Search

Many ambush-foraging snakes move their tails to entice prey within striking range (‘caudal luring’). During ontogeny, the conspicuous hues of caudal lures change to match the cryptic patterning of the body/head. This coincides with decreased luring behaviour and reflects the trade-off between prey acquisition and camouflage as the snake grows. Australo-Papuan death adders (Acanthophis, Elapidae) are unique in that both juveniles and adults use caudal luring, but ontogenetic colour change has not been investigated. We examined the spectral reflectance, microstructure and pigmentation of caudal skin in wild-sourced and captive bred Acanthophis antarcticus ranging in body size (snout-vent length 116–674 mm; mass 3–832 g; N = 33) to test whether colour properties change as snakes grow. We found that lure colour is distinct from the cryptic body skin across the life history, and changes from a matte banding pattern (grey/black) in neonates/juveniles, to uniform and glossy black with a yellow ventral stripe in larger snakes. These colour changes are caused by increases in dermal pigmentation and a transition to a smooth, interlocking epidermal microstructure. To understand the selection pressures that might be driving ontogenetic colour change in this species, further studies should test how different prey types respond to distinct lure morphologies.

We assess the availability of four names proposed by Wells & Wellington (1985) for Australian death adders (Acanthophis). In agreement with previous literature, A. hawkei is an available name, whereas A. armstrongi, A. lancasteri, and A. schistos are not described in conformity with the requirements of Articles 13.1.1 or 13.1.2 of the International Code of Zoological Nomenclature and are therefore considered nomina nuda. Consequently, A. cryptamydros Maddock et al., 2015, is confirmed as the valid name for the Kimberley death adder of Western Australia. We comment on the need for greater clarity in the Code, and emphasise that the responsibility for establishing the availability of new nomina rests with their authors, not subsequent researchers.

The south-eastern distributional limit of many Australian species coincides with northern, and sometimes far-eastern, Victoria. In the mid-19th century, Blandowski’s Lower Murray Expedition sought to study the natural history of this area, specifically north and north-western Victoria. The expedition collected many specimens that are now registered with Museums Victoria, including species that are now extinct, extinct in the state or greatly reduced in distribution. During the expedition, a specimen of the death adder Acanthophis antarcticus was collected at Lake Boga in north-western Victoria. During the 20th and 21st centuries, there has been debate about whether this species persists in Victoria. We review early records of this species, including voucher specimens held by Museums Victoria, one of which we confirm as the specimen collected during Blandowski’s Lower Murray Expedition. We also explore recent claims of sightings of this species in Victoria. We collate names for the death adder used by Aboriginal people in northern and north-western Victoria. Death adders undoubtedly occurred in north-western Victoria in the 19th century and were known to the Aboriginal people, but it is probable that they no longer occur in that part of the state. It is possible that death adders persist in far East Gippsland, east of the Wallagaraugh River, although no substantiating material, such as photographs or specimens, has been collected in that area.

Alpaca (Vicugna pacos), like all other members of the camelid family, produce a unique heavy chain only IgG subclass. This form of IgG has been proposed as having superior neutralising properties and improved safety as compared with conventional mammalian IgG-based immunotherapeutics. The objective of this study was to investigate the potential of alpaca antibodies to neutralise the lethal and procoagulant properties of several Australian elapid snake venoms. Various experimental antivenoms were produced by immunisation of alpaca (Vicugna pacos) with combinations of five Australian elapid snake venoms: tiger snake (Notechis scutatus), eastern brown snake (Pseudonaja textilis), Papuan taipan (Oxyuranus scutellatus canni), mulga snake (Pseudechis australis) and common death adder (Acanthophis antarcticus). Venoms were emulsified in Freund’s Incomplete Adjuvant and alpaca repeatedly immunised. Having previously shown that such alpaca produce persistent venom-specific antibody responses with minimal physiological impact on the animal, the current report demonstrates that polyvalent alpaca antivenom neutralises the lethal effects of three elapid venoms (tiger, brown and Papuan taipan venoms). Such lethality neutralisation was, however, of generally lower potency, but of the same order of magnitude, when compared with bioCSL monovalent antivenoms (brown, tiger and taipan antivenoms). By contrast, the monovalent alpaca tiger and brown snake antivenom were found to be superior to the equivalent bioCSL monovalent antivenoms when considering the neutralisation of the procoagulant effects of the respective immunising venoms. The bioCSL polyvalent antivenom also less potent, when compared with the alpaca taipan monovalent antivenom, against Papuan taipan venom procoagulant neutralisation. These findings support the potential of camelid immunoglobulin for the development of novel elapid specific antivenoms.

Acanthophis laevis Macleay, 1877 (Fig. 32) Type locality. New Guinea. Distribution in the Kei Islands. We collected a single specimen on Kei Kecil and two specimens on Kei Besar. The WAM expedition collected six specimens from Kei Besar, and ZMUC holds five additional specimens from Kei Kecil. Local people are familiar with this lethal snake and report that it is not present on either Tam or Kur. Natural history. Venomous and dangerous. On Kei Besar, we collected this species at two locations in the vicinity of Gunung Daab, one on the ground in a small forest window of bunchgrass within primary forest, and the other was found dead on the road near the trailhead. On Kei Kecil this species was found in disturbed forest habitat. Fig. 32. Close-up in life of head of Acanthophis laevis from Kei Kecil (ALS 150). Field identification. A small to medium brown snake with a viper-like flat, broad, triangular head, distinctly raised horn-like supraoculars, and a relatively short and thin tail with a terminal spine (de Lang, 2013)., Published as part of Karin, Benjamin R., Stubbs, Alexander L., Arifin, Umilaela, Bloch, Luke M., Ramadhan, G., Iskandar, Djoko T., Arida, Evy, Reilly, Sean B., Kusnadi, Agus & Mcguire, Jimmy A., 2018, The herpetofauna of the Kei Islands (Maluku, Indonesia): Comprehensive report on new and historical collections, biogeographic patterns, conservation concerns, and an annotated checklist of species from Kei Kecil, Kei Besar, Tam, and Kur, pp. 704-738 in Raffles Bulletin of Zoology 66 on page 730, DOI: 10.5281/zenodo.5363075, {"references":["Macleay W (1877) The ophidians of the Chevert Expedition. Proceedings of the Linnean Society of New South Wales, 2: 33 - 41.","de Lang R (2013) The Snakes of the Moluccas (Maluku), Indonesia: A Field Guide to the Land and Non-marine Aquatic Snakes of the Moluccas with Identification Key. Frankfurter Beitrage zur Naturkunde. Edition Chimaira, Frankfurt, 417 pp."]}

Parthenogenesis is a form of asexual reproduction by which embryos develop from unfertilized eggs. Parthenogenesis occurs in reptiles; however, it is not yet known to occur in the widespread elapid snakes (Elapidae), which include well-known taxa such as cobras, mambas, taipans and sea snakes. Here, we describe the production of viable parthenogens in two species of Australo-Papuan elapids with divergent reproductive modes: the oviparous coastal/Papuan taipan ( Oxyuranus scutellatus ) and the viviparous southern death adder ( Acanthophis antarcticus ). Analyses of nuclear SNP data excluded paternity for putative fathers and convincingly demonstrated asexual reproduction, thus representing the first evidence of facultative parthenogenesis in Elapidae. Our finding has broad implications for understanding the evolution of reproductive diversity in snakes, as well as managing the conservation of genetic diversity in wild and captive populations.

