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Poisoning due to fungi, plants, and animals 

Poisoning due to fungi, plants, and animals
Poisoning due to fungi, plants, and animals

D Nicholas Bateman

, Robert D Jefferson

, Simon HL Thomas

, John P Thompson

, and J Allister Vale

Page of

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Subscriber: null; date: 13 August 2020

Poisonous fungi


Most fungi are not toxic, but several species (around 100 worldwide) can produce clinical toxicity. Exposures to potentially toxic fungi tend to occur in two main scenarios. Young children, who normally eat only small quantities of raw material, and consumption by adults of larger quantities, often foraged. Misidentification in the latter situation may result in accidental ingestion of a poisonous species and the production of a range of clinical features some of which can be associated with serious sequelae. Some fungal toxins are denatured by heat, but others are not, so it is important to understand the precise nature of the ingestion.

In assessing toxic risk it is useful to have information from a mycologist. It may be helpful to take photographs of any uncooked specimens for transmission for identification by smartphone or e-mail. Information on a number of aspects will also be useful, including the following:

  • At what time were the mushrooms eaten?

  • When was the onset of symptoms after the ingestion?

  • Was more than one kind of mushroom ingested?

  • Are all persons who ate the mushroom ill?

  • Are persons in the group who ate none of the mushroom ill?

  • Was the mushroom eaten raw or cooked?

  • If cooked, how and how long were they cooked (i.e. sautéed, fried, soup, stew, etc.)?

  • Was any alcohol consumed with a meal?

  • Were the mushrooms eaten at more than one meal? If so, were they reheated?

  • Were specimens with old or wormy fruit-bodies gathered?

  • How were the mushrooms stored and transported between collection and preparation?

  • What was the condition of the mushrooms at the time of preparation? Were they cleaned before being put into the basket? (Note: important identifying features may be destroyed during cleaning.)

  • Were the mushrooms put in plastic bags (and did they become slimy)?

  • What was it growing on (i.e. wood, soil, etc.)?

  • In a wild area or a cultivated area?

  • What kind of tree(s) was it growing near?

  • What time of year was the mushroom collected?

It is convenient to divide fungi according to the clinical syndromes they produce. The common species and their toxidromes are outlined in Table 13.1.

Table 13.1 Common fungi and their toxidromes


Responsible species include:

Timing of symptom onset

Summary of symptoms


Amanita phalloides

5–24 hours

Latent phase: a duration of <8 hours is associated with poor outcome

Amanita virosa

5–24 hours post ingestion. Duration: 1–2 days

Phase 1: sudden onset abdominal pain and watery diarrhoea, vomiting, and thirst

Duration: 12–36 hours

Phase 2: phase of ‘well-being’ in which GI symptoms abate; however, liver and renal function may deteriorate. In severe cases this period may not occur

2–6 days post ingestion

Phase 3: hepatic and renal failure, hypoglycaemia, seizures, coma, and death


Coprinus atramentarius

20 minutes–2 hours after ethanol consumption

Disulfiram-like reaction in presence of ethanol. Features include flushing of the face, neck, and chest, metallic taste, nausea, vomiting, tachycardia, headache, anxiety, and hypotension. Toxicity does not develop unless ethanol is consumed.

Can occur up to 5 days after mushroom consumption

GI toxins

Many species

30 minutes–3 hours

Nausea, vomiting, diarrhoea, and abdominal pain, normally resolving within 24 hours


Gyromitra esculenta

2–24 hours (mostly 5–15 hours) post ingestion

Phase 1: bloating followed by abdominal cramps, vomiting and watery diarrhoea (which may persist), headache and lethargy/weakness

36–48 hours post ingestion

Phase 2: seizures, coma, liver toxicity with jaundice, intravascular haemolysis and methaemoglobinaemia, renal failure, and respiratory failure

Immune mechanism (unknown toxin)

Paxillus involutus

Haemolytic anaemia, particularly in patients who have previously ingested the fungus


Inocybe spp.

15–300 minutes post ingestion

Cholinergic features including increased secretions (sweating, salivation, lachrymation) miosis, blurred vision, abdominal pain, watery stools, and asthmatic wheezing. Bradycardia and hypotension in severe cases

Clitocybe rivulosa, Omphalotus olearius

Muscimol (and ibotenic acid which is converted to muscimol)

  • Amanita gemmata

  • Amanita muscaria

  • Amanita pantherina

30–120 minutes. Duration: c.12 hours

Drowsiness, confusion, ataxia, euphoria, fluctuating conscious level, delirium, visual or auditory hallucinations, hyper-reflexia, myoclonus, seizures, coma


Cortinarius spp.

36 hours–17 days post-ingestion

Latent phase: the shorter the latent phase, the more severe the toxicity. If >6 days, long-term effects are unlikely; if <2–4 days, renal failure may be irreversible

Duration: around 7 days

Pre-renal phase: anorexia, nausea and vomiting, headache, chills, sweats (without pyrexia), thirst. and polyuria

7–21 days

Renal phase (50–70% cases): loin pain, anuria, renal dysfunction and renal failure


  • Psilocybe cyanescens

  • Psilocybe semilanceata

30–240 minutes

Nausea, vomiting, abdominal pain, flushing of the face and neck, tachycardia, dilated pupils, impaired judgment, euphoria, ataxia, drowsiness (progressing to sleep)

Fungi producing gastrointestinal features

GI features occur commonly in poisoning with fungi. Several species causing serious toxicity to other organs can also cause GI features. It is important therefore to monitor closely all patients with GI features after ingestion of fungi for clinical and biochemical signs of toxicity affecting other organ systems. Baseline biochemistry is of value in identifying and monitoring future changes. A few of the fungi in the following list are toxic when raw, whereas others can cause symptoms despite having been cooked.

Those fungi generally associated only with GI features include:

  • Agaricus placomyces, A. semotus, and A. xanthodermus (Yellow Stainer)

  • Boletus species such as the Lurid Bolete (B. luridus), the Devil’s Bolete (B. satanus), B. legaliae and B. rhodopurpureus

  • Chlorophyllum molybdites (False- or Green-spored Parasol of North America)

  • Coprinus species such as Hygrophoropsis aurantiaca (False Chanterelle)

  • Entoloma sinuatum (Livid Entoloma)

  • Lactarius helvus (Fenugreek Milkcap), L. torminosus (Wooly Mikcap)

  • Mycena pura (Lilac Bonnet)

  • Omphalotus illudens

  • Pholiota squarrosa (Shaggy Scalycap)

  • Russula emetica (Sickener), R. nobilis (Beechwood Sickener)

  • Scleroderma citrinum (Common Earth-Ball)

  • Stropharia aeruginosa (Verdigris Agaric)

  • Tricholoma sulphureum (Sulphur Knight), and T. saponaceum (Soapy Knight).

Clinical features

Early onset (normally within 3 hours) of nausea, vomiting, diarrhoea, and abdominal pain, normally resolving within 24 hours.

The Common Ink Cap (Coprinus atramentarius) can produce an ‘antabuse’-like reaction caused by the toxin, coprine (or a metabolite of coprine), inhibiting aldehyde metabolism after alcohol ingestion. This may last for up to 5 days. The Club-footed Clitocybe (Ampulloclitocybe clavipes) can cause similar symptoms, but does not contain coprine.


This is generally supportive and symptomatic. Appropriate management of fluid balance is needed. Identification of the causative mushroom will assist in reassuring all involved.

Fungi producing hepatotoxic features

Certain fungi contain cyclopeptides (e.g. amatoxins, phallotoxins, and virotoxins) that are potent hepato-toxins, producing fatty degeneration and centrilobular necrosis. Such fungi include the Amanita species Amanita phalloides (Death Cap) and A. virosa (Destroying Angel). Several Lepiota species contain amatoxins, including Lepiota brunneoincarnata (Deadly Dapperling), as well as some Galerina species, such as Galerina marginata.

Clinical features

A latent period of 5–24 hours is followed by GI toxicity (e.g. nausea, profuse vomiting, cramping abdominal pain and watery diarrhoea hypotension, tachycardia, lactic acidosis and metabolic acidosis, electrolyte abnormalities and renal toxicity). This may be followed temporarily by an apparent recovery period before signs of liver damage may appear after 2–6 days, sometimes progressing to severe jaundice, liver and kidney failure, and death.

The shorter the interval between ingestion and onset of diarrhoea, the worse the prognosis. An interval of less than 8 hours after ingestion appears to indicate poor prognosis.

This GI phase may last for 1–2 days, before a transient improvement occurs for 12–36 hours.

Later feature: hepatic central lobular necrosis occurs after 2–6 days resulting in jaundice and liver failure, the complications of which include coma, hypoglycaemia, disseminated intravascular coagulation, and haemorrhage. Hypoglycaemia may also occur earlier, from direct insulin-releasing effects of the toxins on the pancreas. Acute tubular necrosis leads to renal failure. Tachycardia, hypotension which may be severe, hypocalcaemia, cardiomyopathy, muscle twitching, and convulsions may also occur.


