Journal of the New Zealand Medical Association, 27-February-2009, Vol 122 No 1290
New Zealand’s venomous creatures
Robin J Slaughter, D Michael G Beasley, Bruce S Lambie, Leo J Schep
New Zealand is host to a small but varied group of terrestrial and marine venomous creatures. They range from species which cause only minor injuries, such as bluebottle jellyfish (Physalia utriculus), to creatures which can cause significant systemic envenoming, such as the yellow bellied sea snake (Pelamis platurus). Although envenoming caused by these animals is relatively rare, there are still a sufficient number of cases each year in New Zealand to warrant a broad review and update of current recommendations for management.
In this article we will examine New Zealand’s venomous creatures, including their habitats and distribution, the clinical effects of envenoming, and appropriate first aid and definitive medical treatment.
Description—There are five medically significant genera of spider in the world (Atrax, Hadronyche, Latrodectus, Loxosceles, and Phoneutria). New Zealand has two venomous spiders from the genus Latrodectus: the endangered native katipo (Latrodectus katipo) and an Australian import, the redback spider (Latrodectus hasseltii). Another spider, the “black katipo”, was once thought to be a separate species (Latrodectus atritus) but has been found to be a junior synonym of L. katipo.1 Katipo is a Māori name and means “night stinger”; it is derived from two words, kakati (to sting), and po (the night).2
L. katipo is found throughout coastal regions of New Zealand, including most of the North Island, and south to Greymouth on the west coast and Dunedin on the east coast of the South Island.3,4 Katipo spiders have a highly specialised habitat and are only found near the shoreline amongst sand dunes.4 Redback spiders were first found in the early 1980s in Wanaka and have spread further afield since then.4
The katipo and redback are similar in appearance, both being dark brown to black in colour, with an orange to red jagged stripe running down the length of the dorsal abdomen (Figure 1). Katipo spiders are slightly smaller than redback spiders (~10 mm body length) (Figure 2).
Both spiders have a red hourglass marking on the lower surface, a common trait in many Latrodectus spiders. Female katipo found north of 39°15'S (L. katipo var. atritus) almost always lack the red stripe on the dorsal abdomen.1,4
There are very few reported cases of katipo or redback bites in New Zealand. Historically, there is some evidence of occasional significant symptoms from katipo bites.2 Black katipo bites have not been considered particularly dangerous, although a suspected case from Te Kopuru with mild to moderate symptoms has been reported.2
Bites from these spiders are not common, as by nature they are shy, non-aggressive animals. Additionally, the narrow habitat of the katipo and diminishing population means interaction between humans and the spider is typically minimal. Accidentally disturbing a web or antagonising a spider will likely result in the spider biting in self defence. If the female spider is protecting an egg sac it may act more aggressively.2
Signs and symptoms—Bites produce a syndrome known as latrodectism, which is characterised principally by pain. There may initially be minimal effects associated with the instant of the bite before local redness, diaphoresis, and pain develop. Pain often increases in severity and spreads proximally.5,6
Abdominal, back, or chest pain can occur. Non-specific systemic symptoms may develop, including nausea, vomiting, generalised diaphoresis, headache, lethargy, malaise and hypertension; less commonly other neurologic and autonomic symptoms may occur.5,6
Treatment—To help minimise systemic venom spread, victims should be reassured and persuaded to remain still. The application of a cold pack may help relieve local pain.
All bites should be medically observed in a hospital for at least 6 hours to detect any onset of symptoms.7 Patients can initially be treated with opioid analgesia and benzodiazepines.8,9 If pain is refractory to initial treatment, or if significant signs and symptoms of latrodectism occur, redback antivenom can be considered.
Current limited evidence on safety and efficacy would support antivenom use in cases of latrodectism causing either systemic effects or severe or persistent pain.8 It is likely to be effective for both redback and katipo spider bites.10 Adverse reactions to this antivenom are relatively uncommon11; early anaphylactoid reactions have been reported as occurring in 0.5 to 0.8% of patients, while less than 5% develop serum sickness.12 Severe anaphylaxis or death has not been reported.
