This page provides information about the kinds of toxins found in spider venoms and the relative risk to humans posed by the venoms of some common Australian spider species.
Although the members of the Uloboridae, Scytodidae (spitting spiders) and a couple of very rare families lack venom glands, the great majority of spider species have them and couldn't survive without them. It was initially thought these glands were modified digestive glands but it is now clear this cannot be correct since a spider's digestive glands are mesodermal in origin whereas the venom glands are actually invaginations of the outer tissue layer, the ectoderm. Spiders generally use their venom conservatively as a defence against aggressors and to immobilize prey and keep them in good condition to be eaten at a later date. On the other hand, they produce and use much larger quantities of digestive fluids.
On this page we will examine the chemical and toxicological nature of the main substances found in spider venoms, their actions in the tissues of
victims of spider bites, their potential uses as insecticides, and the medical procedures that are presently in use to help people who are suffering serious
envenomation. It has been enstimated that overall there could be as many as ten million individual toxins in the world's spiders, an 'average' spider
possessing about 100 of them, mostly working synergistically. Exactly which combination of toxins a particular spider uses varies with its habitat,
its usual prey and mode of catching them, and the inevitable changes in venom composition that occur as spiders evolve into new families, genera and species.
Many of the components of spider venoms are highly toxic to arthropods, which is to be expected because the main prey of a typical spider are insects
and other spiders. The reader may therefore wonder why a spider doesn't poison itself before it has even put its venom to use. The answer to this question
is not a simple one because of the variety of toxins in a single venom sample and their chemical and functional diversity.
However, it is probably correct to say that most of them are stored in the venom glands in inactive precursor form. They presumably only become
active as they are being released from the venom glands but there is not much information available as yet as to the actual
activation process. Most probably, the toxin is stored as part of a larger molecule and pieces of this precursor molecule are
enzymically cleaved as the venom is being injected into the victim.
The outer membrane of a neuron (nerve cell) is electrically charged because it contains a sodium-potassium pump system that causes the inside of the neuron to accumulate many more potassium ions than sodium ions and vice versa for the fluid around the neuron. These positively charged ions try to correct their imbalances across the membrane which is therefore given a potential difference (electrical charge). But electrical or chemical stimulation of the neuron can temporarily disrupt this system, allowing some sodium ions to flow into the neuron through specific gated ion channels and causing the membrane to depolarize (i.e. to become stimulated). A wave of depolarization then flows along the neuron until it reaches its specialized ending which we call the synapse.
A small gap (the synaptic cleft) separates the presynaptic end of the neuron from the surface (the postsynaptic membrane) of the nerve, muscle or gland
cell the neuron is attempting to stimulate or inhibit. The synaptic cleft is almost never crossed by direct electrical contact between the presynaptic
and postsynaptic membranes. Instead, the usual way the former acts on the latter is by releasing tiny droplets of a chemical called a neurotransmitter.
Molecules of this substance then diffuse across the the cleft and bind very briefly to specific receptor structures on the postsynaptic membrane, which
therefore becomes stimulated. This release of neurotransmitter droplets is believed to involve the opening of calcium ion pores in the presynaptic membrane
when it depolarizes. All of the above processes are normally of very short duration. The sodium-potassium pump quickly repolarizes the neuron and the
released neurotransmitter is either broken down enzymically or reabsorbed back into the presynapse.
The neurotransmitter used in each synapse varies with the kind of animal involved and the target cell the neuron is trying to influence. In man and
all other vertebrate animals acetylcholine and the catecholamine noradrenaline are the transmitters that are used at synapses outside
the brain and spinal cord but some other substances, including dopamine, serotonin, GABA and glutamate, are employed at certain sites within the central
nervous system. All of these neurotransmitters are found to some extent in various spider venoms and this is one reason why some spiders are
potentially harmful to humans. On the other hand, while acetylcholine is the neurotransmitter we use to drive our skeletal muscles, insects use
glutamate as their general excitatory transmitter. This is a major reason why many spider venoms are highly toxic to insects and other
arthropods but almost harmless to us.
In both insects and spiders the peripheral nerve synapses involved in locomotion have glutamate as the excitatory neurotransmitter rather than the
acetylcholine of vertebrates. The acylpolyamines of spider venoms do not act on these postsynaptic glutamate receptors but if the receptors have already
been activated by glutamate (and some spider venoms contain this transmitter to ensure the receptors are activated) then the acylpolyamine molecules prevent
recovery of the synapse so the muscle system becomes paralysed. This effect helps spiders such as the Araneidae to stop
insects caught in their webs from escaping. The paralysis is long-lasting but does not kill insects as quickly as paralysis does a a human because
insects don't have breathing muscles like the vertebrate ones that must be used constantly. It is for this reason that when humans are bitten by either an araneid or a nephilid spider
the adverse effects produced are normally minor and not life-threatening. It is a fact that humans do use glutamate as a neurotransmitter within
the brain, though not at any peripheral synapses, but polyamine toxins are unlikely to reach these brain synapses because the central nervous system is
protected from most circulating toxins by a highly selective blood-brain barrier.