Treat symptomatically with fluid replacement and correction of acidosis. In some areas of the world specific tests for amatoxins are available to confirm diagnosis, but not in the UK.

Observe asymptomatic patients for a minimum of 24 hours if ingestion of Amanita phalloides is thought likely (beware latent period). It is very important to verify the type of mushroom, if possible by a mycologist.

Treatment with multiple doses of oral activated charcoal is of theoretical benefit because amatoxins are excreted in bile and activated charcoal is likely to interrupt entero-hepatic circulation. However, there are no controlled trials which demonstrate benefit and use is often precluded by severe vomiting. Nevertheless, provided the patient is not vomiting and the airway can be protected, multiple-dose activated charcoal should be considered.

Check U&Es, creatinine, full blood count, and LFTs. Consider checking arterial blood gases in symptomatic patients. Ensure adequate hydration and monitor urine output. If the patient has deranged LFTs, check prothrombin time, which is the single most useful prognostic test of liver failure.

Early convulsions or coma may be due to hypoglycaemia so monitor plasma glucose concentrations.

Correct hypoglycaemia and treat convulsions conventionally. Single brief convulsions do not require treatment.

Penicillin reduces the uptake of amatoxins into the liver in experimental models and benzylpenicillin has been used in the treatment of poisoning. Doses of 300 mg/kg/day (0.5 million units/kg/day) as a continuous infusion for 2–3 days from the day of ingestion, with close monitoring of renal function, have been suggested. NB Giving IV benzylpenicillin too rapidly may cause convulsions. Penicillin allergy should be excluded. The evidence base for this, and other specific treatments is poor. Renal and hepatic damage is managed conventionally, and liver transplantation has been required occasionally.

The following are of no confirmed benefit: constant duodenal aspiration to prevent enterohepatic circulation of amatoxins; intravenous N-acetylcysteine; early plasmapheresis, haemodialysis or haemoperfusion for removal of circulating amatoxins; silibinin; and thioctic acid.

Fungi producing nephrotoxic features

The Deadly Webcap (Cortinarius rubellus), Fool’s webcap (C. orellanus), and some other Cortinarius species contain a range of toxins, including orellanine, a nephrotoxin which can cause interstitial nephritis and acute tubular necrosis after a latent period of 7–21 days. Two north-western US species, Smith’s Amanita (Amanita smithiana) and the Abrupt-bulbed Lepidella (A. abrupta) and also A. proxima (in Spain) and A. pseudoporphyria (in Japan) have also been associated with acute kidney injury after 6–24 hours, probably as a result of an acute tubulopathy. It has been suggested that 2-amino-4,5-hexadienoic acid may be the responsible toxin.

Clinical features

In Cortinarius poisoning features are delayed and occur in three phases:

  • The latent phase lasts for at least 36 hours, but rarely up to 17 days, post ingestion. The shorter the latent phase, the more severe the toxicity. A latent phase of more than 6 days suggests long-term effects are unlikely, while less than 2–4 days suggests that renal failure may be irreversible.

  • The pre-renal phase is predominantly gastrointestinal and lasts for around 7 days. Nausea, vomiting, diarrhoea, abdominal pain, anorexia, and headache are common. A burning sensation in the mouth causes intense thirst, polyuria, and polydipsia. Other features include chills, shivering, sweating, muscle and loin pains, liver damage, paraesthesiae, fatigue, tinnitus, and seizures.

  • The renal phase: usually occurs after 7–21 days (occasionally earlier). 50–70% of patients develop some renal involvement, 10–15% are likely to develop chronic renal failure. The main pathology is interstitial nephritis with leucocyturia, proteinuria, haematuria; oliguria occurs initially followed by anuria.

Damage may be reversible with renal function recovering slowly over 3–4 weeks in mild cases or several months in more severe cases. An initial recovery of renal function may not be sustained, and permanent renal damage can occur.


Symptomatic and supportive. Dialysis may sometimes be required, and renal transplantation has been performed in some cases of chronic renal failure associated with Cortinarius poisoning.

Fungi producing haematological features

The Brown Roll-rim (Paxillus involutus) may cause haemolytic anaemia by an immune mechanism, (involving IgG) particularly in patients who have previously ingested the fungus.

Clinical features

Severe haemolysis and shock may result in acute kidney injury in affected individuals.


Plasma exchange has been used to remove possible immune complexes, and the renal failure is treated conventionally.

Fungi producing toxicity to muscles

Ingestion of Tricholoma equestre (Yellow Knight) also known as T. flavovirens and of Russula subnigricans (the Blackening Russula found in China and North America) have been associated with rhabdomyolysis occurring 24–72 hours later.

Clinical features

Nausea (without vomiting) and muscle pain (especially of the quadriceps), and/or weakness may be accompanied by features of acute myocarditis and hyperthermia.


There are no specific antidotes and management is symptomatic.

Fungi producing cholinergic (muscarinic) features

This toxidrome is produced by the cholinomimetic, muscarine which is present in several fungi, including Clitocybe rivulosa, (False Champignon or Fool’s Funnel), Inocybe, and Omphalotus olearius (Jack-o-Lantern).

Clinical features

Symptoms occur early, often between 15 minutes and 5 hours after ingestion, and reflect the effects of muscarine. These include: increased perspiration, salivation, lachrymation, vomiting, abdominal pain, diarrhoea, urgency of micturition, flushing, bradycardia, hypotension, constricted pupils, and blurred vision.


Supportive and symptomatic. Atropine may be required if peripheral cholinergic features are troublesome.

Fungi producing neuropsychiatric features

The Jewelled Deathcap (Amanita gemmata), Fly Agaric (Amanita muscaria), and Panther cap (Amanita pantherina) contain ibotenic acid (a glutamate receptor agonist), and muscimol (a GABAA receptor antagonist). Psilocybe species such as the Bluing Psilocybe (Psilocybe cyanescens) and the Liberty Cap (P. semilancealata) (‘Magic mushrooms’) contain the hallucinogenic agents psilocybin and psilocin. These fungi are often picked and ingested for these psychoactive effects as agents of misuse. As the quantity of toxin varies with season, variety, and age of the fungus fruiting parts, effects may be unpredictable, and in some cases prolonged.

Clinical features

Amanita gemmata, A. muscaria, and A. pantherina ingestion may result in the early onset (30–120 minutes) of GI symptoms (not always prominent), which may be accompanied by somnolence or agitation, with visual and/or auditory hallucinations. Bradycardia and pyrexia have also been reported. CNS effects usually peak around 2–3 hours post ingestion and usually wear off within 12 hours but may be followed by a deep sleep. Drowsiness may persist for 24 hours. A residual headache may last for days. Retrograde amnesia is a frequent result of poisoning. Delirium, hyper-reflexia, myoclonus, seizures (more commonly in children), and coma have also been noted in more severe poisoning.

Psilocybe cyanescens may also be associated with visual and/or auditory hallucinations that may persist for several days. Physical effects include nausea, vomiting, abdominal pain, flushing of the face and neck, tachycardia, dilated pupils, diastolic hypertension, and drowsiness. Rhabdomyolysis leading to renal failure, arrhythmias, and myocardial infarction have been reported. Methaemoglobinaemia and abnormal LFTs have sometimes been reported after IV abuse of fungal extracts. CNS effects are common initial symptoms including dizziness, confusion, euphoria and ataxia (i.e. resembling alcohol intoxication), myoclonus, hyperkinesia, and seizures. Neuropsychiatric effects vary from restless over-activity with lack of cooperation and aggressiveness to withdrawn, uncommunicative staring. Perceptual abnormalities such as visual hallucinations, distorted body image, sounds, and tactile sensation may occur. Ability to judge heights and distances may be grossly impaired. These effects occasionally persist for some days.


Agitation in adults may necessitate benzodiazepine administration (NB it is normally better to manage agitation without sedation in children). Benzodiazepines may also be needed to treat convulsions. Atropine is not recommended, since it is thought to increase the adverse effects of ibotenic acid. In patients with more severe features, such as hallucinations or psychosis, an antipsychotic such as haloperidol may be required.

Fungi producing neurological features

Gyromitra esculenta (False Morel) contains gyromitrin, which is hydrolysed in the body to monomethylhydrazine (MMH) an inhibitor of GABA synthesis, which may cause convulsions and methaemoglobinaemia. Further MMH metabolism can lead to hepatic damage.

A rare toxidrome consisting of delayed onset of decreased visual acuity, somnolence, weakness, and reduced motor tone and activity occurring 24 hours after the ingestion of Hapalopilus rutilans (Purple-Dye Polypore) mushrooms has been attributed to the toxic effects of polyporic acid, a dihydrorotate dehydrogenase inhibitor. There may be associated hepatic and renal dysfunction.

