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Spider Venoms

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.

The anatomy and physiology of spider venom glands
In mygalomorph species the venom glands are located within the large chelicerae these spiders possess. There are probably muscle fibres in the walls of these glands and the ejection of venom may also be encouraged by the many muscle fibres that fill the chelicerae, these muscles also facilitating penetration of the fangs as the spider bites. Venom secretion is under the control of the nervous system but can be induced in a spider that has been anaesthetized by a brief exposure to an atmosphere of carbon dioxide gas. All that is needed is to stimulate the venom glands with electrical impulses from a pair of small electrodes placed on each side of the chelicerae. Venom collected in this way often looks turbid because the stimulation has caused regurgitation of gut contents but clear, uncontaminated venom may sometimes be obtained by fitting thin plastic tubes to the fangs, assuming the fangs are large enough for this technique to be feasable.

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.

What toxic substances are found in spider venoms?
There are several important classes of chemical agents that serve as toxins in spider venoms and while most of them are used by the members of more than one spider family it does appear that individual families vary in their preferred toxin type. An overview of these differences is presented in the next graphic. Why spiders need so many different venom toxins is at least partly explained by the fact that they use their venom both for defence against predators and as a means of immobilizing their prey, either to prevent its escape or before it does major damage to the spider's web (if any). A few venom components also seem to assist spiders in the extracorporeal (outside the spider) digestion of their prey. These multiple roles of spider toxins provide an explanation for the curious fact that some individual toxins are relatively target-specific. For example, the necrotoxins which make Loxosceles (the American recluse or fiddle-back spider) venom so dangerous for humans, rabbits and guinea pigs are claimed to have comparatively little effect on rats and mice, possibly indicating the latter animals have developed some kind of blocking factors in their circulating blood. This certainly is the case for the Australian funnel-web toxin that is lethal for man and other primates but almost harmless to virually all other kinds of vertebrate animals, these having naturally occurring antibodies in their blood to neutralize the funnel-web toxin before it can cause significant adverse effects.

In the following paragraphs each of the seven toxin categories listed in the above table will will be discussed in more detail. The reader needs to understand that so many different spider toxins have now been described that what is presented below can only be an overview. A comprehensive description of the known toxins would be exceptionally lengthy and would also overwhelm anyone who is not a highly trained biological chemist. At the end of this page are a few excellent reference articles that will provide a more complete description for those who would like it. Since many of the types of toxin molecules used by spiders act on the synapses (nerve endings) that link the victim's nervous system to its muscles, glands, and peripheral nerves it is appropriate to first offer a basic explanation of the functioning of a 'typical' synapse and how it can be disrupted by the presence of a toxic agent of some kind.

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.

So how do each of the major spider toxin classes act?
Although the reality is that the venom of most spiders contains a combination of several kinds of toxins, some of which act synergistically, it is also valid to say that the members of each spider family depend particularly on just one or two of the venom component types listed in the table above. Furthermore, the modes or action of the toxin classes are sufficiently different that it is obvious that the one(s) that has been adopted is the one that will best serve the purposes for which the spider needs a venom. This concept will now be further expalined by examining each of the toxin classes in more detail.

(1) Acylpolyamines. A simplified diagram of the typical acylpolyamine structure is shown below. As the name suggests, these are composed of a string of amino (-NH) groups attached via an amino acid linkage to an aromatic ring structure. There may also be an aryl side chain added, the purpose of which is variable and often uncertain. There are also a number of less well known and probably less significant polyamines in the venoms of many spiders but in order to avoid making this page excessively confusing these will not be discussed further.

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.

(2) Peptides with cystine bridge knot structures. This is easily the largest category of known spider toxins, one review article suggesting about 90% of toxins prsent in spider venoms belong in this category. At least 500 different examples have been isolated so far, these collectively being found in 20 spider families, but there are undoubtedly many more waiting to be discovered. Among the mygalomorph families they definitely are present in significant quantities in the Hexathelidae, Actinopodidae and Theraphosidae and are probably present in all of the other families as well. Of the more successful araneomorph families the Ctenidae, Sparassidae, Lycosidae, Oxyopidae and Miturgidae certainly possess them but in the Araneidae and several other major families they seem be minimal significance. With a molecular size of less than 10,000 Daltons these peptides are much smaller than a typical protein toxin, the normal size of which is more than 1,000,000 Daltons. Another distinguishing characteristic of the peptide toxin molecule is that it contains cysteine at several places along its amino acid strand and the sulfur atoms of pairs of cysteine residues link to form disulfide (-S-S-) bridges which twist the amino acid chain into a knot-like configuration.