All of these cystine bridge peptides are toxic because they disturb synapses within a victim's nervous system. The amino acid sequence in the peptide of each spider species that has this kind of toxin is unique to that species. The actual mode of action of these toxins at synapses also varies and it is for this reason researchers have now given each one a Greek letter prefix to indicate how it works. Thus omega-peptides block the presynaptic calcium ion channels in a synapse, beta-peptides cause excessive and prolonged activation of sodium ion channels, delta-peptides delay inactivation of sodium ion channels, mu-peptides inhibit the functioning of activated sodium ion channels, and kappa-peptides disturb potassium ion channels. On this basis the adverse effects the peptide toxin has on the victim may be excessive stimulation (including spasticity) or flaccid paralysis depending on which of these possible modes of action the toxin has. As a further complication it is clear that many of these toxins are highly poisonous in certain kinds of target animals and almost harmless in others. This is one of the reasons why the majority of spiders that sometimes bite people usually produce only mild and localized adverse effects in them.
In recent years there has been a great deal of interest in using spider venom toxins as bioinsecticides. The cystine bridge peptides have been of particular interest because an advantage of the -S-S- cross-linking within the amino acid strand is that it becomes more resistant to breakdown by peptidases in any creature that ingests it. A major problem with the earlier generations of purely synthetic insecticides such as DDT and the organophosphates has been their toxicity for people and domesticated animals and even for insects such as bees which are considered to be beneficial as pollinators of crops. Hence, the discovery that many spider toxins, and especially some of those in the cystine-bridge peptide class, have powerful and often quite specific toxic actions on desired target insects but almost no adverse effects on humans and higher animals has led to the creation of extensive libraries of toxin structures with potential for use as bioinsecticides.
Spiders produce only very small quantities of venom so the
idea of spraying whole venom onto crops that need protecting is ridiculous. We could never hope to acquire the quantities we need just by raising and milking spiders. Fortunately, we now know how to determine the amino acid sequence of each
peptide molecule and to synthesize it in the laboratory. But once again, this is not an economically feasable way of manufacturing the relatively enormous amounts of
insecticide that are needed for agricultural and domestic purposes. In addition, problems associated with the spraying of simple solutions of spider
peptides include instability of the peptides when used in this way, the inability of water-soluble peptides to pass through the impervious cuticle of
insects, and the almost inevitable collateral environmental damage the peptides would cause.
Researchers have therefore come up with at least two better ways of selectively delivering cystine-bridge peptides to insect pests. Both employ the techniques of genetic engineering, the details of which are much too complex to be described in detail on this page. However, the basis of this technology is to take the toxin-producing genes from a spider's venom and incorporate them into a piece of DNA called a plasmid which can then incorporate itself into the genetic make-up of some other kind of cell. The first method to become widely used was to insert the genes for an insecticidal toxin found in the soil bacterium, Bacillus thuringiensis, into the cells of cotton plants. This makes the plants toxic to any insect (and especially the cotton moth, Heliothis/Helicoverpa) that ate them. Putting the genes for a toxin into an agricultural crop reduces the extent of the damage done to it by insect pests and also eliminates the problem of getting a dissolved toxin across an insect's cuticle. Unfortunately, it also makes the plants potentially toxic to other non-pest creatures that might happen to eat them and the gene insertion process would have to be repeated for every crop that needs protection against insect pests.
For these reasons a second way of delivering cystine-bridge
toxins to insect pests has now received a great deal of attention. This alternative technique involves the insertion of a spider's toxin genes into a microorganism such as a baculovirus and then spraying a suspension
of this onto the crop to be protected. The advantages of this method are that baculoviruses tend to be highly target-specific and easily taken up by the
target insect and there will only be a high toxin concentration present once baculovirus has proliferated within the body of the insect. Clearly, this last
characteristic is desirable in that it greatly reduces the risk of collateral damage to other creatures that are also present in a field that is to be
sprayed. It also has the advantage that people who are opposed to the production of genetically modified (GM) crops will
probably be less concerned about the introduction of this kind of insecticide into agricultural practices.
