Full Text

Molecular, Clinical and Environmental Toxicology.
Volume 2: Clinical Toxicology 233

Edited by A. Luch
© 2010 Birkhäuser Verlag/Switzerland
Venomous animals: clinical toxinology

Julian White
Toxinology Department, Women’s and Children’s Hospital, North Adelaide, Australia
Abstract. Venomous animals occur in numerous phyla and present a great diversity of taxa,
toxins, targets, clinical effects and outcomes. Venomous snakes are the most medically sig-
nificant group globally and may injure >1.25 million humans annually, with up to 100 000
deaths and many more cases with long-term disability. Scorpion sting is the next most impor-
tant cause of envenoming, but significant morbidity and even deaths occur following enven-
oming with a wide range of other venomous animals, including spiders, ticks, jellyfish,
marine snails, octopuses and fish. Clinical effects vary with species and venom type, includ-
ing local effects (pain, swelling, sweating, blistering, bleeding, necrosis), general effects
(headache, vomiting, abdominal pain, hypertension, hypotension, cardiac arrhythmias and
arrest, convulsions, collapse, shock) and specific systemic effects (paralytic neurotoxicity,
neuroexcitatory neurotoxicity, myotoxicity, interference with coagulation, haemorrhagic
activity, renal toxicity, cardiac toxicity). First aid varies with organism and envenoming type,
but few effective first aid methods are recommended, while many inappropriate or frankly
dangerous methods are in widespread use. For snakebite, immobilisation of the bitten limb,
then the whole patient is the universal method, although pressure immobilisation bandaging
is recommended for bites by non-necrotic or haemorrhagic species. Hot water immersion is
the most universal method for painful marine stings. Medical treatment includes both gener-
al and specific measures, with antivenom being the principal tool in the latter category.
However, antivenom is available only for a limited range of species, not for all dangerous
species, is in short supply in some areas of highest need, and in many cases, is supported by
historical precedent rather than modern controlled trials.
Introduction
Venom appears to have been a success story in evolution because venomous

animals are found in such a range of taxa, but the success is muted since most
animals remain non-venomous. Logically it follows that venom is not the
answer to all life’s challenges, so how does it benefit those animals that pro-
duce it? Venom appears to have two main functions; prey acquisition and pro-
cessing, and defence against predators. The value mix between these two com-
peting functions varies between animal groups, but for those venomous ani-
mals most likely to cause venomous harm to humans, notably snakes, scorpi-
ons, spiders, and jellyfish, prey acquisition seems to predominate. The honey
bee, Apis mellifera, is the obvious exception, as the sting, with attached venom
gland, is purely defensive, having no role in prey acquisition, but here it is not
venom toxicity that affects humans, but venom allergy. So vast is the range and
diversity of venomous life on earth that a single chapter cannot cover more than
some key elements and groups, a caveat that readers should be cognisant of.
234 J. White
Epidemiology
For most venomous animals for much of the world, detailed statistics on the
number of humans bitten or stung, envenomed, or killed each year are unavail-
able. Published data are replete with conjecture, estimates, or guesstimates,
with variable validity. It is clear, however, that certain taxa of venomous ani-
mals cause significant morbidity and mortality amongst humans. Top of this
list are venomous snakes, with current estimates of >2.5 million cases and
around 100 000 deaths per year [1]. Subsequent analysis has indicated that
these estimates are likely on the high side, with low estimates nearer 1.2 mil-
lion cases and 20 000 deaths annually [2] (Tab. 1). These figures hide the huge
toll of morbidity after snakebite, which affects far more cases than fatal out-
comes, and often results in long-term suffering, and social and economic loss
[3]. That the snakebite toll is greatest in the rural tropics of the developing
world [4], where poverty, poor education and under-resourced health systems
combine to minimise effective care, is an ongoing tragedy of human existence,
made worse by the effects of natural disasters [5].
After snakebite, scorpion stings likely account for many medically significant
cases and incidence has been estimated as >1.2 million cases each year [6].
Mexico alone documents >200 000 cases requiring hospital care annually [6, 7].
In some regions scorpion stings are more frequent than snakebites; North Africa
is an example. Deaths are increasingly uncommon, perhaps as a result of
antivenom use plus higher standards of hospital care, but children remain at risk
[6–8].
Spiderbite is undoubtedly common [9], as are spiders [10], but most bites
are medically trivial and nearly all medically significant bites can be ascribed
to just a few groups of spiders: widow spiders (Latrodectus), recluse spiders
(Loxosceles), banana spiders (Phoneutria) and Australian funnel-web spiders
(Atrax, Hadronyche) [9, 11–13]. Deaths are rare.
Table 1. Summary of most recent published data on snakebite epidemiology globally [2]
Region Envenoming Deaths
Low estimate High estimate Low estimate High estimate
Asia 237 379 1 184 550 15 385 57 636

Australasia 1099 1260 2 4
Caribbean 1098 8039 107 1161
Europe 3961 9902 48 128
Latin America 80 329 129 084 540 2298
North Africa and Middle East 3017 80 191 43 78
North America 2683 3858 5 7
Oceania 361 4635 227 516
Sub-Saharan Africa 90 622 419 639 3529 32 117
Total 420 549 1 841 158 19 886 93 945
Venomous animals: clinical toxinology 235
Jellyfish encompass a vast range of species that share a common stinging

mechanism, the cnidocil or nematocyst, an individual stinging cell that both
makes and delivers venom [14, 15]. These cells can be numbered in the mil-
lions in the tentacles of large jellyfish, but while most species can induce local
discomfort in humans, few can cause medically significant envenoming and
almost none, lethal stings [14–16]. The clear exception, the Australo-Pacific
box jellyfish (e.g., Chironex fleckeri), still occasionally kills humans, but in
tiny numbers, almost unmeasurable compared to snakebite [14–18]. However,
this threat has resulted in modified human behaviour in some at-risk regions,
with consequent drops in rates of envenoming cases [19].
Stinging fish also will affect large numbers of humans, but while pain, how-
ever brief, can be severe, life is rarely at risk [15, 20].
Venomous animals: Taxonomy
Venomous animals are represented in 6 phyla, across 20 subphyla or classes,

including multiple vertebrate taxa [21]. A detailed discussion of the taxonomy
of venomous animals is beyond the scope of this chapter.
Venoms: A clinical overview
Venom can be defined as compounds or mixtures of toxins that are deleterious

to another organism at a certain dosage [22]. Most venoms contain an array of
toxins, usually with a diversity of actions. A single toxin can have multiple
actions. For any single species of venomous animal, there will be a degree of
variability in the composition of venom between individuals and even a single
individual may have slight variations in venom composition over time
[23–26]. Such variability can be seasonal or ontogenetic. The range of actions
of toxins contained in a venom can reflect the variable types of prey that must
be acquired, but may also reflect natural and rapid experimentation within
populations of venomous animals [24, 25]. With such an array of toxins avail-
able, it might be expected that many would combine to cause toxicity in
humans, but experience has shown that often clinical effects of significance
can be attributed to just a few distinct toxins, or classes of toxins and it is these
that are discussed further [27–29]. Venom classification is therefore consid-
ered below in terms of clinical effects in humans.
Neurotoxins
Paralysis
Paralytic neurotoxins are a recurring theme amongst venomous animals, being
present in such diverse taxa as snakes, ticks, jellyfish, cone snails and octo-
236 J. White
Table 2. Major venomous animal groups commonly associated with neurotoxic paralysis [163]
Type of animal Examples Type of neurotoxin#
Elapid snakes Kraits Pre- and postsynaptic

Coral snakes Postsynaptic
Mambas Dendrotoxins and fasciculins
Cobras (some) Postsynaptic
King cobra Postsynaptic
Selected Australian snakes; tiger snakes, Pre- and postsynaptic
taipans, rough scaled snake, death adders,
copperheads
Sea snakes Postsynaptic
Viperid snakes Mohave rattlesnake (some) Presynaptic
Neotropical rattlesnakes Presynaptic
Sri Lankan Russell’s viper Postsynaptic
Ticks Paralysis ticks, Ixodes and Dermacentor spp. Presynaptic
Cone shells Variety of Conus spp. Conotoxins
Octopusses Blue ringed octopuses, Tetrodotoxin
Hapalochlaena spp.
#
Definite, predominate or most likely major site of action/type of toxin in humans.
puses (Tab. 2). They are well characterised in snakes, where their primary site
of action is the neuromuscular junction (Fig. 1), causing progressive flaccid
paralysis, although the precise mechanism of action varies between toxins,
often with multiple toxin types represented in a single venom [27–29]. The
mode of action can be of great clinical relevance, affecting response to antiven-
om therapy. A number of other taxa possess paralytic neurotoxins, also caus-
ing flaccid paralysis, but their site and mode of action differ, again with clini-
cal implications centred on duration of paralysis.
Excitation
Amongst invertebrate venomous animals, neuroexcitatory toxins predominate,
especially amongst arthropods, but also amongst some marine animals,
notably a few jellyfish species [21, 30]. The structure and mode of action
varies amongst these toxins, but the prime clinical effect is generally similar,
with rapid, sometimes extreme excitation of portions of the nervous system,
most commonly autonomic stimulation resulting in a “catecholamine storm”
effect, which can be rapidly lethal [31].
Myotoxins
Activated myotoxins induce myolysis and fall into two broad groups: the local-
ly acting type and the systemically acting type, with the latter, in particular, able
to cause potentially devastating and lethal effects as a result of secondary renal
Figure 1. Diagrammatic representation of the site of action of principal neuromuscular junction para-
lytic neurotoxins (original photo/illustration copyright © Julian White).
failure, hyperkalaemia and cardiotoxicity [21, 28]. In most cases myotoxins are
modified phospholipase A2 (PLA2) toxins, sometimes closely related to presy-
naptic neurotoxins [27]. In some cases a single toxin, such as notexin from
Australian tiger snake (Notechis scutatus) venom, possesses both myotoxic and
presynaptic neurotoxic activity, residing in separate portions of the molecule
[27, 32]. Most venom myotoxins are found in snake venoms, although only in
a minority of species, but myotoxic activity does occasionally occur with
envenoming by other animals, including widow spider bites and mass hymenop-
teran stings [33–39].
238 J. White
Blood toxins
Coagulants and related toxins

Snakes have evolved a wide array of toxins to attack the complex haemostatic
system (Fig. 2), and in many cases a variety of distinctly different toxins, with
different targets, may coexist within a single venom [40, 41] (Tabs 3 and 4).
However, more often a particular toxin will predominate in clinical effects on
haemostasis. In the majority of species, this predominant activity will be pro-
coagulant, most often causing either clotting through activation of thrombin,
or direct attack on fibrinogen. While in the laboratory this may result in rapid
plasma clotting, in an in vivo setting, like an envenomed human, the effects
may be rather different, such as rapid consumption of all fibrinogen, causing
hypocoagulability and a tendency to bleed [28, 40–45]. Thus, while these tox-
ins may be characterised as potent clotting agents, their clinical effect may
seem quite the opposite, effectively anticoagulating the blood through con-
sumption of fibrinogen. There are exceptions to this, notably the potent clot-
ting toxins in two Caribbean pit-viper venoms, which clinically cause exten-
sive thrombosis, sometimes lethal [46–50]. Snakes are not the only venomous
animals to specifically target haemostasis; a South American caterpillar with
venom-tipped “hairs” can also cause severe procoagulant coagulopathy and
fibrinogen depletion [51, 52]. Coagulopathy is also reported following stings
by a few scorpion species, but is less well defined [53–55].
Anticoagulants
In addition to the secondary anticoagulant effects of some procoagulant tox-
ins, some snake venoms contain potent true anticoagulant toxins that work by
Table 3. Summary of common target points for venoms interfering with the human haemostatic sys-
tem [163]
Class of toxin Specific activity
Procoagulant Factor V activating

Factor X activating
Factor IX activating
Prothrombin activating
Fibrinogen clotting
Anticoagulant Protein C activating
Factor IX/X activating
Thrombin inhibitor
PLA2
Fibrinolytic Fibrin(ogen) degradation
Plasminogen activation
Vessel wall interactive Haemorrhagins
Platelet activity Platelet aggregation inducers
Platelet aggregation inhibitors
Plasma protein activator SERPIN inhibitors
Figure 2. Diagrammatic representation of the human haemostatic pathways within blood vessels and
some common targets where venom toxins can interfere with this process (original photo/illustration
copyright © Julian White).
inhibiting the haemostatic process (Tabs 3 and 4) [40, 41]. This type of coag-
ulopathy is largely restricted to a minority of snake species and, in most cases,
causes less severe clinical problems than procoagulants [41, 56, 57].
240 J. White
Table 4. Major venomous animal groups likely to cause primary coagulopathy
Type of animal Examples Type of venom action
Colubrid snakes Boomslang, vine snake Procoagulant