The binding of compounds to nicotinic acetylcholine receptors is of great interest in biomedical research. However, progress in this area is hampered by the lack of a high-throughput, cost-effective, and taxonomically flexible platform. Current methods are low-throughput, consume large quantities of sample, or are taxonomically limited in which targets can be tested. We describe a novel assay which utilizes a label-free bio-layer interferometry technology, in combination with adapted mimotope peptides, in order to measure ligand binding to the orthosteric site of nicotinic acetylcholine receptor alpha-subunits of diverse organisms. We validated the method by testing the evolutionary patterns of a generalist feeding species (Acanthophis antarcticus), a fish specialist species (Aipysurus laevis), and a snake specialist species (Ophiophagus hannah) for comparative binding to the orthosteric site of fish, amphibian, lizard, snake, bird, marsupial, and rodent alpha-1 nicotinic acetylcholine receptors. Binding patterns corresponded with diet, with the Acanthophis antarcticus not showing bias towards any particular lineage, while Aipysurus laevis showed selectivity for fish, and Ophiophagus hannah a selectivity for snake. To validate the biodiscovery potential of this method, we screened Acanthophis antarcticus and Tropidolaemus wagleri venom for binding to human alpha-1, alpha-2, alpha-3, alpha-4, alpha-5, alpha-6, alpha-7, alpha-9, and alpha-10. While A. antarcticus was broadly potent, T. wagleri showed very strong but selective binding, specifically to the alpha-1 target which would be evolutionarily selected for, as well as the alpha-5 target which is of major interest for drug design and development. Thus, we have shown that our novel method is broadly applicable for studies including evolutionary patterns of venom diversification, predicting potential neurotoxic effects in human envenomed patients, and searches for novel ligands of interest for laboratory tools and in drug design and development.

Adenoviruses are medium-sized DNA viruses with very high host fidelity. The phylogenetic relationships of the adenoviruses strongly resemble that of their hosts, consistent with evolutionary codivergence. The genus Atadenovirus appears to have evolved in squamate hosts. Perhaps the best known of the squamate adenoviruses is Agamid adenovirus 1 (AgAdV1), found most commonly in central bearded dragons (Pogona vitticeps), where it is a prevalent cause of hepatitis/enteritis, especially in young animals. All previous reports of adenoviruses in bearded dragons were AgAdV1. Helodermatid adenovirus 2 (HeAdV2) was first seen in Mexican beaded lizards (Heloderma horridus). Subsequently, partial adenoviral polymerase gene sequence from a western bearded dragon (Pogona minor) in Australia was found to share 99% nucleotide homology with HeAdV2. This article reports the discovery of a virus identical to HeAdV2 in a captive central bearded dragon in Florida and wild Gila monsters (Heloderma suspectum) in Arizona. Additionally, a partial adenoviral polymerase gene sharing 98% homology with this HeAdV2 was discovered in a death adder (Acanthophis antarcticus) in Australia. These findings call into question the provenance of HeAdV2. Further studies of atadenoviral host range, diversity of adenoviruses in captive animals, and characterization of adenoviruses from wild squamates are indicated.

There is limited information on the cross-neutralisation of neurotoxic venoms with antivenoms. Cross-neutralisation of the in vitro neurotoxicity of four Asian and four Australian snake venoms, four post-synaptic neurotoxins (α-bungarotoxin, α-elapitoxin-Nk2a, α-elapitoxin-Ppr1 and α-scutoxin; 100 nM) and one pre-synaptic neurotoxin (taipoxin; 100 nM) was studied with five antivenoms: Thai cobra antivenom (TCAV), death adder antivenom (DAAV), Thai neuro polyvalent antivenom (TNPAV), Indian Polyvalent antivenom (IPAV) and Australian polyvalent antivenom (APAV). The chick biventer cervicis nerve-muscle preparation was used for this study. Antivenom was added to the organ bath 20 min prior to venom. Pre- and post-synaptic neurotoxicity of Bungarus caeruleus and Bungarus fasciatus venoms was neutralised by all antivenoms except TCAV, which did not neutralise pre-synaptic activity. Post-synaptic neurotoxicity of Ophiophagus hannah was neutralised by all antivenoms, and Naja kaouthia by all antivenoms except IPAV. Pre- and post-synaptic neurotoxicity of Notechis scutatus was neutralised by all antivenoms, except TCAV, which only partially neutralised pre-synaptic activity. Pre- and post-synaptic neurotoxicity of Oxyuranus scutellatus was neutralised by TNPAV and APAV, but TCAV and IPAV only neutralised post-synaptic neurotoxicity. Post-synaptic neurotoxicity of Acanthophis antarcticus was neutralised by all antivenoms except IPAV. Pseudonaja textillis post-synaptic neurotoxicity was only neutralised by APAV. The α-neurotoxins were neutralised by TNPAV and APAV, and taipoxin by all antivenoms except IPAV. Antivenoms raised against venoms with post-synaptic neurotoxic activity (TCAV) cross-neutralised the post-synaptic activity of multiple snake venoms. Antivenoms raised against pre- and post-synaptic neurotoxic venoms (TNPAV, IPAV, APAV) cross-neutralised both activities of Asian and Australian venoms. While acknowledging the limitations of adding antivenom prior to venom in an in vitro preparation, cross-neutralization of neurotoxicity means that antivenoms from one region may be effective in other regions which do not have effective antivenoms. TCAV only neutralized post-synaptic neurotoxicity and is potentially useful in distinguishing pre-synaptic and post-synaptic effects in the chick biventer cervicis preparation.

Research into Australian elapid venoms has mainly focused on the seven genera of greatest clinical significance: Acanthophis, Hoplocephalus, Notechis, Oxyuranus, Pseudechis, Pseudonaja and Tropidechis. However, even small species represent a potential for causing severe clinical envenoming. Further, owing to taxonomic distinctiveness, these species are a potential source of novel toxins for use in drug design and development. This is the first study to characterize the venoms of Cryptophis boschmai, Denisonia devisi, Echiopsis curta, Hemiaspis signata and Vermicella annulata. MALDI analysis of each venom, over the range of 4-40 kDa, indicated components in the weight range for three finger toxins (6-8 kDa) and phospholipase A(2) (PLA(2) ; 12-14 kDA). Interestingly, C. boschmai venom was the only venom, which contained components > 25 kDa. All venoms (10 μg/ml) demonstrated in vitro neurotoxicity in the chick biventer cervicis nerve-muscle preparation, with a relative rank order of: H. signata ≥ D. devisi ≥ V. annulata = E. curta > C. boschmai. CSL polyvalent antivenom neutralized the inhibitory effects of C. boschmai venom but only delayed the inhibitory effect of the other venoms. All venoms displayed PLA(2) activity but over a wide range (i.e. 1-621 μmol/min./mg). The venoms of C. boschmai (60 μg/kg, i.v.), D. devisi (60 μg/kg, i.v.) and H. signata (60 μg/kg, i.v.) produced hypotensive effects in vivo in an anaesthetized rat preparation. H. signata displayed moderate pro-coagulant activity while the other venoms were weakly pro-coagulant. This study demonstrated that these understudied Australian elapids have varying pharmacological activity, with notable in vitro neurotoxicity for four of the venoms, and may produce mild to moderate effects following systemic envenoming.