Clinical features

In poisoning with Gyromitra esculenta, GI symptoms (occurring after 2–24 hours) include bloating, abdominal cramps, vomiting, and watery diarrhoea. Headache and lethargy/weakness, tremor, nystagmus, ataxia, slurred speech, mydriasis, delirium, coma and convulsions may also occur. Later features include liver toxicity with jaundice, intravascular haemolysis and methaemoglobinaemia, renal failure, and respiratory failure.


Treatment of Gyromitra esculenta poisoning is supportive and symptomatic. Intravenous pyridoxine may be considered in treating convulsions and possibly also to reduce the risk of, or treat, established hepatic damage. Methylene blue may be indicated if methaemoglobinaemia occurs. Management of poisoning with Hapalopilus rutilansis is also symptomatic and supportive, although repeated-dose activated charcoal has been advocated.

Further reading

Diaz JH (2005). Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med, 33:427–36.Find this resource:

Fungi of Europe: <>.

Kibby G (1997). An illustrated Guide to Mushrooms and other Fungi of Britain and Northern Europe. London: Parkgate Books Ltd.Find this resource:

    Levine M, Ruha A-M, Graeme K, et al. (2011). Toxicology in the ICU Part 3: natural toxins. Chest, 140:1357–70.Find this resource:

    UK Mushrooms: <>.

    Common plant poisonings


    Most accidental ingestions of plant material by small children do not result in more than minor symptoms; however, deliberate ingestion of some plants can cause serious features or even death. All patients who have deliberately ingested toxic plants need referral for psycho-social assessment as well as medical treatment. In some cases collecting wild plants for food has resulted in ingestion of misidentified plants and this can also cause problems.

    When contacting a poisons centre about a plant poisoning it is preferable to have the Latin name of the plant, as many common names can refer to more than one plant, e.g. laurel, oleander. Poisons centres do not generally attempt to identify plants over the telephone. If identification is required then botanic gardens or garden centres may be able to help and photographs of the plant may aid identification.

    In the UK plant poisonings represent less than 1% of enquiries to poisons centres. Table 13.2 shows the most common plant accesses on TOXBASE® in 2011.

    Table 13.2 Most common TOXBASE® plant accesses in 2011 (total 2011 product accesses >1.3 million)



    Capsicum (chillies)


    Amaryllidaceae (daffodil)


    Saintpaulia ionantha (African violet)


    Taxus baccata (yew)


    Laburnum anagyroides


    Lily (supermarket type e.g. Asiatic, Oriental)


    Atropa belladonna (deadly nightshade)


    Valeriana officinalis (valerian)


    Digitalis purpurea (foxglove)


    Laurus nobilis (laurel, bay tree)


    Data from TOXBASE®, 2011, National Poisons Information Service.

    In considering plants and their toxic hazard it may be useful to classify them in various groups depending on their properties. These include either their toxic hazard, low or high, or their mechanism of causing symptoms. This section includes both approaches and provides illustrative examples. Low-toxicity plants are grouped in Box 13.1. Some plants are only available at certain times of the year and cause seasonal exposures (Box 13.2).

    Plants of low toxicity

    • Lilium spp. (stargazer lilies, oriental lilies, Easter lilies)—this includes most of the lilies bought in supermarkets but not lily of the valley, peace lily, calla lily which belong to other families. NB Lilium species are extremely toxic to cats.

    • Saintpaulia ionanthe (African violet) is considered to be of very low toxicity but may cause dermatitis.

    • Sorbus aucuparia (rowan, mountain ash) contains parasorbic acid, which is an irritant. The cooked berries are said to be edible. Ingestion of raw berries may cause mild GI upset.

    • Valeriana officionalis (valerian) is considered to be of low toxicity and is used extensively in herbal preparations. Ingestion may cause drowsiness.

    Plants which cause irritation

    • Aesculus hippocastanum (horse chestnuts, conkers) contain aesculin and ingestion of large quantities is likely to cause GI upset. Allergic reactions have been reported.

    • Capsicum species (chilli peppers) contain capsaicin which is severely irritating to respiratory tract, causing a burning sensation to mucous membranes, eyes, and skin. Inhalation may cause irritation, bronchospasm, and pulmonary oedema. Cold water or vegetable oil may give some relief for skin irritation.

    • Euphorbia spp., e.g. Euphorbia helioscopia (sun spurge), which contains diterpene esters in the sap is very irritant to eyes and skin. Although Euphorbia pulcherrima (poinsettia) was formerly thought to be toxic no serious cases have been reported recently and it is probably less irritating than other members of the Euphorbia spp.

    • Laurus nobilis (laurel, bay tree, sweet bay), is an irritant and is unlikely to cause more than GI upset, if ingested. However, bay leaves used in cooking and accidentally ingested have occasionally lodged in the GI tract, requiring surgical removal.

    Generally ingestion of the above plants and those mentioned in Box 13.1 require only symptomatic treatment. Wash contaminated skin well with soap and water.

    Toxicodendron spp, Rhus spp. (poison ivy, poison sumac, poison oak). All parts of the plant contain urushiol. This plant is generally found in North and Central America but since the onset of symptoms may be delayed patients may report symptoms after returning from holiday. Contact can be direct with damaged plants, indirect with clothing or shoes, or even from smoke from burning plants. Allergic contact dermatitis results in symptoms (redness, pruritus and bullae in severe cases) within 24–48 hours and lasting up to 2 weeks. Washing is only effective within 10 minutes of contact. For moderate cases calamine lotion, cold compresses, and topical corticosteroids may help. In more severe cases systemic corticosteroids should be given early and oral antihistamines may be useful.

    Oxalate containing plants include:

    • Amaryllidacae spp. (daffodil, narcissus)—dermatitis from handling the bulbs; severe nausea and vomiting from eating raw or cooked bulbs (mistaken for onions) may last 3–4 hours. Treatment is symptomatic with an antiemetic if required.

    • Rheum raponticum (rhubarb)—causes dermatitis; ingestion of large amounts of the leaves (cooked or uncooked) has resulted in corrosive features. The systemic features of oxalate toxicity are unlikely, but include hypocalcaemia, tetany, convulsions, renal and hepatic damage, and death.

    • Spathiphyllum spp. (peace lily), Zantedeschia aethiopica (calla lily, altar lily), Monstera deliciosa (swiss cheese plant), Arum maculatum (lords and ladies), and Dieffenbachia (leopard lily) all cause severe irritation of the buccal mucosa with a painful burning sensation and hypersalivation with a risk of obstruction of the airway if oedema occurs. Cold drinks or ice cream may be helpful.

    Plants that cause photosensitization

    Hypericum perforatum (St John’s wort) is of low toxicity if ingested. Over-the-counter tablets are used to treat mild depression. Ingestion of large quantities of the plant (but not skin contact) can cause photodermatitis, i.e. dermatitis which develops after subsequent exposure to the sun, which should be managed conventionally.

    Skin contact with Heracleum mantegazzianum (giant hogweed) results in dermatitis and photosensitization after exposure to sunlight, resulting in erythema, burn-like lesions, and large fluid filled blisters developing over 24–48 hours. All patients even if asymptomatic should be protected by covering the skin or wearing sun-block for at least 48 hours after exposure. Itching may be relieved with tepid baths, cool compresses, calamine lotion, steroid creams, and oral antihistamines. Patients with severe dermatitis should be reviewed by a burns specialist. Hyperpigmentation may occur and does not require treatment but skin may be sensitized for years and sun screen should be used. Ingestion may cause irritation, hypersalivation, GI upset, and also photosensitization. For ingestion manage symptomatically and advise to avoid going out in the sun for at least 12 hours.

    Plants that contain cyanogenic glycosides

    A number of plants contain cyanogenic glycosides and can potentially cause cyanide poisoning in large quantity e.g. members of the Prunus family (Prunus armeniaca (apricot); Prunus dulcis x. amara (bitter almonds); Prunus laurocerasus (ornamental cherry, cherry laurel); Prunus spinosa (blackthorn, sloe)—may also cause thorn injury, see ‘Plant thorn injury’ later in this section). In these cases accidental ingestion of small quantities (e.g. one or two apricot kernels ingested by a child) is unlikely to cause toxicity but may cause obstruction. Apricot kernels contain amygdalin and extracts have been falsely claimed to be a cancer cure (laetrile), and this use has occasionally resulted in cyanide toxicity. Early features may include dizziness and drowsiness leading in severe cases to coma, cardiovascular collapse, respiratory depression, and pulmonary oedema. See Cyanide, pp. [link][link], for further information on cyanide.

    Cotoneaster spp. also contain cyanogenic glycosides but in low concentrations and ingestion of berries does not usually causes more than GI upset. Only symptomatic treatment is required.

