Introduction to Oxyuranus scutellatus canni

Description: A large, fast-moving snake that is typically greyish, dark brown to black above with a broad orange-red dorso-vertebral stripe that extends along most of the back. The belly can be white to orange in colour. The tip of the nose and the sides of the lips are usually creamish. There is local and regional variation in colouration and even specimens from the same location may differ considerably in colour. Head long and distinct from powerfully muscled but slender neck and forebody. Papuan taipans have large distinctive heads that are crudely rectangular; the body is large, long and muscular; the tail is round and tapers to a fine tip. The mouth is large and the lower jaw articulates well back beyond the labial scales giving these snakes an enormous gape and the ability to accommodate very large prey items.

Scalation: Dorsal scales in 21-23 rows at mid-body, and most are keeled, particularly on the neck; 220-250 ventrals; anal single; 60-80 paired subcaudals.

Body Size: Average length: 1.8 metres for females and 2.0 metres for males; maximum length: claimed to be 3.4 metres, but specimens over 2.6 metres long are rarely seen.

Distribution: This species is restricted to grasslands and savannah woodlands in the southern coastal provinces of Milne Bay, Central (including the National Capital District), Gulf and Western provinces. Absent from the lowland rainforest plains between the Purari and Bamu Rivers. Specimens have been recorded from the mainland near Samarai Island in Milne Bay province and are common in areas of open savannah woodland and grassland west through the Magarida (Iruna), Boru, and Marshall’s Lagoon districts. The range extends along the coastal littoral and into the foothills of the Owen Stanley Range near Sogeri, encompasses the National Capital District and continues through Mekeo into the eastern third of Gulf province to just west of Malalaua near Koaru. Slater records that the species also occurs in the isolated grasslands around the Vailala River west of Kerema.

The species is absent from the Kikori Basin but Papuan taipans have been found on both sides of the Fly River, and bites have been recorded in Balimo, Suki, Wipim and Morehead. None could be found on Daru Island during fieldwork in 2004, and there are no hospital records of envenomation originating on the Island. Papuan taipans have been collected by herpetologists in southern West Papua (Indonesia) around Merauke and west to the Wildoman River region. There has also been a confirmed record from Saibai Island (Australia).

Habitat: Inhabits grasslands and savannah woodland to an altitude of around 400 metres. Adapts well to areas of human activity and often lives in village gardens and residential areas. Papuan taipans are relatively common in the suburbs of Port Moresby especially around Gerehu, Waigani, Erima, Korobosea and Kaugere. In both urban and rural areas these snakes are often found close to human settlements or in and around garden plots. In rural areas of Central and Gulf province Papuan taipans are common in areas of kunai (Imperata cylindrica) or pit-pit (Themeda triandra) grassland, melaleuca and acacia scrub, savannah (Eucalyptus spp.) wood land and other ‘dry’ tropical habitats. Papuan taipans often cross gravel roads transecting large expanses of pit-pit cane or kunai grass, especially in the Mekeo, Rigo and Kupiano-Moreguina districts.

Diet: Feeds on warm-blooded prey; primarily rodents and small mammals to the size of bandicoots, but also known to eat ground-dwelling birds. Appears unaffected by the introduction of the cane toad (Bufo marinus), which is thought to be a cause of declines in frog-eating species. As other species continue to decline, the proportion of snakebites by this species will rise.

Reproduction: Oviparous producing 1-2 clutches of 16-22 eggs each year. Mating has been observed between June and July. The normal incubation is 60-66 days, but female snakes usually leave their eggs within a few days of laying them.

Activity: Papuan taipans are usually only active by day. Most are seen moving around between early to late-morning, and then again during the mid to late-afternoon. During research in PNG no specimens were observed later than 6.30 pm. Not enough is known to tell if taipans are more active at different times of the year.

Behaviour: A very shy, extremely nervous snake that tries to avoid human contact, but which will defend itself violently when threatened, making them exceedingly dangerous adversaries. Taipans are capable of ferocious self-defence and may inflict multiple bites in rapid succession using a ‘snap and release’ strategy, where larger amounts of venom are injected with each subsequent bite. Taipans also strike higher than other venomous species; bites to the calves or even above the knee can occur. This is the only snake in PNG likely to ‘attack’ a perceived threat.

Medical importance: The most dangerous species of venomous snake in Papua New Guinea, with the highest venom yield and the longest fangs. There is considerable evidence that this snake causes most of the serious snakebites admitted in Central province. Lalloo et al (1995) showed, using a specific diagnostic test (EIA), that 82.3% of serious snakebites in Central province were caused by Papuan taipans.

