Oxyuranus microlepidotus

   1.1 Scientific Name
   1.2 Family
   1.3 Common Names
   2.1 Main risks and target organs
   2.2 Summary of clinical effects
   2.3 Diagnosis
   2.4 First-aid measures and management principles
   2.5 Venom apparatus, poisonous parts or organs
   2.6 Main toxins
   3.1 Description of the animal
      3.1.1 Special identification features
      3.1.2 Habitat
      3.1.3 Distribution
   3.2 Poisonous/Venomous Parts
   3.3 The toxin(s)
      3.3.1 Name
      3.3.2 Description
      3.3.3 Other physico-chemical characteristics
   3.4 Other chemicals in the animal
   4.1 Uses
   4.2 High risk circumstances
   4.3 High risk geographical areas
   5.1 Oral
   5.2 Inhalation
   5.3 Dermal
   5.4 Eye
   5.5 Parenteral
   5.6 Others
   6.1 Absorption by route of exposure
   6.2 Distribution by route of exposure
   6.3 Biological half-life by route of exposure
   6.4 Metabolism
   6.5 Elimination by route of exposure
   7.1 Mode of action
   7.2 Toxicity
      7.2.1 Human data Adults Children
      7.2.2 Animal data
      7.2.3 Relevant in vitro data
   7.3 Carcinogenicity
   7.4 Teratogenicity
   7.5 Mutagenicity
   7.6 Interactions
   8.1 Material sampling plan
      8.1.1 Sampling and specimen collection Toxicological analyses Biomedical analyses Arterial blood gas analysis Haematological analyses
      8.1.2 Storage of laboratory samples and specimens Toxicological analyses Biomedical analyses
      8.1.3 Transport of laboratory samples and specimens Toxicological analyses
   8.2 Toxicological analyses and their interpretation
      8.2.1 Tests on toxic ingredient(s) of the material Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s)
      8.2.2 Tests for biological specimens Simple qualitative test(s) Advanced qualitative confirmation test(s) Simple quantitative method(s) Advanced quantitative method(s) Other dedicated method(s)
      8.2.3 Interpretation of toxicological analyses
   8.3 Biomedical investigations and their interpretation:
      8.3.1 Biochemical analyses Blood, plasma or serum Urine Other biological specimens
      8.3.2 Arterial blood gas analyses
      8.3.3 Haematological analyses
      8.3.4 Other (unspecified) analyses
      8.3.5 Interpretation of biomedical investigations
   8.4 Other biomedical (diagnostic) investigations and their interpretation
   8.5 Summary of most essential biomedical and toxicological analyses in acute poisoning and their interpretation
   9.1 Acute poisoning/envenomation
      9.1.1 Ingestion
      9.1.2 Inhalation
      9.1.3 Skin exposure
      9.1.4 Eye contact
      9.1.5 Parenteral exposure
      9.1.6 Other
   9.2 Chronic poisoning by:
      9.2.1 Ingestion
      9.2.2 Inhalation
      9.2.3 Skin contact
      9.2.4 Eye contact
      9.2.5 Parenteral exposure
      9.2.6 Other
   9.3 Course, prognosis, cause of death
   9.4 Systemic description of clinical effects
      9.4.1 Cardiovascular
      9.4.2 Respiratory
      9.4.3 Neurological CNS Peripheral nervous system Autonomic Skeletal and smooth muscle
      9.4.4 Gastrointestinal
      9.4.5 Hepatic
      9.4.6 Urinary Renal Other
      9.4.7 Endocrine and reproductive systems
      9.4.8 Dermatological
      9.4.9 Eye, ear, nose, throat: local effects
      9.4.10 Haematological
      9.4.11 Immunological
      9.4.12 Metabolic Acid base disturbances Fluid and electrolyte disturbances Others
      9.4.13 Allergic reactions
      9.4.14 Other clinical effects
      9.4.15 Special risks
   9.5 Other
   10.1 General Principles
   10.2 Relevant laboratory analyses and other investigations
      10.2.1 Sample collection
      10.2.2 Biomedical analysis
      10.2.3 Toxicological analysis
      10.2.4 Other investigations
   10.3 Life supportive procedures and symptomatic treatment
   10.4 Decontamination
   10.5 Elimination
   10.6 Antidote treatment
      10.6.1 Adults
      10.6.2 Children
   10.7 Management discussion
   11.1 Cases and reports from literature
   11.2 Internally extracted data on cases
   11.3 Internal Cases
   12.1 Availability of antidotes
   12.2 Specific preventative measures
   12.3 Other
   13.1 Clinical and Toxicological References
   13.2 Zoological References
    1.  NAME

          1.1  Scientific Name

               Oxyuranus microlepidotus (McCoy)
               Oxyuranus scutellatus (Peters)
               subspecies scutellatus scutellatus
               subspecies scutellatus canni

          1.2  Family


                         Genus:    Oxyuranus

          Note:  Some authors still maintain the junior synonym 
          Parademansia microlepidota for this species, however it is now 
          generally accepted as O. microlepidotus. In some early Australian 
          papers on venomous snakes and snake venom,  O. scutellatus is 
          listed as  Pseudechis scutellatus and Oxyuranus maclennani. 

          1.3  Common Names

               Scientific Name              Common Name

               Oxyuranus microlepidotus     Western Taipan, Inland Taipan,
                                            Fierce Snake, Small-scaled Snake
               Oxyuranus scutellatus        Taipan, Common Taipan
               Oxyuranus canni              New Guinea Taipan

    2.   SUMMARY

          2.1  Main risks and target organs

          Taipans are a relatively minor cause  of snakebites in Australia 
          in relation to numbers of cases, but assume a far more important 
          position due to the extreme hazard of their bites. Without 
          appropriate antivenom treatment up to 75% of taipan bites will be 
          fatal. Indeed, in the era prior to specific antivenom therapy, 
          virtually no survivors of taipan bite were recorded. 

          Main risks are: neurotoxic paralysis, coagulopathy, 
          rhabdomyolysis, acute renal failure. 

          Target organs: neuromuscular junction, coagulation system, 
          skeletal muscle. 

          2.2  Summary of clinical effects

          Locally:   Local effects appear variable, not all cases being 
          significantly painful. Bite marks are usually visible,  due to 
          the moderately large fangs, but in some cases local erythema or 
          oedema may be absent. A complete set of teeth marks including 

          fangs, post-maxillary teeth, pterygopalatine teeth and mandibular 
          teeth may be present (Figure ). However, only minor fang marks 
          may be seen in other cases (Figure ). Local secondary infection 
          is unusual. Venom may spread to draining lymph nodes with 
          consequent pain and/or tenderness and/or swelling. Local  
          symptoms and signs may be  made worse by prolonged use of first 

          Systemic:   headache, nausea, vomiting, abdominal pain, impaired 
          conscious state, occasionally (especially in children) loss of 
          consciousness and convulsions.  Coagulopathy rarely with overt 
          bleeding manifestations. Progressive neurotoxic paralysis. Muscle 
          movement pain. Acute renal failure. 

          2.3  Diagnosis

          Monitor the coagulation profile to establish the presence and 
          extent of coagulopathy and as an index of systemic envenomation. 
          Should be performed at  presentation, on development of symptoms 
          or signs of systemic envenomation, and 1-2 hours after antivenom 
          therapy until sufficient antivenom given to reverse coagulopathy. 

          In the absence of a clotting laboratory, whole blood clotting 
          time in a glass test tube is useful. If a clotting laboratory is 
          available, prothrombin ratio, activated partial thromboplastin 
          time, thrombin clotting time, fibrinogen level, and fibrin(ogen) 
          breakdown products (FDP or XDP) are most useful. 

          Other useful tests include: complete blood picture and platelet 
          count; serum electrolytes, creatinine, urea; serum enzymes, 
          especially creatine phosphokinase; urine output and urine 

          Venom detection using CSL Venom Detection Kit. The best sample is 
          a swab from the bite site (sample swab stick in kit). If the 
          patient has systemic envenomation, urine may also be a useful 
          sample. Blood is not a reliable sample. 

          2.4  First-aid measures and management principles

               First Aid:

                    (a)  If the patient develops evidence of respiratory or 
                         cardiac failure, use standard cardiopulmonary 
                         resuscitation techniques to maintain life. 

                    (b)  The patient should be encouraged to lie still and 
                         reassured to avoid panic. 

                    (c)  A broad compression bandage should be applied over 
                         the bitten area, at  about the same pressure as 
                         for a sprained ankle. This bandage should then be 
                         extended distally, then proximally, to cover as 
                         much of the bitten limb as possible. 

                    (d)  The bandaged limb should be firmly immobilised 

                         using a splint. 

                    (e)  The bite site wound should not be washed, cleaned, 
                         cut, sucked, or treated with any substance. 

                    (f)  Tourniquets should not be used.

                    (g)  The patient should be transported to appropriate 
                         medical care. 

                    (h)  Nil orally unless the patient will not reach 
                         medical care for a prolonged period of time in 
                         which case only water should be given by mouth. No 
                         food should be consumed. Alcohol should not be 

                    (i)  If the offending snake has been killed it should 
                         be brought with the patient for identification. 

                    (j)  Remove any rings, bangles etc from the bitten 

          Treatment principles

                    (a)  Specific: If the patient has systemic 
                         envenomation, give taipan snake antivenom (CSL). 

                    (b)  General: Support of cardiac and respiratory 
                         functions; treatment of shock; maintenance of 
                         adequate fluid load, electrolyte balance, and 
                         renal output; tetanus prophylaxis; treatment of 
                         local sepsis with antibiotics; treatment of 
                         significant blood loss with blood transfusion. 

                    (c)  Local: Do not clean or touch local wound until 
                         appropriate samples taken for venom detection. 
                         Thereafter ensure antisepsis. Early surgical 
                         intervention is generally contraindicated, and is 
                         only rarely indicated in the late stages, in the 
                         unusual event that significant local necrosis has 

          2.5  Venom apparatus, poisonous parts or organs

          Venom is produced in paired modified salivary glands, 
          superficially situated beneath the scales, posterior to the eye, 
          and surrounded by muscles, the contraction of which compress the 
          glands, expelling venom anteriorly via venom ducts to the fangs. 
          The fangs are likewise paired, situated at the anterior part of 
          the upper jaw, on the maxillary bones.  They have an enclosed 
          groove for venom transport, with an exit point near the fang tip.  
          Fang length in adult taipans is variable and dependent on 
          species; O. microlepidotus, 3.5 - 6.2 mm; O. scutellatus, 7.9 -
          12.1 mm.

          Average venom yield is:  O. microlepidotus, 44 mg, max. 110 mg; 
          O. scutellatus, 120 mg, max. 400 mg. Mean venom injected at first 
          bite (defensive strike) is: O. microlepidotus, 17.3 mg, range
          0.7-45.6 mg, with mean venom left on skin 0.6 mg; O. scutellatus, 
          20.8 mg, range 0.6-68.9 mg, with mean venom left on skin 0.9 mg. 

          2.6  Main toxins

          Oxyuranus venom is a complex mixture of protein and non-protein 
          components, not all of which have been fully evaluated. 

                    (a)  Neurotoxins:  both presynaptic (taipoxin) and 
                    (b)  Procoagulants: principally factor Xa analogues, 
                         acting largely independently of cofactors (eg 
                         factor V, calcium, phospholipid), converting 
                         prothrombin to thrombin (meziothrombin). 

                    (c)  Myolysins: second action of presynaptic 
                         neurotoxins (eg taipoxin) which contain a 
                         phospholipase A2 component. 


          3.1  Description of the animal

               3.1.1     Special identification features

          Taipans are large snakes.  Male specimens of O. scutellatus 
          attain  a maximum snout-vent  length of 156 cm. The maximum 
          snout-vent length for females is 144 cm.  O. microlepidotus is 
          only slightly smaller, 132 cm for males, 145 cm for females. 

          Covacevich et al (1981) describe the colour and pattern of each 
          species of Oxyuranus: O. scutellatus unmarked light olive to dark 
          russet brown dorsally (specimens from Tully area, NE Qld, almost 
          black); head usually lighter coloured, especially in the rostral 
          and labial regions; ventrally cream, usually with pink or orange 
          flecking; buccal cavity pink; eye reddish; O. microlepidotus pale 
          to very dark brown dorsally, often with dark flecks which may 
          form distinct bands posteriorly; head glossy black in most 
          freshly collected specimens (this sometimes fades with 
          captivity); ventrally (behind the black neck region) mustard 
          yellow without flecks; buccal cavity in dark specimens blue grey 
          shading to pink, in lighter coloured specimens greyish pink 
          shading to off-white; eye black. 

          The heads of Taipans are large, oblong, almost rectangular (in O. 
          scutellatus) to moderately elongate (in O. microlepidotus). The 
          canthus rostralis is pronounced in O. scutellatus, but not in O. 