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 venom.

What Australian spider neurotoxins are known to be dangerous to humans?
While the venoms of most Australian spiders are yet to be tested for toxicity to humans there is no reason to think they will be much different from the ones that have already been examined and some equivalent overseas species. While many people are unjustifiably afraid of spiders the reality is that there are very few species that are known to be capable of causing anything worse than mild and temporary pain and inflammation at the bite site. The majority of species have fangs that are too small to penetrate human skin deeply and their natural instinct is to run away rather than bite. In addition, large animals are not their normal prey so their venom toxins are mostly designed to act on insects rather than vertebrates.

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:

  • males (especially) of all Atrax and Hadronyche species of funnel-web spiders;
  • females of the redback spider, Latrodectus hasselti, and perhaps some Steatoda species; and
  • males of the actinopodid species Missulena bradleyi.

  • 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.

    What can now be done in instances of severe envenomation by one of these dangerous Australian spiders?
    At the time of writing of this page the only antivenoms available for treatment of spider bite victims in Australia are those specific for bites by the redback and funnel-web species. However, there is some evidence that the funnel-web antivenom is effective against the venom of a male Missulena bradleyi spider and the redback antivenom also benefits victims of brown widow and Steatoda spider bites. The following graphic attempts to show the fundamental steps used in the production of the funnel-web antivenom. Development of the redback antivenom preceded that of the funnel-web one and involved the use of horses rather than rabbits as the antibody producer and a slightly different antibody purification method. Another noteworthy difference between the management of cases of funnel-web and redback envenomation is that in the latter case a compression bandage should not be used because it tends to make the pain generated by the venom unbearably intense.

    Why has no antivenom been developed for any Australian spider apart from the redback and the funnel-web? Well, one reason for this is that an examination of clinical records shows that no Australian spider other than the ones just mentioned has a history of making a human victim severely ill. Also, the cost of production of antivenoms for which the demand will be extremely small is likely to be prohibitively high. And finally, antivenom therapy usually carries a significant risk of inducing anaphylactic shock and therefore is rarely performed (assuming an appropriate antivenom even exists) unless failure to administer it places the envenomated person at a high risk of death despite the use of available alternative treatments. Curiously, although the CSL redback antivenom has been used widely for several decades one researcher reported in February 2015 that there is now clinical evidence that this antivenom does not significantly improve either the chances of survival or the speed of recovery after redback envenomation.

    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
    2. Male funnel-web spiders are glossy black (not matt and not furry) apart from the abdomen, which may have a purple hue
    3. Adult male mouse spiders look like funnel-webs but are shorter and wider and have a pale blue abdominal patch
    4. If the spider clearly is not a redback, funnel-web or mouse spider then it probably cannot inflict a lethal bite
    5. No Australian spider has a proven ability to cause severe skin ulceration except by causing a secondary complication
    6. It is a good idea to try to capture the spider that inflicted the bite so an expert can verify its identity
    7. Where the spider was found (on a web, inside a building, etc.) often indicates what kind it could/could not be
    8. If a biting does occur on an arm or leg a compression bandage (but not for redbck bites) will delay symptom development
    9. No medical assistance is needed for most spider bites but a doctor should be consulted if strong adverse effects develop

    What should Australians know if concerned about living in places where contact with spiders is inevitable?
    The following facts should be helpful for such people:

    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.

    Some related sources of information
    The pages on spider food and hazards faced by spiders contain some information relevant to what is covered in the above paragraphs. In addition, the following are worth reading:

    Vassilevski A.A., Kozlov S.A. and Grishin E.V. (2009) "Molecular Diversity of Spider Venom" Biochemistry (Moscow), 74, 1505-1534.

    Kuhn-Nentwig L., Stocklin R. and Nentwig W. (2011) "Venom Composition and Strategies in Spiders: Is Everything Possible?" in Advances in Insect Physiology, 60, Editor J. Casas, Elsevier Ltd. (ISBN: 978-0-12-387668-3)

    Windley M.J., Herzig V. and Nicholson G.M. (2012) "Spider-Venom Peptides as Bioinsecticides" Toxins (Basel), 4, 191-227.

    Isbister G.K. and Gray M.R. (2003) "White-tail spider bite: a prospective study of 130 definite bites by Lampona species," Med. J. Aust., 179, 199-202.

    Isbister G.K. & Whyte I.M. (2004) "Suspected white-tailed spider bite and necrotic ulcers", Internal Medicine Journal, 34, 38-44


    Email Ron Atkinson for more information.    Last updated 13 May 2016.