Venom: The two most important components of taipan venom are (1) an irreversible neurotoxin that destroys nerve endings, and (2) a powerful activator of a blood clotting factor (prothrombin), which leads to the incoagulable blood seen in many taipan bite patients. In addition to these toxins there are also several other minor components which contribute to the effects of envenoming.

exellent information, I really think that it shoul be a post like this in all species profiles
thanks for this

Interesting information, Mario.
I'd appreciate such articles for other snakes anytime.
Thanks!

Yes this is indeed a good account ... it should be. I am the author!!

Mario, thanks for the reference , David what is your prediction or facts on the LD 50 of Oxyuranus Temporalis , in part i ask this because in case of accidental envenomation should the medical technicians follow the prescribed 12000 units of Taipan antivenom or be prepared to use more im speculating this will also apply to Oxyuranus microlepidotus.

At this stage no data on the LD50 of Oxyuranus temporalis or its neutralisation with commercial antivenom has been made available, so it would be premature to speculate. Suffice to say there is no reason to believe at this time that CSL taipan or polyvalent antivenoms would not be effective.

Daniel, thanks for the prompt reply.

Daniel, this is a serious issue at least in the United States because of the large amount of Elapidae specimens and the advent of captive breeding doubling and tripling captive inventories and if really not the entire world wide range of Elapidae , Question is can you see a day where serum laboratories will come up with an substance to increase the half life of antivenom and or polyvalent for use in treatment of rare accidental envenomations.

i believe in the future as captive breeding evolves in to an industry in Austrailia you will see exports becoming more common as "just one more agricultural sect. product" i would like to see the specific antivenom accompany the sale/export for this to happen add i would like to see the expiration dates increase or become almost infinitum on the serum in order for this opportunity to become feasible to all herpetoculturist who wish to partake of this sophisticated educational skill.

You can clearly see my implications this would be a win win situation for all involved including serum laboratories not to mention added tax revenues.

FDA regulations , changing taste , further economic downward spriral , may delay this from happening in the near future but i believe it will be inevitable in search of new markets in a changing world , Thanks in advance Albert.

Addtl*, Not previously asked and no reply warranted strictly voluntary.

Question being is Acanthophis (Deathadders) venom still strictly neurotoxins, sans. any haemotoxins, cardiotoxins, cytotoxins etc. to include coagulants and or anticoagulants upon the discovery of Ancathophis Wellsi and other Acanthophis species . Thank you .

David Williams or Dr. David Williams.

AVRU-UPNG
Snakebite Research Project
School of Medicine & Health Sciences
University of Papua New Guinea

Australian Venom Research Project
School of Medicine
University of Melbourne

http://www.avru.org

Typo Daniel , for this error i apologize.

David and co. though not of the Oxyuranus section the question is of neither species, it is about the component of these Elapidaes venom well with in the scope of David Williams Work.

Addtl. Thanks, Andrew Hackett of South Africa for this ref.

Hi Brian , I came across this information from http://cat.inist.fr/?aModele=afficheN&cpsidt=15005180 '' Based on early studies on Acanthophis antarcticus (common death adder) venom, it has long been thought that death adder snake venoms are devoid of myotoxicity. However, a recent clinical study reported rhabdomyolysis in patients following death adder envenomations, in Papua New Guinea, by a species thought to be different to A. antarcticus. Subsequently, a myotoxic phospholipase A2 component was isolated from A. rugosus (Irian Jayan death adder) venom. The present study examined the venoms of A. praelongus (northern), A. pyrrhus (desert), A. hawkei (Barkly Tableland), A. wellsi (black head), A. rugosus, A. sp. Seram and the regional variants of A. antarcticus for in vitro myotoxicity. Venoms (10-50 μg/ml) were examined for myotoxicity using the chick directly (0.1 Hz, 2 ms, supramaximal V) stimulated biventer cervicis nerve-muscle preparation. A significant contracture of skeletal muscle and/or inhibition of direct twitches were considered signs of myotoxicity. This was confirmed by histological examination. All venoms displayed high phospholipase A2 activity. The venoms (10-50 μg/ml) of A. sp. Seram, A. praelongus, A. rugosus, and A. wellsi caused a significant inhibition of direct twitches and an increase in baseline tension compared to the vehicle (n = 4-6; two-way ANOVA, p < 0.05). Furthermore, these venoms caused dose-dependent morphological changes in skeletal muscle. In contrast, the venoms (10-50 μg/ml; n = 3-6) of A. hawkei, A. pyrrhus, and regional variants of A. antarcticus were devoid of myotoxicity. Prior incubation (10 min) of CSL death adder antivenom (5 U/ml) prevented the myotoxicity caused by A. sp. Seram, A. praelongus, A. rugosus, and A. wellsi venoms (50 μg/ml; n = 4-7). In conclusion, clinicians may need to be mindful of possible myotoxicity following envenomations by A. praelongus, A. rugosus, A. sp. Seram, and A. wellsi species.