Yamakagashi, red necked keelback Procoagulant
Elapid snakes Selected Australian snakes; tiger snakes, Procoagulant
rough scaled snake, taipans,
brown snakes, broad headed snakes
Selected Australian snakes; Anticoagulant
mulga snakes, Collett’s snake,
black snakes, Papuan black snake
Viperid snakes Saw scaled or carpet vipers Procoagulant, disintegrins,
haemorrhagins
Gaboon vipers and puff adders Procoagulant, antiplatelet,
disintegrins, haemorrhagins
Russell’s vipers Procoagulant, haemorrhagins
Malayan pit viper Procoagulant, antiplatelet,
haemorrhagins
North American rattlesnakes Procoagulant, fibrinolytic,
antiplatelet, disintegrins,
haemorrhagins
North American copperheads Procoagulant, anticoagulant,
fibrinolytic, disintegrins
South American pit vipers Procoagulant, Anticoagulant,
(selected Bothrops spp.) fibrinolytic, disintegrins,
haemorrhagins
Asian green pit vipers Anticoagulant, fibrinolytic,
(selected Trimeresurus spp.) antiplatelet, disintegrins,
haemorrhagins
EuroAsian vipers (selected Vipera spp.) Procoagulant, disintegrins,
haemorrhagins,
Insects Latin American caterpillars, Procoagulant
Lonomia spp.
Haemorrhagins
Synergy between diverse toxins can often result in more devastating effects on
prey, or humans, and this is clearly the case with haemorrhagins, found in a
number of snake venoms, mostly based on a metalloproteinase toxin that
directly damages tissue, especially vascular tissue (Tabs 3 and 4) [40, 41,
58–61]. This direct damage promoting bleeding sites when combined with
procoagulants that defibrinate, so preventing thrombotic repair of bleeding
sites, which can lead to very severe clinical effects, especially locally around
the bite site.
Nephrotoxins
Few primary nephrotoxins have been reported from venoms [62, 63], but sec-
ondary renal damage is very much a clinical problem with many snakebites,
and without renal supportive therapy, such as dialysis, can prove lethal
[64–72]. Secondary renal damage can occur through a variety of venom-medi-
ated mechanisms, including coagulopathy, myolysis and hypotension [27, 29].
A particular syndrome, microangiopathic haemolytic anaemia (MAHA), can
occur after envenoming by some snake species, and is characterised by
intravascular haemolysis, thrombocytopenia and renal failure, but the precise
causative mechanisms in envenoming remain to be elucidated [71, 73].
Necrotoxins
Local tissue injury following bites or stings is a common theme across many
taxa, including snakes, spiders, scorpions (but only a very few species), cen-
tipedes and some marine animals such as the box jellyfish (Chironex fleckeri)
and some of its relatives, and some stingrays [3, 11, 12, 18, 19, 21, 29, 45,
74–79]. The mechanism of injury is incompletely understood in most cases,
although specific necrotoxins, such as sphingomyelinase D (from recluse spi-
ders, Loxosceles spp.), are known [80–84], and the role of myotoxic PLA2 in
snake venom indicates a prime role in local tissue injury [81], while hyalur-
onidases are implicated in other venoms [85]. In many cases it is likely that
local tissue necrosis is mediated by a complex interplay between several toxin
effects and natural defence mechanisms within the victim.
Other toxins
In addition to the specific toxins and effects listed above, most venoms have a
number of other, less well understood components, the clinical significance of
which is usually unknown. This group, which may include the bulk of all toxin
types, includes many low molecular weight toxins, including peptides. The lat-
ter are of increasing interest as potential templates for new pharmaceuticals,
but undoubtedly some have significant clinical actions. Also within this group
can be included a very diverse and important mix of toxins originating in cone
snails (Coniidae; Conus spp. and some related hunting marine snails). Broadly
classified as “conotoxins”, these highly potent toxins are diverse in pharmaco-
logical effects and are already proving a rich area for new drug development
[86].
Envenoming: A management overview
Envenoming will vary in severity, depending on the relative toxicity of the

venom involved, the amount of venom actually delivered, the size of the vic-
tim, any pre-existing medical conditions, and environmental/social considera-
tions [21, 28, 29]. It follows that even for a highly dangerous species, such as
242 J. White
an Australian taipan snake (Oxyuranus scutellatus), the degree of envenoming

and risk to life is not constant; while most cases may develop life threatening
envenoming, often quite rapidly, there will still be some cases who never
develop significant envenoming. Predicting which course each case will take,
in the early stages, may be difficult to impossible, so it is a general rule that
any case of definite or likely bite/sting by a medically significant venomous
animal should be managed initially as a high priority medical emergency.
Inevitably, a number of cases, perhaps the majority in some geographic
regions, will ultimately prove to be only minor, with minimal or no envenom-
ing. This is not a justification for assigning a low initial priority to bite/sting
cases who seem apparently well on presentation. Envenoming can develop
quickly, but can also be delayed in onset, yet still potentially lethal. Health
professionals, except in a few situations, are unlikely to see or treat large num-
bers of bite/sting cases, so maintaining knowledge and skill can be problem-
atic. It follows that in most situations, consultation with a doctor who is an
expert in clinical toxinology is advisable, if optimal patient outcomes are to
be ensured.
First aid
Pre-hospital care can, quite literally, be the difference between life and death
in cases of envenoming, particularly for those species causing rapid severe
effects such as respiratory paralysis and cardiotoxicity. There are few research-
proven first aid methods for envenoming, yet many methods are used or rec-
ommended, most of which have either no benefit, or more commonly, cause
actual harm [87–106]. Appropriate envenoming first aid should follow three
principles; (1) do no harm, (2) immobilise venom to prevent it reaching target
sites, and (3) support vital functions (airway, breathing, circulation) [107]. The
last of these, supporting vital functions, if adopted universally, would likely
save life in many cases of envenoming. It is often overlooked, but the impor-
tance of ensuring airway patency, respiration and circulation cannot be
overemphasised. Avoiding causing harm is a vital principle, also generally
overlooked. Table 5 lists well-known first aid methods that cause actual harm
in envenoming and should not be used. Table 6 lists those few first aid meth-
ods shown to have value in envenoming.
Approach to management
As outlined earlier, two principles should guide care of the definitely or poten-
tially envenomed patient: (1) all cases should be initially managed as poten-
tially severe, and (2) expert advice should be sought at the earliest opportuni-
ty [107]. Locating expert advice will vary between countries, but in most
cases, a major poisons information centre may be a reasonable first choice.
Table 5. Harmful or ineffective first aid methods that should not be used; only some prominent meth-
ods are listed
Method Problems
Tourniquet Direct pressure injury under narrow band tourniquet

Severe pain
Ischaemic limb damage (may include loss of limb)
Potential for massive envenoming on release
Patent suction devices Local tissue injury
Increased local necrosis
Painful
Only minor venom removal
No proven benefit in reducing envenoming
Local scarification, wound Local tissue injury
excision, amputation Painful
May increase rate of envenoming
May introduce local infection
Can cause significant bleeding and blood loss
Electric shock Dangerous
Chemical application Potential toxicity
Snake stone No proven benefit in reducing envenoming
Traditional healers No proven benefit in reducing envenoming
Cause potentially lethal delays in seeking definitive care
Consultant clinical toxinologists are currently a rare commodity within health

systems, but this may improve over time, as training courses output more grad-
uates.
The first priority when assessing a case of bite/sting with definite or poten-
tial envenoming, is to ensure vital systems functioning (airway, breathing, cir-
culation). One must be aware of the possibility that coagulopathy may be pres-
ent or develop, and physical interventions, such as i.v. line insertion, should be
chosen with care to avoid causing uncontrollable bleeding problems. In the
presence of coagulopathy, certain i.v. sites (subclavian, jugular, femoral) and
actions (e.g., i.m. injections, fasciotomy, tracheostomy) are hazardous and
should be avoided if at all possible. The second priority is establishing a work-
ing diagnosis, from which more definitive care, including antivenom therapy,
will follow where indicated and available.
Diagnosis of envenoming
Diagnosis is a crucial early step in managing envenoming [28, 107]. Two parts
of diagnosis can be discerned: (1) determining the cause of envenoming, from
which more specific treatment can follow, and (2) determining the extent of
244 J. White
Table 6. First aid methods considered effective or possibly effective and not harmful
Method Useful for
Immobilisation of bitten All snakebites and other causes of systemic envenoming

limb and whole patient
Australian pressure All non-necrotic or haemorrhagic snakebites, including all
immobilisation Australian snakes, kraits, coral snakes, king cobra, sea snakes,
bandage technique mambas, selected cobras, South American rattlesnakes;
Australian funnel-web spiders;
Possibly (not proven experimentally or by clinical trial):
Buthid scorpions, cone shells, blue ringed octopus
Cardio-pulmonary resuscitation Any bite/sting causing impaired cardiac or respiratory function
Removal of attached organism Any bite/sting, to prevent ongoing envenoming; specifically
important to remove bee sting/venom gland, paralysis tick,
Helodermatid lizard
Hot water (to 45 °C; All venomous fish stings, stingray injuries, jellyfish stings
care to avoid hotter water (not yet proven for box jellyfish stings)
and thermal injury)
Direct wound care/staunching Injuries affecting major blood vessels, such as some stingray
bleeding injuries
Copious fluid irrigation of All cases with venom in the eye, particularly spitting cobras
the eye
Removal of rings, other May reduce the chance of local swelling causing ischaemic
constricting objects from damage
limbs, especially digits
Reassurance Calming the patient and keeping them still may reduce the
rate of onset of envenoming and development of anxiety-
related symptoms
Retrieval of the envenoming If the culprit has been killed or captured and can be safely
animal transported with the patient, do so, as this will assist in
accurate diagnosis;
CAVEAT: Do not waste time or risk further bites/stings to
kill/capture the culprit
envenoming, including severity, progression, systems affected, and evident

complications, which will guide the degree and nature of any therapeutic
response. All three elements of the diagnostic process, history, examination,
and laboratory tests, play a role, but the extent to which each may contribute
varies with the venomous animal concerned. For many species, laboratory
tests may add little to diagnosis and history will be crucial. However, the his-
tory may give no early clue to diagnosis, particularly when the presentation is
symptom-driven, perhaps without any suggestion of a bite/sting occurring or
being causative. Thus, in unexplained cases of coagulopathy, paralysis, neu-
roexcitation, myolysis, renal failure, collapse, convulsions, or local tissue
injury, envenoming may sometimes be an important differential diagnosis
needing consideration and exclusion.
History
Ideally, a toxinological history will answer some or all of the following ques-
tions: (1) is a bite/sting a likely diagnosis, (2) do the circumstances (including
a description of the assailant, if available) and geographic location of the
bite/sting indicate likely assailants, (3) does the patient have any symptoma-
tology suggestive of envenoming, local or systemic, and does the pattern of
symptoms indicate likely assailants, (4) are there any patient-related factors
that might influence diagnosis, severity of envenoming, or outcome, and (5) is
the patient in need of treatment urgently, or likely to need treatment later?
The key areas for questioning are shown in Table 7, but these are designed
to fit all common situations, while in the real world, the list of possible
assailants will likely be narrower and so the range of questions required will
be less. Often the key diagnostic features emerge early and allow a more
directed approach to confirm the likely assailant and therapeutic response
required. However, some caution is required, because any venomous animal
can, on occasion, cause an atypical presentation.
Examination
Examination is directed towards finding evidence that a bite/sting has
occurred, and if any local or systemic envenoming effects are present. Where
the history has not clearly identified a likely assailant, examination findings
may help to narrow diagnostic possibilities. Key areas for examination are
shown in Table 8. As for history, this list is designed to cover many common
possibilities and in the real world, a more directed examination is often possi-
ble. Again, caution is required, to ensure no key signs are missed because early
assumptions are made about the likely culprit.
Laboratory tests
Specific testing for evidence of envenoming is only applicable for some ani-
mals, mostly snakes, while no lab tests are routinely indicated for bites/stings
by many non-snake venomous animals. Key lab tests are shown in Table 9, and
as with history and examination, selection of which tests to request, if any, will
be determined by the circumstances in each case, particularly the possible
assailants to be considered.
Urgent care
The acutely and significantly envenomed patient presents an urgent case requir-
ing prompt, accurate assessment and directed treatment. The patient presenting
in extremis will require immediate life supportive care, then best-guess diagno-
sis of the likely culprit(s) and urgent specific treatment to cover these animals,
followed by more considered assessment and treatment, once the acute emer-
gency is controlled. In such a situation, it may still be possible to rapidly ascer-
tain key diagnostic features, such as presence of coagulopathy, paralysis, myo-
246 J. White
Table 7. Important points in a toxinological history
Area of questioning Relevance
Circumstances of bite/sting May indicate likely degree of envenoming