Acanthophis Daudin, 1803 Type species. Boa antartica (= Acanthophis antarcticus) Shaw & Nodder, 1802, by monotypy. Diagnosis. Species assigned to the genus Acanthophis are moderately large, stout terrestrial elapid species most similar to vipers (Viperidae) from other continents. Species within the genus have distinctive wide and stout heads anterior to a defined narrowing forebody that rapidly broadens to the widest point towards midbody. Tail slender, distal portion laterally compressed terminating in a tail spine. Etymology. From the Greek words acanthi meaning ���spine��� and ophis meaning ���snake���, in reference to the terminal tail spine present on species within the genus. �� 12 0 19 0 17 0 15 0 12 -�� 12 -019 -017 -015 -012 0 12 0 15 0 17 0 19 �� 12 -012 ��ey -015 A. rug��sus g����up -017 A. we����si A. pyrrhus -019 A. cryptamydr��s sp 1 n��v 1 -�� 12, Published as part of Maddock, Simon T., Ellis, Ryan J., Doughty, Paul, Smith, Lawrence A. & W��ster, Wolfgang, 2015, A new species of death adder (Acanthophis: Serpentes: Elapidae) from north-western Australia, pp. 301-326 in Zootaxa 4007 (3) on pages 307-308, DOI: 10.11646/zootaxa.4007.3.1, http://zenodo.org/record/243397, {"references":["Daudin, F. M. (1803) Histoire Naturelle, generale et particuliere des Reptiles. Vol. 5. Dufart, Paris, 365 pp.","Shaw, G. & Nodder, F. P. (1802) Boa antarctica. Naturalist's Miscellany, 13, 535."]}