Description—The white tailed spider (Lampona cylindrata and L. murina) is an Australian native which arrived in New Zealand in the late 19th Century.13 Often found both inside and outside the home, it hides during the day in small crevices in walls, crawl spaces, shoes, bed linen, and under clothes or items left on the floor.7 This spider is distinctive with a dark grey to black cylindrical body, and is readily identifiable by a small white patch at the end of the abdomen, above the spinnerets. It is between 12 and 17 mm long (Figure 3).
A prospective cohort study of 130 cases with confirmed bites was conducted. Patients were included only if there was a clear history of a bite, and the spider was caught at the time of the bite and later identified by an expert arachnologist. None of the 130 cases developed necrotic ulcers. Indeed, the only spiders proven to cause necrotising arachnidism belong to the genus Loxosceles, such as the North American brown recluse spider,19 and are not found in New Zealand.
Signs and symptoms—The bite from a white tailed spider may cause local symptoms of pain, redness, swelling, and pruritus.18 Less commonly minor systemic symptoms of nausea, vomiting, malaise, and headache can also be seen. All these symptoms are generally mild and self-limiting.18 As with any puncture wound, there is a risk of secondary infection.
Treatment—First aid consists of ensuring the wound is cleaned, along with application of an ice pack to reduce pain and swelling.
Further treatment is seldom required but may include simple analgesia and/or antihistamines for symptomatic relief. Patients presenting with a lesion thought to be associated with a spider should be thoroughly investigated for another cause.20 A good history and physical examination should be undertaken.
For severe or persistent necrotic lesions, microbiological investigation should be performed, including cultures for organisms such as fungi and unusual bacteria.21 Alternative diagnoses to spider bite should be considered, as a wide array of conditions have been misdiagnosed as necrotic arachnidism; these include sporotrichosis,22 Pyoderma gangrenosum,23 Mycobacterium ulcerans,24 and even chemical burns.25
Description—Of the numerous jellyfish within New Zealand’s coastal waters, only two species (within the same genus) are considered medically important: the Bluebottle jellyfish (Physalia utriculus) and the Pacific or Portuguese Man-of-War jellyfish (Physalia physalis). The two jellyfish species most dangerous to humans,26 the box jellyfish (Chironex fleckeri) and irukandji jellyfish (Carukia barnesi), are not found in New Zealand.
Bluebottles have a distinctive bright blue floating bladder, measuring about 2–15 cm long, and one main deep blue fishing tentacle which may be up to 10 m in length.27 (Figure 4)
The Pacific or Portuguese Man-of-War is a larger form of the bluebottle; its floating bladder may be up to 25 cm long, and it has up to five main tentacles.28 (Figure 5)
All jellyfish possess microscopic stinging cells called nematocysts. These structures are numerous on the tentacles or body of the animal, and are used to capture prey. A small dose of venom contained within each nematocyst is discharged in response to chemical or mechanical stimulation.29 Nematocysts from many jellyfish do not penetrate human skin and/or their venom is not toxic to humans; encounters with these therefore do not produce a significant reaction. However, Physalia nematocysts do penetrate human skin, and envenoming may lead to systemic effects.
Signs and symptoms—Most victims of Physalia envenoming will display no signs and symptoms other than localised pain and pruritus. Characteristically, stings cause a linear collection of elliptical blanched weals, with a surrounding red flare (resembling a "string of beads").30
Extensive stinging (more likely from larger specimens) may lead to systemic symptoms including nausea, vomiting, headache, chills, drowsiness, breathing difficulties, cardiovascular collapse, or death;31,32 however, systemic symptoms are rare.33 Mild localised hypersensitivity reactions can occur (e.g. rash, urticaria, itching), but anaphylaxis is uncommon.34
Treatment—Initially the victim should be prevented from rubbing the area or performing vigorous muscular activity, as this will lead to greater discharge of attached nematocysts and venom movement into the general circulation.35
On-site first aid consists of flushing the affected area with sea water to help remove any adherent tentacles;28 careful removal of tentacles with forceps may be required.