(brief glancing attack versus chewing
bite/prolonged sting), but even glancing bite
can sometimes cause severe envenoming;
May indicate likely culprit
Geographic location Can narrow range of possible culprits
Description of animal Can help determine likely culprit, but beware
colour variability, especially in snakes
Number of bites/stings Multiple bites/stings may cause increased
envenoming
Immediate symptoms May indicate possible culprit;
May indicate likely severity
First aid, including timing May influence onset of envenoming symptoms
and signs
Onset and nature of any symptoms Can determine pattern and severity of
Specifically enquire about symptoms of: envenoming, which can indicate likely identity
• Paralysis (drooping/heavy eyelids, of culprit and requirement for treatment
slurred speech, drooling, difficulty walking,
moving limbs, holding head up, breathing,
swallowing)
• Myolysis (muscle weakness, pain,
tenderness, red to black urine)
• Coagulopathy (bleeding gums,
haematemesis, haematuria, melaena,
sudden bruising)
• Renal damage (altered urine output, thirst)
• Cardiotoxicity (palpitations, collapse)
• Necrotoxicity (bite/sting site pain,
blistering, bleeding, darkened or
blue-black skin, eschar formation)
• Neuroexcitatory envenoming
(increased sweating, salivation,
lacrimation, piloerection, respiratory
distress with frothing (pulmonary oedema),
fasciculation of muscles, including
tongue, nystagmus)
• Non-specific (headache, nausea, vomiting,
abdominal pain, diarrhoea, dizziness,
collapse, convulsions, metallic taste in
mouth)
Medications May identify medications that might interact
with envenoming or skew interpretation of lab
tests (e.g., warfarin and coagulopathy)
Past history May identify pre-existing conditions of
relevance to envenoming
Allergies Particularly important to determine if there is
a potential allergy to any treatment, such as
antivenom, OR if the symptoms could be more
related to allergy than envenoming
Table 8. Key points in the toxinological examination
Area of examination Relevance
Bite/sting site Is there evidence of multiple bites/stings, ongoing

bleeding (coagulopathy), bruising (coagulopathy),
blistering/bleb formation (necrosis), increased
sweating (neuroexcitatory envenoming), major
swelling (fluid shifts, impending shock), significant
mechanical trauma (stingray), attached tentacle
(jellyfish) or stinger (honey bee)?
Bitten/stung region/limb Is there evidence of venom spread (lymphadenopathy
or tenderness, lymphangitic tracking) or regional
envenoming (spreading blistering/blebs, ecchymosis,
increased sweating)?
Critical systems (cardiac, respiratory) Is there hyper/hypotension, brady/tachycardia, cardiac
arrhythmia, cyanosis/respiratory distress, use of
accessory muscles? What is Glascow coma score
(GCS)?
Neurological systems Is there evidence of paralytic neurotoxicity (cranial
nerve signs like ptosis, ophthalmoplegia, fixed dilated
pupils, drooling, dysarthria, dysphagia, altered
taste/smell, limb muscle weakness, reduced or absent
deep tendon reflexes)?
Is there evidence of neuroexcitatory envenoming
(increased local, regional, or generalised sweating,
piloerection, increased salivation, lacrimation,
muscle fasciculation, including tongue, pulmonary
oedema)?
Haemostasis systems Is there evidence of increased bleeding (oozing from
bite site, i.v. sites, gums, elsewhere, bruising, CNS
signs of intracranial bleeding) OR of thrombotic
problems (deep vein thrombosis, pulmonary embolus,
stroke)?
lysis, or neuroexcitation, which will guide the therapeutic response. The same
rapid assessment techniques can be utilised to effectively triage cases with less
life threatening features. Observation of the patient’s face can often show if they
are in significant pain (grimace), if they have any early developing paralytic
features (ptosis, loss of facial tone, partial ophthalmoplegia; Fig. 3), or neu-
roexcitatory features (increased sweating, lacrimation), or coagulopathy (bleed-
ing bite site, gums; Fig. 4), while a simple check of any i.v. insertion or sam-
pling sites will reveal evidence of coagulopathy (continued ooze, bleeding,
extending bruising), and a check of the bite/sting site will reveal if there is rap-
idly advancing swelling, or early tissue injury features (ecchymotic blistering,
marked dark skin colouration, especially if clear demarcating edges; Fig. 5), or
early neuroexcitation (increased local sweating, piloerection). If major neu-
roexcitatory envenoming is a likely diagnosis, chest auscultation (for signs of
pulmonary oedema) is required. Except where pulmonary oedema is a signifi-
cant risk, most envenomed patients will benefit from early i.v. fluid load.
248 J. White
Table 9. Key laboratory investigations to consider in a case of definite or suspected envenoming. The
actual choice of tests will be determined partly by the type of organism and the clinical setting
Test Relevance Relevant fauna
Whole blood clotting time If substantially prolonged and/or Most snakebites, Brazilian
(WBCT) with weak clot, can indicate Lonomia caterpillars, Iranian
coagulopathy (NOTE: always Hemiscorpius and Nebo
use glass vessel, do control) scorpions, recluse spiders
20-minute WBCT (is blood Simple derivative of WBCT, As above
clotted at 20 minutes?) validated for some snakebites
Coagulation studies Definitive assessment of As above
• INR/prothrombin time coagulopathy; d-dimer may be
• aPPT/PTTK most sensitive early measure
• d-dimer/XDP/FDP of developing coagulopathy
• fibrinogen
Complete blood examination Important in assessing if there As above, plus other fauna
• platelets is haemolysis, MAHA, or that may cause haemolysis,
• haemoglobin (Hb) isolated thrombocytopenia. including severe jellyfish
• blood film for evidence of Early absolute lymphopenia stings, massive hymeno-
haemolysis can be another marker for pteran multiple stings
• white cell and absolute envenoming
lymphocyte count
• reticulocytes (if haemolysis)
Blood chemistry, especially Each parameter specific for Most snakebites, any major
• renal function particular envenoming/complica- systemic envenoming/
• creatine kinase tion, such as renal damage, collapse, envenoming where
(CK, for myolysis) myolysis, haemolysis, haemolysis suspected, such
• electrolytes (particularly K+) hyperkalaemia as mass hymenopteran stings
• bilirubin (if haemolysis)
• glucose (if scorpion sting)
• liver function tests
(LFTs; if haemolysis, myo-
lysis, or if pancreatitis is
suspected after scorpion sting)
Arterial blood gases Principally assessing oxygen- Any bite/sting where
ation, if respiratory compromise, respiratory failure/paralysis
such as in neurotoxic paralysis possible, including selected
snakebites, Australian funnel-
web spider, scorpion, para-
lysis tick, cone shell, blue
ringed octopus, Irukandji
jellyfish envenoming
Bite site wound swabs In Australian snakebites, for Australian snakes;
• venom detection (Australia) venom detection; any infected wound
• culture and sensitivity everywhere, if wound is infected
Specific treatment: Antivenom
In general, the only specific treatment for envenoming is antivenom and this is
only available for some venomous animals.
Figure 3. Ptosis, often the first sign of developing neurotoxic envenoming (Notechis scutatus bite)
(original photo/illustration copyright © Julian White).
Figure 4. Persistent blood oozing from bite area, often indicative of coagulopathy (Pseudechis spp.
bite) (original photo/illustration copyright © Julian White).
250 J. White
Figure 5. Demarcating area of tissue injury, indicative of an area likely of developing necrosis
(Pseudechis australis bite) (original photo/illustration copyright © Julian White).
The era of antivenom therapy for envenoming dates back to the work of
Calmette and others, in the final years of the 19th century [108]. Antivenom is
essentially antibody raised against whole venom(s) or venom fractions in a
domesticated animal (horse, sheep, goat, rabbit) and works by binding to tox-
ins, either at the active site (so rendering them inactive), or elsewhere (allow-
ing clearance) [109, 110]. It follows that a given antivenom contains neutralis-
ing antibody against only those venoms used in the immunising mix, so utili-
ty in treating envenoming by other species is dependent on sufficient antigenic
similarities between venoms [111, 112]. For some venoms, there is consider-
able similarity with venoms from other, usually related, species. This provides
cross-specific protection, therefore a particular antivenom may be effective in
treating envenoming by a number of different species. However, such cross-
specific protection is not a universal, or even particularly common, finding. As
a rule, then, antivenom used in treatment should be proven as specific for a
particular species, or group of species [110].
There are a variety of ways of producing antivenom, although all currently
in use start by hyperimmunising an animal [109, 110, 112]. Nearly all antiven-
oms are based on mammalian IgG antibody, most commonly equine (horse).
The IgG can be refined in a number of ways to eliminate contaminants from
plasma that can stimulate adverse reactions. IgG can be further fractionated to
yield fractions of IgG, each with distinct properties, advantages and disadvan-
tages. Whole IgG and Fab2 antivenoms have a prolonged half life, compared
to Fab antivenoms, so they maintain clinically useful blood levels over sever-
al days, important in neutralising late-released venom from a depot at the bite
site, but their larger size limits extravascular spread. Fab antivenoms have bet-
ter extravascular penetration, but at the cost of short half life, measured in
hours, usually necessitating repeat doses or continuous infusion [113–115].
Few Fab antivenoms are available, the principle ones being for North
American pit viper bite (CroFab®) and European adder bite (Viperatab®), but
early experience with these affinity-column-refined ovine (sheep) antivenoms
shows they are relatively safe and effective, but commonly require repeat dos-
ing to counter short half life [113–118]. In North America, an issue of recur-
rence of coagulopathy has raised questions about effectiveness, since this
recurrence is sometimes resistant to further antivenom doses. However, exam-
ination of case experience with the previous equine whole IgG antivenom
shows recurrence was also an issue and other factors may be at play [114].
Arguments have been mounted that whole IgG antivenoms are the most effec-
tive, but traditional manufacture has been associated with high levels of
adverse effects [119–122]. As a consequence, many producers have moved to
Fab2 antivenoms, which are as effective, but generally have been considered to
have a better adverse effect profile, a view now questioned [119–122].
However, development of caprylic acid treatment of whole IgG antivenoms is
claimed to produce a product with high efficacy and a good adverse effect pro-
file, with a further advantage of lower production cost [123–126]. This may
swing antivenom production back towards predominantly whole IgG product.
Horses are by far the predominant host animal for antivenom production
[109–112, 127–129]. They are relatively easy to manage, provide large plas-
ma volumes with regular venesection or plasma pheresis, are comparatively
safe as vectors of disease transmission, and production techniques are well
established [130, 131]. However, equine antivenoms, especially whole IgG,
have been associated with sometimes very high levels of adverse effects [132].
Because of this, a few producers have explored other animals, notably sheep
[113, 115–117, 133]. Ovine antivenoms are now produced by two major pro-
ducers and have proved safe but, because of an increased risk of disease trans-
mission, particularly viral and prion disease, sheep are only practical in the few
countries with certified safe flocks [131]. If new processing steps that can
guarantee removal of infectious agents are developed, this may make ovine
antivenoms more widespread, but the use of caprylic acid purification of whole
IgG equine antivenoms may render such ovine antivenom developments
unnecessary. Goats have also been used in the past and one producer current-
ly uses rabbits for a low output specialised antivenom [134]. Current research
is investigating camels, as these may be easier than horses in some regions,
252 J. White
such as Africa, and camelid IgG can be more readily fractionated into really
small molecular size antivenoms that may open up possibilities for combined
systemic and local use [135, 136]. This work is purely experimental and it is
at present not known if it will translate to commercial production. Another dif-
ferent approach using hens to produce egg-based IgY antivenoms has also
been explored, but a number of problems, including widespread major immu-
nity to such a product, with the potential for severe adverse reactions, appears
at this time to make commercial IgY antivenoms unlikely [137–140]. The
development of genetically engineered antivenom production, using recombi-
nant methods, is at an early stage of development, with no commercial prod-
ucts available as yet, although research is progressing, both into recombinant
production of immunising toxins, and complete recombinant production of
specific antivenom [141–144].
Antivenom theory
Antivenom works by binding specifically to venom toxins and rendering them
inert and/or speeding clearance from the circulation [109, 112, 145]. To be
effective, antivenom must rapidly bind and inactivate/remove all circulating
venom from the circulation, and as far as possible, the rest of the body. This
requires primary intravascular distribution, which is why antivenom should, in
most cases, be given only i.v., not used locally or as an i.m. injection. There
are a few antivenoms for which i.m. injection is advocated or has shown
favourable results [134, 145–158] with some evidence that it is effective,
although this is controversial in light of recent studies [158–162]. However,
these are for organisms with more slowly developing and, in general, non-
lethal envenomings.
The prime requirement for antivenom is therefore i.v. administration of an
initial dose expected to fully neutralise all circulating venom. Except for Fab
antivenoms, most or all of the antivenom will remain in the circulation, yet for
many venoms, key components will exit the circulation to reach their extravas-
cular targets, such as the neuromuscular junction or skeletal muscle. Toxins
acting on the haemostatic system and haemorrhagins act within the intravas-
cular system, so are readily accessible to antivenom. Concentration gradients
between extravascular and intravascular venom levels are likely to draw
extravascular venom back into the circulation, for neutralisation, as intravas-
cular venom levels fall with neutralisation by antivenom. This mechanism
requires high levels of antivenom, compared to venom, explaining the clinical
requirement for adequate antivenom doses initially. Antivenom administered
i.m. will be slow to reach high intravascular concentrations [160, 162], so will
be far less efficacious, particularly for rapid, acute, severe envenoming, as
caused by many snake species. Similarly, locally injected antivenom is unlike-
ly to reach significant blood levels, so will be ineffective against circulating
and distributed venom. Therefore, even if low molecular weight antivenoms
are developed for local injection, there will still be a critical need for simulta-
neous i.v. administration.
What is antivenom effective for?

