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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.
Katipo and Redback spidersDescription—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.
White tailed spiderDescription—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
JellyfishDescription—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.
StingraysDescription—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
Other venomous marine puncturesDescription—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.
Sea SnakeDescription—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.
SummaryNew 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: robin@poisons.co.nz
References:
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