Acanthophis cryptamydros sp. nov. Kimberley death adders Figs. 5���8 Holotype. WAM R 174083, medium-sized male collected 1 km north-west of Theda Station homestead, Western Australia (14 �� 46 ' 59.10 "S, 126 �� 29 ' 22.02 "E), on 8 March 2014 by R. Ellis, G. Bourke, and R. Barrett. Fixed in 10 % formalin, stored in 70 % ethanol at WAM. Liver samples stored in 100 % ethanol at WAM and SAM. Paratypes. WAM R 70690, sub-adult male, 45 km north-northeast Halls Creek, WA (17 �� 51 '00"S, 127 �� 50 '00"E); WAM R 81245, adult male, Packsaddle Springs, near Kununurra, WA (15 �� 54 '00"S, 128 �� 41 '00"E); WAM R 103755, adult male, Surveyors Pool, Mitchell River National Park, WA (14 �� 39 ' 46 "S, 125 �� 44 ' 34 "E); WAM R 165567, adult male, Koolan Island, WA (16 ��08'04"S, 123 �� 45 '05"E); WAM R 168918, adult female, Boongaree Island, WA (15 �� 4 ' 39.36 "S, 125 �� 11 ' 13.56 "E); WAM R 172034, adult female, north-west Molema Island, WA (16 �� 14 ' 17 "S, 123 �� 49 ' 49 "E). Diagnosis. A moderately stout Acanthophis to 645 mm total length. Distinguished from all other Australian Acanthophis by a combination of midbody scales in 22 or 23 rows, 125���139 ventrals, undivided prefrontal scales, posterior edge of frontal scale not extending beyond posterior edge of supraoculars, laterally flared supraoculars, area of lower secondary temporal scale equal to or smaller than sixth supralabial, anterior dorsal scales with prominent keels, and ventrum unpigmented except for 1���3 rows of spots on ventrolateral edge. Description of holotype (WAM R 174083). A medium-sized male Acanthophis, measurements and counts: ToL 482 mm; SVL 394 mm; TailL 88 mm (22 % of SVL); HeadL 24.9 mm; HeadW 17.4 mm; MBSR 23; AntSR 20; PostSR 17; VS 129; ScST 54; SupLab 6; InfLab 7. From above, head pear-shaped and distinct from neck, widest at interparietal scale angling forward to rostral and back to posterior jaw edge, narrowing to body; tip of snout blunt, broadly rounded; head in profile deepest at interparietal scale, snout convex; top of snout slightly concave where rostral and internasals converge; head scales rugose; rostral scale twice as wide as high, apex rounded, distal edges with low straight sides, ventral edge concave above lingual fossa; nasal scales narrowly separated by two internasals, approximately twice as wide as tall, rugose; nostril centered on nasal scale, opening dorsally and posteriorly, a shallow divot posterior to nostril; internasals as wide as long, in broad contact with each other, narrow contact with rostral, broad contact with nasals and prefrontals; prefrontals 1.5 times long as wide, narrowing laterally, 0.75 times area of frontal, 1.5 times area of internasals; frontal scale roughly rectangular, anterior edge slightly wider than posterior edge, approximately 1.5 times as long as wide (FrL 4.7 mm, FrW 3.0 mm), apex of posterior edge not extending beyond posterior edge of supraoculars; two parietals, as wide as long, anterior edge in contact with posterior angles of frontal, anterior edge of parietal sharing border with posterior edge of frontal, anterolateral edge in broad contact with supraocular, narrow contact with upper postocular, posterior border irregularly scalloped; preocular single, supraocular single, postoculars two, suboculars two; preocular in contact with prefrontal, nasal, third supralabial and anterior subocular scales; supraocular much longer than wide (SupOcL 5.03 mm, SupOcW 2.90 mm), thicker and rugose in appearance to other head scales, angled upwards at 30 ��; primary temporal scales two, lower primary temporal 2.5 times larger than upper, upper primary temporal feebly keeled; secondary temporal scales four, gradually increasing in size from dorsalmost to ventralmost, first and second with moderate keels, third and fourth smooth, fourth secondary temporal larger than prior three, located in the notch formed by fifth and sixth supralabials, two times smaller than sixth supralabial; supralabials six, sixth largest, fifth slightly smaller; first supralabial in contact with rostral and nasal, second in contact with nasal; third in contact with nasal, preocular, primary subocular, secondary subocular; fourth in contact with secondary subocular and lower postocular; fifth in contact with lower subocular, second primary temporal, fourth secondary temporal and sixth supralabial; mental triangular; infralabials seven, fourth infralabial largest, first in contact with postmental scale; anterior chin shields in contact with infralabials one to four; posterior chin shields in contact with fourth infralabial only, anterior and posterior chin shields forming a butterfly-like shape; six rows of intergulars between chin shields and anteriormost ventral. Body width widest at midbody tapering gradually forward to base of head and posteriorly to cloaca; scale rows 23 at midbody (i.e., at 64 th ventral scale from anterior), decreasing to 20 behind the head, 17 anterior to vent; 129 ventral scales; anal scale single; 54 subcaudal scales, first subcaudal paired, anteriormost 29 single, followed by 29 paired; scales on side of body diamond-shaped, scales in vertebral zone more narrow; dorsal keeling strongest on anterior quarter of body, 10���12 longitudinal scale rows wide; keeling weak along remainder of length; dorsolateral and lateral scales weakly keeled to smooth, ventral scales smooth (Figs. 5���7). Tail elongate, TailL 88 mm (22 % of SVL), tapering from cloaca to laterally compressed caudal lure; ScST 54 (ScSS 30, ScSP 24). Caudal lure much higher than wide ending with terminal tail spine. Eyes small with vertically elliptic pupil, iris mottled in appearance, similar in coloration to surrounding ocular scales. Coloration. In life, ground color of dorsal and lateral surfaces pale orange-brown; 33 darker cross-bands (Fig. 5); cross-bands two to four midbody scales wide with dark brown border; dorsal scales edged with black anteriorly; tail coloration same as dorsum with 12 bands; tail tip and terminal spine black with white to cream flecks; first midbody scale dark in center, distal edge pale; ventral scales cream-white and lacking pigmentation other than lateralmost edges; ventral coloration of tail similar in appearance to ventrum with patches of dark pigment in center of posteriormost subcaudal scales prior to black tail tip and terminal spine; supralabials stippled with black, stronger stippling on posterior labials, ventral edge pale white; infralabials pale white with dark oblong vertical blotch in center of scale, on posterior scales the ventral edge of the blotch is angled posteriorly. In preservative, dorsal ground color dull orange brown; overall pattern is subdued with less contrast between light and dark cross-bands (Fig. 6). Variation. SVL up to 555 mm; TailL 15���24 % of SVL, mean 20 % (N = 22). FrW 47���73 % of FrL, mean 59 % (N = 26). Apex of posterior edge terminates equal to (N = 13) or prior to (N = 13) posterior supraocular edge, never post. Fourth secondary temporal equal to (N = 13) or smaller than (N = 13) sixth supralabial. MBSR 22���23 (N = 24), mostly 23 (N = 21), occasionally 22 (N = 3). AntSR 16���23, mean 19 (N = 24), PostSR 16���19, mean 18 (N = 24). Ventral scales 125���139, mean 130 (N = 23). First anterior subcaudal scale usually divided, not separated (N = 9), occasionally undivided (N = 5), divided and separated by two (N = 4), three (N = 3) or one (N = 1) by a small rounded scale. ScST 46���56, mean 50, ScSP 20���40, mean 30 and ScSS 14���32, mean 21 (N = 22). Ground color of dorsal and lateral surfaces variable from dull red-orange, tan-brown or gray in coloration with darker cross bands (Fig 6). Dorsal cross bands 44���61, mean 50 (N = 23); SVL 35���46, mean 39, Tail 9���15, mean 11 (N = 23). Tail tip black with white ventral surface, occasional small white lateral flecks (80 %, N = 16), less often white (15 %, N = 3) or banded (5 %, N = 1). Ventral scales cream-white and lacking pigmentation other than lateralmost edges of ventral scale. Supralabials pale white, mottled in appearance fusing to darker markings on adjacent scales, lower edge of supralabials pale. Infralabials white-edged with dark pigment, both solid and mottled in appearance in center of scale extending to upper edge of scale. Sexual dimorphism is not obvious, although female TailL % of SVL is shorter than males: female TailL 15��� 19 % of SVL, mean 18 (N = 10); male TailL 21���24 % SVL, mean 22 % (N = 10). The tail tapers much more abruptly posterior to the vent in females, whereas in males the tail tapers gradually. The number of ventral and subcaudal scales is similar in both sexes (Table 3). Distribution. Acanthophis cryptamydros sp. nov. is known from the Kimberley region of Western Australia. The species��� range in Western Australia is known to extend from Wotjulum (WAM R 11241) in the west, 45 km north-north-east of Halls Creek in the south (WAM R 70690), and Kununurra in the east (WAM R 137470). Acanthophis cryptamydros sp. nov. is also known to occur on some offshore islands including Koolan, Bigge, Boongaree, Wulalam, and an unnamed island in Talbot Bay (Palmer et al. 2013). A single specimen (NTM R 29109) with incomplete data (no collection date or precise latitude and longitude) is reported as occurring from Adelaide River in the Northern Territory (Fig. 1); however, this locality may be in error. Further collecting from the area may resolve the issue. Habitat and ecology. The holotype (WAM R 174083) was collected early morning towards the end of the ���wet season��� (early March) from among basalt boulders in savannah woodland at the edge of a low plateau near a small sandstone outcrop. Vegetation among the basalt boulder habitat was dominated by Eucalyptus tectifica and Corymbia greeniana amongst mixed shrubs over mixed groundcovers and annual/perennial grasses (Fig. 