          The skulls of O. scutellatus and O. microlepidotus are similar, 
          but they differ in size and proportion and there are minor 
          differences in dentition (Covacevich et al 1981).  The fangs of 

          O. scutellatus are long (7.9 - 12.1 mm) while those of O.
          microlepidotus are of moderate length (3.5 - 6.2 mm). Posterior
          to the fangs on the maxilla in O. scutellatus there is a single, 
          solid tooth. In O. microlepidotus there are several maxillary 
          teeth posterior to the fangs, and these are structurally 
          identical to the fangs (ie they are syringe-like for most of 
          their length) (Figures ). 

               Oxyuranus microlepidotus:  23 (rarely 25) mid-body scales, 
               anal single, ventral 211-224, sub-caudals 54-66 paired. Eye 
               diameter smaller than its distance from the mouth (Figures). 

               Oxyuranus scutellatus: mid-body scales 21-23, anal single, 
               ventrals 220-248, sub-caudals 48-76 paired.  Eye diameter 
               greater than its distance from the mouth (Figures ). 

                    3.1.2     Habitat

               O. scutellatus occurs coastally in open forest, dry closed 
               forests, heathlands, grasslands and cultivated areas. It is 
               well known in and near sugar-cane plantations. 

               O. microlepidotus is confined to vast treeless semi-arid and 
               arid ashy downs remote from the coast. 

                    3.1.3     Distribution

               O. scutellatus is widely distributed in northern and eastern 
               Australia and in southern Papua New Guinea (O. scutellatus 
               canni). In Australia it occurs in northwest Western 
               Australia, in northern parts of the Northern Territory 
               (including near coastal islands), across Cape York Peninsula 
               and throughout coastal Queensland as far south as the 
               Beaudesert area (Figure ___). O. microlepidotus occurs in 
               the drainage systems of Cooper Creek, the Diamantina River 
               and the Georgina River in far western Queensland and north 
               eastern South Australia (Figure ___). 

     3.2  Poisonous/Venomous Parts

          Venom glands (paired) situated superficially in posterior part of 
          head, connected by ducts to forward placed (paired) fangs (Figure 
          3.2.1). Fangs moderate in length (see 3.1), sometimes with 
          multiple reserve fangs (Figure 3.1.1). Fangs may leave small 
          puncture marks (Figure 2.2.2) through to a complete set of teeth 
          marks (Figure 2.2.1), or scratches. 

          3.3  The toxin(s)

                    3.3.1     Name

               Oxyuranus venom; Taipan venom; O. microlepidotus venom; O. 
               scutellatus venom. 


               Neurotoxins:   Taipoxin (O. scutellatus),
                              Paradoxin (O. microlepidotus),
                              O. scutellatus fraction III
                              O. scutellatus fraction IV

               Coagulants:    Direct prothrombin converter (O. scutellatus) 

               Myolysins:     Taipoxin

                    3.3.2     Description

               Whole venom production based on milking specimens, usually 
               in captivity, and lethality (LD50 sc mice). 

      Species                      Average       Maximum     LD50
      Oxyuranus microlepidotus      44 mg         110 mg     0.025
      Oxyuranus scutellatus        120 mg         400 mg     0.099

          3.3.3     Other physico-chemical characteristics


               Taipoxin - presynaptic neurotoxin, phospholipase A2 based, 
               moderately acidic sialo-glycoprotein, MW 45,600, as a 
               ternary complex 1:1:1 with a , b , g subunits. a and b 
               subunits are 120 amino acids long, with 7 disulphide 
               bridges. g subunit has 135 amino acids and 8 disulphide 
               bridges. Only the very basic (pI >10) g-subunit has lethal 
               neurotoxicity. LD50 of complete molecule is 2 mg/kg (IV 
               mouse). 17% of venom. 

               O. scutellatus fraction III - minimal data. Presumed 
               postsynaptic neurotoxin. LD50 100 mg/kg (IV mouse). 47% of 

               O. scutellatus fraction IV - minimal data. Presumed 
               postsynaptic neurotoxin. LD50 100 mg/kg (IV mouse). MW 
               approximately 8,000. 10% of venom. 

               Paradoxin - presynaptic neurotoxin, phospholipase A2 based, 
               essentially identical to taipoxin. It accounts for 12% of 
               crude venom, is a sialo-glycoprotein with three subunits and 
               has an LD50 of 2 mg/kg (IV mouse). Amino acid analysis of 
               paradoxin and taipoxin, both in whole form and as subunits, 
               shows close homology. 


               Prothrombin converters from O. scutellatus venom - a large 
               multichain protein, MW approximately 300,000 D, consisting 
               of an enzymatic unit of 57,000 D and a cofactor of 220,000 
               D, the  latter promoting the prothrombinase activity of the 
               former. Structurally resembles factor Xa-Va complex. 
               Prothrombinase activity is independent of factor V, but 
               enhanced by phospholipid and calcium. The enzymatic unit 
               appears to consist of two chains, each approximately 30,000 
               D, linked by a disulphide bond, while the cofactor has two 
               chains, 110,000 D and 80,000 D. 

               No prothrombin converter has been reported for O. 
               microlepidotus venom. 

               In monkeys, O. scutellatus clearly causes coagulopathy but 
               O. microlepidotus does not.  However, in human envenomation 
               both species can cause marked defibrination-type 


               Taipoxin (see above)

               In  monkeys O. scutellatus venom is myolytic, and O. 
               microlepidotus only mildly myolytic. 

     3.4  Other chemicals in the animal

          Very little information is available on minor components which 
          have a weak haemolytic action. 

          O. microlepidotus has moderate hyaluronidase activity. 


          4.1  Uses

          Venom is used both in antivenom production and for laboratory 
          research. The  neurotoxins in particular have proved valuable in 
          neuromuscular transmission research,  while the procoagulant has 
          been used in assays of prothrombin level in plasma and other 
          studies on blood coagulation. 

          4.2  High risk circumstances

          Children: when playing in areas where taipans are common, either 
          through accidental encounter (ie stepping on snake) or while 
          trying to emulate naturalists (ie trying to catch snake). 

          Adults: when living in areas where taipans are common, and moving 
          around barefoot and without due care, or while putting hands etc 
          into non-reconnoitred potential snake retreats (ie hollow logs 

          Farm workers:  when working in areas where taipans are common. 
          Manual labour cane field harvesting may be a particular high risk 

          Reptile keepers and snake handlers: if due care is not exercised 
          in catching and handling snakes, including venom milking. Taipans 
          are particularly fast and agile snakes, and so may be more 
          difficult to handle safely than most other Australian snakes. 

          Recreation seekers:  camping or walking or playing sport in areas 
          where taipans are common. 

          Homes: around homes in taipan prone areas when water is scarce 
          and free water is available in the garden or home. 

          4.3  High risk geographical areas

           Note distribution of taipans in Australia
          (sections 3.1.2, 3.1.3).

          Some areas of Australia are known to have high populations of 
          snakes, and there are many instances of localities where there 
          are very frequent encounters with potentially dangerous snakes. 
          These high densities with high incidences of sightings of 
          specimens usually occur in spring and early summer, when the 
          snakes emerge from their winter inactivity to search for food or 
          mates. For example, Pseudechis porphyriacus can be very common in 
          the Macquarie Marshes, ME New South Wales and Acanthophis 
          antarcticus is also extremely common in some parts of the 
          Numinbah Valley, SE  Queensland. (Covacevich, unpublished data). 

          In coastal Queensland, the presence of the introduced cane toad, 
          Bufo marinus, may have led to an increase in populations of 
          taipans, O. scutellatus. Shine and Covacevich (1983) have 
          demonstrated that in the period since the introduction of cane 
          toads (ie, in 1935), numbers of taipans donated to the Queensland 
          Museum have increased dramatically in relation to numbers of 
          donations of other potentially dangerous snakes from the same 
          area.  Of course, this is not conclusive evidence that 
          populations have increased.  Such an inference seems reasonable, 
          however, because cane toads are known to have deleterious effects 
          on many species of frog-eating native vertebrates, especially 
          snakes (Covacevich and Archer, 1975). The highly potent body 
          toxins of cane toads make them lethal prey. Taipans (Oxyuranus 
          spp) are not directly affected in this way because they feed 
          exclusively on mammals, a characteristic unique amongst the 
          Australian elapids. 


          5.1  Oral

          No data, but unlikely to be hazardous unless there are open 
          wounds in gastrointestinal tract. 

          5.2  Inhalation


          5.3  Dermal

          No evidence that venom can be absorbed through intact skin. 
          Current first-aid advice is to leave venom on skin for later 
          venom identification. 

          5.4  Eye

          Unlikely, no cases reported.

          5.5  Parenteral

          In human envenomation, venom is always inoculated by the snake 
          biting. Owing to the size of the fangs, venom is most likely to 
          be inoculated cutaneously or subcutaneously. Intramuscular or 
          intravenous inoculation is much less likely. 

          Stings: not possible.

          5.6  Others

          Experimentally, venom may be administered to test animals via 
          subcutaneous, intramuscular, intravenous, intraperitoneal, and 
          intraventricular (CNS) routes, as well as directly applied to 
          target tissues or organs (ie muscle, liver, kidney, plasma). 

    6.   KINETICS

          6.1  Absorption by route of exposure

          The rate and amount of absorption will depend on the quantity of 
          venom injected, the depth of injection, site of injection 
          including vascularity, the activity of the victim, and the type, 
          efficiency of application and length of application of first aid. 

          Clinical evidence from human cases of envenomation suggests that 
          much initial venom movement is via the lymphatic pathways.  This 
          is supported by work in monkeys using RIA to detect whole venom. 

          Direct intravenous injection, rare in man, obviously allows rapid 
          systemic circulation of venom and may result in different effects 
          from normal routes of inoculation, particularly in regard  to 
          coagulation. In sheep given IV tiger snake venom as a bolus, 
          complete coagulation of blood in the heart occurred within 
          minutes,  causing irreversible cardiac arrest.  While similar 
          experiments with taipan venom have not been performed, this venom 
          possesses a more potent procoagulant and a similar outcome might 
          be predicted. 

          6.2  Distribution by route of exposure

          As noted in 6.1, it appears that much venom is transported from 
          the bite site via the lymphatic system, then concentrating in 
          draining lymph nodes, before ultimately reaching the systemic 

          However, experience with a  number of human cases  of taipan 
          envenomation shows that symptoms and signs of envenomation may 
          occur within 15-30 minutes of the bite, especially in children. 
          Such early effects (eg headache, nausea, abdominal pain, 
          collapse) may be due to either rapidly systemically circulating 
          venom toxins, or systemically circulating natural agents released 
          at the bite site by the action of venom on local tissue. 

          Once in the systemic circulation, venom rapidly reaches  high 
          concentrations in the kidneys, whence it is excreted in the 
          urine. Such venom must also exit the circulation, to enter the 
          extravascular space  where  it  binds  within  the  neuromuscular 
          junction (presynaptically and/or postsynaptically) and possibly 
          other nerve junction sites (eg autonomic system, perhaps causing 
          abdominal pain). 

          The kinetics of venom distribution, excretion, and detoxification 
          are incompletely understood. Neurotoxic  paralysis  usually  
          takes 2-4 hours to become clinically detectable. Coagulopathy 
          however may become well established within 30 minutes of a bite. 

          6.3  Biological half-life by route of exposure

          Substantive data in man are not available.

          6.4  Metabolism

          Little information is available on the metabolism of venom 
          components in man, but most components are fully active in whole 
          venom, requiring no further modification for activity. As venom 
          reaches high concentrations in the kidneys, where it is excreted 
          in urine, and does not reach equivalent concentrations in the 
          liver, it could be postulated that little detoxification of venom 
          components occurs, the body instead relying on direct excretion 
          of unaltered venom.  The  fate of specific venom  components, 
          particularly neurotoxins and procoagulants, is unclear. Once 
          fixed at the nerve terminal, it seems unlikely that the 
          neurotoxins would then release, return to the circulation, and 
          exit via the kidney. As the term of paralysis is finite, it seems 
          more likely that these components are progressively detoxified in 

          6.5  Elimination by route of exposure

          As mentioned previously, most venom is eliminated via the 
          kidneys, in urine. 


          7.1  Mode of action

          Neurotoxic paralysis

          Whole venom contains a variable mixture of presynaptic and 
          postsynaptic neurotoxins, the latter poorly defined and much less 
          toxic. Composition of this mixture may or may not be uniform 
          across all populations of taipans. 

          The presynaptic neurotoxins (eg taipoxin, paradoxin) appear to 
          bind directly to the cell membrane of the terminal axon, at the 
          neuromuscular junction.  After a latent period of approximately 
          60-80 minutes, the neuromuscular block becomes detectable (in 
          isolated nerve-hemidiaphragm preparations of mouse), and is 
          rapidly established as essentially complete paralysis.  This  is 
          associated  with a reduction in cholinergic synaptic vesicle 
          number, fusion of vesicles, and damage of intracellular 
          organelles such as mitochondria. There is an increase in the 
          level of free calcium in the nerve terminal.  Thus the 
          neurotransmitter acetylcholine appears to be progressively 
          removed or made unavailable for release, causing paralysis. 
          (Dowdall et al 1977; Eaker 1978; Cull-Candy et al 1976; Datyner & 
          Gage 1973) 

          The postsynaptic neurotoxins cause blockade of the acetylcholine 
          receptor on the muscle end-plate at  the neuromuscular junction. 
          As this action is extracellular, these toxins are more readily 
          reached by antivenom. 