Albert J. Montejo wrote:

Question is can you see a day where serum laboratories will come up with an substance to increase the half life of antivenom and or polyvalent for use in treatment of rare accidental envenomations.

There is already very good evidence that antivenoms retain significant potency long beyond the expiry date written on the label. See for example, the extensions of expiry of US (Wyeth) Micrurus antivenom by the USFDA, and also http://www.ncbi.nlm.nih.gov/pubmed/19144367 for information pertaining to Australian antivenoms. The problem is that from a medico-legal perspective the majority of doctors have their hands tied by law when it comes to administration of an expired antivenom. In the case of the Wyeth product the USFDA extension overs the legal question and use is permissible under US law. In the case of any other expired antivenom however, a US doctor might be justifiably wary about using it on legal grounds (or lack thereof) even if no alternative is available.

Albert J. Montejo wrote:

i believe in the future as captive breeding evolves in to an industry in Austrailia you will see exports becoming more common as "just one more agricultural sect. product" i would like to see the specific antivenom accompany the sale/export for this to happen add i would like to see the expiration dates increase or become almost infinitum on the serum in order for this opportunity to become feasible to all herpetoculturist who wish to partake of this sophisticated educational skill.

Unfortunately in this regard I disagree. I am not at all in favour of seeing extremely dangerous wildlife of any description in private homes & apartments. This of course is based to some extent on my knowledge of just exactly what damage snake venoms can do to people, but I also believe that the examples of careless handling that appear on an almost weekly basis are an argument unto themselves. Certainly the inability of the herpetoculture community to act responsibly and police itself plays right into the hands of animal liberationists and other groups, and my personal view is that just as with most things we are no longer allowed to do freely, the laws regarding the keeping of dangerous animals are only going to get tighter, not more relaxed. This is in part also because the animal liberationist learned quickly that to influence policy they needed seats at the table... which is why government departments that devise laws are nowadays full of people with (discretely concealed) hidden policy agendas.

I cannot see a day in my lifetime when Australia will allow the export of reptiles as "just one more agricultural sect. product". But I do believe that if you are going to keep venomous snakes then you have an obligation to ensure that you have some form of access to effective antivenom - BEFORE - you acquire the species. Whether this be a subscription to an Antivenom Bank, or arranging for the import of the products yourself, the fact is that it is grossly irresponsible to keep a venomous snake in a residential community without having access to appropriate antivenom, and again, it is this behaviour that plays into the hands of the people who want to ban such keeping. Note that my own objections are passive, I'm not in favour of banning anything, but I don't have to agree with it either.

Albert J. Montejo wrote:

Addtl*, Not previously asked and no reply warranted strictly voluntary.

Question being is Acanthophis (Deathadders) venom still strictly neurotoxins, sans. any haemotoxins, cardiotoxins, cytotoxins etc. to include coagulants and or anticoagulants upon the discovery of Ancathophis Wellsi and other Acanthophis species . Thank you .

Acanthophis venoms contain a much wider range of toxins than previously expected, and yes there are anticoagulants, myotoxins, presynaptic neurotoxins and a range of other components present. Previously (~15-20 years ago) it was generally thought that the only medically significant toxins were postsynaptic neurotoxins, sometimes called 3FTx (three-finger toxins - to describe their shape), and to a large extent this still holds true, in the sense that most of the patients bitten by Acanthophis spp., are most at risk as a result of these 3FTx, rather than from the clinical effects of other venom components. Nobody has ever died of anticoagulation induced by a death adder for example, although I am aware of a handful of cases of significant, and in a few, lethal, outcomes dues to the accumulated clinical effects of myotoxicity by Acanthophis laevis in PNG. But for the vast majority it is postsynaptic neurotoxicity that is the over-arching clinical dilemma, and with antivenom, or alternatively, anticholinesterases + atropine, recovery is swift and uneventful.

Cheers


David

David,

Slightly off topic....is there anymore information regarding the Demansia vestigiata death in PNG?