    Pyracantha spp. (firethorn) contain cyanogenic glycosides in low concentrations and ingestion of berries does not usually cause more than GI upset requiring symptomatic treatment. Injury from plant thorns may result in local irritation, erythema, pain, and swelling—see ‘Plant thorn injury’ later in this section.

    Sambucus nigra (elder) does contain cyanogenic glycosides but the flowers and ripe cooked berries are not toxic. Ingestion of raw berries and other parts of the tree may cause weakness, dizziness and numbness. In severe cases consider cyanide toxicity (see Cyanide, pp. [link][link]).

    Toxic plants

    Abrus precatorius (jequirity beans, rosary peas) are used in jewellery due to their bright colour and in Ayurvedic medicine. They contain abrin which is highly toxic. A single seed may pass through, but if chewed, ground, or pierced (as in a necklace) it is potentially fatal. All cases should be managed in hospital and should be discussed with a poisons centre. Initial features are gastrointestinal followed by neurological and in severe cases multiorgan failure occurs resulting in death up to 4 days after ingestion. Treatment of hypotension, ECG abnormalities, convulsions, and metabolic acidosis may be required.

    Aconitum napellus (aconite, monkshood, wolf’s bane) is probably the most toxic of UK plants and contains aconitine, a potassium efflux channel blocker. All parts of the plant are toxic and ingestion causes nausea, vomiting, diarrhoea, paraesthesia, tachyarrhythmias, convulsions, coma, and death. Serious cases should be discussed with a poisons centre. Cardiac resuscitation may be required and conventional management for hypotension, bradycardia, and arrhythmias. If unresponsive, intravenous lipid emulsion may be tried.

    Atropa belladonna (deadly nightshade) contains hyoscyamine (atropine) and scopolamine (hyoscine). Ingestion can cause anticholinergic effects and may require management of hypotension, convulsions, and delirium (see sections in Chapter 3, pp. [link][link]).

    Colchicum autumnale (Autumn crocus) and Gloriosa superba (flame lily, glory lily) both contain colchicine especially in the corms. All patients should be referred to hospital. Features after ingestion may be delayed for 6 hours and can last 7 days or more. Initial features include severe GI upset, hypotension, and cardiogenic shock. Later features after 24 hours may include bone marrow suppression leading to sepsis, acute respiratory distress syndrome, renal failure, DIC, and direct cardiotoxic effects. Management will require treatment of hypotension, hyperthermia, and convulsions. Death is usually the result of intractable hypotension and asystole. For more information see Colchicine, pp. [link][link].

    Cicuta virosa (cowbane, water hemlock) contains cicutoxin, a potent, non-competitive GABA receptor antagonist. All parts of the plant are toxic, especially the roots. Features usually start within 1 hour of ingestion but can be delayed for 10 hours and may last up to 4 days. Poisoning is characterized by severe convulsions. There may also be cardiac features and neurological complications. Intensive supportive treatment will be required with management of convulsions, hypotension/hypertension, bradycardia, agitation, hyperthermia, metabolic acidosis, and rhabdomyolysis.

    Conium maculatum (hemlock) contains toxic alkaloids including coniine and all parts of the plant are toxic. Initial features develop within 15 minutes–3 hours after ingestion and include irritation, and tachycardia followed by bradycardia, and muscular paralysis leading to respiratory failure. Rhabdomyolysis and convulsions may also occur. Treatment may require management of hypotension, bradycardia, convulsions, and rhabdomyolysis. Death has occurred within 2 hours of ingestion.

    Digitalis purpurea (foxglove) contains cardiac glycosides and causes poisoning similar to digoxin (see Digoxin, pp. [link][link]). All patients should be referred to hospital. Initial features within 6 hours include GI features and later marked bradycardia and arrhythmias which may require treatment with digoxin-specific antibodies. Management of hypo/hyperkalaemia, metabolic acidosis, hypotension, and cardiac arrhythmias may be required. Note when requesting a digoxin concentration it is important to specify that it is due to plant material since methods vary. Similar features occur with Nerium oleander (pink oleander), Thevetia peruviana (yellow oleander), Convollaria majalis (lily of the valley), and Drimia maritime (sea squill) which also contain cardiac glycosides. In serious cases where considering the use of digoxin-specific antibodies consult a poisons centre for dosage.

    Laburnum anagyroides is generally considered to be toxic but few serious poisonings have occurred in recent years. While all parts of this tree are potentially toxic (especially the pods and seeds) it contains cytosine which is an emetic and this may limit toxicity. Common effects are nausea, vomiting, and abdominal pain and if these do not develop within about an hour subsequent toxicity is unlikely. In more severe cases there may be convulsions and cardiac effects which should be managed conventionally. Clinical effects may last up to 48 hours.

    Ricinus communis (castor oil plant, castor beans) contains ricin in the seeds (see Ricin and abrin, pp. [link][link]). Swallowing the beans whole may not cause problems but fatalities have occurred after chewing and swallowing beans. All patients should be referred to hospital. However, ricin is less toxic by ingestion than by inhalation or injection. Contact with the beans may also cause allergic reactions. GI upset usually occurs within a few hours of ingestion followed by drowsiness, confusion, convulsions, intravascular haemolysis, metabolic acidosis, and ECG abnormalities. Allergic reactions have been reported following inhalation and skin contact with castor bean dust. Note that the plant Fatsia japonica is also known as the castor oil plant but is much less toxic and is expected to cause only mild GI upset.

    Taxus baccata (yew) contains taxane alkaloids (used clinically as cytotoxics). All parts of the plant are toxic with the exception of the fleshy red part of the berry. Ingestion of the whole berry or the fleshy red part of the berry is unlikely to cause more than nausea and vomiting. Chewing the berries or seeds or ingestion of other parts of the tree can result in hypotension, bradycardia, cardiac arrhythmias, respiratory depression, convulsions, coma, and death. Cardiac monitoring and pacing may be required.

    Plants that may be abused

    Cannabis sativa and Cannabis indica both contain tetrahydrocannabinol. Adults are unlikely to require treatment after ingestion or smoking but agitation should be controlled with diazepam or haloperidol. Children who have accidentally ingested cannabis may develop coma and all children should be observed for 6 hours after ingestion. Advice of a paediatrician should be sought in serious cases.

    Catha edulis Forsk (khat) contains cathinone, norpseudoephedrine, norephedrine, sympathomimetic alkaloids, and tannins. Khat is commonly used in African and Middle Eastern countries for its mildly euphoric properties. Leaves are chewed and the liquid swallowed giving effects lasting 20 minutes to several hours. Euphoria is followed by irritability, depression, anorexia, and insomnia. A variety of side effects may occur from single and chronic use and management of agitation, hypo- or hypertension, tachycardia, and hyperthermia may be required. Note that a drug of abuse screen will be positive for amfetamines.

    Datura stramonium (jimson weed, thorn-apple) contains atropine, scopolamine, and hyoscyamine, especially in the seed pods and is abused for its hallucinogenic potential. Features after ingestion are those of anticholinergics (see The anticholinergic syndrome, pp. [link][link]). Brugmansia spp. (angel’s trumpet) contains scopolamine, hyoscyamine, and atropine, and produces similar effects.

    Ephedra spp. (Ma Haung) are used in herbal preparations for asthma and fevers, in dietary supplements, and in some herbal ecstasy tablets. Sympathomimetic features (see The stimulant syndrome, pp. [link][link]) are expected and substance dependence has developed.

    Myristica fragrans (nutmeg) is abused for its hallucinogenic features (reported from one to three nutmegs or 5–20 g of ground nutmeg). Symptoms appear within 1–8 hours of ingestion and may last at least 36 hours. There may be GI, cardiovascular, and CNS effects and management of agitation and hypertension may be required.

    Lophophora williamsii (peyote cactus) contains mescaline and is abused for its hallucinogenic effects which are similar to LSD (see Psychedelic agents, pp. [link][link]). GI effects occur within 30–60 minutes and hallucinogenic effects in 1–2 hours lasting 12–18 hours. Management of agitation, hypertension, hyperthermia, and rhabdomyolysis may be required.

    Ipomoea purpurea (morning glory) seeds contain an indole alkaloid similar to LSD. Clinical features including restlessness and heightened awareness, auditory and visual hallucinations, disorientation, anxiety, violent behaviour, and flashbacks. Agitation should be managed with diazepam or haloperidol (see Delirium (acute confusional state) pp. [link][link]).

    Herbal products

    Licensed herbal products are unlikely to cause toxicity. Some herbal products have been banned in the UK (< restrictedherbalingredients/index.htm>), e.g. Aristolochia spp. (renal failure and cancers), Piper methysticum (kava kava) permitted for external application—hepatic failure and acute dystonic reactions reported after oral use.