9). Shrub cover was dominated by Grevillea mimosoides, Grewia retusifolia, Indigofera sp. and Olearia arguta (Fig. 9). The specimen was observed retreating to grass tussocks after being disturbed. The specimen was tightly coiled within the grass tussock before attempting to move to another tussock when disturbed. WAM R 145216 was collected from thick grasses on a creek bank subjected to minor sheet flooding at Little Mertens Falls. Collection notes and accession data of other specimens describe individuals collected from among grasses or leaf litter in sandstone habitats. One specimen was collected from under a rock in a vine thicket near a beach on an unnamed island in Talbot Bay (WAM R 172034), and another from leaf litter in Acacia woodland on Wulalam Island (WAM R 172035). Two specimens were collected from roads or tracks (WAM R 70690, WAM R 165567). Examination of the stomach contents of two specimens revealed a mixture of frogs, lizards, and mammals. A juvenile specimen (WAM R 1251 B) had an adult Heteronotia species (aff. H. binoei). In the gut of an adult specimen (WAM R 141552), a subadult Lophognathus species (L. gilberti), an adult Litoria species (aff. L. nasuta or L. watjulumensis), and hair belonging to a native murid species, Pseudomys sp. (aff. P. johnstoni or P. delicatulus) were found. Two small reptilian eggs were also collected from the adult, possibly from the Lophognathus ingested. Accession data for WAM R 116934 identified a Ctenotus pantherinus (WAM R 117001) from examination of its stomach contents. An ecological study of Australian and Papuan death adders by Shine et al. (2014) included five specimens of A. cryptamydros; however, examination of stomach contents revealed no prey items, only a small quantity of dirt. Examination of the gut contents of other northern Acanthophis species indicated a diet consisting of a wide range of vertebrate species, especially lizards but also including frogs, mammals, and some birds (Shine et al. 2014). Examination of reproductive organs of an adult female specimen (WAM R 106033) revealed 13 well-developed follicles approximately 10 x 14 mm in size (month of collection unknown). Comparison with other species. Distinguished from A. pyrrhus by higher average MBSR (23 vs. 21), fewer ventral scales (125���139 vs. 136���158), pigment on lateral periphery of ventral scales (vs. no pigment on ventral scales), presence of pigment patches on infralabials (infralabials unpigmented in A. pyrrhus), less prominent dorsal keeling (strongly keeled in A. pyrrhus, tapering to a sharp point on posterior edge), head scales less rugose, posterior edge of frontal scale not extending beyond posterior edge of supraoculars (equal to or beyond in A. pyrrhus), and undivided pair of prefrontal scales (divided in A. pyrrhus). A. cryptamydros sp. nov. A. ' rugosus group' Character N = 23 N = 14 (9 ♂, 7 ♀) (9 ♂, 5 ♀) SVL 428 �� 57 (322���555) N = 20 486 �� 97 (375���690) ♂♂ N = 9 ♀♀ N = 7 ♂♂ N = 9 ♀♀ N = 5 412 �� 41 468 �� 54 434 �� 57 581 �� 82 (374���496) (392���555) (375���530) (482���690) TailL 86 �� 9 (72���110) N = 20 94 �� 11 (80���110) ♂♂ N = 9 ♀♀ N = 7 ♂♂ N = 9 ♀♀ N = 5 90.6 �� 9 81.4 �� 5 92 �� 11 98 �� 9 (79���110) (76���89) (79���110) (85���108) TailL/SVL 0.20 �� 0.03 (0.15���0.24) N = 20 0.20 �� 0.03 (0.15���0.23) ♂♂ N = 9 ♀♀ N = 7 ♂♂ N = 9 ♀♀ N = 5 0.22 �� 0.01 0.18 �� 0.01 0.21 �� 0.01 0.17 �� 0.03 (0.21���0.24) (0.15���0.19) (0.20���0.23) (0.15���0.22) HeadL 26.1 �� 2.4 (22.7 ���32.0) N = 20 31.1 �� 5.5 (25.5���42.3) HeadW 16.4 �� 2.2 (13.8���20.2) N = 20 19.4 �� 4.6 (13.1���27.1) HeadW/HeadL 0.63 �� 0.05 (0.54���0.71) N = 20 0.60 �� 0.04 (0.51���0.66) VS 130 �� 4 (125���139) N = 20 127 �� 4 (123���136) ScST 50 �� 3 (46���56) N = 20 46 �� 6.14 (29���55) ♂♂ N = 9 ♀♀ N = 7 ♂♂ N = 9 ♀♀ N = 5 53 �� 2 49 �� 2 47 �� 7 45 �� 3 (51���56) (46���51) (29���55) (42���49) MBSR 22.9 �� 0.3 (22���23) 22.0 �� 0.9 (21���23) AntSR 19.2 �� 1.3 (16���23) 20.3 �� 0.6 (19���21) PostSR 17.8 �� 0.9 (16���19) 18.0�� 0.7 (17���19) PreOc 1.0��0 (1) 1.1 �� 0.3 (1���2) SupOc 1.0��0 (1) 1.1 �� 0.3 (1���2) PostOc 2.0�� 0.2 (2���3) 2.1 �� 0.3 (2���3) SubOc 2.2 �� 0.4 (2���3) 2.7 �� 0.5 (2���3) Ptemp 2 ��0 (2) 2.0��0 (2) Stemp 4.4 �� 0.5 (4���5) 4.0�� 0.4 (3���5) SupLab 6.0��0 (6) 6.0��0 (6) InfLab 7.0��0 (7) 7.1 �� 0.3 (7���8) FrL 5.6 �� 0.5 (4.7���6.7) N = 20 7.2 �� 0.9 (6.0���9.0) FrW 3.3 �� 0.3 (2.6���4.1) N = 20 3.4 �� 0.5 (2.8���4.4) FrW/FrL 0.59 �� 0.06 (0.47���0.73) N = 20 0.48 �� 0.02 (0.45���0.52) SupOcL 5.5 �� 0.5 (4.8���6.4) N = 20 6.4 �� 0.7 (5.2���7.4) SupOcW 3.1 �� 0.3 (2.8���3.7) N = 20 3.7 �� 0.5 (3.0��� 4.6) Differs from A. wellsi by higher midbody scale rows (22���23 vs. 19���21), less prominent dorsal keeling, posterior edge of frontal scale not extending beyond posterior edge of supraoculars (equal to or beyond in A. wellsi), and more laterally flared supraocular (absent or less prominent in A. wellsi). Differs from melanistic forms of A. wellsi by the absence of prominent black coloration on head and black dorsal bands. Distinguished from A. antarcticus by higher average MBSR (23 vs. 21), more ventral scales (125 + vs. 124 -), and more prominent anterior dorsal keeling (vs. smooth or very weakly keeled in A. antarcticus). Most similar to A. rugosus group in appearance, but differs through higher average ventral scale counts (130 vs. 127), despite considerable overlap in range, lacking dark pigment on the ventrum other than lateral edge (vs. distinct blotching of dark pigment), posterior edge of frontal scale not extending beyond posterior edge of supraoculars (beyond in 13 of 14 specimens, equal in one specimen) and size of lower secondary temporal not larger than sixth supralabial in area (A. cryptamydros equal in 13 specimens, smaller in 13 vs. A. rugosus equal in 10, larger in 4). See Table 3 for further details. Comparisons of A. cryptamydros sp nov. to the A. rugosus group are complicated by the likely existence of a number of undescribed species within the latter, which greatly increases variation within this complex. We comment on morphological characters that are useful in distinguishing these two taxa. Etymology. The specific epithet is modified from the Greek words kryptos (cryptic, hidden) and amydros (indistinct, dim) in reference to the cryptic nature of the species and its indistinct appearance relative to its surroundings making its presence unknown to predators and prey. Used as a noun in apposition. Remarks. The A. rugosus group is likely to contain a number of undescribed species. Taxonomic resolution of this group will further define differences between individual species within the group and A. cryptamydros sp. nov. The discovery of A. cryptamydros sp. nov. as a previously undescribed major lineage within Acanthophis highlights the incompleteness of our understanding of phylogenetic structure and species limits within the genus. At the same time, it also highlights the importance of the Kimberley region of Western Australia as a center of endemism (Doughty 2011; Oliver et al. 2012; Pepper & Keogh 2014). Lethal ingestion of the cane toad (Rhinella marina) has been documented in previous studies on Acanthophis specimens from the Kimberley region and Northern Territory (Phillips & Shine 2007; Hagman et al. 2009; Phillips et al. 2010; Pearson et al. 2014) indicating the species is likely to be at risk of significant decline as cane toads continue to move west across the Kimberley region. A detailed assessment on potential threats to the species including cane toads will identify the need for listing as a species requiring protection under state or federal legislation., Published as part of Maddock, Simon T., Ellis, Ryan J., Doughty, Paul, Smith, Lawrence A. & W��ster, Wolfgang, 2015, A new species of death adder (Acanthophis: Serpentes: Elapidae) from north-western Australia, pp. 301-326 in Zootaxa 4007 (3) on pages 308-315, DOI: 10.11646/zootaxa.4007.3.1, http://zenodo.org/record/243397, {"references":["Palmer, R., Pearson, D. J., Cowan, M. A. & Doughty, P. (2013) Islands and scales: a biogeographic survey of reptiles on Kimberley islands, Western Australia. Records of the Western Australian Museum, 81 (Supplement), 183 - 204. http: // dx. doi. org / 10.18195 / issn. 0313 - 122 x. 81.2013.183 - 204","Oliver, P. M., Doughty, P. & Palmer, R. (2012) Hidden biodiversity in rare northern Australian vertebrates: the case of the clawless gecko (Crenadactylus, Diplodactylidae) of the Kimberley. Wildlife Research, 39, 429 - 435. http: // dx. doi. org / 10.1071 / WR 12024","Pepper, M. & Keogh, J. S. (2014) Biogeography of the Kimberley, Western Australia: a review of landscape evolution and biotic response in an ancient refugium. Journal of Biogeography, 41, 1443 - 1455. http: // dx. doi. org / 10.1111 / jbi. 12324","Phillips, B. & Shine, R. (2007) When dinner is dangerous: Toxic frogs elicit species-specific responses from a generalist snake predator. The American Naturalist, 170, 936 - 942. http: // dx. doi. org / 10.1086 / 522845","Hagman, M., Phillips, B. L. & Shine, R. (2009) Fatal attraction: Adaptations to prey on native frogs imperil snakes after invasion of toxic toads. Proceedings of the Royal Society B, 276, 2813 - 2818. http: // dx. doi. org / 10.1098 / rspb. 2009.0192","Phillips, B. L., Greenlees, M. J., Brown, G. P. & Shine, R. (2010) Predator behaviour and morphology mediates the impact of an invasive species: cane toads and death adders in Australia. Animal Conservation, 13, 53 - 59. http: // dx. doi. org / 10.1111 / j. 1469 - 1795.2009.00295. x","Pearson, D. J., Webb, J. K., Greenlees, M. J., Phillips, B. L., Bedford, G. S., Brown, G. P., Thomas, J. & Shine, R. (2014) Behavioural responses of reptile predators to invasive cane toads in tropical Australia. Austral Ecology, 39, 448 - 454. http: // dx. doi. org / 10.1111 / aec. 12102"]}