          Procoagulants and coagulopathy

          Procoagulants have been isolated from O. scutellatus venom and O. 
          microlepidotus venom. They are proteins, with a MW of about 
          200,000 D, and achieve their action in a manner analogous to 
          factor Xa, causing conversion of prothrombin, through 
          intermediates, to thrombin.  However, they  are direct 
          prothrombin converters, working largely independent  of cofactors 
          in the absence of factor V, calcium and phospholipid. The 
          thrombin product then converts fibrinogen to fibrin clots in 
          vitro. (Walker et al, 1980, Speijer et al, 1986) 

          In human envenomation there is widespread consumption of  
          fibrinogen resulting  in defibrination and hypocoagulable blood. 
          Any damage to blood vessels then causes increased bleeding, 
          although spontaneous bleeding is not often seen. Usually 
          platelets are not consumed, but factors V, VIII, Protein C and 
          plasminogen all show acute reductions in human envenomation. 
          While major clots are not seen in man, some fibrin cross linkage 
          and stabilisation does occur in vivo, as XDP levels rise sharply 
          in human envenomation. (White 1983c; White 1987c; White 
          unpublished data) 


          Some of the presynaptic neurotoxins are also directly myolytic  
          (eg taipoxin) and cause major destruction of skeletal  muscle,  
          locally  and systemically,  both in experimental animals and 
          occasionally in human envenomation. The phospholipase A2 

          components of these toxins may hydrolyse muscle cell surface 
          membrane phospholipids (Mebs & Samejima 1980).  Not all muscle 
          cells are equally affected, skeletal muscle being most 
          susceptible, and immature muscle cells appear resistant. In 
          experimental animals muscle cell destruction may occur in only a 
          few hours, within 3 days the process is complete and cell 
          regeneration commences, with complete  regeneration taking 3-4 
          weeks (Harris et al 1975). Following acute muscle damage there is 
          a progressive rise in serum levels of creatine phosphokinase (CK 
          or CPK) peaking at between 10 to 20 hours post-bite. Myoglobin 
          levels also rise and are excreted in the urine, causing the 
          typical dark brown discolouration. (Sutherland et al, 1981b, 
          Brigden & Sutherland, 1981). 

          Renal damage

          No specific nephrotoxins have been detected in taipan venom, but 
          a few cases of renal function impairment have been reported in 
          humans envenomed by O. scutellatus (Brigden & Sutherland, 1981; 
          White unpublished data). In one case this was apparently 
          secondary to renal damage by myoglobin. Other possible causes 
          include: breakdown products of fibrin released secondary to the 
          coagulopathy; breakdown products of red cells secondary to venom-
          induced haemolysis; deposition of venom and immunoglobulin 
          complexes in the kidney; vascular impairment in the early stages, 
          eg secondary to "shock". 

          7.2  Toxicity

                    7.2.1     Human data


                    The human lethal dose for taipan venom is unknown. 
                    However, without antivenom treatment, a significant 
                    number of taipan bites may be fatal. 


                    No data available, but clearly their smaller body mass 
                    ensures that children are more likely to receive a 
                    lethal dose than adults. 

                    7.2.2     Animal data

               LD50 mg/kg (18-20g mice), subcutaneous injection of dried 
               venom in mice (Broad et al, 1979, Sutherland 1983b) 

                                          Saline       Bovine Serum

               Oxyuranus microlepidotus   0.025          0.010
               Oxyuranus scutellatus      0.099          0.064

               7.2.3     Relevant in vitro data

               No data available.

          7.3  Carcinogenicity

          No data available.

          7.4  Teratogenicity

          No data available.

          7.5  Mutagenicity

          No data available.

          7.6  Interactions

          No data of clinical significance.


          8.1  Material sampling plan

            8.1.1     Sampling and specimen collection

        Toxicological analyses

                    For venom detection: swab from bite site moistened in 
                    sterile saline. If systemic envenomation also collect 
                    urine (5ml in sterile container). 

                    For venom analysis (research only using 
                    radioimmunoassay). 5ml blood; 5ml urine, frozen. 

                    At autopsy collect vitreous humor, lymph nodes draining 
                    bite area, excised bite site. 

                    (For other laboratory tests see 10.2.1)

              Biomedical analyses

                    For standard tests (eg. serum/plasma electrolytes, CK, 
                    creatinine, urea) collect venous blood in a container 
                    with appropriate anticoagulant as issued by the 
                    laboratory (usually heparin). 

             Arterial blood gas analysis

                    Collect arterial blood by sterile arterial puncture 
                    into a container as issued by the laboratory. 

             Haematological analyses

                    For whole blood clotting time as a "bedside" test 
                    collect 5-10 ml of venous blood without anticoagulant 

                    (either in the collection syringe or from a central 
                    line or other venous access line that may have 
                    anticoagulant ) and place in a glass test tube. 
                    Carefully observe the time till a clot appears. 

                    For standard tests (eg. coagulation studies, complete 
                    blood picture) collect venous blood in appropriate 
                    containers with anticoagulant as issued by the 
                    laboratory ensuring that the right amount of blood is 
                    used (for coagulation studies citrate will usually be 
                    the anticoagulant; EDTA will be used for complete blood 

                    8.1.2   Storage of laboratory samples and specimens

       Toxicological analyses

               For samples for standard venom detection: 

               Short term (less than 24 hrs) ordinary fridge is acceptable 
               -(4C), in sterile container. 

               Long term, store frozen (-20C or lower).

      Biomedical analyses

               For samples for venom analysis (research) store frozen
               (-200C or lower). 

               For samples for standard tests refer to laboratory. In 
               general keep at 4C, particularly for samples for 
               coagulation studies. 

          8.1.3     Transport of laboratory samples and specimens

      Toxicological analyses

               Use insulated container.

          8.2  Toxicological analyses and their interpretation

                8.2.1     Tests on toxic ingredient(s) of the material

             Simple qualitative test(s)

                    Simple qualitative test for presence of snake venom and 
                    designation of species/genus group, corresponding to 
                    the most appropriate monovalent anti-venom. This test 
                    is a commercial test sold by antivenom manufacturer as 
                    a kit (Snake Venom Detection Kit; CSL Melbourne) 
                    (Coulter et al 1980; Chandler & Hurrell 1982; Hurrell & 
                    Chandler 1982). 

                    (1)  Principle of test

                    The kit uses an enzyme-linked immunosorbent assay 
                    technique with specific antibodies raised to each of 
                    the five main venom types in Australia. If venom is 
                    present in the test sample it will cause a colour 
                    change in the relevant well of the kit, indicating the 
                    presence of venom for that species. 

                    (2)  Sampling

                    See section 8.1. The best samples are a swab from the 
                    bite site (swab stick etc. included in kit), or urine 
                    (only if patient has systemic envenomation). Blood has 
                    not proved a reliable sample (White 1987d). 

                    (3)  Chemicals and Reagents

                    All reagents needed for the test are included in the 
                    kit. The kit should be kept at 4C (standard fridge) 
                    and has a shelf life of 6 months. A control is built 
                    into the kit. If this fails the test results are 

                    (4)  Equipment

                    Virtually all equipment required for the test is 
                    provided in the kit. The only item not provided is a 
                    timer, but an ordinary watch is sufficient, each step 
                    taking approximately 10 minutes. An empty specimen 
                    container in which to discard waste fluid at each step 
                    is a useful addition. 

                    (5)  Specimen preparation

                         Not applicable

                    (6)  Procedure

                         Refer to instructions in kit.

                    (7)  Calibration procedure

                         Not applicable.

                    (8)  Quality control

                         Included in kit

                    (9)  Specificity

                    Where testing for snake venom using a bite site swab or 
                    urine no interference with a result is expected. If 
                    snake venom is present it will react with specific 
                    antibody in one of the wells, resulting finally in a 
                    colour change in that well. After a further delay all 
                    wells will then change colour. It is therefore 

                    important to carefully watch the wells in the last 
                    stage and note which tube changes colour first. 

                    A few snakes may cause simultaneous colour change in 
                    two wells initially. Yellow faced whip snakes may cause 
                    positive venom detection in either wells indicating 
                    brown snake venom or tiger snake venom (Williams and 
                    White, 1990) 

                    (10) Detection limit

                    The manufacturer states the kit will detect as low as 
                    10ng venom per ml. 

                    (11) Analytical assessment

                     Not applicable.

                     (12) Medical interpretation.

                    If the test is positive, it will indicate the presence 
                    of snake venom and the species/genus of snake and 
                    therefore the appropriate monovalent antivenom to 
                    neutralize the effects of that venom. 

                    If the test sample was a bite site swab, a positive 
                    result does not indicate either the presence of 
                    systemic envenomation, or the need to administer 
                    antivenom. Other clinical criteria are required in this 
                    situation (see sections 9 and 10). 

                    If the test sample was urine a positive result 
                    indicates present or past systemic envenomation and 
                    together with other clinical and laboratory criteria 
                    may be used to determine the need for antivenom 

             Advanced qualitative confirmation test(s)

                    As for

             Simple quantitative method(s)

                    Not applicable.

             Advanced quantitative method(s)

                    A radioimmune assay has been developed by staff at the 
                    Commonwealth Serum Laboratories, Melbourne to detect 
                    small quantities of many Australian snake venoms. It is 
                    primarily a research tool, being too time-consuming to 
                    be practical in determining emergency treatment of 
                    snakebite victims. It has proved useful in 
                    demonstrating snake venom either at autopsy or after 

                    patient recovery. 

               8.2.2     Tests for biological specimens

             Simple qualitative test(s)

             Advanced qualitative confirmation test(s)


             Simple quantitative method(s)

                      Not applicable

             Advanced quantitative method(s)

             Other dedicated method(s)    
               8.2.3     Interpretation of toxicological analyses               
               For venom detection as for subsection (12): 
               If the test is positive, it will indicate the presence of 
               snake venom and the species/genus of snake and therefore the 
               appropriate monovalent antivenom to neutralize the effects 
               of that venom. 

               If the test sample was a bite site swab, a positive result 
               does not indicate either the presence of systemic 
               envenomation, or the need to administer antivenom. Other 
               clinical criteria are required in this situation (see 
               sections 9 and 10). 

               If the test sample was urine a positive result indicates 
               present or past systemic envenomation and together with 
               other clinical and laboratory criteria may be used to 
               determine the need for antivenom therapy. 

               For venom analysis refer to the laboratory performing the 

          8.3  Biomedical investigations and their interpretation:

               8.3.1     Biochemical analyses

           Blood, plasma or serum

                    Electrolytes: Look for imbalance, particularly evidence 
                    of dehydration, hyponatraemia (inappropriate ADH 
                    syndrome?), hyperkalaemia (renal damage, 

                    Urea, creatinine: Look for evidence of renal function 

                    CK: If high may indicate rhabdomyolysis, usually 
                    greater than 1000 u/l. 


                    Output: Low output may indicate renal damage or poor 
                    fluid input. 

                    Myoglobin: If present indicates rhabdomyolysis, and may 
                    be missed as the red colouration of urine may be 
                    mistaken for haematuria (both may be positive on dip 
                    stick testing). 

                    Electrolytes if indicated (eg. inappropriate ADH 

             Other biological specimens

                    Not applicable.

               8.3.2     Arterial blood gas analyses

               Performed in the setting of impaired respiratory function, 
               usually secondary to neurotoxic paralysis; look for evidence 
               of poor oxygenation and its sequelae. 

               8.3.3     Haematological analyses

               Whole blood clotting time: If greater than 10 mins suspect 
               presence of coagulopathy and if no clot after 15 mins then 
               significant coagulopathy present. If no clot after 30 mins 
               then full defibrination is likely. 

               Coagulation studies: If possible these should be performed 
               as well as or instead of whole blood clotting time as they 
               will give a more comprehensive picture of any coagulopathy. 
               The principal defect likely is a defibrination-type 
               coagulopathy which will render the blood unclottable. This 
               will usually result in the following key results: 

               Prothrombin ratio /INR >12 (normal about 0.8-1.2).

               APTT >150 secs (normal <38 secs).

               Thrombin clotting time (TCT) > 150 secs (normal <16 secs).

               Fibrinogen <0.1 g/l (normal 1.5-4.0 g/l).

               Fibrin(ogen) degradation products grossly elevated 
               (including D-Dimer). 

               Platelet count normal.

               If the patient exhibits the above picture in the context of 
               a snakebite then they have a defibrination-type 

               This will require specific antivenom therapy (see section 
               10) and repeated tests of coagulation status to define 
               progress of the coagulopathy and titrate antivenom therapy 
               against resolution. The earliest sign of resolution will be 
               a rise in fibrinogen level and this may first be seen as a 
               reduction in the TCT from > 150 secs, often to 80 secs or 
               less. This may occur before there is a detectable rise in 
               fibrinogen titre. It indicates that the pathologic process 
               of venom-induced defibrination has ceased implying that all 
               circulating venom has been neutralized, at which point 
               further antivenom therapy can be withheld until the trend of 
               improving results is confirmed, in which case no further 
               antivenom therapy for the coagulopathy is indicated (unless 
               there is a subsequent relapse). 