    Chinese herbal medicine and Ayurvedic medicine are becoming more popular in the West and medicines brought from developing countries or over the Internet may contain pharmaceuticals, disallowed herbals, and heavy metals.

    Other sources of plant poisoning


    There have been reports of poisoning from honey where the bees have collected nectar from poisonous plants but this has not been reported in the UK. The plants involved include those containing:

    • Pyrrolizidine alkaloids (e.g. Senecio jacobaea, ragwort). Poisoning with these is more common in animals. Toxicity is more likely following chronic ingestion. Liver function tests should be checked.

    • Grayanotoxins (e.g. Rhodendron spp., azalea) which are sodium channel agonists. Ingestion of the flowers, decoctions of the plant, or honey from bees that fed on the plants has lead features such as nausea, vomiting, dizziness, hypotension, and cardiac complications which may required treatment with atropine.

    Plant thorn injury

    Plant thorn injury may occur from hairs or thorns from, for example, cacti, rose bushes, blackthorn, etc. Damage may be mechanical with intense pain and a histamine-like reaction. Thorns should be removed completely, otherwise secondary infection and ulceration may develop over days or weeks, which may require topical steroids and antibiotics.

    Essential plant oils

    These are used in aromatherapy and the pure oils (undiluted) are highly toxic. Doses of up to 10 mL clove oil have caused serious toxicity in children, Symptoms start within 30 minutes–4 hours and all children and adults should be observed for at least 6 hours after ingestion. Hypoglycaemia, metabolic acidosis, convulsions, and liver and renal failure may occur in severe cases. Aspiration may cause pneumonitis. Splashes in the eye may cause severe irritation and corneal damage (Essential oils, pp. [link][link]).

    Red kidney beans

    Red kidney beans contain a phytohaemagglutinin, which is destroyed on adequate cooking. Ingestion of raw or partially cooked beans causes acute gastroenteritis within 1–2 hours, and lasting 3–4 hours.

    Where to get advice

    Plants may be identified by Botanic Gardens or a local garden centre. Advice on management may be obtained from a poisons centre (or public health advice call centre if appropriate) or TOXBASE® (if registered).

    Further reading

    Chan TY (2009). Aconite poisoning. Clin Toxicol, 47:279–85.Find this resource:

    Dauncey EA (2010). Poisonous Plants – A Guide for Parents and Childcare Providers. London: The Royal Botanic Gardens.Find this resource:

      Frohne D, Pfänder H (2005). Poisonous Plants: A Handbook for Pharmacists, Doctors, Toxicologists, Biologists and Veterinarians, 2nd edition. London: Manson Publishing.Find this resource:

        Jansen SA, Kleerekooper I, Hofman ZL, et al. (2012). Grayanotoxin poisoning: ‘mad honey disease’ and beyond. Cardiovasc Toxicol, 2:208–15.Find this resource:

        Krenzelok EP, Mrvos R (2011). Friends and foes in the plant world: a profile of plant ingestions and fatalities. Clin Toxicol, 49:142–9.Find this resource:

        Schep LJ, Slaughter RJ, Becket G, et al. (2009). Poisoning due to water hemlock. Clin Toxicol, 47:270–8.Find this resource:

        The Royal Botanic Gardens (2000). Poisonous Plants and Fungi in Britain and Ireland. CD-ROM. London: The Royal Botanic Gardens.Find this resource:

          Venomous animals—spiders and scorpions


          Venomous snakes are the single most important group of toxin-producing animals worldwide; however, venomous arthropods have a significant impact on human health, particularly in the tropics and subtropics. Fortunately only small subsets of known spider and scorpion species are proven causes of harm to human health, but this small subset can cause major and sometimes lethal envenoming. In Europe scorpions and spider envenomation is most commonly from ‘pets’. Occasionally returning travellers present with later features, particularly from spider bite.


          Spiders, like scorpions, are obligate predators, and virtually all species possess paired fangs and venom glands. Most spiders are too small to bite effectively and envenom, even if their venom was toxic to humans. There are a very small number of exceptions, spiders that contain toxins in their venom that targets humans and causes medically significant effects. These represent only a tiny fraction of the huge diversity of spider species. Spiders are, with very few exceptions, members of one of two major groups (suborders); Mygalomorphae (the more ‘primitive’ spiders), and Araneomorphae (most other spiders). Species capable of harming humans are found in both these groups.

          Epidemiology of spider bites

          There are few reliable studies of the incidence of spider bites to humans. In the UK these are from ‘pets’ or rarely on imported products. In Australia, spider bite calls are the commonest call to poison centres (~5000 per annum), and widow spider bite is common, with around 1000 cases a year receiving antivenom. Conversely, the far more dangerous funnel web spiders cause few bites.

          In parts of South America recluse spiders are a common problem. In North America, widow spiders and, to a lesser extent, recluse spiders cause medically significant bites, but such bites are uncommon and are largely restricted to southern and eastern USA. In Africa, notably southern Africa, widow spiders and recluse spiders are medically important.

          Spider venom

          Spider venoms capable of harming humans fall into the same two broad groupings as scorpion venoms: excitatory neurotoxins and locally necrotic cytotoxins.

          Neuroexcitatory spider venoms

          The structure of spider neuroexcitatory venoms varies, but the effects are similar, and the target is a nerve cell membrane ion channel. The most potent spider toxin against humans is the atracotoxin group from funnel web spiders. These are low-molecular-weight toxins (around 4–5 kD) targeting potassium channels. Widow spider toxins (latrotoxins) are far larger (around 130 kD).

          Cytotoxic spider venoms

          Only recluse spiders (Loxosceles spp.) are clearly associated with local necrosis in humans. The component of most importance is a sphingomyelinase-D that causes both direct tissue damage, and indirect damage by attracting neutrophils which then also cause tissue damage.

          Clinical effect of spider venoms

          Medically significant spider bites are either neuroexcitatory or cytotoxic. Other spiders can bite humans and cause temporary local pain, but no significant local or systemic effects.

          Neuroexcitatory envenoming

          Neuroexcitatory envenoming produces a range of clinical presentations, depending on the type of spider venom. It is more distinctive than seen with scorpion stings.

          Australian funnel web spiders (genera Atrax and Hadronyche, found in eastern Australia) are the most dangerous of all spiders and without adequate treatment envenoming can cause death, even in adults. Because of large fangs, local bite-site pain is common, increased by the spider ‘hanging on’, and the acidity of the venom. When systemic envenoming occurs it develops rapidly, within minutes to an hour. Patients bitten by a funnel web spider symptom-free for 4 hours have not been effectively envenomed. First symptoms of systemic envenoming can occur from 5 minutes post bite, commencing with peri-oral tingling and sometimes tongue fasciculation. This rapidly progresses, in significant cases, to one or more of: headache, nausea, profuse sweating, lacrimation, salivation, piloerection, hypertension, tachycardia. In the most severe cases there may be rapid progression to: pulmonary oedema, hypoxia, intracranial hypertension, coma. In severely envenomed untreated patients the pulmonary oedema phase is often fatal, but if survived, then progresses through generalized muscle fasciculation to hypotension, bradycardia, cardiac arrhythmia, to terminal cardiac arrest. Specific antivenom changes the clinical picture as it effectively reverses envenoming. The rate and severity of envenoming from funnel webs varies between species.

          Bites by the closely related mouse spiders (genus: Missulena) rarely cause problems, but when significant envenoming does occur it is similar to funnel web spiders.

          Widow spiders (genus: Latrodectus) occur almost worldwide and the syndrome of envenoming, latrodectism, is sufficiently uniform to be considered a single entity. Other related theriid spiders (family: Theriidae) can cause milder forms of latrodectism; e.g. cupboard spiders (genus: Steatoda). Classic widow spider bite causes only minor bite-site pain. In significant cases increasing pain develops in the bite area about 15–45 minutes (or more) post bite, with associated local erythema, sometimes local central blanching, and local profuse sweating. Over a variable time period the pain can track centrally, sometimes causing severe regional pain, associated with profuse sweating in some cases, tender and/or enlarged draining lymph nodes. Nausea, malaise, and hypertension also occur. In the most severe cases the pain can be excruciating, come in waves, involve much of the body, with profuse sweating, and occasionally severe hypertension. This systemic pain can mimic myocardial infarction, or an acute abdomen. Without treatment the pain and other features may persist beyond 1 week. Irrespective of bite site, if inadequately treated pain may devolve to burning pain in the soles of both feet and severe pain and profuse sweating of both legs below the knee. Death directly from envenoming is unlikely; rarely pulmonary oedema occurs. Debilitation secondary to envenoming may cause secondary fatal illness, particularly in children, the elderly, or infirm.

          Banana spiders (genus: Phoneutria) cause phoneutrism which is a common toxinological cause of hospital attendance in parts of Central and South America, notably Brazil. Phoneutrism is similar to latrodectism, with sometimes severe pain and sweating, but is generally less severe. In young males priapism is a common envenoming effect, unlike latrodectism, where it occurs only rarely. Envenoming resolves over hours to days and is rarely fatal. Risks increase in the very young, old, and infirm, in whom antivenom is recommended.