The utilization of venom in predatory and defensive contexts is associated with benefits regarding minimization of energetic expenditure on hunting, maximization of success in prey acquisition and avoidance of injury from dangerous prey and aggressors. Multiple characteristics suggest that venom is quite expensive to produce, thereby creating a tradeoff between advantages and disadvantages associated with its possession. The metabolic costs of venom production have rarely been studied and no information on the detailed metabolic processes during venom replenishment exists. Where costs of venom production have been studied they are often not in context with other components of the energy budget of the study organism. Using flow-through respirometry, we examined changes in metabolic rate in the Australian elapid Acanthophis antarcticus after venom expenditure and feeding as well as during preparation for shedding to establish a comparison of the magnitude of energetic expenditure during venom replenishment and other common physiological processes. We also defined the temporal pattern of metabolic processes during venom replenishment at a higher resolution than has previously been attempted in snakes. Our results suggest that total costs of venom replenishment are relatively small when compared to costs of digestion and shedding. We conclude that, in spite of the manifold factors suggesting a high cost of venom in snakes, its production is less energetically costly than often assumed. Until further research can clarify the reasons for this more caution should therefore be applied when assuming that costs of venom production exert strong selection pressures on the ecology, behavior and evolution of venomous taxa.

While Australo-Papuan death adder neurotoxicity is generally considered to be due to the actions of reversible competitive postsynaptic alpha-neurotoxins, the neurotoxic effects are often poorly reversed by antivenom or anticholinesterases. This suggests that the venom may contain a snake presynaptic phospholipase A(2) (PLA(2)) neurotoxin (SPAN) that binds irreversibly to motor nerve terminals to inhibit neurotransmitter release. Using size-exclusion liquid chromatography under non-reducing conditions, we report the isolation and characterisation of a high molecular mass SPAN complex, P-elapitoxin-Aa1a (P-EPTX-Aa1a), from the venom of the common death adder Acanthophis antarcticus. Using the chick biventer-cervicis nerve-muscle preparation, P-EPTX-Aa1a (44,698Da) caused inhibition of nerve-evoked twitch contractions while responses to cholinergic agonists and KCl remained unaffected. P-EPTX-Aa1a also produced significant fade in tetanic contractions and a triphasic timecourse of neuromuscular blockade. These actions are consistent with other SPANs that inhibit acetylcholine release. P-EPTX-Aa1a was found to be a heterotrimeric complex composed of alpha, beta and gamma-subunits in a 1:1:1 stoichiometry with each subunit showing significant N-terminal sequence homology to the subunits of taipoxin, a SPAN from Oxyuranus s. scutellatus. Like taipoxin, only the alpha-chain produced any signs of neurotoxicity or displayed significant PLA(2) enzymatic activity. Preincubation with monovalent death adder antivenom or suramin, or inhibition of PLA(2) activity by incubation with 4-bromophenacyl bromide, either prevented or significantly delayed the onset of toxicity by P-EPTX-Aa1a. However, antivenom failed to reverse neurotoxicity. Early intervention with antivenom may therefore be important in severe cases of envenomation by A. antarcticus, given the presence of potent irreversible presynaptic neurotoxins.

Signal design can reflect the sensory properties of receivers. The death adder, Acanthophis antarcticus, attracts prey by wriggling the distal portion of its tail (caudal luring). To understand the design of this deceptive signal, we explored perceptual processes in a representative prey species: the Jacky dragon, Amphibolurus muricatus. We used 3D animations of fast and slow death adder luring movements against different backgrounds, to test the hypothesis that caudal luring mimics salient aspects of invertebrate prey. Moving stimuli elicited predatory responses, especially against a conspicuous background. To identify putative models for caudal luring, we used an optic flow algorithm to extract velocity values from video sequences of 61 moving invertebrates caught in lizard territories, and compared these to the velocity values of death adder movements. Caudal lures had motion characteristics that matched common invertebrate prey speeds, each corresponding to a peak in a bimodal distribution. Subsequent video playback tests using animations of crickets showed that significantly more attacks were evoked by stimuli moving at common than at rare invertebrate speeds. Overall, these results suggest that biases in the nervous system of the receiver, originally selected for prey recognition, might have been exploited by the design of the caudal luring signal. We suggest that viewing caudal luring from this perspective, rather than thinking of it as aggressive mimicry per se, may help us understand the function and evolutionary origin of this behaviour.

We report a 60 year old male bitten by snakes from the Acanthophis genus (Death adder) on two occasions who developed high titres of human IgG antibodies to Acanthophis venom detected at the time of the second bite. The patient was bitten by Acanthophis antarcticus (common death adder) on the first occasion, developed non-specific systemic effects and did not receive antivenom. Three months later he was bitten by Acanthophis praelongus (northern death adder) and he developed significant local myotoxicity associated with a moderate rise in the creatine kinase (maximum 4770 U/L). He was given antivenom 55 h after the bite and recovered over several days. Death adder venom was detected in serum at the time of the first bite, but not the second bite. Human IgG antibodies to death adder were detected on the second admission but not the first. However, despite the presence of antibodies to death adder venom and free venom not being detected, the patient still developed significant local myotoxicity.

Many prey species use chemical cues to detect predators. According to the threat sensitivity hypothesis, prey should match the intensity of their antipredator behaviour to the degree of threat posed by the predator. Several species of lizards display antipredator behaviours in the presence of snake chemical cues, but how species specific are these responses? In Australia, most snake species eat lizards, and are therefore potentially dangerous. Hence, we predicted that lizards should display generalized rather than species-specific antipredator behaviours. To test this prediction, we quantified the behavioural responses of velvet geckos, Oedura lesueurii, to chemical cues from five species of elapid snakes that are syntopic with velvet geckos but differ in their degree of danger. These five snake species included two nocturnal ambush foragers that eat geckos (broad-headed snake Hoplocephalus bungaroides, and death adder, Acanthophis antarcticus), two active foragers that eat skinks (but rarely eat geckos) and that differ in their activity times (nocturnal small-eyed snake, Cryptophis nigrescens, and diurnal whip snake, Demansia psammophis), and a nocturnal nonthreatening species that feeds entirely on blind snakes (bandy-bandy, Vermicella annulata). Geckos showed similar antisnake behaviours (tail waving, tail vibration), and a similar intensity of responses (reducing activity, freezing), to chemical cues from all five snake species, even though the snakes differed in their degree of danger and foraging modes. Our results suggest that velvet geckos display generalized antipredator responses to chemicals from elapid snakes, rather than responding in a graded fashion depending upon the degree of threat posed by a particular snake species. © 2009 The Association for the Study of Animal Behaviour.

Death adder envenomation is rare in humans and there is only one brief report previously in dogs. This paper details three cases of canine common death adder (Acanthophis antarcticus) envenomation and one case of bardick (Echiopsis curta) envenomation which were responsive to death adder antivenom. The available literature on death adder envenomations is also reviewed. The main clinical sign in the four dogs was severe lower motor neuron paralysis. There was no clinical evidence of coagulopathy or myopathy. Use of a snake venom detection kit was essential for selection of appropriate antivenom. Death adder and bardick envenomation in dogs potentially has a good prognosis if sufficient antivenom is administered and intensive supportive care is available.

Death adder (genus Acanthophis) venoms display neurotoxic activity but were thought to be devoid of myotoxic components. Studies from our laboratory have shown that some species (i.e. Acanthophis rugosus and Acanthophis sp. Seram) possess venom with myotoxic activity [Wickramaratna JC, Fry BG, Aguilar M, Kini RM, Hodgson WC. Isolation and pharmacological characterisation of a phospholipase A2 myotoxin from the venom of the Irian Jayan death adder (A. rugosus). Br J Pharmacol 2003;138:333-342; Wickramaratna JC, Fry BG, Hodgson WC. Species-dependent variations in the in vitro myotoxicity of death adder (Acanthophis) venoms. Toxicol Sci 2003;74:352-360]. The present study describes the isolation and characterisation of two myotoxins (acanmyotoxin-2 and acanmyotoxin-3) from A. sp. Seram venom. Venom was fractionated into approximately 12 major peaks using reverse phase high performance liquid chromatography. Two components caused concentration (0.1-1 microM) dependent inhibition of direct (2 ms, 0.1 Hz, supramaximal V) twitches and an increase in baseline tension in the chick biventer cervicis nerve-muscle. Histological examination of the muscle confirmed damage. PLA2 activity was detected in both acanmyotoxin-2 (390.2+/-19.7 micromol/(min mg); n=4) and acanmyotoxin-3 (14.2+/-7.7 micromol/(min mg); n=4). In comparison, A. sp. Seram whole venom had a specific activity of 461.3+/-90.4 micromol/(min mg) (n=3). Mass spectrometry analysis indicated acanmyotoxin-2 had a mass of 13,082 Da and acanmyotoxin-2 13,896 Da. Acanmyotoxin-2 and acanmyotoxin-3 accounted for approximately 7 and 4% of total venom composition, respectively. N-terminal sequencing of the first 30 amino acids of each toxin indicated they shared some sequence homology with known myotoxins. In conclusion, clinicians should be aware that symptoms of envenoming by some species of death adder may include signs of myotoxicity as well as neurotoxicity. Future studies will investigate the efficacy of the current antivenom treatment against the myotoxic components of A. sp. Seram venom.