Antivenom is an effective antidote against venom components that are specifi-
cally covered as antigens for a given antivenom [163]. This implies that antiven-
om must be specific for the type of venomous animal involved, or have proven
cross protection for that animal. It also implies antivenom must be able to
access the venom. This may be difficult for locally sequestered venom, such as
in the bitten limb. It follows that in general, antivenom is far more effective at
neutralising systemic effects than local effects, except for low molecular weight
antivenoms (Fab), which more readily reach extravascular sites. However,
antivenom cannot repair injured tissue, it can only bind to venom with appro-
priate antigenic matching. Therefore, some venom effects that involve damage
to target tissue, such as presynaptic neurotoxicity (terminal axonal damage),
myotoxicity (damage to muscle cells), renal toxicity (direct or indirect renal
damage) and secondary damage from coagulopathy, are not reversible with
antivenom therapy. For this reason it is important to detect systemic envenom-
ing at the earliest opportunity and commence appropriate antivenom therapy,
before such tissue damage is extensive. Equally, this explains why late antiven-
om therapy to remedy such tissue injury is ineffective and generally not war-
ranted. A caveat is that continuing venom absorption from the bite site, causing
ongoing envenoming, requires maintenance of adequate antivenom levels,
which may warrant repeat dosing, even for whole IgG or Fab2 antivenoms.
Clinically, this seems applicable for continuing myolysis. A list of clinical
effects and their responsiveness to antivenom is given in Table 10.
The indications for administering antivenom in a case of envenoming are,
to some extent, specific for each type of venomous animal, and discussing
requirements for each species or antivenom is beyond the scope of this chap-
ter. There are, however, some broad principles that apply in many circum-
stances. Firstly, antivenom should only be given if there is evidence of signif-
icant envenoming, either systemic, or in some settings, local. It is rarely justi-
fied giving antivenom to a patient who exhibits no evidence of envenoming.
Bites/stings by nearly all venomous animals have a significant and variable
rate of “dry bites”, where bite/sting marks may be present, but insufficient
venom is injected to cause medically significant envenoming effects. Just
because a bite/sting is from a highly dangerous species does not mean signif-
icant envenoming will develop. Secondly, in most settings, antivenom should
be given as soon as there is evidence of systemic envenoming developing.
There are exceptions, particularly for those venomous animals that cause pre-
dominantly local effects, but not necrosis, and/or non-specific systemic effects
with a low likelihood of threat to life (e.g., headache, nausea, vomiting, diar-
rhoea, abdominal pain, dizziness). Systemic effects that are virtually always
worrying will usually indicate the need for antivenom (Tab. 11).
Choosing an antivenom
The ideal antivenom will be safe and efficacious at neutralising target venoms.
In regions where polyvalent antivenoms predominate, covering all major med-
254 J. White
Table 10. Key clinical envenoming effects and their responsiveness to antivenom
Toxin activity type Clinical effects and responsiveness to antivenom
Paralytic neurotoxin Flaccid paralysis

• Presynaptic • Resistant to late antivenom therapy
• Postsynaptic • Often reversal with antivenom therapy
• Anticholinesterase • Muscle fasciculation
Excitatory neurotoxin Often causes “catecholamine storm”, massive stimulation of
autonomic nervous system; can be very responsive to antivenom,
but in some cases (some scorpions) must be given early to be
effective
Myotoxin Systemic skeletal muscle damage; may respond to antivenom,
but damage pre-antivenom will remain, causing symptoms and lab
test changes (mainly elevated creatine kinase, CK)
Haemostatic system toxins Interfere with normal haemostasis, causing either bleeding or
thrombosis; often respond to antivenom, as only effective
treatment, but not effective for all venoms
Haemorrhagins Damage vascular wall, causing bleeding; role of antivenom
uncertain, may be helpful
Nephrotoxins Direct renal damage; value of late antivenom uncertain
Cardiotoxins Direct cardiotoxicity; role of antivenom uncertain, controversial
Necrotoxins Direct tissue injury at the bite site/bitten limb; antivenom, given
early, may be of some value, but overall results are not
encouraging
Non-specific systemic Often indirectly mediated; antivenom often very effective at
effects (headache, controlling symptoms
vomiting etc.)
Table 11. Indicators for antivenom. Note only some indicators will be theoretically applicable for any
particular species of venomous animal [191]
Indicators
Any degree of developing or progressing neurotoxic paralysis

Any significant disturbance of haemostasis (except pure secondary disseminated intravascular
coagulation, DIC)
Any degree of significant myolysis
Acute renal damage
Acute haemolysis
Prolonged collapse or convulsions in confirmed envenoming
Major and progressive local swelling
Developing necrosis (except if presenting days later)
ically important species of snakes, there is no absolute need to determine the

type of snake in choosing an antivenom. However, in this setting, knowledge
of the type of snake may allow better prediction of likely progress, complica-
tions and prognosis, all valuable for the patient and the therapeutic process.
In regions where there is a choice of several different antivenoms, without

one that covers all possible snakes in the region, there is an absolute need to
determine the type of snake with a sufficient level of confidence to allow
choice of an appropriate antivenom. There are several possible methods for
determining the type of snake. All have advantages and risks and wherever
possible, combination of several methods is preferred, to assure better accura-
cy of the result. Venom detection has been used as an experimental technique
for many years [164–175]. In Australia and New Guinea there is a unique
commercial snake venom detection kit (SVDK), designed specifically to deter-
mine the most appropriate antivenom to use [176–185]. While certainly use-
ful, it is not useful in every case and suffers from both false-positive and false-
negative results, the likelihood of which are increased with certain test sample
choices. This SVDK was not designed to act as a diagnostic screen for
snakebite and should not be used as such. It is possible that similar snake
venom detection systems may be developed for other regions for which no sin-
gle universal polyvalent snake antivenom is available.
Given the problems of identifying the snake, if a polyvalent antivenom is
not available, why would producers choose to make monovalent or limited
polyvalent antivenoms instead of full polyvalent antivenoms? One reason is
the practical mechanics of antivenom production. If the range of snakes to be
covered is large, and cross protection between species limited, there may be
more different venoms required than is practical, both from an immunising and
vial size perspective. Inevitably a polyvalent antivenom, covering a number of
species, will generally be of higher volume than specific or monovalent
antivenoms for each species. That higher volume may translate into higher
costs or lower costs (reduced range of products required), but will inevitably
result in a higher risk for the patient, because a higher volume of antivenom
must be injected, only some of which is actually therapeutically useful (the
antibody fraction against the particular snake involved in envenoming that
patient). Delayed (type III) hypersensitivity reactions (serum sickness) can
occur with any antivenom, but are more common with high volume antiven-
oms such as polyvalents [109, 117, 121, 136, 139, 148, 152, 160, 163, 186–
190]. Therefore, for the patient, to reduce adverse effects and, in some cases,
cost, a specific or monovalent antivenom is a better choice, providing the iden-
tity of the snake can be reliably determined. Australia and New Guinea have
both specific/monovalent and a polyvalent antivenom against regional snakes.
The SVDK allows preferential use of specific/monovalent antivenoms, rather
than polyvalent antivenom, in most cases, which reduces rates of adverse
effects and cost to the health system. Another option in parts of Australia,
where the range of important venomous snakes is limited, is to use a mixture
of two specific/monovalent antivenoms to cover possible species, where iden-
tity of the snake is not assured [134]. A similar approach is possible in some
other regions.
For each region, clear delineation of the envenoming profile for each impor-
tant species can provide the basis for diagnostic algorithms, as used in Australia
256 J. White
(Fig. 6), which can assist in determining the species involved and is a useful
confirmatory procedure, even if venom detection is available [134, 191].
While the discussion above has been directed to antivenoms against ven-
omous snakes, the principles apply to all antivenoms. However, for most other
venomous animals, if an antivenom exists, it is a specific/monovalent product,
because the range of species required to be covered in any region often does
not warrant a polyvalent antivenom. There are exceptions to this, such as poly-
valent anti-scorpion and/or anti-spider antivenoms, particularly in parts of
South America, North Africa and the Middle East [127–130]. Advising on spe-
cific choice methods for antivenoms in each region is beyond the scope of this
chapter.
Administering antivenom
As discussed earlier, in most settings, acute and rapidly severe envenoming
mandates i.v. administration of antivenom to ensure rapid, therapeutically ade-
quate blood levels. For those few antivenoms where the producer recommends
an i.m. route, the clinician treating the patient should determine if this is advis-
able in the individual circumstances, if necessary in consultation with an
expert (e.g., through a poisons centre or a clinical toxinology service).
The method of i.v. administration will be dictated by several factors: (1) the
volume of the antivenom at the selected dose, (2) the size of the patient, (3)
pre-existing health problems for the patient, (4) the availability of i.v. adminis-
tration equipment, such as sterile i.v. giving sets, i.v. fluids, i.v. pumps etc.
High-volume antivenoms in small children may pose fluid overload issues,
exacerbated by the common practice of diluting antivenom in an i.v. carrier
solution, up to 1:10, such as normal saline or Hartman’s solution. In general,
where practical, such dilution and administration through a giving set is advan-
tageous, because it allows precise control of rate of infusion and may make
adjustments for adverse reactions easier. There are other methods which are
also validated, particularly direct slow i.v. injection of antivenom at the bed-
side, easiest if the total volume is not high [191]. This approach has several
advantages; it requires less equipment, so is generally easier and cheaper, par-
ticularly in less well resourced health systems, and it forces the doctor, who
must give the injection, to be present at the bedside throughout administration.
This makes it far more likely that any adverse reaction will be detected early
and the injection stopped and the reaction promptly treated. With diluted i.v.
infusions there is a risk that staff will start the infusion and then be occupied
with other duties or patients, potentially missing early signs of reactions and so
missing the opportunity to treat early, when treatment will likely be more effec-
tive. In a well-managed hospital setting such risks can be avoided and it is the
author’s practice, in most cases, to give antivenom by diluted i.v. infusion.
Selection of the dose of antivenom is beyond the scope of this chapter,
because it will vary between antivenoms, organisms causing envenoming, and
degree of envenoming. There is one important principle that is universal; dose
is not determined by patient size, therefore children receive the same dose as
Figure 6. Diagnostic algorithms for Australian snakebite; an example of what may be possible if
detailed profiling of envenoming by snake species is undertaken in a given geographic region (origi-
nal photo/illustration copyright © Julian White).
258 J. White
adults. There is no paediatric dose for antivenom. Doses should never be

reduced because the patient is a child.
Adverse reactions
All antivenoms are, by definition, foreign antigens when they are administered
and all have the potential for adverse reactions, both early and late [134, 163,
191, 192]. The more highly purified the antivenom, in general, the lower the
rate of reactions, but as noted earlier, whole IgG antivenoms purified with
caprylic acid, may enjoy comparatively low reaction rates, especially com-
pared with simple whole IgG antivenoms.
The causes of adverse reactions to antivenom are multiple, but contaminat-
ing components in the antivenom are of great importance and may include
pyrogens from bacterial or other contamination, other plasma components as
contaminants, such as albumin, Fc components of fractionated IgG, and ele-
ments of equine plasma that cause allergic responses [109, 119, 121, 136, 191,
192]. In addition, prior exposure to the antivenom or the host animal used in
immunising may stimulate an allergic response, even IgE production in rare
cases. Modern production methods should exclude contamination with live
bacteria or viruses, but prions are harder to exclude, hence the requirement,
particularly applicable to ovine antivenoms, that the host animal is from a
flock/herd certified free of prion disease [131, 132].
The principle early reactions, in order of frequency and severity, are an ery-
thematous rash, by itself of little consequence, rigors indicative of a pyrogenic
reaction, and least common, a significant systemic allergic reaction, often
characterised as “anaphylaxis”, although true IgE involvement occurs only in
the minority of cases, with complement activation by the antivenom being a
more common aetiology. The principle delayed reaction is serum sickness and
this is partly dependent on the volume of antivenom administered; the higher
the volume, the greater the risk.
For early reactions, other than simple rash, the first response should be to
stop the antivenom infusion. If there is a major systemic allergic reaction, clas-
sic treatment for anaphylaxis is warranted, including adrenaline (epinephrine),
i.v. fluids, resuscitation, as indicated. Detailed discussion of the management
of anaphylaxis is beyond the scope of this chapter and readers are referred to
current published reviews on this topic [193]. Once the reaction is controlled,
antivenom infusion can be cautiously restarted, sometimes requiring titration of
rate against blood pressure response and i.v. diluted adrenaline infusion [134].
The development of an anaphylactic reaction to antivenom is not a justification
for abandoning antivenom therapy in that patient. If antivenom has been com-
menced on sound clinical grounds, because of major or life threatening enven-
oming, those grounds remain valid. Nevertheless, it is prudent to re-evaluate
the extent/severity of envenoming before committing to restarting antivenom.
For late reactions, notably serum sickness, the patient will often have been
discharged prior to onset, so it is essential that all patients receiving antivenom,
whatever the type, amount, or route, be informed of the possibility of serum
sickness and presenting symptoms, to maximise the probability they will