               In the patient seen late or treated initially elsewhere 
               there may be no abnormal clotting time, with an INR < 2.0, 
               but fibrinogen may be low associated with raised degradation 
               products. In this case the results may indicate a minor or 
               resolved coagulopathy not requiring antivenom therapy. 

               Note that the platelet count (complete blood picture) will 
               usually be normal despite the intense defibrination. 

               In a few cases the platelet count may start to fall as or 
               after resolution of the defibrination occurs. This is 
               usually associated with renal damage and renal function 
               should be assessed. In this setting the thrombocytopenia may 
               well be secondary to the renal damage. 

               8.3.4     Other (unspecified) analyses

               8.3.5 Interpretation of biomedical investigations

               The interpretation of the above tests should be made in the 
               context of total patient assessment including clinical 
               evidence of pathology such as paralysis, myolysis, 
               coagulopathy and renal damage. 

          8.4  Other biomedical (diagnostic) investigations and their 

          While other investigations are not usually required to make the 
          primary diagnosis of snakebite envenomation, they may be 
          indicated in response to secondary effects of envenomation. If 
          there is either renal failure or severe rhabdomyolysis there may 
          be a hyperkalaemia, hence an ECG may be appropriate. If the 
          patient is unconscious, especially in the presence of a severe 
          coagulopathy, then a CT head scan may be appropriate to determine 
          if there is intracranial pathology such as a haemorrhage. 

          8.5  Summary of most essential biomedical and toxicological 
          analyses in acute poisoning and their interpretation 

          Overall interpretation of the results of the above tests will 
          depend on the clinical setting. Results should never be 
          interpreted in isolation from an overall clinical assessment. 

          A patient with positive venom detection from either the bite site 
          or urine and a significant coagulopathy clearly is envenomed and 
          will usually require antivenom therapy. 

          A patient with positive venom detection from the bite site only 
          and with no clinical symptoms or signs of envenoming and all 
          other tests negative is not significantly envenomed at that point 
          in time and does not require antivenom therapy. However this 
          situation may change and so careful observation and repeat 
          testing would be indicated. 

          A patient presenting some hours after the bite with positive 
          venom detection from the urine but clinically well and with all 
          other tests either normal or showing a resolved coagulopathy, 
          probably had a minor degree of envenomation, now resolved and 
          will usually not require antivenom therapy. However they should 
          be observed carefully for evidence of relapse. 


          9.1  Acute poisoning/envenomation

                    9.1.1     Ingestion

                    No data available.

                    9.1.2     Inhalation

                    No data available.

                    9.1.3     Skin exposure

                    If skin surface intact, no effects.

                    9.1.4     Eye contact

                    No data available.

                    9.1.5     Parenteral exposure

               In practical terms, this is the only likely route of entry, 
               by s.c. or i.d. injection. 

               Early symptoms, usually in the first six hours. 

               Local: pain, mild to severe; oedema, mild; ecchymosis, 
               variable, mild; persistent bleeding from wound, variable; 
               pain or swelling of draining lymph nodes (may take 1-4 hours 
               to develop). 

               Systemic: collapse, unconsciousness, convulsions may all 
               occur, especially in children, occasionally as rapidly as 15 
               minutes after the bite. Headache, nausea, vomiting, 
               abdominal pain, and visual disturbance may all occur. 

               Early signs of neurotoxic paralysis such as ptosis, 
               diplopia, dysarthria may develop within 1-3 hours of the 

               Coagulopathy may develop within 30 minutes of the bite. 

               Delayed symptoms

               Local: rarely a small area of superficial necrosis may 
               develop, particularly if first aid left in place more than 4 
               hours, or if a tourniquet used (Sutherland 1981, 1983a; 
               White 1987d;). 


               Paralysis: progressive up to complete paralysis. 

               Coagulopathy: bleeding from all puncture wounds. 

               Myolysis: muscle weakness and movement pain.  Dark urine. 

               Renal impairment: oliguria or anuria.

                    9.1.6     Other

                    No data available.

          9.2  Chronic poisoning by:

                    9.2.1     Ingestion

               No data available.

                    9.2.2     Inhalation

               No data available.

                    9.2.3     Skin contact

               No data available.

                    9.2.4     Eye contact

               No data available.

          9.2.5 Parenteral exposure

               No data available.

          9.2.6 Other

               Not applicable.

          9.3  Course, prognosis, cause of death

          Initially the patient will usually be anxious, knowing they have 
          sustained a snakebite. The subsequent course will depend on (a) 
          amount of venom injected, (b) size of patient relative to venom 
          load (ie children may be worse affected), (c) degree of activity 
          of patient after bite (physical activity hastens venom 
          absorption), (d) timing, type, effectiveness of first aid, (e) 
          speed and nature of specific medical treatment given, if systemic 
          envenomation ensues, (f) pre-existing health factors for each 
          patient (ie past renal problems, allergic problems etc). 

          Minor envenoming: little or no venom injection, no development of 
          system envenomation, no need for antivenom treatment, no likely 
          sequelae or complications. 

          Moderate envenoming: bite usually at least slightly painful, with 
          some local reactions, subsequent development over next few hours 
          of some or all of the following: headache, nausea, vomiting, 
          abdominal pain, collapse, convulsions (especially in children), 
          early signs of paralysis, such as ptosis, diplopia, and 
          laboratory evidence of coagulopathy. Antivenom treatment at this 
          stage will usually arrest or reverse the various manifestations 
          of systemic envenomation. Without antivenom treatment, in most 
          such cases the symptoms and signs will show progressive 
          worsening, with deepening coagulopathy and an increased chance of 
          secondary haemorrhage (beware intracranial haemorrhage), 
          progressive paralysis which may ultimately progress to complete 
          respiratory paralysis, about 18-24 hours post-bite; progressive 
          myolysis and muscle movement pain; secondary renal failure; 
          secondary complications of the above, particularly pneumonia; 
          ultimate outcome may be death, more than 24 hours post-bite. 

          Severe envenoming: most likely if bite either multiple, or 
          associated with chewing bite and numerous teeth marks. Local 
          reactions such as ecchymosis, oedema and pain likely. Rapid 
          development of headache, collapse, convulsions (especially 
          children), sometimes within 30 minutes of bite. Subsequent 
          symptoms may include headache, nausea, vomiting, abdominal pain, 
          and evidence of progressive paralysis, coagulopathy, myolysis and 
          renal impairment. Ptosis and diplopia may be evident within 2 
          hours of bite; coagulopathy may be detectable within 30 minutes 
          of bite; myolysis may take several hours to develop. Renal damage 
          may occur early. Prompt antivenom treatment required as soon as 
          nature of envenomation evident. In some circumstances paralysis 
          may be sufficiently advanced at a cellular level that antivenom 
          cannot prevent severe paralysis. In this situation, intubation 
          and assisted ventilation may be required for a variable period 
          (up to several weeks). The coagulopathy may only reverse 
          following large amounts of antivenom. The myolysis may not be 
          preventable, and may result in widespread muscle damage, which 
          will eventually resolve. Renal damage is usually reversible, 

          after a period of haemodialysis. 

          Without antivenom treatment such cases will almost certainly die. 

          Special notes

          Children are more likely to develop severe envenomation than 
          adults, and do so more rapidly. 

          Bites to the trunk or face are harder to manage with first aid, 
          and so may cause earlier development of envenomation. 

          Secondary infection of the local bite wound may occur. 

          Physical activity after a snakebite increases the rate of 
          absorption of venom and so hastens the onset of envenomation. 
          This situation often occurs in bites to children. 

          Multiple bites nearly always are associated with potentially 
          lethal envenomation. 


          As noted above. Overall up to 75% of all taipan bites will prove 
          fatal if no antivenom treatment is used (based on statistics from 
          cases prior to specific taipan antivenom becoming available; 
          modern intensive care facilities may improve this figure 
          significantly). Insufficient data are available on fatality rate 
          with antivenom treatment, but deaths do still occur. 

          Causes of death

          Coagulopathy   primary eg cerebral haemorrhage;
                         secondary eg renal failure.

          Paralysis      primary eg respiratory failure;
                         secondary eg pneumonia

          Renal Failure  includes secondary complications such as

          Anaphylaxis    acute allergic reaction to venom in a
                         patient previously exposed to taipan
                         snake venom (eg reptile keeper).

          Cardiac complications likely to be secondary

          9.4  Systemic description of clinical effects

               9.4.1     Cardiovascular

               Collapse, presumably due to hypotension, is common in the 
               early stages of systemic envenomation, especially in 
               children. The mechanism is uncertain but may be due to 
               release of vasoactive substances from or by the venom. 

               Specific cardiac abnormalities due to taipan snake 
               envenomation in man have not been described. 

               9.4.2     Respiratory

               No primary effects of taipan snake venom on the respiratory 
               system in man are not reported, with the exception of 
               respiratory muscle paralysis (see below). 

               9.4.3     Neurological


                    While no direct CNS toxins have been reported for 
                    taipan snake venom, early collapse and convulsions do 
                    occur, especially in children. Their aetiology remains 

             Peripheral nervous system

                    Effect of venom uncertain and of little clinical 


                    Abdominal pain.

             Skeletal and smooth muscle

                    Best documented effects of taipan snake venom are at 
                    the neuromuscular junction, both experimentally and 
                    clinically. Both presynaptic and postsynaptic 
                    neurotoxins present, causing progressive neuromuscular 
                    paralysis, up to complete paralysis of all muscles of 

               9.4.4     Gastrointestinal

               Nausea and vomiting may occur. In the presence of a venom-
               induced coagulopathy, haematemesis and even melaena may 
               occur, though they appear rare, even in severe envenomation. 
               Abdominal pain is sometimes described. 

               9.4.5     Hepatic

               Direct hepatic effects of taipan snake venom have not been 
               noted clinically. 

                9.4.6     Urinary


                    No direct nephrotoxin has been reported from taipan 
                    venom, but renal failure has been reported in a few 
                    cases, and is a very serious complication of 
                    envenomation, with a significant mortality, despite 

                    antivenom treatment. The nature of the renal injury and 
                    its cause are poorly documented, but acute tubular 
                    necrosis seems most likely.  Renal cortical necrosis 
                    has not been reported, but has been seen in one case 
                    (White unpublished records). 


                    No data available.

               9.4.7     Endocrine and reproductive systems

               No data available.

               9.4.8     Dermatological

               The local bite site may be painful, though not significantly 
               so in all cases. Similarly, while local oedema and even 
               ecchymosis may occur, it is not universal. Teeth marks are 
               variable, from single fang puncture to multiple tooth 
               punctures and scratches. Local necrosis may occur, but is 
               usually minor if present, unless a tourniquet is used as 
               first aid. Secondary infection may occur (White 1983b). 

               9.4.9     Eye, ear, nose, throat: local effects

               No data available.

               9.4.10 Haematological

               A major clinical effect of taipan envenomation in man is 
               coagulopathy caused by potent procoagulants in the venom, 
               which cause prothrombin activation and secondary fibrinogen 
               consumption. The resulting defibrination is associated with 
               hypocoagulable blood, and persistent bleeding from any 
               vascular injury, including venepuncture sites. Without 
               antivenom treatment, this may occasionally resolve. 

               However, as the venom is not apparently vasculotoxic, in the 
               absence of vascular injury bleeding does not occur, thus in 
               many patients the coagulopathy proves relatively benign. 

               An early neutrophil leukocytosis may occur in some patients. 

          9.4.11 Immunological

               Significant depletion of circulating lymphocytes may occur 
               in the early stages of envenomation, with resultant 

          9.4.12 Metabolic

            Acid base disturbances

                    No changes.

            Fluid and electrolyte disturbances

                    Secondary fluid and electrolyte disturbances due to 
                    renal failure if present. Inappropriate ADH (anti-
                    diuretic hormone secretion) syndrome should be 
                    considered. In this situation, otherwise acceptable 
                    intravenous fluid loads may result in significant 
                    electrolyte imbalance and other sequelae. 


                    Rise in serum levels of liver enzymes, cardiac enzymes, 
                    plus CK (if rhabdomyolysis). A rise in CK to below 1000 
                    IU/l is not indicative of rhabdomyolysis. True venom-
                    induced rhabdomyolysis causes CK levels well above 1000 

               9.4.13 Allergic reactions

               May occur due to allergy to venom or antivenom, and 
               resultant anaphylaxis may prove fatal. 

               Reptile keepers previously bitten by taipans are also at 
               risk of acute anaphylactic allergic reactions on subsequent 
               bites, which may cause collapse within minutes of the bite. 
               Fatalities have occurred due to this mechanism (Sutherland 
               1983; White 1987 b,d). 