(3) Neurotoxic proteins. These are only known to be present in the venoms of some of the larger members of the Family Theridiidae. Why they
apparently are not used by other spider families remains to be discovered. The theridiid toxins that have received the greatest amount of attention from researchers are two large protein molecules:
alpha-latrotoxin and a latroinsectotoxin. Both of these work in essentially the same way but alpha-latrotoxin is toxic to man and other vertebrates
whereas the insectotoxin only exerts strong effects on small arthropods like insects. The fundamental action (though apparently not the only action) of
alpha-latrotoxin is to cause strong presynaptic influx of calcium ions which then induces excessive release of acetylcholine and other neurotransmitters.
Some glands are also stimulated to secrete inappropriately. In a severely envenomated human the consequences of this excessive stimulation include
muscular spasm or tremors in many parts of the body, tachycardia, hypertension, and intense pain plus excessive salivation, sweating and secretion of tears.
In insects the main effect of overstimulation by a latroinsectotoxin is paralysis, which is obviously helpful while the spider is using its spinnerets
and tarsal combs to securely wrap up prey it has just caught.
(4) Linear Cytolytic peptides. There are many of these among the world's spiders and they vary greatly in structure. The 'typical' linear peptide molecule is 18-48 amino acids in length and is more or less extended when in solution. The cell membrane (outer wall) of most animal and microbial cells is a phospholipid double layer, the fatty acid parts of the phospholipid molecules in each layer occupying the centre of the bilayer and the more polar (water -soluble) phosphate 'head' of each molecule comprising the outer and inner portions of the membrane. When in the vicinity of such a cell membrane a linear cytolytic peptide molecule tends to transform into a helical (spiral) configuration such that its positively charged amino acid residues are mainly on one side of the molecule. This side, being somewhat hydrophobic/lipophilic, is attracted to the lipid-rich centre of the membrane bilayer while the other side of the molecule has a greater affinity for the cell's phosphate residues and the aqueous environment in which the cell is living. The result of this toxin binding is that the integrity of the cell wall is compromised and the cell eventually breaks open and immediately dies. The following diagram is a greatly simplified illustration of this phenomenon, which is many respects is similar to the way detergents remove insoluble soluble fatty residues from dishes in the kitchen sink.
Any venom that contains large quantities of potent cytotoxic peptides has the potential to cause widespread cell lysis throughout a victim's body. This is likely to lead to the victim's death. For example, if the victim is human the cytolysis of large numbers of tissue cells may release enough potassium ions into the blood plasma to disturb the electrical properties of the heart muscles, thus causing dysrhythmias or even complete cessation of the heart beat. But is this a common occurrence? Almost certainly not. The highest levels of cytotoxic peptides found so far in spider venoms have been in some members of the Families Lycosidae and Zodariidae but there are no confirmed reports of a human or large animal suffering death or near-lethal harm following a bite by any Australian lycosid or zodariid spider. Curiously, at least one research paper states that the venom of Loxosceles reclusa (Family Sicariidae) can cause fatal systemic haemolysis. Presumably, as explained further in the next section of this page, this involves a mode of action quite unlike the one described above for the linear cytolytic peptides.
It is possible that cytolytic peptides may play a secondary role in a spider's extracorporeal digestion of its prey but it is now widely believed that
these peptides mainly have a useful antimicrobial role when present in a spider's venom. The suggested mode of action of these peptides on cell bembranes described
above applies not only to the eukayrotic cells of animals but also to the prokaryotic cell walls of bacteria. On this basis it is proposed that these
peptides have an antiseptic role during the digestion of prey but also help keep the fangs and mouth parts free of pathogenic microorganisms.
(5) Histolytic enzymes. At the time of writing of this page the only spiders proven to have venom with the ability to induce long-lasting skin
lesions in humans are Loxosceles species (Family Sicariidae, the recluse or fiddle-back spiders). Loxoxceles venom
contains phospholipases and hyaluronidase but also sphingomyelinase D and this last enzyme is considered to be the primary reason why some victims
of fiddle-back spider bite develop necrotic skin lesions that normally take months to heal and often expand to a life-threatening extent. Sphingomyelin is
a type of phospholipid found in animal cell membranes but especially in those of the myelin sheaths around nerve fibres and in the walls of red blood cells.
Loxosceles species are almost non-existent in Australia yet there are still quite frequent reports of skin ulceration that seems likely to be secondary
to a spider bite and the species that is usually blamed by the popular media is Lampona cylindrata (Family Lamponidae).