promptly return for treatment. A detailed discussion of management for serum
sickness is beyond the scope of this chapter, but oral corticosteroids such as
prednisolone, and oral antihistamines are generally the mainstays of treatment.
Some doctors advise a short (about 5–7 days) course of oral corticosteroids
after administration of antivenom, to reduce the likelihood of serum sickness.
This is not a clinical trial-proven therapy, but logically may be of some benefit.
There is a considerable amount of literature on use of prophylaxis prior to
antivenom, in an attempt to reduce the rate of adverse reactions. Several key
points have emerged. Firstly, sensitivity testing prior to antivenom is a non-
predictive and dangerous procedure, which should never be undertaken, even
though some antivenom producers still recommend it [163, 191]. Secondly,
there is no convincing evidence that antihistamines or steroids such as hydro-
cortisone prevent adverse reactions [163, 194]. There is highly conflicting evi-
dence that subcutaneous adrenaline may be useful, but most recent studies and
advice from leading authorities is that adrenaline as premedication for antiven-
om is inappropriate [163, 195].
Other antidotes
Antivenoms are only available to cover some of the more dangerous venomous
animals. Even where antivenom is available, there may be other treatments that
can be effective as ancillary care, although not as a replacement for antivenom.
For neurotoxic paralysis caused by purely post-synaptic neurotoxins, anti-
cholinesterases are theoretically attractive and have shown efficacy for enven-
oming by some species. By reducing the rate of acetylcholine destruction with-
in the neuromuscular junction (Fig. 1), it is sometimes possible to overwhelm
the effect of the toxin in blocking the muscle end-plate acetylcholine receptor,
thus reducing the extent of paralytic features. In selected cases this may be
enough to wean the patient off the need for ventilatory respiratory support, but
frequent re-dosing is usually required. This ancillary treatment has been suc-
cessful in treating paralysis following bites by Philippines cobras (Naja philip-
pinensis), death adders (Acanthophis spp.) and sea snakes (New Caledonia;
species not certain) and is likely applicable to a wider range of snakes
[196–199]. However, recent research indicates at least some death adders also
have pre-synaptic neurotoxins in their venom, which may explain cases refrac-
tory to both antivenom and anticholinesterase treatment.
For scorpion stings causing neuroexcitatory envenoming, some clinicians
report that prazosin is highly effective [200–206]. Experimental studies also
indicate prazosin may be effective in countering Irukandji jellyfish (Carukia
barnesi) envenoming, in cases with significant cardiac involvement [207, 208].
In both these settings there is a form of “catecholamine storm”. However, the
cardiovascular collapse caused by severe box jellyfish (Chironex fleckeri)
envenoming is not responsive to prazosin [209, 210].
260 J. White
General treatment
For most cases with significant envenoming it is a reasonable and common

practice to give an initial i.v. fluid load (crystalloids), the degree of loading
being tempered by patient factors such as presumed degree of dehydration (if
any), patient age, size and pre-existing infirmity (such as cardiac disease)
[134]. Particularly in children it is important not to overload with fluid.
Analgesia will depend on both the type of envenoming and patient factors
[107]. Many envenomings will not result in significant pain, so routine anal-
gesia is not required and where indicated, oral analgesia should be used before
considering parenteral analgesia. In all cases, it is best to avoid narcotic anal-
gesia that may cause respiratory depression [107, 163, 211]. However, some
forms of envenoming are routinely associated with severe pain, requiring
prompt and vigorous analgesia, such as use of i.v. fentanyl for Irukandji stings
[212], or regional nerve blocks for intransigent pain from stingray or ven-
omous spined fish wounds [20, 213]. In some cases, antivenom will be the
most effective “analgesic”, such as in widow spider bites and stonefish stings
[9, 20, 134, 152, 214].
Most envenoming cases do not develop significant secondary infection, so
routine antibiotic use is generally not warranted [9, 191]. As the organisms
involved in those cases that do become infected are highly variable, wherever
possible culture and sensitivity should be performed prior to commencing ini-
tial antibiotic therapy, often with broad spectrum cover. Some envenomings,
notably some snakebites in South America by Bothrops jararaca, B. jarara-
cusu and related species can develop significant local sepsis and abscess for-
mation, so routine antibiotic therapy may be appropriate in such bites,
although is not always effective [215–219].
All bites and stings are potential sources for tetanus [191, 220, 221] and it
is important to ensure current tetanus immunisation status, but care should be
taken when giving i.m. tetanus immunisation updates in the presence of active
coagulopathy, as caused by many snake species [191, 222–224]; the coagulo-
pathy must first be under control.
Major local limb swelling is a common sequelae of envenoming by many
snake species [163, 191, 225, 226]. In the past it has been assumed by some
doctors that compartment syndrome would commonly occur, so fasciotomies
were frequently performed. This invariably resulted in damaging scarring,
which often progressed to long-term functional disability. It is now clear that
true compartment syndrome is an infrequent complication of such local snake
envenoming and fasciotomy should only be performed in cases where two cri-
teria are met: (1) there is confirmation of compartment syndrome by direct
measurement of intracompartmental pressure, and (2) any coagulopathy asso-
ciated with envenoming has been reversed [163, 191, 225, 226].
Debriding necrotic wounds, should in most cases be done in the first few
days, except for loxoscelism (recluse spider bites), where early debridement
may spread venom and extend the area of necrosis [9, 227–229]. In these cases
it is advisable to wait until the area of necrosis has stabilised. For deep pene-
trating wounds, such as with some stingray injuries, after debriding damaged
and necrotic tissue, it is important to allow wounds to heal by secondary inten-
tion [230].
Specific groups of venomous animals
In the following accounts, only selected groups or representatives are dis-

cussed, as the vast array of venomous animals is too great to cover in a chap-
ter such as this. Similarly, the range of possible data sources is immense, so
readers are referred to a few key texts [15, 22, 27–29, 127–130, 134, 163, 191,
211] and a website (www.toxinology.com), rather than listing many hundreds
of further references for individual species or species groups in the remaining
portion of this chapter.
Venomous snakes
As discussed earlier, venomous snakes represent the single most important

venomous animal group from a medical perspective, accounting for more mor-
tality and serious morbidity than all other groups combined. Amongst the
snakes, the majority of species fall into the four broad families containing ven-
omous species [1–3, 163], but true venomous species represent only a minor-
ity of the snake fauna, and species dangerous to humans an even smaller pro-
portion.
Colubrid snakes (Colubridae)

Family Colubridae comprises a diverse assemblage of over 1850 snake spe-
cies, with some recent taxonomic work indicating that the family could be split
into an array of further families [231, 232]. The majority of colubrid snakes are
considered technically “non-venomous” and lack distinct venom apparatus or
fangs [233]. However, it is clear that many other colubrid snakes can produce
toxic oral secretions that some authors argue constitutes venom, a view possi-
bly supported by apparent DNA coding for toxins [234]. This issue of what
constitutes “venomousness” in colubrid snakes is an ongoing and unresolved
issue that will not be further canvassed here. Among those few colubrid snakes
with definite venom-producing glands and distinct enlarged teeth (some con-
sidered as fangs) for venom delivery, in all cases situated towards the middle
to back of the upper mouth (so-called “back-fanged” or opisthoglyphous), sev-
eral species are capable of causing severe, even lethal systemic envenoming,
usually associated with deranged blood coagulation and a bleeding tendency.
Colubrid snakes are global in distribution.
Boomslang (Dispholidus) and vine snakes (Thelotornis): These southern
African arboreal snakes have caused a number of fatalities associated with
262 J. White
coagulopathy. A specific antivenom is available in South Africa for the boom-

slang.
Keelbacks (Rhabdophis): The keelbacks and yamakagashi were originally
thought to be harmless, but several severe, even fatal bites confirmed their
potential to cause major envenoming and coagulopathy. A specific antivenom
is available in Japan.
Other venomous and toxic colubrids: A number of other colubrid snakes
have caused bites with varying degrees of envenoming, although generally not
lethal. As more cases are accumulated it is probable that further colubrid spe-
cies will be added to this list and it is no longer valid to assume a colubrid
snake, not previously associated with significant bites, will be always harm-
less. However, those species that are small in size are less likely to inflict sig-
nificant bites, although some large species of colubrids are not known to cause
medically significant bites. No antivenoms are available for these snakes.
Elapid snakes (Elapidae)

Elapid snakes are, without exception, venomous, possessing well-developed
venom glands and paired anterior placed proteroglyphous fangs. Many elapid
snakes are small and may not be capable of significantly envenoming humans,
but there are also many large species very capable of inflicting lethal bites. The
range of elapid snakes is global, reaching a peak of diversity in Australia.
Cobras (Naja, Hemachatus, Walterinnesia): Cobras represent the single
largest, most widely distributed group of elapid snakes of major medical
importance, causing mortality and morbidity in thousands to tens of thousands
of humans every year. They cover several genera, but most fall within the sin-
gle genus Naja, with recent taxonomic changes moving several related genera
into Naja. Clinically cobras divide into two broad types of envenoming: (1)
predominantly local envenoming with necrosis, mild to moderate neurotoxici-
ty, and (2) predominantly neurotoxic envenoming, without major local effects.
The former group contains many species in Africa and Asia capable of spitting
venom and causing severe venom ophthalmia. A variety of antivenoms are
available for cobra envenoming, i.e., for covering more common species only,
specific for particular species, species groups, or regions. Not all important
species are covered and it is important to use the most specific antivenom
available, particularly noting differences between African, West Asian and
East Asian species, each covered by different products.
King cobra (Ophiophagus): The king cobra, although certainly cobra-like in
origin and appearance, is separated because of its sheer size, at over 4 m, the
longest of all venomous snakes. Found in much of eastern Asia, this snake
causes both local effects and severe paralysis. Several specific king cobra
antivenoms are available.
Kraits (Bungarus): As we understand more about snakebite epidemiology it
becomes clear just how important kraits are in Asia as a cause of lethal enven-
oming. The numerous species are widely distributed and are generally noctur-
nal hunters, common in rural, even urban areas, where they mostly bite at
night, with a painless bite and later development of progressive severe paraly-
sis, often associated with abdominal pain and, at least for some species,
myotoxicity as well. Most, but not all, species show some degree of body
banding. Antivenom is available for some krait species.
Coral snakes (Micrurus, etc.): Coral snakes are of most medical signifi-
cance in the Americas, especially in South and Central America, where they
can cause severe paralysis and/or myolysis, with minimal local effects. There
are a few species found in the southern USA, but throughout their range they
are an infrequent, although sometimes fatal cause of bites. Several specific
coral snake antivenoms are available in South and Central America.
Mambas (Dendroaspis): The African mambas (Fig. 7) have a ferocious rep-
utation, but available data indicates they likely cause relatively few bites,
although some species have a high lethality potential. The venom causes com-
plex neurotoxicity, leading to both muscle fasciculation and paralysis, but gen-
erally few local effects. At least one African polyvalent antivenom covers
mambas.
Australian and New Guinea elapids (Pseudonaja, Pseudechis, Notechis,
Tropidechis, Austrelaps, Hoplocephalus, Acanthophis, Oxyuranus, Micro-
pechis): Australian and New Guinea elapid snakes have developed rather sep-
arately from elapids elsewhere and present a distinct set of clinical problems.
Local effects of bites vary, depending on species, from trivial to moderate
swelling, but it is systemic effects that dominate, again varying between spe-
cies, but including pre- and post-synaptic paralysis, severe myotoxicity, coagu-
Figure 7. Black mamba, Dendroaspis polylepis (original photo/illustration copyright © Julian White).
264 J. White
lopathy and haemorrhage, renal failure and cardiotoxicity. Several “monova-

lent” and a polyvalent antivenom are available for Australian snakes.
Sea snakes: Long considered a separate family, sea snakes are now includ-
ed within Elapidae and are thought to have evolved from early Australasian
elapids. They are subdivided into two broad groups; the purely marine
Hydrophiinae, encompassing the bulk of species, and the Laticaudinae that
come onto land during their breeding cycle. Both groups have potent venoms,
principally neurotoxins and/or myolysins, this being reflected in clinical
envenoming, with both flaccid paralysis (post-synaptic) and systemic myotox-
icity possible, either separately, or both together. The myolysis can cause sec-
ondary renal failure and cardiac toxicity and be severe enough to cause weak-
ness that can mimic true neurotoxicity. Only one sea snake antivenom is cur-
rently available, but while it is made against venom from just one species, it
appears to be effective for bites by most other sea snake species.
Other elapids (Paranaja, Pseudohaje, Boulengerina, Aspidelaps, Elapso-
idea, Homoroselaps): This mixed group of elapids do not collectively cause
significant numbers of bites, but some species can cause moderate to severe
envenoming and have lethal potential. The taxonomic status of some genera is
in flux; some are proposed to be subsumed within Naja (the cobras). There are
no antivenoms available for these snakes.
Atractaspid snakes (Atractaspididae)