               9.4.14 Other clinical effects


               Due to direct action of presynaptic neurotoxins (eg 
               Taipoxin) on muscle cells, causing widespread muscle damage. 
               This causes muscle weakness, muscle tenderness, muscle 
               movement pain, diminished deep tendon reflexes, rise in 
               serum CK, and frank myoglobinuria (dark brown urine). If 
               muscle damage is severe, recovery may take weeks, although 
               full functional recovery is possible. Severe muscle wasting 
               may be apparent, and intensive physiotherapy is required to 
               prevent contractures in the early stages, and to promote 
               rapid muscle regeneration in the later stages. 

          9.4.15    Special risks

               No data available.

          9.5  Other

          No data available.


          10.1 General Principles

          All patients suspected of having sustained a taipan bite should 
          be admitted to hospital for observation over the first 24 hours. 
          While all such cases should be treated as potentially fatal not 
          all cases will develop envenomation. Management of cases with 
          systemic envenomation may be divided into specific, symptomatic, 
          and general treatment. 

               The aims of treatment are:

                    (a)  Maintain life through maintenance of
                         vital bodily functions.
                    (b)  Neutralise inoculated venom.
                    (c)  Correct venom-induced abnormalities.
                    (d)  Prevent or correct secondary

          Specific treatment

          If there is evidence of systemic envenomation, antivenom therapy 
          is the most important treatment. Once the snake has been 
          identified (eg by venom detection) give specific antivenom (CSL 
          Taipan Snake Antivenom). ( White 1981; 1987d; Sutherland 1983; 
          Trinca 1963). 

               Symptomatic and general treatment

               Support of cardiorespiratory systems.
               Treatment of shock.
               Maintain adequate renal perfusion.
               Replace major blood loss due to
               coagulopathy induced haemorrhage (but use blood
               products only with great caution until
               coagulopathy resolved).
               Tetanus prophylaxis.
               Avoid respiratory depressant
               medications (eg morphine).
               Avoid antiplatelet medications (eg aspirin).

          10.2 Relevant laboratory analyses and other investigations 

               10.2.1    Sample collection

               Venom for venom detection: use CSL Venom Detection Kit; best 
               sample is swab from bite site (swab stick etc in kit); if 
               systemic envenomation present then urine useful; 
               serum/plasma less reliable. If a bandage has been applied 
               over the bite site as first aid, keep the bandage adjacent 
               to wound because this may have absorbed venom; it can be 
               tested to identify venom (after elution) if all other 
               samples negative in presence of significantly envenomed 

               Blood: Initially collect for complete blood count (EDTA 
               sample), clotting studies (citrated sample), electrolytes 
               and enzymes (heparin and/or clotted sample) and possibly, 
               group (type) and screen serum (clotted sample). In 

               anticoagulated blood samples ensure correct ratio of blood 
               to anticoagulant (especially citrate samples) and proper 
               mixing. If laboratory facilities unavailable, collect for 
               whole blood clotting time (ie 5-10 ml in glass test tube, 
               and measure time to clot). Samples for clotting studies in 
               particular should be kept cold during transportation. 

               Urine: Measure urine output, visual check for 
               haemoglobinuria or myoglobinuria (dark red-brown urine); if 
               suspect myoglobinuria collect samples at intervals for 
               subsequent laboratory confirmation (5-10 ml). 

               10.2.2    Biomedical analysis

               Venom detection: Venom at the bite site confirms only the 
               species of snake, but venom in the urine indicates systemic 

               Coagulation studies: In the absence of a haematology 
               laboratory, whole blood clotting time is a useful test, for 
               both the presence of a coagulopathy, and its progress and 
               resolution with adequate antivenom therapy. 

               If a laboratory is available, the most useful tests for 
               presence and extent of coagulopathy are: Prothrombin 
               time/ratio; Activated partial thromboplastin time; Thrombin 
               clotting time; Fibrinogen assay; Fibrin(ogen) breakdown 
               products assay. 

               In addition, a complete blood count should always be 
               performed concurrently, particularly for a platelet count. 

               Other blood tests:

                   Electrolytes (eg Na, K etc);
                   Renal function (eg creatinine, urea);
                   Enzyme levels, especially CK;
                   Arterial blood gas, if appropriate (ie impaired 
                   respiratory function).

               Urine: For haemoglobinuria and myoglobinuria

                         10.2.3    Toxicological analysis

               Venom detection, see section 8.

                         10.2.4    Other investigations

                              As indicated medically.

          10.3 Life supportive procedures and symptomatic


          In severe cases of systemic envenomation by taipans, where 

          antivenom treatment has been delayed, paralysis may progress to 
          complete or near complete respiratory paralysis. In this 
          situation early intervention by endotracheal intubation and 
          artificial ventilation is lifesaving. Such respiratory support 
          may be needed for hours, days, or even weeks, until adequate 
          respiratory function returns. 

          Once established, such severe paralysis may not be reversed by 
          antivenom therapy. 


          The principal method of treatment of taipan envenomation 
          coagulopathy is the neutralisation of all inoculated venom by 
          antivenom. Until this is achieved, use of clotting factor blood 
          products (eg fresh frozen plasma, cryoprecipitate, fibrinogen) 
          may only deepen the degree of coagulopathy, by providing more 
          substrate on which the venom may act. Once all venom is 
          neutralised normal homeostatic mechanisms quickly return 
          coagulation towards normal, without the need for replacement 
          therapy. The possible exception would be where there is major 
          bleeding as a result of the coagulopathy (eg cerebrovascular 
          accident), when replacement therapy should be considered once 
          adequate antivenom has been given.  Heparin has no proven value 
          in this situation and there is evidence it may be harmful. 

          In cases of severe envenomation a central venous pressure (CVP) 
          line may be highly desirable for patient management, but in the 
          presence of coagulopathy should be inserted with great caution, 
          due to the likelihood of significant haemorrhage from the 
          insertion site if the insertion attempt is unsuccessful. 

          In such cases frequent testing of coagulation will be necessary 
          to titrate antivenom therapy. A CVP line will allow frequent 
          sampling without further breaches of veins, an important 
          consideration in severe coagulopathy where venepuncture may 
          result in bleeding for hours. For similar reasons, venepuncture 
          from major veins, such as the femoral, should be avoided, and 
          used only as a last resort. 

          Following resolution of the coagulopathy there may be rebound 
          hyperfibrinogenaemia at about 2-4 days post resolution. There is 
          a theoretical potential for hypercoagulability at this time, 
          particularly in the immobile paralysed ventilated patient, and 
          the possibility of thrombus formation and emboli, including 
          pulmonary emboli, should not be forgotten. 


          Apart from antivenom therapy, maintenance of adequate renal 
          throughput and, in the latter stages during recovery, appropriate 
          diet (high protein) and physiotherapy. 

          Renal failure

          First priority is to avoid renal injury by ensuring adequate 

          renal perfusion. In all cases of significant systemic 
          envenomation, catheterisation of the bladder to monitor urine 
          output constantly is advisable. In severe cases of envenomation, 
          the use of a CVP line will assist in adjusting IV fluid load to 
          ensure adequate blood volume and renal perfusion. 

          Once renal injury is established, standard techniques of medical 
          management should apply. Haemodialysis may be required. Renal 
          biopsy should be avoided at least until the coagulopathy is 
          completely resolved. 

          Local bite site

          The bite site should be cleaned only after adequate sampling for 
          venom. Local infection may occur, but is not usual, and thus 
          prophylactic antibiotic therapy is not appropriate. Tetanus 
          prophylaxis should be ensured. If there is minor local necrosis, 
          this can usually be successfully treated conservatively. Only 
          rarely will local skin necrosis be sufficient to warrant 
          debridement and grafting, and this is best left until the acute 
          phase of envenomation is over, and the area of injury clearly 
          delineated. Taipan bites do not apparently cause sufficient local 
          reaction to justify surgical decompression. If compartment 
          syndrome is suspected, then it should be confirmed by 
          intracompartmental pressure measurement prior to any surgical 



          May be necessary, though most cases will need no more than 
          paracetamol. Morphine should be avoided (CNS depressant effect). 
          Platelet-active drugs should be avoided (eg aspirin). 


          May be useful in treatment of severe allergic reactions, or in 
          the prophylaxis of serum sickness, but their role in the general 
          treatment of taipan snake bite is doubtful. 

          10.4 Decontamination

          Not applicable.

          10.5 Elimination

          Not applicable.

          10.6 Antidote treatment

               10.6.1 Adults

          Taipan snake antivenom (CSL, Melbourne) is the specific treatment 
          of taipan snake bite. It should only be used if there is definite 
          systemic envenomation. (Trinca 1963; Sutherland 1974, 1983b; 

          White 1981, 1987d) 

          The antivenom is a refined horse serum (Fab2 fragments), with all 
          the potential hazards of that product. One ampoule contains 
          12,000 units of activity against taipan snake venom. This is 
          sufficient to neutralise the "average" amount of venom produced 
          by a single milking of one snake (Oxyuranus scutellatus). In a 
          severe bite, and multiple bites, several ampoules of antivenom 
          may be necessary. The average volume of antivenom (horse serum) 
          per ampoule is 40 ml, but the precise volume varies from batch to 

          Taipan antivenom is used to counter the potentially life-
          threatening systemic effects of venom and must be given 

          Since skin testing is unreliable and hazardous, there is no place 
          for pre-therapy sensitivity testing of antivenom. (Sutherland 
          1983b; White 1987d). 

          Acute allergic reactions up to and including potentially fatal 
          anaphylaxis may occur during antivenom therapy. Precautions 
          should be taken to reduce the risk to the patient. These include: 

          Only give antivenom if staff, drugs and equipment to treat severe 
          anaphylaxis, including intubation facilities are available 
          (preferably in an intensive care unit), unless in extreme 

          Always have adrenaline injection prepared and ready to use. 

          Always have a good reliable IV line inserted.

          Always maintain adequate monitoring of patient during and after 
          antivenom therapy, especially blood pressure. 

          Dilute antivenom (1:5 to 1:10) in IV carrier solution (normal 
          saline; dextrose or Hartmann's). 

          Give antivenom initially very slowly, and increase rate if no 
          reaction, aiming to give whole dose over 15-20 minutes. 

          Premedication is proposed by some. (Sutherland 1983b) Suggested 
          premedications are subcutaneous adrenaline and intravenous 
          antihistamine. The author of this monograph does not routinely 
          use such premedication. (White 1987d) Antihistamine may make the 
          patient drowsy or irritable, and thus interfere with the ongoing 
          assessment of envenomation, especially in children. Adrenaline is 
          potentially hazardous, especially in older patients or those with 
          coagulopathy, and as acute severe allergic reactions may be 
          delayed up to an hour or more, such premedication is of doubtful 
          value. A patient with known or likely allergy to horse serum 
          presents a special case, where premedication as above, possibly 
          with the addition of steroids, is worthy of active consideration. 
          Similarly a sole country medical practitioner managing a severe 
          snakebite, where antivenom must be given before an aeromedical 

          evacuation team can arrive, may well consider premedication with 
          subcutaneous adrenaline a worthwhile precaution. 

               In the presence of mild to moderate systemic envenomation 
               (ie no or minor paralysis, no active bleeding from 
               coagulopathy etc) initially give one ampoule of antivenom 
               (dependent on species of tiger snake, see table below). 
               Follow up with further ampoule(s) if progression of symptoms 
               and signs, or if no resolution of coagulopathy. Resolution 
               of coagulopathy may be used to titrate antivenom therapy. 
               (White 1983c; 1987 c,d) 

               In the presence of severe envenomation, initially give 2 
               ampoules of antivenom, and be prepared to give more, as 
               above. If using the resolution of coagulopathy to titrate 
               antivenom therapy, aim to retest coagulation (see section 
               10.2.1) about 1 - 1.5 hours after completion of antivenom 
               dose. First evidence of impending resolution may be a 
               reduction in the thrombin clotting time, often accompanied 
               by a slight rise in fibrinogen level. If there is no 
               significant improvement, give further antivenom. If there is 
               significant improvement, repeat test in a further 1-2 hours 
               and reassess. 

               There is no mandatory upper limit on antivenom dosage, but 
               only rarely will more than 4-5 ampoules be required (also 
               dependent on species/subspecies of taipan snake). 

               10.6.2 Children

               The dosage of antivenom is identical in children to adults. 
               However, in small children fluid volume considerations may 
               force lower dilutions of antivenom. For any given bite the 
               degree of envenomation will be worse in children due to 
               lower body mass. 

               Following antivenom therapy there is a possibility that the 
               patient may develop serum sickness. This should be explained 
               to the patient so that if symptoms develop, they will seek 
               appropriate treatment. 

               If large volumes of antivenom are used (eg 50-100 ml or 
               more) then prophylaxis for serum sickness should be 
               considered (eg oral steroid therapy for 2 weeks). 

          10.7 Management discussion

          Controversies in management exist in several areas 

          First aid

          Tourniquet versus pressure/immobilisation: the latter is now well 

          accepted as the method of choice. (Balmain & McClelland 1982, 
          Fisher 1982, Murrell 1981, Sutherland 1983b; Sutherland et al 
          1981 a,b; White 1987d) 

          Suction of wound: No proven value.