But in fact there is now compelling evidence
that L. cylindrata venom does not cause significant skin necrosis in human victims and neither does the venom of other popular candidates such as the black
house spider (Badumna insignis, Family Desidae) and the wolf spider (Lycosa godeffroyi, Family Lycosidae). And yet skin lesions that somewhat resemble
those caused by Loxosceles do occur in this country so how are they actually induced? There probably is no single cause. Some people have 'fragile'
skin because of other medical conditions such as diabetes mellitus or an immune/autoimmune response and others may have a secondary microbial infection at the bite site, the spider's
only role being to create a breach of the skin that allows entry of some kind of 'flesh-eating' bacteria or similar pathogen.
(6) Digestive enzymes. There have been a number of published reports suggesting that venoms from at least 14 spider families have been found to
contain digestive enzymes, notably
collagenase and the so-called 'spreading factor' hyaluronidase, but many other researchers have concluded that most of the apparent instances of
digestive enzymes in spider venom samples are there only because of contamination of the venom by spider gut secretions during collection of the venom.
It is quite likely that some kinds of spiders do release venom and digestive secretions almost simultaneously into their prey and any digestive enzymes
present may then facilitate the actions of the venom toxins. The author of this page personally tested the 'crude' (electrically stimulated) venoms of
Nephila edulis (Araneidae), Eriophora transmarina (Araneidae), Lycosa godeffroyi (Lycosidae), and Holconia immanis (Sparassidae) on both mouse and human
skin and found that an extensive 'ungluing' of the skin cells was present after six hours. However, in no case was this same skin cell dissociation
induced when venom gland extracts were used and neither was there any cell disruption of skin exposed to venom collected cleanly by capillary tubes from
the mygalomorphs Hadronyche infensa (Hexathelidae), Euoplos species (Idiopidae), and Namea salanitri (Nemesiidae).
(7) Small acids and amines. In addition to the major toxins already mention above, spider venoms contain a variety of small substances that mostly seem to serve as inflammatory mediators and agents that potentiate the actions of the more potent toxins. In at least a few venoms the concentration of potassium ions is high enough to disturb the functioning of excitable membranes in insects and other small animals. Citric acid is another venom component that lowers the venom pH to 5.3-6.1 and thus functions as a pain producer and as an inhibitor of bacterial growth. Simple amino acids like glutamate and gamma amino butyric acid (GABA), as well as amino acid derivatives such as histamine, serotonin, and noradrenaline are also common venom components, their functions being to cause pain and in some cases to inappropriately stimulate parts of a victim's nervous system.
About 40 years ago nicotine was sprayed onto crops as an insecticide because many of an insect's nerve synapses use nicotinic cholinergic receptors.
This practice ceased because of the toxicity of nicotine in farmers who were spraying it but the effectiveness of nicotine as an insecticide showed that acetylcholine, the normal neurotransmitter
at nicotinic synapses, is present in insect nervous systems and hence can be expected to occur occasionally in spider venoms as well. And finally, mention
must be made of some nucleotides and nucleosides and also a few simple polyamines such as spermine, spermidine and putrescine that occasionally are detected in spider venoms.
The actions of these as venom toxins are uncertain but probably varied in different species. Some modify gated ion channels in nerve pathways and others
influence tissue cell survival but in general their overall effect seems to be to potentiate the actions of the major peptide toxins in a spider's
It probably is not a good idea to handle any of the larger Australian spiders such as the huntsmen, wolf spiders and some of the orb weavers, but most of them can be left in peace unless they have built their webs in inconvenient places or have ventured a bit too far into our personal space. A few others, possibly including the males of one or two theraphosid species (true tarantulas) and the male of the barychelid, Idiommata iridescens, may indeed have venom capable of causing significant illness in a human victim but these so rarely come in contact with people that the chances of a biting are too small to worry about.
So what seriously dangerous spiders do Australians have to be wary of? The list appears to be remarkably short:
It is important to realize that while the venoms of these spiders are highly toxic to humans we are not their normal prey so they are only biting as a defensive measure and many of their bites will be 'dry' ones. This means their fangs penetrate the skin but little or no venom is injected, a very common occurrence in the case our most dangerous spiders, the Australian funnel-webs. But what are the adverse effects of a bite that does indeed involve the injection of a substantial amount of venom? Severe envenomation by a funnel-web spider can lead to symptoms in less than 30 minutes and because the human body has no natural antibodies against this toxin the victim's condition will continue to deteriorate for many hours. Fortunately, the prompt wrapping of a compression bandage over the bite site can greatly impede the speed with which the venom reaches any vital internal organs. Prior to the development of the funnel-web antivenom by the Commonwealth Serum Laboratories people who were severely envenomated often died within a few days despite the best efforts of hospital emergency staff.