Burrowing or mole “vipers” have been the subject of considerable taxonomic
instability, but currently are considered a distinct family of habitually subter-
ranean venomous snakes, limited to Africa and the Middle East, mostly small
and generally not involved in envenomings in humans. There are several larg-
er species within genus Atractaspis that have potent venoms and do cause
human envenoming and are potentially lethal. Within this group the unique
sarafatoxins, similar to human endothelins, can cause severe or lethal cardiac
effects. However, local tissue injury and sometimes necrosis is a far more com-
mon consequence in envenomed humans. They are adapted for a subterranean
existence, burrowing in search of prey and have evolved a unique fang struc-
ture allowing side-swiping envenoming.
Viperid snakes (Viperidae)

Vipers comprise a diverse assemblage of venomous snakes, with a wide glob-
al distribution. They have front-placed fangs on rotating modified maxillae,
allowing the fang to be folded against the roof of the mouth, then erected
when biting, an arrangement that permits development of long fangs, and
referred to as solenoglyphous dentition (Fig. 8). In some viperids, fangs can
exceed 2.5 cm in length and these large fangs are often combined with large
venom glands, able to effectively deliver a substantial venom load. While
many viper venoms may not be as toxic as selected elapid venoms, this is fre-
quently counterbalanced by their ability to deliver more venom. Viperid
snakes are the single most important cause of snakebite to humans globally,
Figure 8. An eastern diamondback rattlesnake, Crotalus atrox, with mouth open and fangs moved to
erect position, but with fang sheath not yet retracted (original photo/illustration copyright © Julian
White).
ahead of elapids. There are two subfamilies of viperid snakes, Viperinae and
Crotalinae.
Viperinae
This subfamily contains classic vipers, found throughout much of the “old
world” and responsible for a substantial portion of the human snakebite toll,
particularly groups like the carpet vipers (genus Echis), Russell’s vipers (genus
Daboia) and African adders (genus Bitis).
Classic vipers and adders (Vipera, Macrovipera, etc.): These small vipers
(or “adders”) have a wide distribution from Europe right across northern Asia
and south into North Africa and the Middle East. While they can cause severe,
even fatal envenoming, in most cases envenoming is less severe and mostly
local, with swelling, pain, bruising, and uncommonly necrosis. Systemic
effects can include shock, coagulopathy and renal damage, with occasional
mild neurotoxic features, such as ptosis, although at least one species (Vipera
ammodytes) can cause more severe paralysis. Several antivenoms are avail-
able.
266 J. White
Puff adders (Bitis): These African vipers range from small species to large
snakes such as the Gaboon viper, Bitis gabonica and the notorious puff adder,
Bitis arietans, an important cause of sub-Saharan snakebite. These snakes
cause severe local envenoming, including swelling, pain, bruising, blistering
and necrosis, plus systemic effects including shock, coagulopathy and haem-
orrhage. Several antivenoms covering the puff adder are available, but not
specifically for other species, although cross-reactivity is likely among some
of these.
Russell’s vipers (Daboia): Russell’s vipers, Daboia russelii and D. siamen-
sis, are the most important members of this genus and are found from Sri
Lanka, through the Indian subcontinent, to Southeast Asia, Indonesia and
Taiwan. Throughout their range they cause a significant number of often
severe or fatal bites, characterised by both severe local effect, including blis-
tering and necrosis, and severe systemic effects, including coagulopathy,
haemorrhage, shock and renal failure. Some populations, particularly in
Myanmar and parts of India, can also cause anterior pituitary infarction, result-
ing in Sheehan’s syndrome. Other populations, notably those in Sri Lanka, can
cause myolysis and paralysis. This diversity of venom actions and clinical
effects, even intra-species, means that antivenom choice is crucial; the antiven-
om, to be effective, must be against the particular population of snakes caus-
ing the bite. Using specific anti-Daboia antivenom from one region, to treat
bites by the same species from a different region, can result in treatment fail-
ure and death.
Carpet vipers (Echis): Carpet or saw-scaled vipers, genus Echis, are com-
mon, relatively small vipers, with a range extending from west Africa to India,
covering a number of species that collectively likely cause more snakebite
fatalities than any other genus of snakes. Their bites cause severe local effects,
including blistering, haemorrhage and necrosis, plus severe systemic coagulo-
pathy and haemorrhage. Venom variability between species means that anti-
venom must be sourced from the correct region and species; Indian anti-Echis
antivenom will not be effective in Africa and vice versa.
Other vipers (Eristocophis, Cerastes, Causus, Pseudocerastes, Atheris,
Montatheris, Proatheris, Adenorhinos, Azemiops): A variety of lesser viperids
exist, some of which are not known to cause significant envenoming in
humans, while others, such as the horned vipers, Cerastes spp., can cause
severe, even life-threatening envenoming characterised by coagulopathy and
haemorrhage. Antivenoms covering these species are mostly unavailable,
although a few antivenoms cover some taxa.
Crotalinae
The other viper subfamily, Crotalinae, contains all the “pit vipers”, those
vipers with two heat sensing pits on the anterior head, allowing detection of
prey by infra-red. Pit vipers occur in both the Old World and New World, alt-
hough they predominate in the latter, throughout the Americas, where they are
the dominant cause of snakebites to humans.
Rattlesnakes (Crotalus, Sistrurus): The rattlesnakes, genus Crotalus

(Fig. 9), and the related genus of “pigmy” rattlesnakes, genus Sistrurus, are the
leading cause of North American snakebite, but are also important in Central
and South America. The North American species cause often severe local
envenoming, with swelling, bruising, pain, sometimes blistering/bleb forma-
tion and occasionally necrosis, particularly for bites to digits. There may be
associated shock, and with some species, major coagulopathy. A few species
can cause at least minor neurotoxic paralytic features, such as ptosis, but some
populations of the Mojave rattlesnake, Crotalus scutulatus, can cause severe
paralysis, as their venom contains a potent presynaptic neurotoxin. Some rat-
tlesnakes, such as canebrakes, Crotalus horridus atricaudatus, can cause
major myolysis and secondary renal failure and cardiotoxicity. A single
antivenom covering all North American pit vipers is available. In Central and
South America, rattlesnake bites have a quite different clinical pattern; major
local effects are not common, but severe systemic envenoming is common,
including neurotoxic paralysis, myolysis, coagulopathy and renal failure. A
variety of South and Central American antivenoms cover one or more of these
rattlesnake species.
Figure 9. Blacktail rattlesnake, Crotalus molossus (original photo/illustration copyright © Julian

White).
Lance head pit vipers (Bothrops, Bothriechis): Snakes of the genus

Bothrops are the single most important cause of snakebite in South and Central
America. Most of the major species cause severe local and systemic effects,
268 J. White
including local tissue injury/necrosis in the bitten limb and systemic coagu-
lopathy and shock. Some species commonly cause local infection with abscess
formation. Renal failure, including permanent injury (bilateral renal cortical
necrosis) is described. Two species in the Caribbean, Bothrops lanceolatus and
B. caribbeus, cause thrombotic problems, as discussed earlier in this chapter.
A variety of antivenoms are available in South and Central America to cover
some of the major species of Bothrops, but it is important to select an antiven-
om with coverage for the species involved in a bite. Many of the lesser
Bothrops species, although capable of causing envenoming, seem rarely to do
so and are not specifically covered by any antivenom. The same applies to the
variety of smaller pit vipers, such as the eyelash viper, Bothriechis schlegeli.
Some polyvalent antivenoms, particularly from Central America, may provide
some cross neutralisation for some of these species.
Bushmasters (Lachesis): The bushmasters are formidable snakes, of large
size, but throughout most of their range, bites are infrequent. Moderate to
severe local effects occur, including bruising, but necrosis is uncommon, while
systemic effects include shock, coagulopathy and haemorrhage. Several
antivenoms covering these snakes are available.
Copperheads, mokasins and cantils (Agkistrodon): In parts of North
America, bites by some Agkistrodon spp. are common and, while not general-
ly as severe as rattlesnake envenoming, can still cause potentially lethal
effects, particularly in children. Moderate to severe local effects are common,
including tissue injury, but major systemic effects are less common. They are
covered by the North American polyvalent antivenom.
Mamushi, etc. (Gloydius, Deinagkistrodon): The snakes currently assigned
to genus Gloydius, restricted to Asia, were formerly in genus Agkistrodon, and
some species are important as a cause of snakebite, particularly the mamushis
of Japan (Gloydius blomhoffii blomhoffii) and China (G.b. brevicaudus). The
Japanese subspecies can cause both severe local effects, including blistering,
and systemic effects, including shock, coagulopathy, haemorrhage, renal dam-
age and mild neurotoxicity. The Chinese subspecies causes similarly severe
systemic effects and possibly myolysis as well, but less severe local effects.
Bites by other members of this genus are less well understood. Antivenoms
against the mamushis are available in China and Japan. The hundred pace
snake, Deinagkistrodon acutus, also found in parts of Asia, can cause severe or
lethal envenoming, characterised by severe local effects, including blistering
and necrosis, and systemic effects such as shock, coagulopathy and haemor-
rhage. Specific antivenom is available in China and Taiwan.
Malayan pit viper (Calloselasma): In Southeast Asia the Malayan pit viper
is a most important cause of severe and lethal bites. It causes major local
effects, including blistering and necrosis, and systemic effects including
shock, coagulopathy and haemorrhage. Several antivenoms covering this spe-
cies are available.
Green pit viper (Trimeresurus, Protobothrops, Crypteletrops, Viridovipera,
Popeia, Garthius, Parias, Peltopelor): These Asian pit vipers, mostly previ-
ously contained within the single genus Trimeresurus, have recently been
split into eight distinct genera [235–237]. They encompass a diverse range of
mostly arboreal snakes, some of which are important causes of snakebite
within their specific distribution. Clinical effects vary between species, from
trivial local and no systemic effects, to extensive local swelling and bruising,
with systemic coagulopathy and haemorrhage, to severe local effects includ-
ing necrosis, plus shock, with or without coagulopathy. This latter group
includes the habu, Protobothrops flavoviridis and Protobothrops mucrosqua-
matus. Antivenoms are available for some of the more medically significant
species.
Hump nose vipers (Hypnale): Hump nosed vipers from India and Sri Lanka
are now recognised as a cause of significant bites, causing both local effects,
including blistering, but not necrosis, and systemic effects including shock,
coagulopathy, haemorrhage, renal damage and MAHA, although most bites
may be less severe. No antivenom is available at present.
Other crotalines (Atropoides, Cerrophidion, Ermia, Ophryacus, Ovophis,
Porthidium, Tropidolaemus): A number of other New World and Asian pit
vipers in several genera can cause bites but are mostly considered of compar-
atively minor medical importance. None are covered by specific antivenoms.
Venomous lizards
Until recently, only two species of lizards, Heloderma suspectum and H. hor-
ridum, family Helodermatidae, were considered venomous. These large
lizards, from arid areas of Mexico and southwestern USA, have venom glands
in the lower jaw, which connect to the base of sharp grooved teeth. The venom
is likely used in prey acquisition, but bites to humans can result in excruciat-
ing local pain and mechanical injury, and in some cases, major systemic
effects, including hypotension and shock, but not paralysis, myolysis, or coag-
ulopathy. Treatment is symptomatic and supportive, as no antivenom is avail-
able.
Recent controversial research has indicated that several other groups of
lizards, notably the varanids/goannas (family Varanidae) and the dragons
(family Agamidae) have genes for venom production and may produce oral
secretions containing toxins [234]. Some researchers consider that for at least
large varanids, such as the massive Komodo dragon (Varanus komodoensis),
these toxic oral secretions are effectively venom and are used in prey acquisi-
tion. Further research is needed to confirm the validity of this work.
Scorpions
Most of the nearly 2000 described species of scorpions are of no medical sig-
nificance, their stings causing either no effects in humans, or minor or short-
270 J. White
lived local pain, rarely with any systemic effects, and the latter are of a minor
and self-limiting nature. However, several hundred species, nearly all within
family Buthidae, can cause envenoming, varying from mild to severe, even
lethal, depending on species and the size of the victim.
Buthid scorpions of medical importance

