particularly pediatrics, has increased the ability of doctors to accurately diagnose and give appropriate therapy for snake envenomation (Mead and Jelinek 1996, White 1987, White 1998). Veterinarians often make an educated guess as to the species of snake involved and a recent survey indicated the use of venom detection kits is minimal (Heller et al 2004), one study indicating that they were only used in 1.1% of suspected veterinary snake bite cases (Mirtschen 1998). This leaves a large amount of inaccuracy in diagnosis of the species snakebite in Australian veterinary with geographical distribution, clinical signs and local knowledge seemingly playing a large part in the identification of the responsible species.

While SVDKs are able to be used in samples taken from a bite site, in a veterinary situation plasma or urine is the more practical alternative sample. Venom is eventually excreted and concentrated in the urine, and after subcutaneous injection reaches a peak concentration in plasma in 2 hours and is unable to be detected reliably within 8 hours of a bite (Moisidis et al 1996). Urinary venom is unreliably detected in urine before 6-8 hours reaching a peak at 6 hours before declining to undetectable levels at 24-40 hours post bite (Moisidis et al 1996). Plasma may have been a more appropriate sample to use for the SVDK with case 1 as the sample was collected only three hours after the bite occurred.

The other common therapy in the veterinary treatment of snakebite in Australia is intravenous fluids (Best 1998, Mirtschin et al 1998, White 2001, Heller et al 2004). Respiratory support, in the form of ventilation or supplemental oxygen, may be needed even with administration of appropriate antivenom (Best 1998) and if the patient is presented after a prolonged period after the envenomation occurred the active constituents, in particular the post synaptic neurotoxins, may have bound to the target tissues and the patient not respond to antivenom administration (Sutherland and Tibballs 2002). Neither case presented had clinical indications of hypoventilation, though analysis of blood gases or measurement of oxygen saturation and end tidal carbon dioxide may have been warranted in case 2.

Antibiotics are routinely administered to veterinary cases by one author (Best 1998) to avoid pyothorax developing in feline cases. It is likely that pyothorax is an extension from a lower respiratory tract infection possibly due to aspiration, and so antibiotics would also be appropriate in dogs to guard against aspiration pneumonia when there is lower motor nerve dysfunction as with case 2. Best (1998) also advocates the use of atropine, as necessary, for treatment of bradycardia, AV blocks and to dry bronchial secretions and frusemide to assist with possible pulmonary edema due to excessive fluid administration, circulatory dysfunction and immobility.

Snake envenomation in domestic animals is a common and potentially fatal condition. The ability to diagnose and treat appropriately is currently hampered by inability to correctly identify the correct antivenom for therapy. It is this and other factors to do with the nature of the envenomations in veterinary practice, such as time from bite to presentation and the ability to provide first aid, that produce such a poor record of success when it comes to treatment of the condition in comparison to that achieved in human medicine.

A recent study shows that the Red Bellied Black snake has been a much underestimated cause of snake envenomation in dogs in NSW in the past (Heller et al 2004) and without identification of the snakes involved in the cases presented it is likely that they would have been attributed to the incorrect species of snake. The more widespread use of SVDKs will help identify the appropriate antivenom therapy and this should aid in the survival of snake bite in veterinary practice.

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Table 1. Hematology approximately 3 hours post bite Case 1 (Macquarie Pathology, Sydney)

Red cells: normal

White cell smear : normal

Platelets: normal on smear

Table 2 Biochemistry and clotting profile 3 hours post bite Case 1 ( Macquarie Pathology, Sydney) 

Table 3. Urinalysis from voided sample 3 hours after the bite Case 1 (Macquarie Pathology, Sydney)

Table 4 Hematology 18 hours after the bite Case 1 (Macquarie pathology, Sydney)

Red cells : Anisocytosis +

Platelets: Clumps ++

Table 5. Biochemistry and clotting profile 18 hours after bite Case 1 (Macquarie Pathology, Sydney)

Table 6 voided urinalysis 18 hour after the bite Case 1 ( Macquarie Pathology, Sydney)

Table 7 coagulation profile 42 hours after the bite Case 1 (Macquarie Pathology, Sydney)

Table 8 urine catheterised sample at presentation Case 2 (in house laboratory)

Table 9 Idex blood results at presentation Case 2

Table 10 voided 28 hours after presentation Case 2 (in house laboratory)