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Collett's snake (Pseudechis colletti) envenoming in snake handlers

G.K. Isbister , M.R. Hooper , R. Dowsett , G. Maw , L. Murray , J. White
DOI: http://dx.doi.org/10.1093/qjmed/hcl007 109-115 First published online: 24 January 2006

Abstract

Background: Collett's snake (Pseudechis colletti) is a member of the black snake genus and occurs in a warm temperate to sub-tropical region of central Queensland, Australia. There are no reports of bites occurring in the wild, and bites were previously thought to cause only minor effects. They are a popular snake among zoos and exotic snake keepers.

Aim: To investigate the clinical effects of severe envenoming by Collett's snake, and possible treatment options.

Design: Case series.

Methods: Clinical and laboratory features are described for six bites, all in snake handlers.

Results: All six bites were from captive snakes, resulting in severe envenoming in four. Two patients were treated early with black snake antivenom, and only developed an anticoagulant coagulopathy and mild myolysis. Two developed anticoagulant coagulopathy and severe rhabdomyolysis associated with acute renal failure, requiring haemodialysis; both received antivenom >10 h after the bite, and initially received minimal fluid replacement. Other effects included thrombocytopenia, non-immune haemolytic anaemia and a marked leukocytosis.

Discussion: Collett's snake envenoming is characterized by early generalized systemic effects (nausea, vomiting, abdominal pain, diarrhoea and headache) and an anticoagulant coagulopathy, followed in some cases by rhabdomyolysis and acute renal failure in untreated patients within 24 h. Early initiation of fluid therapy and treatment with black snake antivenom should be undertaken in all envenomed patients.

Introduction

Collett's snake (Pseudechis colletti) is a member of the Australian black and mulga snake genus. Their colouration is distinctive, with pink, orange, or light brown speckled patterning on a darker brown background, but in body form they are similar to mulga snakes (P. australis) and can exceed 2 m in length. They occur in a warm temperate to sub-tropical region in central Queensland in Australia, but are rarely seen in the wild.1 There are no reports of bites occurring in their natural environment. They are a popular snake for zoos and snake enthusiasts, and are now kept throughout Australia and other parts of the world.

Originally, it was believed that Collett's snake was only moderately dangerous and that systemic envenoming was unlikely. It was initially classified with the red-bellied black snake (P. porphyriacus) and thought unlikely to cause major systemic envenoming, with the recommended treatment being tiger snake antivenom. However, following the first case reported here,2 it was recognized that this snake could cause severe envenoming and that the envenoming syndrome was more like mulga snake envenoming. We present six cases of definite Collett's snake bite that all occurred in snake handlers and caused severe envenoming in four cases.

Case reports

Case 1

A 41-year-old male herpetologist was bitten by a 1.97 m Collett's snake on the right index finger (Figure 1) while feeding the snake in February 1996. The snake hung on and had to be manually removed. He had immediate local pain, developed abdominal pain within 5 min, had an episode of diarrhoea and started vomiting. A headache developed 30 min after the bite. The finger and arm were bandaged and immobilized, and he was transported to hospital, arriving 70 min after the bite. He had no past medical history and had not previously been bitten by a snake.

Figure 1.

An adult Collett's snake (Pseudechis colletti). This is the specimen involved in case 1. (Original photo copyright © Dr Julian White)

On arrival at hospital, he had ongoing abdominal pain, vomiting and headache. The bite site was tender (Figure 2). There was no evidence of paralysis, muscle pain or external haemorrhage. He was commenced on i.v. fluids. Initial bloods 1.5 h post-bite were INR >12, aPTT 62 s, fibrinogen 4.7, undetectable D-dimer, normal creatine kinase (CK) and normal creatinine (Table 1). Following the second abnormal INR result, one ampoule of CSL black snake antivenom was administered. Within 1 h, the abdominal pain and vomiting resolved and only a mild headache remained. Coagulation studies were normal 90 min after antivenom. There was a moderate increase in CK, peaking at 4000 IU 15 h post-bite, but no muscle tenderness or pain, no myoglobinuria and normal renal function. He had persistent pain in the finger with swelling, paraesthesia and tenderness for 7 days, and loss of the sense of smell.

View this table:
Table 1

Laboratory tests for case 1

Time after bite (h) …1.536.58.51215
INR (0.9–1.3)>12>121.11.11.11.1
aPTT (25–36 s)625824262727
WCC (4.0–11 × 109/l)20.024.630.829.724.2
CK (24–200 IU)1082511803258029754000
Cr (60–120 μM)10070707070
  • Normal ranges are shown in parentheses. INR, international normalized ratio; aPTT, activated partial thromboplastin time; WCC, white cell count; CK, creatinine kinase; Cr, serum creatinine.