          Cutting or excising wound: of no practical value and potentially 


          Use of premedication: not universally accepted. (Sutherland 1975, 
          1977 a,b,c; 1983b; White 1987d) 

          Use of skin pretesting: not appropriate.


          Use of fibrinogen, fresh frozen plasma etc as primary treatment: 
          No proven benefit and potentially very dangerous.  (White 1987d) 

          Use of heparin: of no proven benefit and potentially dangerous. 

          Non-antivenom treatment

          Based on the assumption that it is paralysis which kills the 
          patient and this can be managed adequately in an intensive care 
          unit by artificial ventilation, therefore antivenom is not 
          required, thus avoiding antivenom allergy problems. This ignores 
          the danger of coagulopathy, best managed by antivenom therapy, 
          and the fact that early antivenom therapy may avoid severe 
          paralysis and the hazards of artificial ventilation. 


          There are many aspects of taipan snake venom worthy of further 
          research, at a basic science level, as well as studies at a more 
          clinical level. 


          11.1 Cases and reports from literature

     Flecker, 1940

          General paper on snakebite, including 3 cases of definite or 
          probable taipan bite. 

          (i)  A 49 year-old man was bitten on the right hand by a large 
          snake, thought to be a taipan. He was initially treated by 
          incision and tourniquet. At 1.5 hours post-bite he developed
          nausea and vomiting, but remained otherwise well, except for the 
          bitten limb. This remained with a tourniquet in place for 7.5 
          hours, leaving the arm swollen and numb. He remained drowsy and 
          weak for several days, without paralysis being noted, and lost 
          both taste and smell, neither of which returned to normal.  He 

          made an otherwise complete recovery. No antivenom treatment. 

          (ii) A 35 year-old Aboriginal man was bitten on the leg while on 
          a bicycle, by a snake thought to have been a taipan. Shortly 
          thereafter he had a convulsion from which he recovered, but then 
          commenced vomiting and 6 hours post-bite had 3 more convulsions, 
          and died.  No antivenom treatment. 

          (iii)     A 39 year-old man was bitten on the leg while fishing. 
          On presentation at hospital 5 hours later he was cyanosed, 
          comatose, with severe paralysis and dilated pupils.  Death 
          occurred 6 hours post-bite.  No antivenom treatment. 

     Flecker, 1944

          (i)  Adult male bitten through trousers on right leg by 2.3 m 
          taipan, applied tourniquet, and remained symptom free until 1.1/2 
          hours after the bite, when he suddenly had a seizure, followed by 
          continual seizures and profuse perspiration, continuing until his 
          death, 5 hours after the bite. 

          (ii) Adult male bitten on the leg, while working in cane fields, 
          by a large brownish snake thought to be a taipan (never 
          confirmed). Initially symptom-free, but after a few hours (time 
          not stated) became unwell, with vomiting, then paralysis of 
          tongue and pharynx, then had convulsions and died. 

          (iii)     A 20 year-old female Aborigine was bitten at 11 pm 
          while walking down a town street, by a large brown snake thought 
          to be a taipan. She was bitten on the dorsal aspect of the foot, 
          immediately ran for home, and collapsed unconscious 90 seconds 
          later, and had convulsions.  She died shortly afterwards. Death 
          was reported due to asphyxia, with blood issuing from nose and 

     Reid and Flecker, 1950

          A detailed case report with recovery.  A 19 year-old Aboriginal 
          boy bitten on the right ankle while stacking timber. Snake killed 
          and confirmed as taipan. Bite occurred through boot  and thick 
          socks, initially treated with tourniquet and incision. Between 
          15-30 minutes post-bite was unable to open eyes, then developed 
          nausea (?vomiting), dyspnoea, and drowsiness.  By 4 hours post-
          bite he was semiconscious, shocked, restless, and tiger snake 
          antivenom was sought and used without great success. By the 
          following day he  was drowsy,  restless, not shocked, breathing 
          spontaneously, but with ptosis, facial weakness, dysphagia, and 
          tongue paresis, although no ocular paresis was detected, and 
          pupils were reactive to light. DTRs sluggish, and limb weakness 
          was present.  He made little improvement over the next 24 hours, 
          and thereafter a slow improvement until on day 7 he developed 
          serum sickness, from which he recovered over several days, being 
          discharged 19 days after the bite. 

     Benn, 1951

          A 20 year-old amateur herpetologist was bitten on his left hand 
          by a taipan (identity confirmed), the bite initially treated with 
          a tourniquet. He remained well initially, with  continued use of 
          a tourniquet, and received tiger snake antivenom. About 2 hours 
          post-bite the tourniquet was removed and at 4.5 hours post-bite
          he developed blurred vision, vomiting, headache, ptosis, and 
          facial weakness. At this time the hand was red and swollen. 
          Paralysis extended over the next 4 hours, with medial rectus 
          palsy and severe ptosis, tongue paralysis,  dysphagia,  
          dysarthria,  and  some decreased intercostal movement, and by 9.5
          hours post-bite there was complete facial paralysis and minimal 
          respiratory capacity, requiring  attempts at  artificial  
          respiration  (in a respirator).  The patient resisted this 
          treatment, and maintained some respiration overnight, but with 
          developing cyanosis. At 23 hours post-bite he had a rigor. At 26 
          hours post-bite respiratory movements ceased, and he was again 
          put in the respirator. At 27 hours post-bite he died, possibly of 
          cardiac arrest. At autopsy the only finding noted was an area of 
          dry gangrene around the bite site. 

     Lester, 1957

          (i)  A detailed report, with the first successful use of the 
          newly available taipan antivenom.  A 10 year-old boy was bitten 
          on the right knee by a snake thought to be a taipan (not 
          confirmed). He became unconscious almost immediately, recovering 
          consciousness spontaneously within 30 minutes, at which time he 
          was noted as pale, drowsy, without paralysis, and was given tiger 
          snake antivenom.  He remained apparently stable until 19 hours 
          post-bite, when severe ptosis, dilated pupils, marked drowsiness, 
          abdominal pain, vomiting, and blood oozing from the wound were 
          noted. The paralysis progressed such that by 24 hours post-bite 
          he had almost complete ptosis, almost complete ophthalmoplegia, 
          dilated pupils almost unreactive to light, dysarthria, but no 
          respiratory distress. At 24.5 hours post-bite he received taipan 
          antivenom, suffering an allergic  reaction controlled by 
          adrenaline. Within 1.5 hours a definite clinical improvement was
          apparent, though marked ptosis remained. The bite site wound 
          continued to ooze. The ophthalmoplegia and ptosis had virtually 
          resolved by day 5 post-bite, though the wound still oozed, this 
          resolving the following day.  He made a complete recovery. 

          (ii)      An adult male, aged 19 years, suffered a bite from a 
          taipan (identity confirmed), subsequently developing vomiting of 
          "coffee grounds and bright blood", then ptosis, generalised 
          weakness, and finally respiratory paralysis ending fatally. 

          (iii)     An adult male, aged 52 years, suffered a bite from a 
          possible taipan (identity not confirmed), remaining symptom-free 
          for 4 hours, then developing respiratory distress, dysarthria, 
          and ptosis, progressing to death some 12 hours post-bite. 

     Sutherland et al, 1980

          A 4 year-old boy sustained multiple bites from a taipan (positive 
          identification of venom), with rapid development of drowsiness, 

          vomiting, then collapse, death occurring within 60 minutes. No 
          specific findings were noted at autopsy, other than evidence of 
          multiple fang punctures (12), and venom in tissues (2 mg/g of 

     Brigden and Sutherland, 1981

          A 39 year-old man presented with a one hour history of nausea and 
          vomiting, at no stage believing he might have been bitten by a 
          snake. Six hours later he developed fixed dilated pupils, ptosis, 
          and  progressive paralysis, ultimately requiring intubation and 
          artificial ventilation. No snake bite marks were found. 
          Coagulation studies revealed a severe coagulopathy. He was 
          hypertensive. He was given 4 ampoules of polyvalent antivenom. 
          Over the ensuing 12 hours he developed oliguria, and a grossly 
          elevated creatine kinase (19,600 IU/L), but the coagulopathy 
          reversed.  He required ventilatory support for 19 days, and 
          peritoneal dialysis for renal failure, but made a complete 
          recovery, being discharged 27 days post-bite. Subsequent testing 
          of early urine samples was positive for taipan venom and 
          myoglobin (serum samples negative for venom). 

     Campbell, 1967

          Details of experience with six taipan bites in Port Moresby, 
          Papua New Guinea. 

          (i)  A male, aged 10 years, bitten on leg, developed vomiting at 
          1.5 hours post-bite, then tender groin nodes, then mild
          paralysis. Given taipan antivenom, with  slight worsening of 
          paralysis but eventual recovery. 

          (ii) A man, aged 20 years, bitten on the ankle, did not develop 
          any evidence of envenomation, though was given antivenom. 

          (iii)     A man, aged 35 years, bitten on the ankle, became 
          unconscious 30 minutes post-bite, with recovery, then later 
          vomiting and abdominal pain, bleeding problems, and severe 
          paralysis. Given antivenom, but paralysis progressed requiring 
          tracheostomy and  artificial ventilation for 10 days, with 
          eventual recovery. 

          (iv) A man, aged 20 years, bitten on the foot, developed 
          epigastric pain and tenderness, and vomiting, without paralysis 
          being noted, received antivenom, and made a complete recovery. 

          (v)  A man, aged 40 years, bitten on the ankle, developed a 
          headache at 30 minutes, nausea at 1 hour, tender groin nodes, 
          haemoglobinuria, albuminuria, and a coagulopathy. Recovered after 
          antivenom therapy. 

          (vi) A woman, aged 20 years, bitten on the leg, developed 
          vomiting, headache,  dysarthria, groin pain, and generalised 
          muscular paralysis. Antivenom was given with  "no response", and 
          the patient required a tracheostomy and artificial ventilation, 
          with eventual recovery. 

     Trinca, 1969, and Sutherland et al, 1978

          A detailed case report of a bite by what was subsequently shown 
          to be O. microlepidotus.  A 46 year-old male amateur 
          herpetologist was bitten by a 1.5 m brownish snake in a remote
          part of south-west Queensland, while catching the snake. He 
          sustained 2 bites to the right thumb. He incised the wounds and 
          applied a tourniquet. 50 minutes post-bite he collapsed, 
          unconscious, with faecal and urine incontinence. He regained 
          consciousness within 15 minutes.  He remained stable, but with 
          muscle pain for several hours,  then developed nausea and 
          vomiting. By 6 hours post-bite he had dysphagia and dysarthria, 
          and the bite site was swollen and cyanosed  (tourniquet still in 
          place, with intermittent release).  During the next 3 hours he 
          became agitated, confused, (while in transit in a Flying Doctor 
          aircraft) and on landing, about 9 hours post-bite, suffered a 
          cardiac arrest, from which he was successfully resuscitated. As 
          he had (incorrectly) identified the snake as a brown snake 
          (Pseudonaja) he was given brown snake antivenom (which is not 
          protective for taipan bites).  He had a past history of severe 
          allergy to  horse serum, though  no anaphylaxis developed on 
          antivenom administration.  He was subsequently placed on a 
          ventilator.  Ptosis and ophthalmoplegia were present, but he 
          could move all limbs. At 17.5 hours post-bite he had a 
          hypotensive episode, with haematuria and bloody diarrhoea.  By 24 
          hours post-bite the bleeding had subsided. He developed episodes 
          of frequent ventricular extrasystoles during aspiration of his 
          endotracheal tube, which continued intermittently, along with 
          transient hypertension. He made a slow recovery, requiring 
          ventilator support for several (unspecified)  days. Subsequently  
          the dead  snake was identified as a taipan (Oxyuranus 
          scutellatus) and later as a western taipan (O. microlepidotus). 

          Mirtschin et al, 1984

          A 37 year-old amateur herpetologist was bitten on his left middle 
          finger by a juvenile O. microlepidotus (between 445 and 490 mm in 
          length, less than 1 month old) while attempting to force feed the 
          snake.  At 20 minutes post-bite he complained of severe headache, 
          feeling flushed, and chest discomfort. No paralysis was noted.  
          Shortly thereafter he received one ampoule of taipan antivenom, 
          and made an uneventful recovery. There is no indication that 
          either coagulopathy or myolysis were tested for in this case. 

          11.2 Internally extracted data on cases

               Case 1 (from White, 1987)

          A 10 year-old boy was bitten on his left middle finger by a large 
          snake (later shown to be a taipan by identification of the venom 
          from bite site). Pressure/immobilisation first aid was applied 40 
          minutes later.  By 1.5 hours post-bite he complained of nausea,
          the bite site was swollen and black, but no evidence of paralysis 
          was found. At 4.5 hours post-bite he commenced vomiting, had
          axillary adenopathy, and a marked defibrination type coagulopathy 

          was noted.  He was given polyvalent antivenom at 5 hours and 7 
          hours post-bite, but by 10 hours  post-bite  the  coagulopathy  
          had worsened, now with thrombocytopenia. At 13 hours post-bite he 
          was given one ampoule each of taipan and polyvalent antivenom. At 
          15 hours post-bite the coagulopathy showed substantial 
          resolution, and platelets were now normal.  The child made a 
          continued recovery, the swelling and discolouration of the bitten 
          finger settling after 24 hours. Paralysis was not detected at any 
          stage. Of importance in this case is testing for venom. Initially 
          blood was tested for venom, without success. Later the bite site 
          was tested, giving a positive result for taipan venom. Blood is 
          often unreliable as a test sample for venom detection using the 
          CSL Venom Detection Kit. Using the VDK to test blood for systemic 
          envenomation is not advisable practice. 