Buthid scorpions (Fig. 10) capable of causing medically important envenom-
ing occur in the Americas, Africa, the Middle East and Asia. All cause a form
of neuroexcitatory envenoming, in many cases characterised as a cate-
cholamine storm effect. A wide variety of scorpion toxins have now been fully
elucidated and these include potent potassium and sodium channel neurotox-
ins. In some regions, such as North Africa, scorpion sting is both more com-
mon, and of greater medical importance, than snakebite. In Mexico around
280 000 scorpion sting cases are admitted to hospital every year. With ade-
quate antivenom therapy, mortality is now low, even in those at most risk,
younger children, in regions where it is widely used. In contrast, some regions
not using antivenom still have significant mortality from scorpion stings.
Antivenoms are available for only some major scorpion species, sourced in
their native regions. However, the management of scorpion envenoming is
controversial, with several different approaches extant. Some clinicians con-
sider antivenom ineffective, instead emphasising both supportive intensive
care and use of cardiovascular drugs such as prazosin. Confusing studies sug-
gesting antivenom is ineffective have created more uncertainty about treat-
ment. Nevertheless, evidence from countries including Mexico and Brazil,
Figure 10. Androctonus australis (original photo/illustration copyright © Julian White).

where severe scorpion stings are very common, indicates that the widespread
use of antivenom has been associated with a dramatic fall in mortality.
Non-Buthid scorpions of medical importance

The most important non-Buthid scorpion is undoubtedly Hemiscorpius lep-
turus, found in Southwest Iran [238–240]. This scorpion, uniquely within all
scorpions, causes local sting-site necrosis and often a systemic syndrome of
haemolysis, coagulopathy, renal failure and shock, which can be lethal. It does
not cause neuroexcitatory envenoming, unlike other medically important scor-
pions. A polyvalent scorpion antivenom, which is claimed effective against
Hemiscorpius, is available in Iran.
Spiders
Spiders undoubtedly cause large numbers of bites to humans, most of which

are trivial, requiring no medical treatment, but a few species can cause major
effects, and one group is potentially lethal. Spiders are generally grouped into
two suborders, Mygalomorphae and Araneomorphae. These two groups can be
distinguished by anatomical features and both contain species of medical
importance.
Mygalomorphs
These spiders, often described as “primitive”, are generally large spiders of
robust build, with comparatively long fangs. Most cause minor local effects
only on biting humans, but one group, the Australian funnel-web spiders and
related mouse spiders are lethal to humans. Some others cause dermal and
ophthalmic irritation through shedding abdominal hairs.
Australian funnel-web spiders: These spiders, of genera Atrax (Fig. 11) and
Hadronyche, found only in Australia, are the World’s most dangerous spiders.
While “dry” or trivial bites are common, they can cause rapidly lethal enven-
oming, even in healthy adults, with death in less than 30 minutes in some cases
in the pre-antivenom era. Envenoming is a rapid, fulminant neuroexcitatory
type, with catecholamine storm effects, similar to major scorpion envenoming.
It responds rapidly to antivenom, even given late, and since antivenom was
introduced, fatalities are now essentially unknown. This specific antivenom
actually is effective for all funnel-web species. The related mouse spiders,
genus Missulena, have a similar venom, also responsive to funnel-web spider
antivenom, but clinically significant envenoming is very rare, so antivenom is
generally not required for bites by these spiders.
Other mygalomorphs: A number of other large mygalomorph spiders can
cause at least local effects such as intense pain, sometimes with non-specific
systemic effects, usually mild and of limited duration, but for the majority of
species there is no evidence, despite their large size and long fangs, that they
are of any medical significance.
272 J. White
Figure 11. The Sydney funnel-web spider, Atrax robustus (original photo/illustration copyright ©
Julian White).
Aranaeomorphs
The bulk of all described spider species are araneomorphs. These diverse spi-
ders span a wide array of families, body size and shape and prey capture meth-
ods, the latter ranging from classic web capture, to hunting and stalking. Most
are of no medical significance, but a few groups can cause problem bites.
Widow spiders (Latrodectus): Widow spider bite is probably the most com-
mon medically important form of spider bite globally. Widow spiders, mostly
of the genus Latrodectus, are distributed across most continents, are often
common and adapt well to human habitation, so opportunities for bites can be
many. In Australia more patients are treated with antivenom for widow spider
(red back spider) bite than all other types of envenoming combined (including
snakebite). Although widow spiders are reported to have caused fatalities,
available evidence suggests this is most likely a result of secondary problems,
not direct primary venom toxicity, but there is no doubt that significant widow
spider envenoming, latrodectism, is an unpleasant problem for affected
patients. The venom causes neuroexcitatory envenoming, but usually without
the severe and life threatening systemic effects seen with scorpion and funnel-
web spider envenoming. Instead, envenoming is characterised by local, then
regional or generalised pain, often with associated sweating, sometimes nau-
sea and hypertension, lasting up to several days. A number of antivenoms are
available and evidence suggests any anti-latrodectus antivenom will be effec-
tive against bites by all widow spider species. Recent research has questioned
the effectiveness of antivenom for latrodectism, but further research will be
required to resolve this issue, as there is a large body of published case expe-
rience (but not randomised control trials) suggesting antivenom is the only
effective treatment.
Banana spiders (Phoneutria): Banana spiders are restricted to South and
Central America, but cause most problems in Brazil, where they are, by far, the
most common cause of major spider bite. Effects are similar to widow spiders
and most distressing for patients, but with low lethality potential. An antiven-
om is available in Brazil, but most patients are managed conservatively, includ-
ing analgesia, without antivenom.
Recluse spiders (Loxosceles): Recluse spiders (Fig. 12) are global in distri-
bution, but a more restricted group cause medical problems, which are quite
distinctive. An effective bite, although rarely felt at the time, will cause either
just local effects, principally necrosis of skin (cutaneous loxoscelism), plus
some self limiting systemic effects, or these local effects plus a potentially
lethal systemic illness (viscerocutaneous loxoscelism), characterised by
haemolysis, coagulopathy, renal failure and shock. An antivenom is available
in Brazil, although its effectiveness, given the usual very late presentation, is
doubtful. Most cases elsewhere, such as in the USA, are managed conserva-
tively. Early debridement of necrotic areas is generally inadvisable as it can
extend the necrotic area. Loxoscelism is sometimes characterised as “necrotic
Figure 12. North American recluse spider, Loxosceles reclusa (original photo/illustration copyright ©
Julian White).
274 J. White
arachnidism” (spider bite causing skin necrosis), but is an over-diagnosed con-

dition in some countries, notably the USA, and also in Australia (where
Loxosceles is not a native species and is likely present, if at all, in very restrict-
ed areas and numbers).
Other aranaeomorphs: A number of other larger araneomorph spiders can
cause mild local envenoming, usually just local pain and/or swelling, occa-
sionally with mild self-limiting general symptoms. None require antivenom.
Ticks and mites
There are many tick and mite species, all parasites of various hosts, sometimes
mammals, but also birds, reptiles, even spiders and insects. Very few produce
saliva with toxin (venom) effects in humans. Indeed, medically, ticks are far
more important as vectors of disease transmission.
Australian paralysis ticks

Hard bodied ticks of the genus Ixodes, limited to eastern Australia, produce a
potent paralysing neurotoxin in their saliva, so that when an adult female tick
attaches to a human, enough toxic saliva may be inoculated, over several days,
to cause a slowly progressive, but potentially lethal, flaccid paralysis. More
people have died from tick paralysis in Australia than from funnel-web or red
back spider bite. Once the tick is removed, paralysis can still progress for up
to 48 hours, before slowly resolving. Severe paralysis can cause respiratory
failure, requiring mechanical ventilation. This is the current treatment, as the
previously available antivenom was of doubtful effectiveness and has been dis-
continued.
North American paralysis ticks

North American paralysis ticks are hard bodied species, principally
Dermacentor andersoni (western North America) and D. variabilis (eastern
and central North America), causing progressive flaccid paralysis, which
regresses immediately on tick removal. No antivenom is available and respira-
tory support is the mainstay treatment in those rare cases with full respiratory
paralysis, often required for only a brief period.
Other paralysis ticks

Tick paralysis is less well described outside North America and Australia,
although it is reported to occur, probably rarely, in Africa, possibly elsewhere.
Centipedes
Centipedes have paired fangs and venom glands adjacent to the head, in the
maxillipedes; the apparent “venomous” spines at the tail region are not ven-
omous. Bites from large species can cause local mechanical trauma and
intense pain from the venom, but systemic effects are not generally seen and
local effects usually settle quickly. However, secondary infection is a risk. No
antivenom is available or required.
Insects
Insects comprise a large proportion of animal species diversity, so it is hardly

surprising some utilise venom for defence or offence. However, comparative-
ly few cause medically significant effects from venom and in most of these, it
is allergy, not primary venom toxicity, that is the risk.
Hymenopterans (bees, wasps, ants)

With a few notable exceptions, all the important venomous insects are hy-
menopterans, either bees, wasps, or stinging ants. In all of these, a single sting
in the tail, with an intra-abdominal venom gland, can deliver a small quantity
of venom, containing potent and often highly allergenic peptides. Most sting-
ing hymenopterans can sting multiple times, but the honey bee, Apis mellifera,
is only able to sting once, resulting in the death of the bee, with the sting and
pumping venom gland left behind in the skin of the victim. While mass
attacks, involving many hundreds, more usually thousands of stings, can result
in primary, even lethal venom toxicity, often with fulminant haemolysis, shock
and renal failure, these events are generally rare. In a few areas, such as
Vietnam and Brazil, such mass attacks by hymenopterans are more common
and cause occasional deaths. For most people and regions, it is allergy from a
single sting that causes most concern, and most fatalities. In many western
countries, bee sting anaphylaxis is considered to kill more people than any
form of envenoming. Not all bees sting, nor do all wasps, but some wasps, par-
ticularly the large communal species, such as European wasps and North
American and Asian hornets, regularly sting humans, either singly, or multi-
ply. Most ants lack effective stinging capacity, although bites can cause local
pain and some species can spray venom under pressure from abdominal venom
glands. Some species do sting and can cause intense local pain, irritation, red-
ness, and allergic responses in some humans. The pain can last many hours,
with “sores” developing around each sting site, which can take days to resolve.
A few of these stinging ants, such as the jumping and inch ants (Myrmecia
spp.) of Australia, can cause major anaphylaxis, more potent than even honey
bees. Similarly, the fire ants (Solenopsis spp.), originally from South America,
but now well established in North America, Australia and elsewhere, can cause
intense local pain, sore formation, and major allergic reactions.
Lepidopterans (caterpillars)
Most caterpillars, moths and butterflies are of no medical significance, but the
caterpillars of some species have locally irritant hairs and in some cases, notably
276 J. White
Lonomia spp. in Brazil, can cause major, even lethal envenoming, on skin con-
tact with these hairs. Lonomia caterpillars cause potentially fatal coagulopathy,
with potent procoagulants in their venom; there is a specific antivenom in
Brazil. Contact with the hairs of some other caterpillars, across several conti-
nents and many species, either through touching the caterpillar, or through shed
hairs in the air, can cause not just local skin irritation, but in the eyes, corneal
irritation, and if inhaled, bronchial irritation, and potentially severe allergic reac-
tions are also possible. The term lepidopterism is used to cover these diverse
clinical effects. In some species, the hairs may be present on the outside of
pupae and adverse effects from contact with these is known as erucism.
Coleopterans (beetles)
A variety of beetles can produce toxic secretions, which can cause injury to
humans, most commonly skin irritation, staining, blistering or necrosis. Of
particular note are beetles of the family Meloidae, the “blister beetles”, some-
times known as “Spanish fly”. These beetles produce the potent toxin can-
tharadin, exuded from limb joints (they have no specific venom gland), and
direct contact with human skin can cause classic blistering and skin necrosis.
Similarly Staphylinidae beetles can cause local effects by squirting toxins,
notably pederin, under high pressure from anal glands. These are defensive
actions by the beetles, not primary prey acquisition. Management of such local
lesions is symptomatic and supportive. No antivenom is available.
Other insects
While a variety of other insect species, across diverse families, possess suck-
ing mouthparts and can attack humans, often as a food source, they are not pri-
marily venomous, though their saliva may contain substances that might be
considered toxic. They will not be further discussed here.
Venomous mammals
Several species of mammals, across two suborders, produce toxic secretions.