We analyze the phylogeny of three genera of Australasian elapid snakes (Acanthophis-death adders; Oxyuranus-taipans; Pseudechis-blacksnakes), using parsimony, maximum likelihood, and Bayesian analysis of sequences of the mitochondrial cytochrome b and ND4 genes. In Acanthophis and Pseudechis, we find evidence of multiple trans-Torresian sister-group relationships. Analyses of the timing of cladogenic events suggest crossings of the Torres Strait on several occasions between the late Miocene and the Pleistocene. These results support a hypothesis of repeated land connections between Australia and New Guinea in the late Cenozoic. Additionally, our results reveal undocumented genetic diversity in Acanthophis and Pseudechis, supporting the existence of more species than previously believed, and provide a phylogenetic framework for a reinterpretation of the systematics of these genera. In contrast, our Oxyuranus scutellatus samples from Queensland and two localities in New Guinea share a single haplotype, suggesting very recent (late Pleistocene) genetic exchange between New Guinean and Australian populations.

Maddock et al. (2015) described a supposedly new species of death adder (Squamata, Elapidae) from northwestern Australia as Acanthophis cryptamydros. However, Maddock et al. (2015: 307) themselves admitted that this name was a junior synonym of Acanthophis lancasteri Wells & Wellington, 1985: “Since the only existing name applicable to this taxon, Acanthophis lancasteri Wells & Wellington, 1985, is a nomen nudum (Aplin & Donnellan 1999), we describe it as a new species below (...)”.

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 microg/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 microg/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

It has long been thought that death adder venoms are devoid of myotoxic activity based on studies done on Acanthophis antarcticus (Common death adder) venom. 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. Consequently, the present study examined A. rugosus (Irian Jayan death adder) venom for myotoxicity, and isolated the first myotoxin (acanmyotoxin-1) from a death adder venom. A. rugosus (10–50 μg ml−1) and acanmyotoxin-1 (MW 13811; 0.1–1 μM) were screened for myotoxicity using the chick directly (0.1 Hz, 2 ms, supramaximal V) stimulated biventer cervicis nerve-muscle (CBCNM) preparation. A significant contracture of skeletal muscle and/or inhibition of direct twitches were considered signs of myotoxicity. This was confirmed by histological examination. High phospholipase A2 (PLA2) activity was detected in both A. rugosus venom (140.2±10.4 μmol min−1 mg−1; n=6) and acanmyotoxin-1 (153.4±11 μmol min−1 mg−1; n=6). Both A. rugosus venom (10–50 μg ml−1) and acanmyotoxin-1 (0.1–1 μM) caused dose-dependent inhibition of direct twitches and increase in baseline tension (n=4–6). In addition, dose-dependent morphological changes in skeletal muscle were observed. Prior incubation (10 min) of CSL death adder antivenom (5 units ml−1; n=4) or inactivation of PLA2 activity with 4-bromophenacyl bromide (1.8 mM; n=4) prevented the myotoxicity caused by acanmyotoxin-1 (1 μM). Acanmyotoxin-1 (0.1 μM; n=4) displayed no significant neurotoxicity when it was examined using the indirectly (0.1 Hz, 0.2 ms, supramaximal V) stimulated CBCNM preparation. In conclusion, clinicians may need to be mindful of possible myotoxicity following death adder envenomation in Irian Jaya. British Journal of Pharmacology (2003) 138, 333–342. doi:10.1038/sj.bjp.0705046

I staged replicate encounters between unrestrained lizards and snakes in outdoor enclosures to examine size-dependent predation within the common garden skink (Lampropholis guichenoti). Yellow-faced whip snakes (Demansia psammophis) forage widely for active prey and most often consumed large skinks, whereas death adders (Acanthophis antarcticus) ambush active prey and most often consumed small skinks. Small-eyed snakes (Rhinoplocephalus nigrescens) forage widely for inactive prey and consumed both small and large skinks equally often. Differential predation may reflect active choice by the predator, differential prey vulnerability, or both. To test for active choice, I presented foraging snakes with an inert small lizard versus an inert large lizard. They did not actively select lizards of a particular body size. To test for differential prey vulnerability, I quantified variation between small and large lizards in behavior that is important for determining the outcome of predator--prey interactions. Snakes did not differentiate between integumentary chemicals from small and large lizards. Large lizards tend to flee from approaching predators, thereby eliciting attack by the visually oriented whip snakes. Small lizards were more mobile than large lizards and therefore more likely to pass by sedentary death adders. Additionally, small skinks were more effectively lured by this sit-and-wait species and less likely to avoid its first capture attempt. In contrast, overnight retreat site selection (not body size) determined a lizard's chances of being detected by small-eyed snakes. Patterns of size-dependent predation by elapid snakes may arise not because of active choice but as a function of species-specific predator tactics and prey behavior. Copyright 2002.

Death adders (genus Acanthophis) are unique among elapid snakes in both morphology and venom composition. Despite this genus being among the most divergent of all elapids, the venom has been historically regarded as relatively quite simple. In this study, liquid chromatography/mass spectrometry (LC/MS) analysis has revealed a much greater diversity in venom composition, including the presence of molecules of novel molecular weights that may represent a new class of venom component. Furthermore, significant variation exists between species and populations, which allow for the LC/MS fingerprinting of each species. Mass profiling of Acanthophis venoms clearly demonstrates the effectiveness of this technique which underpins fundamental studies ranging from chemotaxonomy to drug design.

Death adders (genus Acanthophis) differ from most other elapid snakes, and resemble many viperid snakes, in their thickset morphology and ambush foraging mode. Although these snakes are widely distributed through Australia and Papua New Guinea, their basic biology remains poorly known. We report morphological and ecological data based upon dissection of >750 museum specimens drawn from most of the range of the genus. Female death adders grow larger than conspecific males, to about the same extent in all taxa (20% in mean adult snout-vent length, = SVL). Most museum specimens were adult rather than juvenile animals, and adult males outnumbered females in all taxa except A. pyrrhus. Females have shorter tails (relative to SVL) than males, and longer narrower heads (relative to head length) in some but not all species. The southern A. antarcticus is wider-bodied (relative to SVL) than the other Australian species. Fecundity of these viviparous snakes was similar among taxa (mean litter sizes 8 to 14). Death adders encompass a broad range of ecological attributes, taking a wide variety of vertebrate prey, mostly lizards (55%), frogs and mammals (each 21%; based on 217 records). Dietary composition differed among species (e.g. frogs were more common in tropical than temperate-zone species), and shifted with snake body size (endotherms were taken by larger snakes) and sex (male death adders took more lizards than did females). Overall, death adders take a broader array of prey types, including active fast-moving taxa such as endotherms and large diurnal skinks, than do most other Australian elapids of similar body sizes. Ambush foraging is the key to capturing such elusive prey.