Figure 2.

The bite site in case 1, demonstrating fang marks, and serous ooze. (Original photo copyright © Dr Julian White)

Six months later, he had ongoing swelling of the distal interphalangeal joint with limited flexion, tenderness, paraesthesia and reduced sensation. His sense of smell remained absent, except for noxious smells. Three years after the bite he still had swelling, limited movement and reduced sensation of the bitten finger. His sense of smell remained abnormal, with most odours either undetectable or present only as an ‘unpleasant decaying smell’.

Case 2

A 64-year-old male snake handler was bitten on the right wrist by an adult Collett's snake while cleaning its cage on 30 January 2004. He immediately put an arterial tourniquet on, and a pressure immobilization bandage was applied. He was transported to hospital by ambulance. He had nausea but was otherwise well. He had previously been treated with antivenom for tiger and brown snake envenoming without allergic reactions. On examination he was anxious and vomiting with normal observations. There were puncture marks on the anterior and posterior aspects of the wrist. The forearm was swollen and erythematous, with no bleeding. Sensation was normal but the hand was cold with no capillary return, so the arterial tourniquet was removed. He was given metoclopramide and developed an urticarial rash within 5 min. One litre of intravenous fluids was started by ambulance officers. The initial bloods taken 45 min post-bite included: INR 1.2, aPTT 73 s, normal biochemistry and CK (Table 2). The patient's nausea was controlled with ondansetron, but no further intravenous fluid was given, nor antivenom.

View this table:
Table 2

Laboratory tests for case 2

Time after bite (h) …0.755.751727.538.5118
INR (0.9–1.3)1.21.21.21.31.21.0
aPTT (25–36 s)736329323112
WCC (3.7–9.5 × 109/l)6.830.349.544.147.426.7
CK (24–204 IU)186303792910 86712 190706
Cr (60–125 μM)104149225369465505
  • Normal ranges are shown in parentheses. INR, international normalized ratio; aPTT, activated partial thromboplastin time; WCC, white cell count; CK, creatinine kinase; Cr, serum creatinine.

Repeat blood tests included elevated urea, creatinine and CK, so one ampoule of black snake antivenom was administered 11 h after the bite. At 15 h post-bite, he first passed 200 ml of urine, which was described as ‘chocolate coloured’. Repeat blood tests 17.5 h post-bite showed worsening renal function, CK of 7929 I/U and platelets of 57 × 10−9. Over the next 5 h, the patient became anuric and complained of abdominal pain. A second ampoule of black snake antivenom was given 20 h after the bite. His renal function continued to deteriorate, CK peaked on day 2 at 11 236 IU, and he had severe thrombocytopenia. Haemodialysis was commenced initially daily and then second-daily. On day 6, he started passing small amounts of urine. Haemodialysis was stopped on day 13, and he was discharged from hospital after 25 days.

Case 3

A 40-year-old male snake handler presented 1 h after being bitten on the left little finger by an adult female Collett's snake on 5 February 2005. The snake had to be removed from the finger, and a PIB was applied by the patient and then again by the ambulance service. He had been drinking alcohol prior to the incident. He had pain at the bite site, felt dizzy and had blurred vision for several minutes. He developed nausea and had one vomit. He had a past history of asthma and a traumatic bowel perforation. He reported two previous snake bites (red-bellied black snakes), neither of which had required treatment with antivenom.

On admission to hospital, he had local pain, diarrhoea, nausea and vomiting. On examination he was shivering and tachycardic (110 bpm). His initial blood tests revealed an APTT of 75 s and INR of 1.1, but normal derived fibrinogen, CK and creatinine. He was admitted to the emergency observation ward for observation, analgesia and serial blood tests. Over the next 12 h, he had persistent vomiting, diarrhoea and bite site pain. The latter was relieved with regular analgesia. The APTT remained elevated at twice normal, but CK and electrolytes were not repeated.

Twenty-two hours after the bite, he complained of muscle aches. Repeat blood tests revealed rhabdomyolysis and acute renal failure (Table 3). One ampoule of black snake antivenom was administered approximately 28 h after the bite, and the patient received aggressive fluid resuscitation. Despite over 11 l of intravenous fluid and increasing doses of frusemide, mannitol and aminophylline, he remained oliguric, with increasing creatinine. He was commenced on continuous venovenous haemofiltration (CVVH) at 3000 ml/h ultrafiltrate with blood pump speed 200–300 ml/min, using a highly biocompatible synthetic membrane with a surface area of 2 m2. Anticoagulation was achieved with heparin. CK continued to rise and peaked at 82 000 IU. He developed a moderate thrombocytopenia (lowest platelet count 60 × 109/l) and a non-immune haemolytic anaemia (lowest haemoglobin 75 g/l). The blood film demonstrated large numbers of spherocytes and echinocytes (Figure 3). Associated bloods were 1.8% reticulocytes, haptoglobin <0.01 g/l, LDH peaked at 2800 IU, bilirubin 30 and direct Coomb's test negative. The APTT remained elevated, with a raised APTT NP 50% not relating to a heparin effect. He was given two further ampoules of black snake antivenom 50 h after the bite.