This lethal funnel-web toxin causes a generalized stimulation at synapses all over the body so the victim develops severe muscle twitching and
cramping, rapid and irregular beating of the heart (and eventually cardiac arrest), hypertension, nausea, excessive secretion by the salivary, tear
and sweat glands, severe pulmonary oedema, pain, and eventually coma leading to death. At present it seems that the main toxin in the venom of
Missulena bradleyi (and perhaps some other mygalomorphs) has most of the same effects in the human body though to a lesser extent. The alpha-latrotoxin of
redback spider venom also overstimulates the human nervous system but because it is a much larger molecule than the funnel-web one it is slower to move
away from the bite site and its most noteworthy effect is to cause intense and long-lasting pain.
Unfortunately, Australians do get bitten by spiders from time to time and they often don't even know the identity of the offending spider. So what, if anything, should they do to minimize the chances of a bad outcome? Well, knowing the following facts may help:
1. Adult female redbacks are totally black apart from a distinctive red stripe and red mark on the upper and lower abdomen
1. Male funnel-webs are our greatest spider threat but most localities in Australia will not have them because funnel-webs only thrive in moist forest
habitats. Furthermore, the females remain in burrows in the ground so they will only present a risk if accidentally excavated and even this risk is small
because their venom is much less potent than that of the males. Adult male funnel-webs do wander above ground and into dwellings but only during their
breeding season and usually on cool, rainy evenings. Anyone who is concerned that they may have funnel-webs in their backyard should look for the
characteristic burrow entrance this species builds. If there is no sign of these burrows the probability that funnel-webs will be there is very low, though
it is always possible some individuals might wander in from a neighbouring property. Funnel-web spiders take a long time to create their burrows so they
are rarely present in garden beds or farm land where frequent cultivation occurs. Males are attracted to sources of water (swimming pools, leaking taps,
etc.) and they take several days to drown if they fall into a swimming pool.
2. Checking for the presence of redback spiders in a domestic backyard is a little harder than for funnel-webs. They normally hide in a tangled web in low shrubs or under ledges (including the rims of plant pots) but the presence of their distinctive spherical, off-white egg sacs makes their nests easier to locate. Like funnel-webs they do not normally move far into a domestic dwelling but whereas funnel-webs take a long time to return after being eradicated from a property redbacks will often be back in just a few months.
3. Mouse spider burrows are comparatively rare in most parts of Australia, although they have been found in quite high numbers in a few localities. Their burrows have a door on top and are therefore very difficult to find. Their overall behaviour is otherwise quite similar to that of funnel-webs.
4. If you discover a large dark brown spider behaving as though it might be a funnel-web the chances are it is actually a member of the trapdoor family (Idiopidae) or a 'false' funnel-web (Nemesiidae and Dipluridae) since both of these are much more common in suburban and rural backyards than true funnel-webs and mouse spiders. They are usually brown to dark chocolate in colour but never a glossy pitch-black and while they may behave as aggressively as a male funnel-web they have not been shown to have venom that is seriously toxic to humans.
5. Australia has no above-ground garden spiders that are capable of inflicting a life-threatening bite apart from the redback spider. Many of the orb weavers (Araneidae) are large spiders and tend to construct their webs in places that are inconvenient for humans but all of them prefer to run away rather than attack someone who gets close to them. Only the Salticidae and Oxyopidae can jump in a horizontal direction but many other kinds of spiders may appear to jump when they drop out of their web in an attempt to escape. Some garden spiders, and notably the Salticidae, will bite if trapped against the skin but the result of such a bite is normally only temporary local pain and inflammation at the bite site.
6. Spiders that often venture into houses, sheds and even mail boxes are often a cause for concern to the people who find them. Huntsman spiders
(Sparassidae) are large and very good at running up internal walls and hiding behind doors. They very often pay the supreme penalty for invading someone's
personal space but the reality is they are virtually harmless and can often be captured in a large jar and released unharmed at a remote site. A few
theridiid spiders such as Parasteatoda tepidariorum, Steatoda grossa, and Nesticodes rufipes and also the daddy-long-legs spider (Pholcus phalangioides)
have a tendency to take up residence in and around houses and probably do need to be eradicated from time to time but the reason for this is more the
fact that they build untidy webs than that they are dangerous to humans. And finally, many people occasionally discover a 'plague' of white-tailed
spiders (Lampona species) in their house and are alarmed because they still believe the media reports (now discredited) about the
skin ulceration this kind of spider can cause. In most cases, white-tailed spider infestations resolve themselves spontaneously but
sometimes the intervention of a pest control man is justified.
Email Ron Atkinson for more information. Last updated 13 May 2016.