The common (A. antarcticus), northern (A. praelongus) and desert (A. pyrrhus) death adders are species belonging to the Acanthophis genus. The present study compared some pharmacological aspects of the venoms of these species and examined the in vitro efficacy of death adder antivenom. Neurotoxicity was determined by the time to produce 90% inhibition (t(90)) of indirect (0.1 Hz, 0.2 ms, supramaximal voltage) twitches in the chick biventer cervicis nerve-muscle (3-10 microg/ml) and mouse phrenic nerve-diaphragm (10 microg/ml) preparations. A. praelongus venom was significantly less neurotoxic than A. antarcticus venom but was not significantly different from A. pyrrhus venom. In the biventer muscle, all three venoms (3-10 microg/ml) abolished responses to exogenous ACh (1 mM) and carbachol (20 microM), but not KCl (40 mM), indicating activity at post-synaptic nicotinic receptors. All venoms (30 microg/ml) failed to produce significant inhibition of direct twitches (0.1 Hz, 2.0 ms, supramaximal voltage) in the chick biventer cervicis nerve-muscle preparation. However, A. praelongus (30 microg/ml) venom initiated a significant direct contracture of muscle, indicative of some myotoxic activity. The prior (10 min) administration of death adder antivenom (1 unit/ml), which is raised against A. antarcticus venom, markedly attenuated the twitch blockade produced by all venoms (10 microg/ml). Administration of antivenom (1.5 units/ml) at t(90) markedly reversed, over a period of 4 h, the inhibition of twitches produced by A. praelongus (3 microg/ml, 72+/-6% recovery) and A. pyrrhus (3 microg/ml, 51+/-9% recovery) but was less effective against A. antarcticus venom (3 microg/ml, 22+/-7% recovery). These results suggest that all three venoms contain postsynaptic neurotoxins. Death adder antivenom displayed differing efficacy against the in vitro neurotoxicity of the three venoms.

While snakebite numbers are decreasing in temperate Australia, snakebite remains an important cause of morbidity in tropical Australia and of mortality in Papua New Guinea and Irian Jaya. The Australasian elapid snakes have complex mixtures of venom components, with distinct clinical syndromes defined for the potentially lethal species. Life-threatening scenarios are progressive neuromuscular paralysis with taipan (Oxyuranus spp.) and death adder (Acanthophis spp.) envenoming and early hypotensive collapse and severe coagulopathy with fibrinogen depletion and major bleeding (especially intracranial haemorrhage) with brown snake (Pseudonaja spp.) bites. The ‘brown snake paradox’ is that textilotoxin is one of the most potent neurotoxins known, yet neurotoxicity is uncommon in brown snake envenoming. Prospective studies using assays of serial patient serum venom levels will provide better evidence for efficacy or otherwise of various first-aid methods used and help define appropriate doses of antivenoms for specific clinical scenarios. Financial and distribution constraints have resulted in antivenoms being unavailable for use in most regions of Papua New Guinea and Irian Jaya.

Objective: Recently it has been recommended that a combination of brown snake and tiger snake antivenom be given to a patient envenomed by an unidentified snake in Perth, except when the bite occurred in the areas where the death adder is prevalent. We present the first reported case of envenomation by a death adder (Acanthophis antarcticus) in Perth, with a view to examining the appropriateness of that recommendation. Clinical features: A 36 year old woman, bitten in a suburb of Perth where death adders are not usually seen, presented with progressive paralysis. Intervention and outcome: Rapid and complete recovery immediately after one ampoule of death adder antivenom confirmed the diagnosis of death adder envenomation. Conclusion: The recommendation is appropriate. Death adder envenomation is in effect “the exception that proves the rule”. Vigilance for this rare envenomation is necessary.

The phospholipase A2 enzyme, acanthoxin, found in the venom of the common death adder (Acanthophis antarcticus) as with other snake PLA2 enzymes displays neurotoxic activity. It is unclear whether this neurotoxic activity particu- lar to some snake PLA2 enzymes is a result of structural differences solely within the catalytic sites or at a distant location upon the molecules. We have predicted the three-dimensional structure of one of the two predominant isoforms of acanthoxin (A1) using comparative protein modeling tech- niques. Given the high degree of homology and the availability of a high quality crystallographic struc- ture, notexin was used as a molecular template to construct an all atom model of acanthoxin. The model was made using the program MODELLER3 and then refined with X-PLOR. Comparison be- tween the predicted structure of acanthoxin and several X-ray structures of toxic and nontoxic PLA2 enzymes has led to a testable two-step proposal of neurotoxic PLA2 activity; involving the favorable binding to acceptor molecules followed by enzy- matic intrusion upon the target membrane. The electrostatic potentials across the molecular sur- faces of toxic and nontoxic PLA2 enzymes were calculated (GRASP) and it was found that the toxic PLA2 enzymes possessed a charge distribution on the noncatalytic surface not identified in the non- toxic PLA2 enzymes. Thus we have identified resi- dues potentially involved in the interaction of the PLA2 enzymes with their acceptor molecules. Fur- thermore, the proposed acceptor molecule recogni- tion site is distant from the catalytic site which upon binding of the PLA2 to the acceptor molecule may enhance the enzymatic ability of the toxic PLA2 enzymes on particular cell types. Proteins 1999

Venom of Acanthophis antarcticus, a common death adder, exhibits potent antiplatelet effects. By a combination of gel-filtration, cation-exchange, and reversed-phase chromatographic methods, two inhibitors of platelet aggregation, named acanthin I and II, were purified to homogeneity as assessed by capillary electrophoresis and electrospray mass spectrometry. These isoforms exhibit the most potent antiplatelet activity known thus far, with IC50 values of 7 nM for acanthin I and 4 nM for acanthin II in human whole blood when collagen was used as an agonist, whereas with ADP the IC50 values were 10 and 12 nM, respectively. Acanthin I and II are basic proteins with pIs of 10.2 +/- 0.1 and 10.4 +/- 0.1 and molecular weights of 12,844.58 +/- 0.61 and 12,895.63 +/- 0.48, respectively, as determined by electrospray mass spectrometry. They exhibit phospholipase enzyme activity, and acanthin I and II hydrolyzed 51. 57 +/- 1.30 and 46.85 +/- 2.90 micromol of phosphatidylcholine/min/mg, respectively. The complete amino acid sequences of acanthin I and II showed that they have a high homology with each other and with other elapids' phospholipase A2 neurotoxin, especially pseudexin A.

Envenoming by a number of species of snake may affect the myocardium or cause electrocardiographic changes; several different mechanisms have been proposed. In a prospective study of snake bite in Papua New Guinea, electrocardiographic changes were observed in 36 of 69 patients (52%) envenomed by the taipan (Oxyuranus scutellatus), 2 of 6 (33%) envenomed by death adders (Acanthophis sp.) and one envenomed by the brown snake (Pseudonaja textilis). Septal T wave inversion and bradycardias, including atrioventricular block, were the commonest abnormalities. There was no haemodynamic deterioration. The cause of these changes is uncertain; only 2 of 24 patients (8.3%) with electrocardiographic changes had markedly elevated plasma concentrations of cardiac troponin T, a sensitive and specific marker of myocardial damage. This suggests that myocardial damage is uncommon following bites by these species. Electrocardiographic abnormalities are most likely to have been caused by a direct toxic effect of a venom component upon cardiac myocyte function; in taipan bites, taicatoxin, a calcium channel blocker, might be responsible.