View this table:
Table 3

Laboratory tests for case 3

Time after bite (h) …1.254.25111424364872
INR (0.9–1.3)1.11.11.11.01.01.10.91.2
aPTT (25–36 s)7571605648413578
Platelets (140–400 × 109/l)385343117ND821067862
Haemoglobin (135–180 g/l)149151127ND1141229988
WCC (4–11×109/l)10.720.633.4NDND28.623.219.9
CK (<200 U/l)83109NDND46 80081 90070 10029 400
Cr (70–120 μM)112102NDND334306209270
  • Normal ranges are shown in parentheses. INR, international normalized ratio; aPTT, activated partial thromboplastin time; WCC, white cell count; CK, creatinine kinase; Cr, serum creatinine; ND, not done.

Figure 3.

Blood film from case 3 showing spherocytes and echinocytes.

He remained in oliguric renal failure with rhabdomyolysis 72 h after the bite, despite CVVH. A 7-l plasma exchange (two plasma volumes) with 4% human albumin was therefore performed over 12 h, with a resultant fall in CK to 29 400 U/l. CVVH was continued thereafter; the CK continued to fall and his renal function recovered slowly. The haemolytic anaemia and thrombocytopenia resolved with no specific treatment. He was discharged home 16 days after the bite, with a creatinine of 0.431 mmol/l. Four weeks following discharge he had normal renal function. Four months after the bite he still has no sense of smell. The finger still felt different and was more sensitive to temperature. The patient also reported problems with short-term memory loss.

Cases 4–6

There was far less clinical information available for the last three cases, but they are included because of the limited number of cases reported in the literature. Cases 4 and 5 were reported to CSL with limited details and laboratory studies.

A 39-year-old male was bitten on his hand by his pet Collett's snake at 1900 h on 14 May 1995. He developed local pain, erythema, vomiting, abdominal pain and lymphadenopathy. He was treated with one ampoule of black snake antivenom with good effect, and did not develop coagulopathy or renal failure.

A 41-year-old male was bitten by his pet Collett's snake on his left index finger at 1815 on 10 November 1997. He had previously been bitten by mulga and Papuan black snakes. He immediately developed a macular rash, nasal congestion and tachycardia, thought to be an acute allergic reaction to venom. He had bite site pain and developed vomiting after 1 to 2 h. No coagulopathy was reported. He was treated with one ampoule of black snake antivenom 2.5 h post-bite. He developed myolysis, evidenced by myoglobinuria and a peak CK of 6003 IU, but had normal renal function throughout.

A 31-year-old snake collector presented to hospital 1 h after being bitten on the right middle finger by a hatchling Collett's snake approximately 30 cm long on 30 March, 2005. He had a CK 199 IU and normal coagulation studies, and remained asymptomatic overnight.

Discussion

This series demonstrates the potential for severe envenoming following Collett's snake bites, and the variability in the clinical syndrome that includes anticoagulant coagulopathy, myolysis and in some cases acute renal failure. In this series, bites by two of five adult snakes resulted in rhabdomyolysis and acute renal failure. In cases 1 and 5, renal failure did not develop, which may have been due to early administration of antivenom and appropriate intravenous fluid therapy or may simply represent the variability in the clinical syndrome. Two previous cases of severe envenoming where there were CK rises >10 000 IU/l were not associated with renal failure. However, no details of fluid resuscitation or hydration status were supplied in these two cases.3 In addition, the severity of the renal failure was out of proportion to the rise in CK in cases 2 and 3, compared to rhabdomyolysis resulting from other Australian snakes such as mulga4 and tiger snakes.5 This may be a result of dehydration, because both patients initially received only maintenance intravenous fluid therapy, but a primary nephrotoxic effect cannot be ruled out.