Vinegar, which is used successfully to treat box jellyfish stings in north Australia,28 is contraindicated in New Zealand as it causes additional discharge of Physalia nematocysts, leading to a greater envenoming.36 Fresh water may also cause a discharge of nematocysts to a lesser extent, but it is acceptable to initially flush the area with fresh water if sea water is not available.
Traditionally, ice or cold packs were recommended for pain relief following Physalia stings;37 however, a recent randomised controlled trial has shown significant benefit of hot water over cold packs.33 Hot water immersion or showers should now be considered the treatment of choice for Physalia envenoming. The technique as described (below) for fish stings should be followed, or alternatively a hot shower may be all that is required to alleviate pain.
Further treatment consists of ensuring adequate pain relief with topical anaesthesia and simple analgesics (e.g. paracetamol), or parenteral administration of an opioid in severe cases. Infection, hypersensitivity reactions, or systemic symptoms are rare complications; monitoring and supportive care should be undertaken if required. There is no antivenom available for Physalia stings.
Description—Stingrays are found throughout New Zealand’s coastal waters, generally in shallow intertidal areas such as sheltered bays, river mouths, and other sandy regions.38 They are cartilaginous fish with a characteristic round, flattened body, and a thin tail (Figure 6). The tail contains at least one serrated spine on the dorsal surface; each spine has two ventrolateral glandular grooves containing the venom glands surrounded by the epidermis.38,39
Stingrays are not belligerent and do not attack humans if unprovoked. The majority of stingray injuries are to the lower limbs and usually occur when swimmers or divers accidentally step on them. Injuries can also occur when fishermen find stingrays in their nets or on their lines.40
Signs and symptoms—The most significant concerns following a stingray strike are the risk of traumatic injury, envenoming, and bacterial wound contamination.41,42 Such strikes may cause lacerations or puncture wounds, which may involve direct injury to tendons, muscles, nerves, blood vessels or internal organs.39 Associated envenoming may cause intense local pain, oedema, and muscle cramps; local blistering or necrosis can also occur and may be extensive.40,41 Serious injury or death, though rare, has occurred due to exsanguination or direct trauma to vital organs (venom may contribute to the internal organ damage from such injuries), and from complications such as septicaemia or tetanus infection.41,43–45 Systemic symptoms, though uncommon, may include nausea, vomiting, diarrhoea, hypotension, syncope, salivation, tremor—and in rare cases convulsions, arrhythmias, or circulatory collapse.46
Treatment—First aid consists of flushing the affected area with fresh water (sea water will suffice if fresh water is unavailable). Flushing assists in the removal of venom and barb fragments. Any haemorrhage must be controlled with local pressure. Stingray venom is heat labile,47 and much pain relief can therefore be achieved through the application of heat to the wound.42 Hot water immersion can be of considerable benefit and should be trialled at an optimum temperature of around 45°C for 15 to 20 minutes, taking care not to cause a thermal burn.48 The water temperature should be checked before immersion to ensure water temperature is bearable without injury.
If pain subsides, immersion should continue for up to 2 hours. Ensure the water remains at around 45°C. However, if pain relief is not achieved in the first 15 to 20 minutes, the procedure should be abandoned.
Early exploration and debridement of the wound is essential in all cases. All patients should be transported to a hospital as soon as practical for definitive wound management. Secondary infection is a significant cause of morbidity.41,49
All foreign matter, including retained sting fragments and any non-viable tissues, must be removed.50 Local anaesthesia or a regional nerve block should be used, but avoid adrenaline as this delays microvascular clearance of venom, thereby aggravating necrosis.46 Deep wounds may require debridement under general anaesthesia. Spines are usually radiopaque, and X-ray examination should be used to ensure removal of all fragments. Ultrasound may be required if there are still doubts regarding retained spines.39 Following debridement, the area should be thoroughly cleaned and left open to granulate and heal by secondary intention.41
Infiltration of the wound area with local anaesthetic may be required in the event of severe pain.41 Regional nerve block and/or parenteral opioids may also be required.51 There is no specific antivenom available. Supportive care should be undertaken for any systemic symptoms.