          Case 2 (from Covacevich, Pearn, White, 1988)

          A 65 year-old herpetologist was bitten on the chest by a large O. 
          microlepidotus, while attempting to catch same for his reptile 
          park. He had a past history of numerous snakebites and allergy to 
          antivenom. He used "cut and suck" as first aid, then attempted to 
          walk for assistance, suffering headache, nausea, and collapse 
          shortly thereafter. He spontaneously recovered from the collapse 
          and unconsciousness, and when seen medically 3.5 hours post-bite
          was stable, but with vomiting and slight ptosis. At this time he 
          was approximately 1,000 km from hospital and, in view of this, 
          his history of antivenom allergy, and stable condition, antivenom 
          therapy was postponed until he was in a medical facility well 
          able to manage complications.  During the medical evacuation 
          flight to hospital in Adelaide he became hypertensive and 
          recommenced vomiting, but no worsening of his then minimal 
          paralysis occurred until arrival in Adelaide some 7 hours post-
          bite.  At this stage testing revealed a severe defibrination type 
          coagulopathy and worsening ptosis (figure 11.2.1), with slight 
          dyspnoea not sufficient to require ventilation. He was promptly 
          treated with taipan antivenom, which totalled 6 ampoules over  
          the next  few hours,  ultimately reversing his coagulopathy, and 
          with lessening of degree of paralysis. He suffered the expected 
          allergic reaction to initial antivenom therapy, with rash (figure 
          11.2.2), bronchospasm, and hypotension, well-controlled by IV 
          adrenaline and subsequent steroid therapy. The only other 
          problems noted were development of non-anuric renal impairment 
          (rise in creatinine) and progressive mild thrombocytopenia, both 
          of which resolved over the next few days. He was discharged at 
          one week post-bite, on steroid therapy, and did not suffer serum 
          sickness. A mild rise in CPK, with myoglobinuria, was noted in 
          the first few days, possibly indicative of mild venom-induced 

               Case 3

          A 29 year-old female amateur herpetologist was bitten on her 
          right thenar eminence (figure 2.2.1) by a 1.7 m newly purchased
          O. scutellatus. No first aid was used.  On presentation to 
          hospital about 15-30 minutes later she was vomiting, with frank 
          haematemesis (note removal of wisdom teeth 2 days previously) and 

          agitated, with developing  ptosis. Shortly  thereafter  she  
          lapsed  into unconsciousness, despite normal BP (130 systolic), 
          lasting 30-40 minutes, by which time she had been intubated and 
          taipan antivenom commenced.  Samples taken at 30 minutes post-
          bite already showed severe defibrination type coagulopathy, and 
          she continued to have significant blood loss from failed IVT 
          insertion sites (figure 11.2.3) and her mouth over the next 3-4 
          hours until the coagulopathy was reversed by sufficient taipan 
          antivenom (6 ampoules). Shortly thereafter, about 7 hours post-
          bite, urine was negative for venom (VDK).  Despite prompt 
          aggressive specific antivenom therapy she developed severe 
          paralysis requiring artificial ventilation for 4 weeks.  Ptosis 
          and ophthalmoplegia resolved after 2 weeks, with return of limb 
          muscle power, respiratory muscle power being the last to 
          satisfactorily resolve. A mild degree of myolysis was noted.  No 
          renal problems developed. After resolution of the coagulopathy, 
          and not before, a mild thrombocytopenia developed, resolving 
          within one week. Due to significant blood loss in the early 
          stages as described above, a significant anaemia developed, 
          requiring  transfusion. Steroids were given to reduce the chance 
          of serum sickness, which did not occur. Intermittent chest pains 
          during the third to fifth week were thought possibly due to mild 
          pulmonary embolism, hence the patient was commenced on a three 
          month course of warfarin. Eventual recovery was complete. The 
          patient was discharged after 5 weeks. 

          Case 4

          A 72 year-old female amateur herpetologist was bitten on the 
          right index finger by a 2.1 m O. scutellatus while feeding the
          snake. She arrived in hospital shortly thereafter, apparently 
          well, and at 30 minutes post-bite no coagulopathy was present. 
          She was observed over the next 2 hours by staff who noted 
          development of a headache and vomiting, but no paralysis, and as 
          she also had a "flu" like illness, the significance of the 
          symptoms was not appreciated.  At 4 hours post-bite, when further 
          advice was sought, she was hypertensive (170 systolic), with mild 
          ptosis, intractable vomiting, and tests revealed a mild 
          coagulopathy. She was promptly treated with taipan antivenom (2 
          ampoules), with rapid resolution of the coagulopathy. However it 
          was then noted she was anuric, and over the next 24 hours anuric 
          renal failure was clearly established.  This became her major 
          problem, necessitating prolonged dialysis and hospital stay. 
          Renal biopsy showed renal cortical necrosis. However, over a 
          period of 6 months, she showed a slow resolution, with return of 
          sufficient renal function to allow cessation of dialysis. At no 
          stage was significant paralysis or myolysis noted, the 
          coagulopathy was mild, and apart from the severe renal failure, 
          this case would be described as minor envenomation for a taipan 
          bite. As she had no past history of renal dysfunction the cause 
          of the renal failure remains uncertain, though a primary effect 
          of the venom would have to be considered. More likely is a 
          combined effect of dehydration, influenza, possible mild shock, 
          and a local angiopathic effect of the mild venom induced 

          11.3 Internal Cases


          12.1 Availability of antidotes

          Specific taipan antivenom and venom detection kits available 
          directly from the manufacturer, Commonwealth Serum Laboratories, 
          45 Poplar Road, Parkville, Victoria 3052, Australia (telephone 
          (03) 389 1911, telex AA 32789, Fax (03) 389 1434, International 
          Fax +61 3 389 1434). 

          12.2 Specific preventative measures

          Avoid exposure to taipans. If working in areas where these snakes 
          exist, be alert, wear appropriate footwear and clothing, do not 
          place hands or other parts of body in places where snakes may be 
          present (eg down holes, in rubbish etc). If handling or catching 
          snakes use appropriate techniques and equipment, regularly 
          checked to ensure peak performance, carry first aid equipment (eg 
          bandages, splint), never work alone, and have an emergency plan 
          documented and tested. If allergy history or known allergy to 
          horse serum ensure this is documented adequately. 

          12.3 Other

          No data available.


          13.1 Clinical and Toxicological References

          Balmain R & McClelland KL (1982) Pantyhose compression bandage: 
          first aid measure for snakebite. Med. J. Aust, 2: 240-241. 

          Barnes JM & Trueta J (1941) Absorption of bacteria toxins and 
          snake  venoms from the tissues: importance of the lymphatic 
          circulation. Lancet, 1: 623-626. 

          Benn KM (1951) A further case of snakebite by a taipan ending 
          fatally. Med. J. Aust, 1: 147-149. 

          Brigden MC & Sutherland SK (1981) Taipan bite with myoglobinuria. 
          Med. J. Aust., 2: 42-43. 

          Broad AJ, Sutherland SK & Coulter AR (1979) The lethality in mice 
          of dangerous Australian and other snake venoms. Toxicon, 17: 661-

          Broad A, Sutherland SK, Tanner C & Covacevich J (1978) 
          Electrophoretic enzyme and preliminary toxicity studies of the 
          venom of Parademansia microlepidotus  (the Small-scaled Snake),  
          with additional data on its distribution (Serpentes: Elapidae).  
          Mem. Qld. Mus., 19(3): 319-329. 

          Campbell CH (1964) Venomous snake bite and its treatment in the 
          territory of Papua and New Guinea. Papua New Guinea Medical 
          Journal, 7(1): 1-11. 

          Campbell CH (1964) Venomous snakebite in Papua and its treatment 
          with  tracheostomy, artificial respiration, and antivenene. 
          Transactions of the Royal Society of Tropical Medicine & Hygiene, 
          58(3): 263-273. 

          Campbell CH (1967) The taipan (Oxyuranus scutellatus) and the 
          effect of its bite. Med. J. Aust., 1: 735-739. 

          Campbell CH (1967) Antivenene in the treatment of Australian and 
          Papuan snake bite. Med. J. Aust., 2: 106-110. 

          Campbell CH (1979) Snake bite and snake venoms: their effects on 
          the nervous system. In: Vinken, P.J. & Bruyn, G.W. Eds. Handbook 
          of Clinical Neurology, Vol. 37, Intoxications of the Nervous 
          System, North Holland Publishing Co. 

          Campbell CH (1979) Symptomatology, pathology, and treatment of 
          the bites of elapid  snakes. In Handbook  of  Experimental 
          Pharmacology, Vol. 52, Snake Venoms, Springer Verlag. 

          Chandler HM & Hurrell JGR (1982)  A new enzyme immunoassay system 
          suitable for field use and its application in a snake venom 
          detection kit. Clinica Chimica Acta, 121: 225-230. 

          Chester A & Crawford GPM (1982) In vitro coagulant properties of 
          venoms from Australian snakes. Toxicon, 20(2): 501-504. 

          Coulter AR, Sutherland SK & Broad AJ (1974) Assay of snake venoms 
          in tissue fluids.  Journal of Immunological Methods, 4: 297-300. 

          Coulter AR, Cox JC, Sutherland SJ & Waddell CJ (1978)  A new 
          solid phase sandwich radioimmunoassay and its application to the 
          detection of snake venom. Journal of Immunological Methods, 23: 

          Coulter AR, Harris RD & Sutherland SK (1980) Enzyme immunoassay 
          for the rapid clinical identification of snake venom. Med. J. 
          Aust., 1: 433-435. 

          Covacevich J (1987) Two taipans.  In Covacevich J, Davie P & 
          Pearn J Eds. Toxic Plants and Animals: A Guide for Australia, The 
          Queensland Museum. 

          Covacevich J, Pearn J & White J (1988) The world's most venomous 
          snake. In Pearn J & Covacevich J Eds. Venoms and Victims, The 
          Queensland Museum and Amphion Press. 

          Cull-Candy SG, Fohlman J, Gustavsson D, Lullmann-Rauch R & 
          Thesleff S (1976) The effects of taipoxin and notexin on the 
          function and fine structure of the murine neuromuscular junction. 
          Neuroscience, 1: 175-180. Denson KWE (1969) Coagulant and 

          anticoagulant action of snake venoms. Toxicon, 7: 5-11. 

          Doery HM & Pearson JE (1961)  Haemolysins in venoms of Australian 
          snakes. Biochem. J., 78: 820-827. 

          Dowdall MH, Fohlman J & Eaker D (1977) Inhibition of high 
          affinity choline transport in peripheral cholinergic endings by 
          presynaptic snake venom neurotoxins. Nature, 269: 700-702. 

          Eaker D (1978) Studies of presynaptically neurotoxic and myotoxic 
          phospholipases A2. In LI, C.H. Ed. Versatility of Proteins, 
          Academic Press. 

          Fairley NH (1929) The present position of snakebite and the snake 
          bitten in Australia. Med. J. Aust., 1: 296-313. 

          Fisher M (1982) First aid in envenomation. Med. J. Aust., 1: 198. 

          Flecker H (1940) Snake bite in practice. Med. J. Aust., 2: 8-13. 

          Flecker H (1944)  More fatal cases of bites of the Taipan 
          (Oxyuranus scutellatus). Med. J. Aust., 2: 383-384. 

          Fohlman J, Eaker D, Karlsson E & Thesleff S (1976) Taipoxin, an 
          extremely potent presynaptic neurotoxin from the venom of the 
          Australian taipan. European Journal of Biochemistry, 68: 457-469. 

          Fohlman J (1979) Comparison of two highly toxic Australian snake 
          venoms: the taipan (Oxyuranus scutellatus) and the fierce snake 
          (Parademansia microlepidotus). Toxicon, 17: 170-172. 

          Fohlman J, Eaker D, Dowdall MJ, Lullmann-Rauch R, Sjodin T & 
          Leander S (1979)  Chemical modification of taipoxin and the 
          consequences for phospholipase  activity, pathophysiology, and 
          inhibition of high-affinity choline uptake. European Journal of 
          Biochemistry, 94: 531-540. 

          Harris JB & Maltin CA (1982)  Myotoxic activity of the crude 
          venom and the principal neurotoxin, taipoxin, of the Australian 
          taipan, Oxyuranus scutellatus. Br. J. Pharmac., 76: 61-75. 