          Cytotoxic envenoming

          Recluse (brown recluse, violin) spiders (genus: Loxosceles) have a wide global distribution, but are not native to all areas. These are the only spiders proven to regularly cause skin damage, with a toxin that induces damage (sphingomyelinase-D). The bite occurs most often at night, may be felt, but often goes unnoticed. Local symptoms may take more than 12 hours to develop, starting as local discomfort and redness, progressing over hours to days to a classic target lesion of central blue-black skin, surrounded by blanched skin, and an outer ring of erythema. There may pain, sometimes severe. In some there is blister or bleb formation. As the lesion develops the patient may develop a concurrent systemic illness, with fever. Full-thickness skin necrosis of large areas can occur, with skip lesions. In most cases the concern is the local tissue injury; cutaneous loxoscelism. In a minority systemic effects can be prominent, severe, or even lethal; viscerocutaneous loxoscelism. The latter can include intravascular haemolysis, thrombocytopenia, DIC, renal failure, or multi-organ failure. When first described (in Chile) mortality rate was 30%. Venom-induced local necrosis results, this may be exacerbated by secondary infection. Venom-induced skin necrosis is difficult to treat and slow to heal, potentially taking months to resolve. It is clear that many alleged loxoscelism cases are due to other causes, e.g. infection.

          Diagnosis of spider bite

          Diagnosis of spider bite often relies on recognizing a distinctive pattern of envenoming, both local and systemic. An actual spider will be seen in a minority of cases.

          There are no clear diagnostic tests and no venom detection kits. Blood tests are diagnostically unhelpful. In widow spider bite creatine kinase may rise, but is neither diagnostic nor influences treatment. In recluse spider bite it is, conversely, important to undertake serial blood tests to ensure viscerocutaneous loxoscelism is not missed, including: full blood count, renal and liver function, and coagulation studies. Necrotic skin lesions should also be swabbed for culture/sensitivity.

          Treatment of spider bite

          The approach varies with spider. Most bites are from species of no medical significance, not requiring treatment. For medically important species, only a minority develop significant envenoming. A few species cause rapid and life-threatening envenoming and where they occur (e.g. Australia) the first aim of treatment is to ensure any at-risk case is urgently assessed and managed. This has resulted in a triage algorithm in Australia that separates out bites by ‘big black spiders’, which might be funnel webs, from all other spider bites.

          Treating neuroexcitatory envenoming

          Depending on the type of spider, antivenom may be: the mainstay of treatment (Australian funnel web spiders); a common treatment used in all significantly symptomatic cases (widow spider bite in Australia); or a treatment reserved for high-risk severe cases (banana spiders, widow spiders in many regions). The only other currently accepted treatments for neuroexcitatory spider envenoming are secondary or symptomatic, but clear evidence on best practice is generally absent.

          For Australian funnel web spider bite all possible (i.e. bite by unidentified ‘big black spider’ within known range) and definite funnel web bites: urgently transport to hospital, urgently triage and assess, and observe for 4 hours post bite. If no evidence of significant envenoming occurs, safely discharge. If envenoming consistent with funnel web spiders develops, specific antivenom should be given IV and expert clinical toxinologist consultation sought regarding the dose and need for further doses.

          For patients presenting with either a clear history of widow spider bite in Australia (red back spider), or an envenoming syndrome consistent with latrodectism, patients should seek medical help only if symptomatic, because envenoming generally is not rapidly progressive, and many cases never develop effects. If significant envenoming develops patients are offered specific red back spider antivenom IM, or IV (IV two vials). Antivenom seems effective and safe. In most other regions with widow spider antivenom available, it is only used in severe cases in high-risk patients (young, elderly, infirm). This reflects concern about the risk of fatal ADRs to antivenom treating a non-fatal illness. This approach is controversial. The Australian antivenom has been used in clinical studies in North America, and used successfully to treat severe bites by the related cupboard (Steatoda spp.) spiders.

          In Brazil, bites by banana spiders are managed by an escalating protocol. For most cases treatment is symptomatic, using analgesia, often local anaesthetic injection. In the minority developing severe envenoming, IV antivenom is considered.

          For other spiders reassurance or symptomatic care is warranted.

          Treating cytotoxic envenoming

          Treating cytotoxic spider bite is controversial. Since diagnosis and treatment is delayed more than 24 hours post bite, and cellular damage has occurred, antivenom is unlikely to reverse this. Steroids, dapsone, and surgery are of no benefit. Treatment should be symptomatic, recovery may be long and incomplete.

          Prevention of spider bite

          In areas with potentially lethal spiders, simple modification of human behaviour may reduce the risk of bites.


          Scorpions are obligate predators with a venom delivery apparatus in their ‘tail’ (the telson), but have pincer-like ‘claws’. One group have large powerful ‘claws’, though their sting may cause pain this is generally not a threat to life. The other group have evolved more potent venom. Many are small and slightly built, and are the scorpions of most threat to human health. Nearly all the dangerous scorpions fall within a single grouping, family Buthidae. Within this group there are more similarities than differences in the clinical pattern of envenoming caused to humans.

          Epidemiology of scorpion sting

          In some parts of the World, scorpion sting is of greater medical impact than snakebite. Examples include Mexico, North Africa, and parts of the Middle East. However, not all scorpion sting hot-spots are in arid regions; thus scorpion stings are important in parts of Brazil including urban environments.

          In Mexico, scorpion stings (annual hospital presentation rates approaching 300,000) are far more than for snakebite. It is likely that a similar or higher number of cases occur across North Africa and the Middle East. Though it receives less attention than snakebite, in parts of SW USA medically significant scorpion sting may also be comparatively common, compared to snakebite. The most recent global estimate is more than 1 million stings per year with about 3000 fatalities.

          Scorpion venom

          Much research has been focused on venoms (especially ion channel toxins) of medically significant scorpions. Detailed exposition on this topic is beyond the scope of this section. There is little information on Hemiscorpius lepturus venom, but so far no sphingomyelinase-D toxin, which is found in recluse spider venom, has been identified despite the strong similarity in envenoming between these two disparate arthropods. Studies suggest metalloproteinase activity of venom may be involved in necrosis. Though apparently not significant in human envenoming, a calcium channel neurotoxin (hemicalcin) has been isolated.

          Clinical effects of scorpion stings

          The clinical pattern of scorpion sting envenoming can be divided into two classes; neuroexcitatory, as caused by nearly every medically significant scorpion species, all within family Buthidae, and cytotoxic, caused by a very limited group of scorpions in family Hemiscorpiidae (formerly family Scorpionidae).

          Neuroexcitatory scorpion envenoming

          The vast majority of medically significant scorpions, and scorpion stings, fall into this category. Some major genera/species are shown in Table 13.3. This form of envenoming has a distinctive pattern, with initial severe pain at the sting site, rapidly followed by progressive systemic envenoming with gross excitation of portions of the nervous system, sometimes described as ‘catecholamine-storm-like’, resulting in peripheral autonomic effects (increased sweating, salivation), hypertension, tachy- or bradycardia, cardiac dysfunction, pulmonary oedema, nystagmus, coma. Gastrointestinal symptoms/signs are common. Cardiac problems include acute myocarditis and cardiac failure; myocardial perfusion abnormalities are documented, for Tityus spp. stings in Brazil. Transitory myocardial ischaemia has been postulated as contributory to cardiac problems in scorpion envenoming, possibly secondary to the catecholamine storm. Severity is greater in children who are at risk of a lethal outcome; adults generally have non-lethal envenoming. The emphasis of clinical features varies between scorpions within this group. For instance, rotary nystagmus and ocular movement abnormalities are prominent in stings by Centruroides spp. scorpions in SW USA and parts of Mexico. A study in Tunisia reported on cases in ICU, with 62% pulmonary oedema, 21% cardiogenic shock, 39% elevated blood sugar, 80% leucocytosis, 74% GI tract signs, and there was a 7.5% mortality rate. In this study poor prognosis was associated with age less than 5 years, fever greater than 38.5° C, and the presence of pulmonary oedema, leucocytosis higher than 25×103/mm3, and GCS less than 8. The effects of scorpion sting in pregnancy are poorly documented, but antepartum fetal death is reported. There are rare reports of cerebral infarction following scorpion sting, notably in India, possibly due to severe hypertension, or coagulopathy.

          Table 13.3 Some medically important scorpion groups

          Scientific name


          Clinical effects

          Family Buthidae

          Leiurus quinquestriatus + other Leiurus spp. (common name—yellow scorpion)

          North Africa to Middle East

          Neuroexcitatory envenoming

          Androctonus spp.