Stingray strikes may introduce a range of marine bacteria into a wound, or the spine may break and contaminate the site. Sequelae to these events include ulceration, infection, necrotizing fasciitis, and osteomyelitis.41,49 Broad-spectrum prophylactic antibiotics are not necessary for all wounds.42 However, they are indicated where there is considerable foreign material present, if there is a delay of 6 hours or more in wound debridement, or if the wound is deep.41,42
If infection is evident, then a broad spectrum parenteral antibiotic regimen is advised.52 Subsequent culture results should be used to determine the best antibiotic for continued management (specify seawater involvement when submitting a swab or specimens for microbiological analysis).53 Ensure tetanus prophylaxis is up to date following any stingray wound. All patients require medical review within 1 to 2 days, to detect any early evidence of wound necrosis or infection.41
Description—New Zealand’s coastal waters are host to a range of venomous fish and sea urchins. Most of these fish are classified within the Scorpaenidae family (scorpion fish) (Figure 7) and come in a wide variety of sizes, shapes, and colours.
Apart from stingrays, further common venomous fish in New Zealand include spiny dogfish (Squalus acanthias) (Figure 8) and elephant fish (Callorhinchus milii) (Figure 9), plus the brown bullhead catfish (Ameiurus nebulosus)—an introduced freshwater catfish (Figure 10).
These venomous fish have external spines, which, depending on the species, may be located on a variety of positions on the fish including the dorsal (common), pectoral, shoulder, pelvic, opercular, anal, and caudal regions.
The different fish venoms have not been studied extensively, but are considered to be heat labile and all produce a similar toxic course.47
Puncture wounds can also be caused by a variety of sea urchins, including kina (Evechinus chloroticus) (Figure 11) which are grouped within the Echinodermata phylum. Sea urchins have two venom apparatus: external spines and pedicellariae (small grasping organ that is covered by venom-producing glandular tissue).54 Injuries typically occur to the feet or hands after victims step on or handle fish or sea urchins.55–57
Signs and symptoms—Symptoms are generally restricted to severe local pain, which can spread to the whole of the affected limb.56,58,59 Mild, non-specific systemic effects can also occur (including nausea, diaphoresis, and hypotension).55,60 Systemic symptoms are thought to be the result of circulating venom.61 In rare instances, sea urchin stings induce a delayed type hypersensitivity reaction. Clinical effects include local pruritus and erythema—along with vesicular eruptions, paraesthesia, malaise, and myalgia.62,63
Treatment—Initial first aid consists of flushing the affected area with fresh water, control of any haemorrhage, and hot water immersion (as outlined for stingray stings). While it is unusual for fish spines to break off, spines of sea urchins can commonly fracture and remain lodged in the wound. Protruding sea urchin spines can be removed using forceps. Fish and sea urchin spines are typically radiopaque and an X-ray or ultrasound can help identify any difficult-to-remove foreign material. If there is evidence of retained fragments, surgical exploration and debridement must be undertaken.
It is especially important for sea urchin stings that all foreign material is removed, as long-term lesions—such as chronic granulomas of various aetiologies and histologies (including sarcoidal)—can occur.64,65 These granulomas are sometimes accompanied by fibrosis, necrosis, or microabscesses. Some represent non-specific foreign body inflammatory reactions, and others are considered delayed type hypersensitivity reactions to an unknown antigen.65
Further treatment of fish and sea urchin injuries includes adequate pain relief, control of infection, tetanus prophylaxis, and (if required) supportive care for any systemic symptoms.
Description—Sea snakes are a diverse group of front-fanged venomous snakes that belong to the Elapidae family. They vary in both size and colour, with most species growing to 1.2 to 1.5 m in length (Figure 12). Sea snakes are distributed mainly in warm tropical waters of the Indian and Pacific Oceans, with the majority found either close to the shore or around coral reefs.
One pelagic species, the yellow bellied sea snake (Pelamis platurus), is widely distributed from the east coast of Africa across the Indian and Pacific Oceans, south to New Zealand and across to the western coast of the Americas.66 Another species, the banded or yellow-lipped sea krait (Laticauda colubrina), has a wide distribution throughout the Pacific.