Cheers,
Scott

Basically the man was bitten in the garden, killed the snake (which was brought to the hospital and preserved in alcohol), and appears from the case notes to have developed an upper airway obstruction due to presumed evolving paralysis and died as a result.

It is of course possible, though improbable that this chap had venom-induced anaphylaxis which might have led to the airway obstruction, but this is unlikely given the time course. It is equally possible death could have been due to drug-induced anaphylaxis, as he had been given antibiotic on presentation, but again, the time course from administration to death suggests otherwise. Envenoming appears to be the most likely cause of his demise.

Cheers


David

Thanks go out to Mario Lutz, Venomland Founder, David Willams , Scott Eipper and Andrew Hacket of South Africa.

addtl. Thanks, for the update guys, i found that i was 15-20 years behind on the components of the Australasian , Australian Elapidae venom in particular the species discussed.
i leave you with some ref. you may find helpful. Albert.

Clinical Management of Snakebite in Papua New Guinea
Introduction

This text arose from the need to develop a national training course in the clinical management of snakebite for Papua New Guinea's many rural health workers and doctors. The inaugural PNG Snakebite Management Course was run at the University of Papua New Guinea School of Medicine & Health Sciences in September 2004 by a volunteer faculty comprising experts in snakebite and emergency medicine from Australia, New Zealand and Papua New Guinea.

This handbook was produced to provide participants with a comprehensive reference that could be available beyond the duration of the training course.

Table of Contents


Cover pages
Table of contents
Acknowledgements
Chapter 1: Snakebite in Papua New Guinea: facts & fiction
David Williams
Chapter 2: The snakes of Papua New Guinea
David Williams
Chapter 3: The composition and actions of Papua New Guinean snake venoms
David Williams & Ronelle Welton
Chapter 4: Symptoms and signs of snakebite in Papua New Guinea
Dr Simon Jensen
Chapter 5: First aid for snakebite in PNG
Benjamin Bal & David Williams
Chapter 6: Patient assessment and diagnosis
Dr Bill Nimorakiotakis, Dr Evelyn Lavu & Dr Simon Jensen
Chapter 7: Treatment overview
Dr Simon Jensen
Chapter 8: Clinical assessment and treatment of neurotoxicity
Dr Gertrude Didei
Chapter 9: Clinical assessment and treatment of coagulopathy
Dr Antony Chenhall & David Williams
Chapter 10: Treatment of other effects of envenomation
Dr Kenny Limbo Aaron, David Williams & Dr Simon Jensen
Chapter 11: The role and use of antivenom in Papua New Guinea
Dr Kenneth D Winkel, Dr Forbes McGain, Dr Bill Nimorakiotakis & David Williams
Chapter 12: Anticholinesterase therapy
Dr Kenneth D Winkel, Dr Forbes McGain, Dr Bill Nimorakiotakis & David Williams
Chapter 13: Managing the respiratory effects of snake envenomation
Dr Antony Chenhall
Chapter 14: Management plans for snakebite patients
Dr Simon Jensen & David Williams
Appendix: CSL venom detection kits
Tim Carroll
Glossary of medical terms

Contact Details

Independent Publishing Pty Limited
PO Box 168
Port Moresby, NCD, PAPUA NEW GUINEA
Telephone: +675 325 9908
Facsimile: +675 325 2506
Email: independent@independent.com.pg
Editors:

David J Williams
School of Public Health & Tropical Medicine
James Cook University
Douglas, Qld, 4811.
AUSTRALIA

Email: david.williams1@jcu.edu.au Dr Simon D Jensen
School of Medicine & Health Sciences
University of Papua New Guinea
Taurama Campus
Boroko, NCD, PAPUA NEW GUINEA.

Email: simondjensen@hotmail.com Dr Kenneth D Winkel
Australian Venom Research Unit
University of Melbourne
Melbourne, Vic, 3010.
Australia

Email: kdw@unimelb.edu.au

I thoroughly enjoyed the discussion of this particular species. It really opened my eyes, to what would have been a somewhat difficult species to manage in captivity, owing to it's extremely "nervous" disposition.

There was the opportunity only one time in my life to raise this species. And I had a very limited idea as to it's toxicity and behaviour. I followed all of the safe handling protocols with it, but did not "imagine" a juvenile would mistakenly strike at it's own body and die, as I mentioned in another thread.

It is a beautiful specimen that brings violent convulsions and death to many who are bitten, and doesn't waist time deciding to bite the unfortunate people that inhabit the territories mentioned above. It is "proactive" in defending itself to be sure.

These guy's kil a lot of people in PNG but I don't know the snake bite states for that area of the world.