There are five previous reports of Collett's snake bite with limited details of clinical effects (not including case 1 here)3 and studies of the venom in animals.6–12 The first case reported a 35-year-old male snake collector bitten on his left ring finger in 1985, who developed mild coagulopathy and evidence of haemolysis. He was not treated with antivenom, because of his past history of anaphylactic reactions, and the pressure immobilization bandage was left on for 16 h. His CK rose to 10 000 IU/l, and renal failure was not reported.3 Three cases were reported in 1991, with limited details. The first was a 34-year-old herpetologist reported to have severe envenoming that responded to tiger snake antivenom. The second was a 20-year-old herpetologist who suffered from vomiting and severe headache, and recovered after being given antivenom. The third was another herpetologist who had an allergic reaction to the venom. He was given no antivenom and his CK peaked at 31 560 IU/l, but was not reported to have any other effects.3 The only other case simply reported a herpetologist losing his sense of smell permanently after a bite.3

Collett's snake venom appears to cause an anticoagulant coagulopathy, similar to that of the mulga snake but different from the procoagulant effects of most Australian snakes.1,,13 In unpublished preliminary studies, whole venom was highly anticoagulant, and had only weakly procoagulant activity at very high concentrations.2 The more important clinical effect is myolysis, which occurred in four adult snake bites and was associated with acute renal failure in two patients. Early work on the venom identified myotoxic components7 in P. colletti venom that caused myoglobinuria in mice. The whole venom of P. colletti also caused a CK elevation in rats similar to that seen with P. australis (mulga snake) venom.14 More recent in vitro animal studies with whole venom from black snake species confirmed that the whole venom of P. colletti had a similar myotoxic effect to the mulga snake (P. australis)9 and was also neurotoxic.8

It is assumed that acute renal failure is secondary to rhabdomyolysis, but it occurred in two of five cases. This differs from the mulga snake, often regarded as having the most myotoxic venom, where acute renal failure is a rare complication and haemodialysis is rarely required. In 15 mulga snake bites with myotoxicity treated in Tropical Northern Territory, only one patient developed renal failure following multiple bites and late presentation (Bart Currie,4 personal communication). These cases cannot exclude the possibility that the renal failure resulted from the combination of myotoxicity and pre-renal renal failure due to dehydration.

The third patient also developed a mild haemolytic anaemia, which on blood film appeared to be consistent with a direct (non-immune) venom mediated effect (Figure 3). Haemolysis has been reported in one previous Collett's snake bite.3 This appearance is uncommon in Australian snake envenoming, although it has previously been reported with black snakes.15,,16 Pseudechis venoms have previously been reported experimentally as more haemolytic than other Australian snake venoms.17 A direct effect on erythrocytes causing spherocytosis and hyperviscosity has been previously reported with Taipan.18 This differs from the recently reported microangiopathic haemolytic anaemia that has been seen occasionally in association with the procoagulant coagulopathy and renal failure of brown snake (Pseudonaja spp.) envenoming, and also the Saharan horned viper.19 Thrombocytopenia occurred in the two severe cases, and leukocytosis occurred with all bites.

Prior to the occurrence of the first case in this series, Collett's snake was not considered to be highly dangerous, and tiger snake antivenom was recommended for treatment.20 In all five cases treated in this series, CSL black snake antivenom was used and appeared to be effective, particularly if administered early. Prophylactic treatment with black snake antivenom prevented myotoxic effects of P. colletti venom in animal studies.9 Although tiger snake antivenom prevented myotoxicity with most Pseudechis species, it was less effective for P. colletti and P. australis.9 Black snake antivenom appears to be the more appropriate treatment for Collett's snake bite.

Collett's snakes are beautiful and distinctive snakes, making them popular for zoos and private collections throughout the world. Although all these cases were reported in Australia, where the snake is indigenous, all cases reported occurred in snake handlers, outside the normal distribution of the snake. A bite by an uncommon Australian snake, the broad-headed snake (Hoplocephalus bungaroides) has previously been reported in Sweden,21 and there are numerous cases of other exotic snake bites in the literature.19,,22 With the increasing spread of exotic snakes, it will be important to identify snakes such as Collett's snake that are popular with collectors, and make available information for their treatment. In the case of Collett's snake, this is made more difficult by the rarity of bites, as the snake is almost never encountered in the wild.

Based on these few cases and previous experience with mulga snake envenoming, we recommend early administration of antivenom in the majority of cases of Collett's snake bite where there is systemic envenoming—vomiting, abdominal pain, diarrhoea, headache and anticoagulation. Although the patient may initially appear to have only mild envenoming with only generalized symptoms and a mild anticoagulant coagulopathy, they can develop severe rhabdomyolysis over 12–24 h. Early administration of antivenom may prevent myolysis, and rapidly reverse other venom-mediated effects. Early appropriate intravenous fluid therapy and careful monitoring of renal function are essential.

Acknowledgments

JW is employed by the Women's and Children's Hospital, Adelaide, which is paid by CSL Ltd to provide a consultant clinical toxinology service for users of CSL antivenom and venom detection products. GKI is supported by an NHMRC Clinical Career Development Award ID300785.

References

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