These two snakes are not common in New Zealand’s coastal waters, but they may occasionally beach themselves around the northern coast of New Zealand.67 It is estimated that only about a handful of these snakes wash up each year.68 Worldwide sea snake bites are encountered very infrequently and, to our knowledge, no cases of envenoming have been reported in New Zealand. Even so, there is a risk that envenoming could occur if a beached specimen is handled.
Signs and symptoms—All species of sea snake possess similar venom and therefore cause similar signs and symptoms; several attributable to myotoxins. Although it is estimated that 80% of bites result in no or trivial envenoming, there is the risk of severe and life-threatening effects occurring following bites.69 If envenoming does occur, there is often an asymptomatic time interval, ranging from one to several hours, before the onset of systemic symptoms.
Systemic toxicity is usually heralded by myolysis; patients typically develop significant muscle aches and pain, sometimes in association with weakness. Associated myoglobinuria may lead to renal effects including acute renal failure. Patients can also develop a flaccid paralysis with ptosis, ophthalmoplegia, and depressed or absent deep tendon reflexes. This may progress to more severe paralysis leading to full respiratory arrest.66,69,70
Treatment—Following envenoming, appropriate first aid consists of applying a pressure immobilisation bandage as early as possible to retard venom transport via the lymphatic system.71
Pressure immobilisation, particularly the immobilisation, appears to be the most effective method to minimise the systemic spread of snake venom.72 It consists of applying a broad compression bandage over the bitten area (as firmly as that used for a sprained ankle) followed by a second firm bandage applied from the tip of the limb heading proximally toward the body to cover as much of the limb as possible. A splint or sling should then be used to immobilise the affected region. The patient should remain completely immobilised for transport to hospital.73
If there is evidence of systemic envenoming, definitive treatment consists of administering antivenom. CSL Polyvalent Snake Antivenom is suitable and this resource is available from the Auckland Hospital Pharmacy. Supportive care of an envenomed patient is probably necessary; this can include management of myolysis, paralysis, and their complications.
IV fluids to help maintain urine output are required should myolysis become evident, and urinary alkalinisation may also be helpful. However, any developing renal failure or hyperkalemia may mandate haemodialysis. Atropine and neostigmine may provide short-term reversal of respiratory paralysis.74 In the event of respiratory compromise, early consideration for intubation and artificial ventilation is recommended. Following appropriate treatment the prognosis is good.
New Zealand has a very small number of venomous creatures, and mortality from envenoming is low. In some circumstances, however, there is the potential for prolonged morbidity if appropriate treatment is not initiated. Because these cases of envenoming are uncommon, this review has been written to assist the healthcare provider to identify the species in cases of likely envenoming, and provide the appropriate first aid and definitive treatment to ensure a satisfactory outcome for the patient.
Competing interests: None known.
Author information: Robin J Slaughter, Poison Information Officer; New Zealand National Poisons Centre, University of Otago, Dunedin; D Michael G Beasley, Medical Toxicologist, New Zealand National Poisons Centre, University of Otago, Dunedin; Bruce S Lambie, Emergency Physician, Dunedin Hospital, Dunedin;
Leo J Schep, Poison Information Specialist, New Zealand National Poisons Centre, University of Otago, Dunedin
Acknowledgements: We thank Dr John Fountain (New Zealand National Poison Centre) for his helpful suggestions; Justine Schep for copyediting the manuscript; Dr Phil Bishop and Ken Miller (Department of Zoology, University of Otago) and Mike Barker (Department of Marine Science, University of Otago) for assistance with the photographs. We also wish to acknowledge contributions of photographs and the helpful suggestions of Malcolm Francis from the National Institute of Water and Atmospheric Research Ltd.
Correspondence: Robin J Slaughter; New Zealand National Poisons Centre, University of Otago, P. O. Box 913. Dunedin, New Zealand. Fax: +64 (0)3 4770509; email: firstname.lastname@example.org
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