          North Africa to Middle East

          Neuroexcitatory envenoming

          Buthus spp.

          Mediterranean region

          Neuroexcitatory envenoming

          Centruroides spp.

          North and Central America

          Neuroexcitatory envenoming

          Tityus spp.

          South America

          Neuroexcitatory envenoming

          Parabuthus spp.

          Southern Africa

          Neuroexcitatory envenoming

          Mesobuthus spp.

          Middle East to India

          Neuroexcitatory envenoming

          Family Hemiscorpiidae

          Hemiscorpius lepturus

          SW Iran

          Moderate to severe local necrosis + in some cases systemic organ damage

          Cytotoxic scorpion envenoming

          This form of envenoming is rare amongst scorpions, principally in a scorpion restricted to SW Iran (Khuzestan), Hemiscorpius lepturus. A few related species cause less severe cytotoxic envenoming. H. lepturus, though not the most frequent cause of stings in Iran (12%), cause the majority of fatal stings (95%) and predominate during winter. 95% of H. lepturus stings affect the skin, with indurated purpuric changes, oedema and necrosis (47%), and bullous reactions (19%). The initial sting may cause only minor discomfort, unlike other scorpion stings, but as necrosis develops, pain can become severe. Necrotic ulcers develop over several days with cellulitis, bullae, or blue-black skin discolouration, and may take months to heal. Necrosis is less common in young children than in older children and adults, but young children are more likely to develop severe systemic effects, including intravascular haemolysis, cardiac toxicity and arrest, CNS problems, and renal failure. Non-specific systemic symptoms (in order of frequency) include malaise, dry mouth, dizziness, nausea, thirst, headache, fever, vomiting, anorexia, tachycardia, hypotension, sweating, vertigo, restlessness, haemolysis, and haematuria.


          In most cases of scorpion sting (neuroexcitatory species) the diagnosis will be obvious: the patient will have had severe local pain from the time of the sting and often have seen the scorpion. In cases where none was seen, sudden onset of severe local pain consistent with a scorpion sting, in a setting where stings are possible, and the subsequent effects consistent with scorpion envenoming, point to the diagnosis. However, snakebite, centipede, or spider bite may also need to be considered in this scenario. There are no diagnostic laboratory tests in neuroexcitatory scorpion envenoming.

          Treatment of scorpion envenoming

          Though controversial, specific antidote therapy using appropriate antivenom is the mainstay of managing major scorpion envenoming in most regions where antivenom is available. Some areas use a clinical score for assessing severity of scorpion stings but utility of this score system is uncertain.

          Treating neuroexcitatory scorpion envenoming

          The major risk group in neuroexcitatory scorpion envenoming is children. Efficacy of antivenom remains unclear. Some maintain antivenom is ineffective citing it cannot: target key venom effects; be given soon enough to be effective; there are other more effective safer therapies. Clinicians in countries such as Mexico who use scorpion antivenom claim dramatic reductions in fatality rate in children; 86.5% reduction in mortality in one study. A recent study of antivenom versus placebo in the US reported that antivenom was clearly effective.

          Experience in Saudi Arabia and Brazil indicates that one problem with antivenom use may have been under-dosing and an inappropriate route (IM), while higher doses given IV appear effective. IV is the preferred route for scorpion antivenom.

          Antivenom is not available in all areas so other treatments should be considered. In India, prazosin is used to manage cardiac toxicity following Mesobuthus spp. envenoming. However, two recent Indian studies indicate that antivenom is more effective than prazosin alone. Prazosin should be reserved for cases developing severe hypertension and pulmonary oedema, as an adjunct to antivenom. Where antivenom is not available prazosin is preferable to dobutamine as first-line therapy. Addition of dobutamine in severe cases with left ventricular failure may be beneficial. Captopril has also been suggested and used in India.

          A novel treatment, but not available for human use, is monoclonal bispecific antibody against selected toxins.

          Treating cytotoxic scorpion envenoming

          This type of envenoming is essentially restricted to SW Iran, where a local polyvalent antivenom, covering several Iranian scorpions, is used, but not documented by clinical trials. However, given the delayed presentation of H. lepturus stings, so delayed antivenom therapy, there are reasons to doubt effectiveness. At present it would seem reasonable to use antivenom at the earliest opportunity, at least two vials, IV (not IM as the manufacturer suggests).

          Prevention of scorpion stings

          Given the frequency and importance of scorpion stings in some regions, with associated costs to the health system, prevention is a worthwhile exercise. Thus in areas where rural workers are at risk of stings, such as corn pickers in Mexico, use of gloves can dramatically reduce sting incidence.

          Venomous ticks

          There is a vast array of ticks and mites, many of which can bite humans, and a number are vectors for disease. A few produce salivary toxins that can envenom humans, causing progressive flaccid paralysis. Only these latter will be considered here.

          Epidemiology of tick envenoming

          Tick paralysis is well documented in Australia, North America, and southern Africa. Paralysis cases are largely restricted to the known range of these ticks in eastern Australia. Children are at highest risk. In North America the incidence of tick paralysis does not appear to closely track the distribution of these ticks.

          Tick venom

          Australian paralysis tick venom has been well studied and a presynaptic neurotoxin has been identified.

          Clinical effects of tick venom

          Most bites do not result in envenoming. Paralysis occurs when a mature female tick attaches to the skin and commences feeding; these are easily overlooked. It may be several days before paralytic symptoms develop. Most commonly these commence as an ascending flaccid paralysis first manifest as ataxia, but potentially progressing to complete paralysis; progression varies from hours to days. Effects may be local, e.g. an apparent Bell’s palsy if the tick is attached near the facial nerve.

          For North American ticks, once the tick is removed, paralysis declines, but for Australian ticks the paralysis may progress for up to 48 hours post removal.

          Diagnosis of tick envenoming

          There are no definitive diagnostic tests for tick paralysis, though clearly finding a tick in a patient with progressive paralysis is strongly suggestive. If no tick is found, other paralytic bites and Guillain–Barré syndrome should also be considered.

          Treatment of tick envenoming

          Tick paralysis requires supportive and secondary treatment; no specific antidote (antivenom) is available. All ticks are located and removed, using specific tick-removal devices; it is important not to squeeze the engorged body or leave mouth-parts behind. If paralysis is severe then respiratory support may be required for a period of hours to a few days. In Australia it is essential that a patient with partial tick paralysis be observed for 2 days post tick removal. This is not required in North America. Where appropriate, check for evidence of tick borne diseases such as Lyme disease.

          Prevention of tick envenoming

          Preventing tick paralysis essentially consists of limiting opportunities for ticks to attack, e.g. ensuring clothing minimizes exposure and possibly the use of pesticides.

          Further reading

          Chippaux J-P, Goyffon M (2008). Epidemiology of scorpionism: a global appraisal. Acta Tropica, 107:71–9.Find this resource:

          Daly F, White J (2005). Widow and related Latrodectus spiders. In: Brent J, Wallace K, Burkhart K (eds) Critical Care Toxicology, pp. 1187–94. Philadelphia, PA: Elsevier Mosby.Find this resource:

            Isbister GK, White J (2004). Clinical consequences of spider bites: recent advances in our understanding. Toxicon, 43(5):477–92.Find this resource:

            Miller MK, Whyte IM, White J, et al. (1999). Clinical features and management of Hadronyche envenomation in man. Toxicon 38:409–27.Find this resource:

            White J (1995). Clinical toxicology of tick bites. In: Meier J, White J (eds), Clinical Toxicology of Animal Venoms and Poisons, pp. 191–203. Boca Raton, FL: CRC Press.Find this resource:

              White J, Cardoso JL, Fan HW (1995). Clinical toxicology of spider bites. In: Meier J, White J (eds), Clinical Toxicology of Animal Venoms and Poisons, pp. 259–329. Boca Raton, FL: CRC Press.Find this resource:

                Marine envenoming


                Venomous marine creatures cause envenoming with a specialized venom apparatus. Specialized glands produce venom which is injected, or applied to another organism. Most marine creatures cause ‘stings’ rather than ‘bites’. Marine stings are rare, except in some coastal regions. The most important are jellyfish, which sting by skin-contact with their tentacles, and venomous fish which have spines that cause penetrating injuries. Less common are stings from sea urchins, sponges, and sea snakes.

                Jellyfish stings

                There are more than 100 medically important jellyfish (cnidariae) around the world. In general, jellyfish stings cause similar types of stings.

                Mechanism of injury

                Jellyfish have millions of stinging cells (nematocysts), mainly on the tentacles. Each stinging cell contains a small amount of venom and a coiled harpoon-like mechanism to inject it. Physical or chemical stimuli trigger the cell to fire off and inject venom.


                Excepting a few species of jellyfish such as Physalia physalis, the type of jellyfish that sting is dependent on the geographic location. Local expertise will be required in more severe cases.