          Harris JB (1983)  Myotoxicity of Animal Toxins. In Mebs, 
          Habermehl Eds. Proceedings of the 5th European Symposium on 
          animal, plant and microbial toxins, Hanover. 

          Hurrell JGR & Chandler HW (1982) Capillary enzyme immunoassay 
          field kits for the detection of snake venom in clinical 
          specimens: a review of two years' use. Med. J. Aust., 2: 236-237. 

          Karlsson E (1979) Chemistry of protein toxins in snake venoms. In 
          Handbook  of experimental pharmacology, Vol. 52, Snake Venoms, 
          Springer Verlag. 

          Kellaway CH & Williams FE (1929)  The venoms of Oxyuranus 
          maclennani and Pseudechis scutellatus. Amer. J. Exp. Biol. & Med. 
          Sci., 6: 155-174. 

          Lee CY & Ho CL (1982)  The pharmacology of phospholipases A2 
          isolated from snake venoms, with particular reference to their 
          effects on neuromuscular transmission. In Yoshida, Hagihara & 
          Ebashi Eds. Advances in  pharmacology and therapeutics II,  Vol. 
          4, Biochemical Immunological Pharmacology, Oxford, Pergamon 

          Lester IA (1957) A case of snake bite treated by specific taipan 
          antivenene. Med. J. Aust., 2: 389-391. 

          Marshall LR & Herrmann RP (1983) Coagulant and anticoagulant 
          actions  of Australian snake venoms. Thrombosis & Haemostasis 
          Research (Stuttgart), 50(3): 707-711. 

          Mebs D (1978)  Pharmacology of Reptilian Venoms. In Gans, C. Ed 
          Biology of the Reptilia, Vol. 8, Physiology B, London, Academic 

          Mebs D & Samejima Y (1980) Purification from Australian elapid 
          venoms and properties of phospholipases A which cause 
          myoglobinuria in mice. Toxicon, 18: 443-454. 

          Mirtschin PJ, Crowe GR & Thomas MW (1984) Envenomation by the 
          inland taipan, Oxyuranus microlepidotus.  Med. J. Aust., 141: 

          Morrison JJ, Pearn JH & Coulter AR (1982) The mass of venom 
          injected by two elapidae: the taipan (Oxyuranus scutellatus) and 
          the Australian tiger snake (Notechis scutatus). Toxicon, 20: 739-

          Morrison JJ, Pearn JH, Covacevich J & Nixon J (1983)  Can 
          Australians identify snakes? Med. J. Aust., 2: 66-70. 

          Morrison J, Pearn J, Covacevich J, Tanner C & Coulter A (1983-84)  
          Studies  on the venom  of Oxyuranus microlepidotus. Clinical 
          Toxicology, 21(3): 373-385. 

          Murrell G (1981) The effectiveness of the pressure/immobilization 
          first aid technique in the case of a tiger snake bite.  Med. J. 
          Aust., 2: 295. 

          Reid CC & Flecker H (1950)  Snake bite by a taipan with recovery. 
          Med. J. Aust., 1: 82-83. 

          Speijer H, Govers-Riemslag JWP, Zwaal RFA & Rosing J (1986) 
          Prothrombin activation by an activator from the venom of 
          Oxyuranus scutellatus (Taipan Snake).  J. Biol. Chem., 261(28): 

          Su MJ & Chang CC (1984)  Presynaptic effects of snake venom 
          toxins  which have  phospholipase A2 activity (B-Bungarotoxin, 
          Taipoxin, Crotoxin). Toxicon, 22: 631-640. 

          Sutherland SK (1974)  Venomous Australian creatures:  the action 

          of their toxins and the care of the envenomated patient. 
          Anaesthesia and Intensive Care, 2(4): 316-327. 

          Sutherland SK (1975) Treatment of snake bite in Australia:  some 
          observations and recommendations. Med. J. Aust., 1: 30-32. 

          Sutherland SK (1977) Serum reactions: an analysis of commercial 
          antivenoms and the possible role of anticomplementary activity in 
          de-novo reactions to antivenoms and antitoxins.  Med. J. Aust., 
          1: 613-615. 

          Sutherland SK (1977) Antivenoms: better late than never. Med. J. 
          Aust., 2, 813. 

          Sutherland SK (1977)  Acute untoward reactions to antivenoms. 
          Med. J. Aust., 1: 841. 

          Sutherland SK, Broad AJ, Tanner C & Covacevich J (1978) 
          Australia's  potentially  most  venomous snake,  Parademansia 
          microlepidotus. Med. J. Aust., 1: 288-289. 

          Sutherland SK, Coulter AR & Harris RD (1980) Rapid death of a 
          child after a taipan bite. Med. J. Aust., 1: 136. 

          Sutherland SK (1981) When do you remove first aid measures from 
          an envenomed limb. Med. J. Aust., 1: 542-543. 

          Sutherland SK (1983) Prolonged use of pressure/immobilization 
          after snake bite. Med. J. Aust., 1: 58. 

          Sutherland SK (1983) Australian Animals Toxins, Melbourne, Oxford    
          University Press. 

          Sutherland SK, Campbell DG & Stubbs AE (1981) A study of the 
          major Australian snake  venoms  in  the monkey  (Macaca 
          fascicularis): II: Myolytic and haematological effects of venoms. 
          Pathology, 13: 705-715. 

          Sutherland SK, Coulter AR, Broad AJ, Hilton JMN & Lane LHD (1975) 
          Human snake-bite victims: the successful detection of circulating 
          snake venom by radioimmunoassay.  Med. J. Aust., 1: 27-29. 

          Sutherland SK & Coulter AR (1977)  Snake bite: detection of venom 
          by radioimmunoassay. Med. J. Aust., 2: 683-684. 

          Sutherland SK, Coulter AR & Harris RD (1979) Rationalisation of 
          first-aid measures for elapid snakebite. Lancet, 183-186. 

          Sutherland SK, Coulter AR, Harris RD, Lovering KE & Roberts ID 
          (1981) A study of the major Australian snake venoms in the monkey 
          (Macaca fascicularis); In the movement of injected venom; methods 
          which retard this movement, and the response to antivenoms. 
          Pathology, 13: 13-27. 

          Sutherland SK & Lovering KE (1979)  Antivenoms: use and adverse 
          reactions over a 12 month period in Australia and Papua New 

          Guinea. Med. J. Aust., 2: 671-674. 

          Theakston RDG, Lloyd-James MJ & Reid HA (1977) Micro-Elisa for 
          detecting and assaying snake venom and venom antibody. Lancet, 2: 

          Thesleff S (1979)  Reptile neurotoxins and neurotransmitter 
          release.  In Chubb IW & Geffen LB Eds. Neurotoxins: fundamental 
          and clinical advances, Adelaide University Union Press. 

          Trinca JC (1963) The treatment of snakebite. Med. J. Aust., 1: 

          Trinca JC (1969)  Report of recovery from Taipan bite.  Med. J. 
          Aust., 1: 514-516. 

          Walker FJ, Whyte GO & Esmon CT (1980) Characterization of the 
          Prothrombin Activator from the Venom of Oxyuranus scutellatus 
          scutellatus (Taipan Venom). Biochemistry, 19: 1020-1023. 

          White J (1981)  Ophidian envenomation:  a South Australian 
          perspective. Records of the Adelaide Children's Hospital, 2(3): 

          White J (1983)  Patterns of elapid envenomation and treatment in 
          South Australia. Toxicon, Suppl. 3: 489-491. 

          White J (1983)  Local tissue destruction and Australian elapid 
          envenomation. Toxicon, Suppl. 3: 493-496. 

          White J (1983)  Haematological problems and Australian elapid 
          envenomation. Toxicon, Suppl. 3: 497-500. 

          White J, Pounder D, Pearn JH & Morrison JJ (1985) A perspective 
          on the problems of snakebite in Australia. In Grigg, G., Shine, 
          R. & Ehmann, H. Eds. Biology of Australasian Frogs and Reptiles, 
          Royal Zoological Society of New South Wales. 

          White J (1987)  Elapid  snakes:  venom production and  bite 
          mechanism. In Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic 
          Plants & Animals: a Guide for Australia, Brisbane, Queensland 

          White J (1987) Elapid snakes: venom toxicity and actions. In 
          Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants & 
          Animals: a Guide for Australia, Brisbane, Queensland Museum. 

          White J (1987)  Elapid snakes:  aspects of envenomation. In 
          Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants & 
          Animals: a Guide for Australia, Brisbane, Queensland Museum. 

          White J (1987)  Elapid  snakes:  management  of bites.  In 
          Covacevich, J., Davie, P. & Pearn, J. Eds. Toxic Plants & 
          Animals: a Guide for Australia, Brisbane, Queensland Museum. 

          White J & Pounder DJ (1984)  Fatal snakebite in Australia. 

          American Journal of Forensic Medicine & Pathology, 5(2): 137-143. 

          Wiener S (1961) Snakebite in a subject actively immunized against 
          snake venom. Med. J. Aust., 1: 658-661. 

          13.2 Zoological References

          Cogger HG (1975) Reptiles and Amphibians of Australia, Sydney, 
          Reed, A.H. & A.W. 

          Cogger HG (1987)  The venomous land snakes. In Covacevich, J., 
          Davie, P. & Pearn, J. Eds. Toxic Plants & Animals: a Guide for 
          Australia, Brisbane, Queensland Museum. 

          Cogger HG, Cameron EE & Cogger HM (1983) Zoological Catalogue of 
          Australia, Volume I: Amphibia and Reptilia, Canberra, Australian 
          Government Publishing Service. 

          Covacevich J (1988) Australia's dangerous snakes. In Pearn, J. & 
          Covacevich, J. Eds. Venoms and Victims, Brisbane, Queensland 

          Covacevich J & Wombey J (1976)  Recognition of Parademansia 
          microlepidotus (McCoy) (Elapidae), a dangerous Australian Snake. 
          Proc. Roy. Soc. Qld., 87: 29-32. 

          Covacevich J & Archer M (1975)  The distribution of the Cane 
          Toad, Bufo marinus, in Australia and its effects on indigenous 
          vertebrates. Mem. Qld Mus., 17(2): 305-310, pl. 41. 

          Covacevich J, McDowell SB, Tanner C & Mengden G (1981)  The 
          relationship of the taipan  (Oxyuranus scutellatus)  and  the 
          small-scaled snake (Oxyuranus microlepidotus), Serpentes:  
          Elapidae. In Banks, C.B. & Martin, A.A. Eds. Proceedings of the 
          Melbourne Herpetological Symposium, Zoological Board of Victoria. 

          Longmore R (1986) Atlas of elapid snakes of Australia, Canberra, 
          Australian Government Publishing Service. 

          McDowell SB (1985)  The terrestrial Australian elapids: general 
          summary. In Grigg G, Shine R & Ehmann H Eds. Biology of 
          Australasian Frogs and Reptiles, Royal Zoological Society of New 
          South Wales. 

          Mengden GA (1985) Australian elapid phylogeny: a summary of the 
          chromosomal and electrophoretic data. In Grigg G, Shine R & 
          Ehmann H Eds. Biology of Australasian Frogs and Reptiles, Royal 
          Zoological Society of New South Wales. 

          Schwaner TD, Baverstock PR, Dessauer HC & Mengden GA (1985)  
          Immunological evidence for the phylogenetic relationships of 
          Australian elapid snakes. In Grigg G, Shine R & Ehmann H Eds. 
          Biology of Australasian Frogs and Reptiles, Royal Zoological 
          Society of New South Wales. 

          Shine R (1985) Ecological evidence on the phylogeny of Australian 

          elapid snakes. In Grigg G, Shine R & Ehmann H Eds. Biology of 
          Australasian Frogs and Reptiles, Royal Zoological Society of New 
          South Wales. 

          Shine R & Covacevich J (1983) Ecology of highly venomous snakes: 
          the Australian genus Oxyuranus (Elapidae). J. Herpetology, 17(1): 

          Storr GM (1985)  Phylogenetic relationships of Australian elapid 
          snakes: external morphology with emphasis on species in Western 
          Australia. In Grigg G, Shine R & Ehmann H Eds. Biology of 
          Australasian Frogs and Reptiles, Royal Zoological Society of New 
          South Wales. 

          Wallach V (1985)  A  cladistic analysis of the terrestrial 
          Australian elapidae. In Grigg G, Shine R & Ehmann H Eds. Biology 
          of Australasian Frogs and Reptiles, Royal Zoological Society of 
          New South Wales. 

          Wilson SK & Knowles DG (1988)  Australia's Reptiles, Sydney, 
          Collins, 447pp. 


               Author(s):     Dr Julian White
               State Toxinology Services
               Adelaide Children's Hospital
               North Adelaide 5006

               Tel: 61-8-2047000
               Mobile phone: 61-18-832776
               Fax: 61-8-2046049

               Ms Jeanette Covacevich
               Senior Curator (Vertebrates)
               Queensland Museum
               PO Box 300
               South Brisbane 4101

     Date:          June 1989

     Review:   Singapore

     Date:          November 1989

     Peer Review: Singapore, November 1991

    See Also:
       Toxicological Abbreviations