In the case of monotremes, the Australian platypus, Ornithorhynchus anatinus,
a hind leg spur attached to a venom gland is used in male:male combat and in
defence, with accidental stings to humans causing intense local pain lasting
many hours. Treatment is symptomatic and no antivenom is available. Toxic
oral secretions from shrews can cause local effects in bitten humans, but these
are generally minor and managed symptomatically.
Venomous birds
Until 1990, birds were not considered as toxin producers, but the discovery of
toxin-producing birds in Papua New Guinea, the pitohuis and infritas, which
principally contain batrachotoxins in their feathers and skin, has changed this
view. However, in these birds, the toxin is used only in defence, when in con-
tact with the bird. There is also uncertainty about the origin of the toxin (is it
made by the bird or concentrated after uptake from the environment). For the
present, then, these birds should be considered poisonous rather than veno-
mous.
Venomous amphibians
As with the birds, mentioned above, those frogs possessing toxic secretions are
generally considered poisonous, not venomous. Interestingly, some venomous
frogs, such as larger Bufo toads, can squirt toxic secretions from posterior
parotid glands in the head-neck region, as a defensive measure. This can
almost be considered venomous, not just poisonous. Toxic secretions in
amphibians, including species of frogs (and toads) and newts, can be highly
potent, such as the batrachotoxins, pumiliotoxins, samandarines and bufotox-
ins, many being low molecular weight alkaloids affecting nerve transmission
or cardiac function. Many are lethal to humans, even at a low dose, but humans
rarely come in contact with these toxins. Most recent reported human deaths
from amphibian toxins follow ingestion of herbal medicines or extracts used
for recreational drugs containing toad toxins such as bufotoxin and bufogenin.
Some of the highly toxic poison arrow frogs from the New World are very
colourful and popular in captivity, but generally loose their toxicity after a
period of captive care, supporting the environmental origin of the toxins.
Venomous fish
There are numerous fish with venomous spines, in a diverse array of families,
in all cases using the venom and spines predominantly for defence, not prey
acquisition. Venom glands envelop spines, which are often grooved, and when
contact is made with a potential target, as the spine enters the tissue, the gland
may be compressed and venom forced subcutaneously into the target. This is
particularly effective in fish such as the stonefish (Synaceia trachynis), the
most venomous of all fish, when a human steps on the dorsal spines. Here, as
with other venomous spined fish, the venom causes local pain, which may be
excruciating and crippling. Similar, but lesser pain can occur with other spe-
cies, when stepped on or picked up in the hand. The location of spines varies
with species and includes dorsal, ventral, lateral, tail fins and behind the head.
Some species, such as lionfish (Pterois spp.) can have many spines providing
a defensive screen around the fish. Only a few of these fish venoms have been
studied, notably the most toxic to humans, the stonefish, which has a potent
neurotoxin, although this does not cause paralytic features in envenomed
humans.
278 J. White
There are no substantial data on rates of venomous fish stings, but it is like-
ly that minor stings are very common, while severe stings are uncommon to
rare. For most of these fish stings, symptomatic care is the only treatment, with
hot water immersion widely recommended as both first aid and hospital treat-
ment to abate pain. A specific antivenom is available for stonefish stings and
may be useful for severe effects by some closely related species, although this
is unproven.
Cnidarians: jellyfish
Jellyfish occur in vast numbers, often in swarms, that can be encountered by

swimming humans, often off popular beaches and in bays in summer. The total
number of stings to humans is almost certainly measured in the many millions
per year, but apart from local pain and wheal formation, generally of short
duration and not requiring medical treatment, the vast majority of these stings
are of no consequence. However, medically, a few species commonly cause
significant effects, even potentially lethal envenoming in the case of the
Australian box jellyfish, Chironex fleckeri, and Irukandji jellyfish (covers sev-
eral species, including Carukia barnesi).
The box jellyfish (Fig. 13), clearly the most deadly jellyfish globally, can
inject large amounts of venom rapidly, some thought to directly enter capillar-
Figure 13. The Australian box jellyfish, Chironex fleckeri (original photo courtesy of Jamie Seymour).
ies, because of its large size and great tentacle length. As with other jellyfish,
venom is produced in and injected by individual stinging cells, nematocysts
(cnidocils), found in vast numbers on the surface of tentacles (Fig. 14). A major
box jellyfish sting can inoculate venom from millions of nematocysts instant-
ly. As the tentacle contacts the skin, a trigger on the surface of each nematocyst
initiates extrusion at high speed of the everted stinging tube, through the skin,
ejecting venom along the extrusion track. A sting is invariably painful, often
with distinctive ladder track marks and the pain can be excruciating.
Sometimes local necrosis and scarring can occur along tentacle contact tracks.
Box jellyfish venom includes toxins that are cardiotoxic and in a major sting,
within a few minutes even an adult human can suffer cardiac arrhythmia and
arrest, so death can occur within 5 minutes of being stung, probably the most
rapid and dramatic lethal envenoming of any venomous animal. This has result-
ed in great fear of box jellyfish stings, but in reality, such a dire outcome is only
likely if the area of tentacle contact is large, usually from a large specimen.
Nets around swimming beaches exclude such large specimens and the majori-
ty of human box jellyfish stings are comparatively minor. Close relatives of the
box jellyfish exist in waters north of Australia and there are reports of fatal jel-
lyfish stings around Southeast Asia, Indonesia and the Philippines. An antiven-
om is available for Australian box jellyfish stings, but there is recent evidence
that while it neutralises the venom effectively, it cannot be given soon enough
Figure 14. Photomicrograph of a jellyfish tentacle showing embedded unfired nematocysts (original
photo courtesy of Jamie Seymour).
280 J. White
to be effective in a clinical setting, although until further research is performed,

this is not a reason to cease using it in severe cases.
The Irukandji syndrome, caused by stings from a variety of jellyfish spe-
cies, not just Carukia barnesi, causes a very different pattern of envenoming.
The sting itself may be trivial or not even felt, and involve a tiny area of only
a few cm2. Many, but not all of these Irukandji jellyfish are tiny, so are not
excluded by protective nets around beaches. A variable time after the sting, but
usually within an hour, systemic effects develop, notably severe muscle pain
in the back, limbs, or elsewhere, often accompanied by severe hypotension,
sweating, and in severe cases, pulmonary oedema. The whole syndrome is
similar to a catecholamine storm and is potentially, but very rarely, lethal.
Treatment is supportive and symptomatic, including strong analgesia. There is
no antivenom available.
The Portuguese Man-of-War or bluebottle (Physalia spp.), is a very common
colony organism “jellyfish” that invades swimming areas in mass swarms in
summer months mainly, sometimes causing large numbers of humans to be
stung. In most cases, local pain, sometimes intense, but usually short lived,
often with wheal formation, is the only effect. In a small number of cases, aller-
gy may be stimulated and rarely, anaphylaxis can occur. Recent research indi-
cates that hot water, most commonly a hot shower, can dramatically reduce
symptoms, more so than other first aid or treatments. No antivenom is available.
Venomous molluscs
Snails are slow moving, so it is perhaps surprising that more predatory species
are not venomous, at least as far as currently known.
Cone snails (Conus)

Of the known venomous predatory marine snails, the vast array of species of
cone snails, Conus spp., is the most important medically, and the best studied.
These snails divide into three broad groups, based on major prey type; fish
eaters, snail eaters and worm eaters. All use a system of venom-coated fired
“harpoon” like radula “teeth” to acquire prey, but some have such potent
venom that they can extrude it into the surrounding water to immobilise or dis-
orient prey such as fish, to facilitate capture. In some cases this may involve
stunning multiple small fish simultaneously. To achieve capture of fast moving
fish, venom must act almost instantly, which may explain why cone snails have
evolved such a diverse and rich array of small peptide-based specialist toxins.
These conotoxins are proving of interest as models for new pharmaceutical
agents, and have an almost bewildering range of activities and targets, mostly
within the nervous system, but often very highly specific, hence their immense
value as neuropharmacological tools in research.
Most cone snails appear unable to effectively or significantly envenom
humans, but a few species can cause severe or lethal envenoming, although
reported cases are few. So from a human epidemiological perspective, their

importance is trivial. Most cases occur in the Indo-Pacific, particularly around
the Philippines. Envenoming occurs when the snail is interfered with or picked
up, with rapid venom inoculation from the fired radula tooth, which may cause
either local pain, or minimal local symptoms. Systemic envenoming can devel-
op rapidly, with flaccid paralysis a particular risk. In severe cases, without res-
piratory support, death may ensue. Treatment is supportive and symptomatic.
No antivenom is available.
Blue ringed octopus (Hapalochlaena)

The blue ringed octopuses, genus Hapalochlaena, are common in waters
around Australia and to the north. They are small and derive their name from
dramatic blue rings that form in the skin when the octopus is alarmed. Their
saliva contains tetrodotoxin, a potent and rapidly acting neurotoxin that targets
sodium channels on nerves, causing flaccid paralysis. It is now considered
likely the octopus does not produce the toxin itself, but accumulates it, or a
precursor, from the environment. Bites are often apparently trivial, with little
or no pain, but in a minority of cases, systemic neurotoxic paralytic envenom-
ing occurs within 10–30 minutes. Without respiratory support, death can rap-
idly follow. Treatment is supportive. Antivenom is not available.
Other marine venomous animals
A wide variety of marine animals use toxins in defence, to establish territory

(such as sedentary corals to maintain or expand living space against competi-
tion), or in prey acquisition. However, they are generally of minor or no med-
ical importance and are not discussed further here.
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Molecular, Clinical and Environmental Toxicology.

Volume 2: Clinical Toxicology 233

Venomous animals: clinical toxinology

Venom appears to have been a success story in evolution because venomous

Region Envenoming Deaths

Low estimate High estimate Low estimate High estimate

Asia 237 379 1 184 550 15 385 57 636

Jellyfish encompass a vast range of species that share a common stinging

Venomous animals: Taxonomy

Venomous animals are represented in 6 phyla, across 20 subphyla or classes,

Venoms: A clinical overview

Venom can be defined as compounds or mixtures of toxins that are deleterious

Type of animal Examples Type of neurotoxin#

Elapid snakes Kraits Pre- and postsynaptic

Coagulants and related toxins

Class of toxin Specific activity

Procoagulant Factor V activating

Table 4. Major venomous animal groups likely to cause primary coagulopathy

Type of animal Examples Type of venom action

Colubrid snakes Boomslang, vine snake Procoagulant

Envenoming: A management overview

Envenoming will vary in severity, depending on the relative toxicity of the

an Australian taipan snake (Oxyuranus scutellatus), the degree of envenoming

Tourniquet Direct pressure injury under narrow band tourniquet

Consultant clinical toxinologists are currently a rare commodity within health

Method Useful for

Immobilisation of bitten All snakebites and other causes of systemic envenoming

envenoming, including severity, progression, systems affected, and evident

Table 7. Important points in a toxinological history

Area of questioning Relevance

Circumstances of bite/sting May indicate likely degree of envenoming

Table 8. Key points in the toxinological examination

Area of examination Relevance

Bite/sting site Is there evidence of multiple bites/stings, ongoing

Test Relevance Relevant fauna

Specific treatment: Antivenom

What is antivenom effective for?

Toxin activity type Clinical effects and responsiveness to antivenom

Paralytic neurotoxin Flaccid paralysis

Any degree of developing or progressing neurotoxic paralysis

ically important species of snakes, there is no absolute need to determine the

In regions where there is a choice of several different antivenoms, without

adults. There is no paediatric dose for antivenom. Doses should never be

sickness and presenting symptoms, to maximise the probability they will

For most cases with significant envenoming it is a reasonable and common

Specific groups of venomous animals

In the following accounts, only selected groups or representatives are dis-

As discussed earlier, venomous snakes represent the single most important

Colubrid snakes (Colubridae)

coagulopathy. A specific antivenom is available in South Africa for the boom-

Elapid snakes (Elapidae)

lopathy and haemorrhage, renal failure and cardiotoxicity. Several “monova-

Atractaspid snakes (Atractaspididae)

Viperid snakes (Viperidae)

Rattlesnakes (Crotalus, Sistrurus): The rattlesnakes, genus Crotalus

Figure 9. Blacktail rattlesnake, Crotalus molossus (original photo/illustration copyright © Julian

Lance head pit vipers (Bothrops, Bothriechis): Snakes of the genus

Buthid scorpions of medical importance

Figure 10. Androctonus australis (original photo/illustration copyright © Julian White).

Non-Buthid scorpions of medical importance