                Overview of jellyfish stings

                There are two major clinical syndromes that result from jellyfish stings—linear or tentacle-like stings and Irukandji-like stings. The majority of stings are the former with variations in severity and range of effects.

                Linear/tentacle-like stings

                Stings typically cause immediate pain that lasts minutes to hours, associated with a linear erythematous or urticarial eruption. Systemic effects are rare, usually non-specific symptoms such as nausea, vomiting, and headache.

                Irukandji-like stings

                Symptoms are usually delayed 20–30 minutes after the sting. There is minimal local pain and erythema, but severe generalized pain, abdominal, back, chest, and muscular, commonly associated with nausea, vomiting, headache, and hypertension. Myocardial injury and pulmonary oedema occur rarely.

                Specific jellyfish

                Physalia species

                Physalia species are widespread, the commonest jellyfish stings worldwide, causing thousands of stings in North America and Australia and are referred to as Portuguese man-o-war, Pacific man-o-war, or blue bottles. Few cases present to hospital. Physalia stings cause immediate localized and intense pain, lasting 1 or more hours. There are linear erythematous marks at the sting site lasting 1–2 days. Systemic effects are rare. Delayed localized bullous reactions can occur but scarring is rare.


                Tentacles should be removed by washing them off with seawater or by hand. Hot water immersion (45° C) for 20 minutes is the recommended treatment for local pain. Test the water temperature first. Alternatively use a hot shower or a constant flow of hot water. Vinegar may increase the pain and is not recommended. Rarely analgesia, or local dressings for skin reactions are required.

                Chironex fleckeri (box jellyfish)

                Chironex fleckeri from northern Australia is often referred to as the most venomous creature in the world. Over 70 deaths have resulted from stings, mostly in children.

                C. fleckeri have a box shape with multiple long tentacles on each corner. Most stings are minor, similar but more severe than other jellyfish. Potentially life-threatening adult stings are associated with several metres of skin contact; just over 1 metre resulted in the death of a child.

                Immediate local pain is associated with linear erythematous eruptions, ‘whip-like’ marks. Stings are often multiple causing severe and longer lasting pain. Local necrosis can occur, rarely resulting in permanent scarring. Delayed papular urticarial reactions occur along the sting sites in about half to two-thirds of cases. Severe envenoming is characterized by cardiovascular collapse and potentially death within 20–30 minutes.


                In severe envenoming pre-hospital first aid and resuscitation are essential. Survival depends on early cardiopulmonary resuscitation. First aid (tentacle removal by hand or seawater, and the sting sites covered in vinegar) should occur simultaneously with basic life support. Vinegar stops further nematocyst discharge and prevents severe envenoming, but not pain.

                Minor stings require simple analgesia, initially with ice packs. The utility of hot water immersion for C. fleckeri stings remains uncertain. Treat severe pain with oral or parenteral opioids. Most stings do not require local treatment except if there is necrosis, which requires local dressings. Systemic envenoming develops rapidly with an hour. Treat cardiovascular collapse as for any cardiac arrest, with cardiopulmonary resuscitation and advanced life support; consider intravenous antivenom and magnesium.

                There is increasing evidence box jellyfish antivenom is unlikely to be effective in human envenoming, thus only consider its use in patients with severe envenoming.

                Irukandji syndrome

                Irukandji syndrome, first reported in northern Australia, is now recognized in most parts of Australia and in other parts of the world. Irukandji syndrome refers to the constellation of clinical effects that was first reported for Carukia barnesi. It is characterized by the delayed onset of generalized pain and systemic effects, with minimal local effects at the time of the sting. One death is reported in Irukandji syndrome.

                There are normally minimal local effects and in many cases no evidence of a sting. After 20–30 minutes severe generalized abdominal, back, chest, and muscular pain develops, associated with systemic symptoms (nausea, vomiting, and diaphoresis), anxiety, agitation, tachycardia, and hypertension. Cardiac toxicity occurs in severe cases. ST segment depression and T wave changes on the ECG and elevated troponin indicate myocardial injury. Rarely cardiogenic pulmonary oedema occurs.


                The majority of stung patients require hospital treatment for severe pain, often associated with other systemic symptoms. Titrated intravenous opiates, morphine or fentanyl, with antiemetics should be given. Benzodiazepines may be used for anxiety and agitation.

                An ECG and troponin should be done in all patients. If patients are pain free with a normal ECG and troponin they can be discharged after 6 hours. If there is cardiac involvement continue monitoring. Admit to critical care unit if patients are unstable or there is evidence of acute pulmonary oedema. Standard supportive care is appropriate.

                Other jellyfish stings

                There are many other species of jellyfish that cause medically important stings; clinicians need to be aware of jellyfish in their local region. In most cases the jellyfish will not be identified and treatment is based on history of, and clinical effects consistent with, a jellyfish sting. Most jellyfish cause local immediate pain and linear eruptions, and in the vast majority of cases the effects are minor and similar to Physalia stings. Systemic effects are rare.


                • Feather hydroids are the most numerous of the hydrozoa group and are plume-like animals that cause minor effects—painful itching and urticaria.

                • Millepora or fire corals cause minor effects.

                • Gonionemus spp. occur in both Russia and Japan and are reported to cause an Irukandji-like envenoming syndrome.

                • Olindias spp. occur in South America and cause effects similar to Physalia.


                • Hair jellyfish (Cyanea spp.) occur in open or colder waters. The tentacles can break off and still cause stings. Stings to the eye or cornea are reported.

                • Catastylus spp. (blubber jellyfish) common jellyfish that rarely cause stings

                • Chrysaora quinquecirrha (sea nettle) occur in the Americas, Japan, and the Philippines. The best known is C. quinquecirrha, common in the Chesapeake Bay. Clinical effects are as for Physalia.

                • Mauve stinger (Pelagia spp.) are reported in the Mediterranean and Australia and cause minor effects such as local pain and urticaria.

                • Linuche unguiculata (thimble jellyfish) larvae occur in the Atlantic and can cause a vesicular pruritic dermatitis that lasts days and resolves spontaneously. Often referred to incorrectly as ‘sea lice’ it usually occurs in areas covered by bathing suits.

                Cubozoa (other box jellyfish)

                • Hawaiian box jellyfish (Carybdea alata) cause large numbers of stings in Hawaii. Clinical effects are similar to Physalia but may be more severe. Hot water immersion is reported to be effective for pain.

                • Chiropsalmus quadrigatus is reported to have caused deaths in the Philippines and Japan, but there is limited information.

                • Chiropsalmus quadrumanus is found along the Atlantic coast of the USA and generally causes minor effects. One unusual death in a child has been reported.

                • Jimble and other box jellyfish (Chiropsalmus bronzeii) occur in Australia and cause minor effects.


                This is the largest group of jellyfish and includes sea anemones. Anemones generally cause very mild effects but can cause local pain associated with local erythema.

                Treatment for other jellyfish

                Treatment is similar to Physalia, but there is less evidence for topical treatments and geographical variation in treatment approaches. In all cases the tentacles should be removed by washing with sea water or removing by hand. Hot water immersion is likely to be effective and has not been tested for jellyfish other than Physalia. Vinegar is not recommended because it may increase the pain. Hospital treatment is only required for severe local effects or systemic envenoming.

                Penetrating venomous marine injuries

                The other major type of marine envenoming is from penetrating marine injuries which includes venomous fish stings, stingray injuries, and sea urchin injuries.

                Mechanism of injury

                Penetrating marine injuries occur when a spine that is usually covered by a sheath ruptures as the spine penetrates the skin. In most cases there is venom between the spine and sheath which is injected as the spine enters the skin. Spines come from fish, stingray tail spines, and sea urchin spines; the latter does not have a sheath.

                Venomous fish

                Worldwide the important venomous fish include catfish, stonefish, bullrout, lesser and greater weever fish, and the scorpion fish group (e.g. lionfish, zebra fish). Venomous fish are found throughout coastal waters and fresh water.

                Clinical effects

                The predominant symptom is localized pain due to the puncture wound, but severity varies based on size of the puncture and amount of venom injected. More severe and persistent pain occurs with stonefish, bullrout, weever fish, or marine catfish where large amounts of venom may be injected. Bleeding is usually minimal but there may be significant swelling and oedema. The spines rarely remain in the wound but small amounts of foreign material can. Secondary infection is a risk; systemic effects are likely to be secondary to severe pain.


                Fresh water and marine stingrays occur throughout the world. Most injuries occur when people tread on stingrays in shallow water; rarely severe thoraco-abdominal trauma occurs when divers swim too close to them.

                Clinical effects

                In general, stingray injuries cause more trauma than other venomous fish due to their size, including severe local pain and bleeding. The pain may be more severe due to venom, and local necrosis may occur in some cases. Secondary infection is a risk, particularly in larger wounds.

                Sea urchins

                Sea urchins occur worldwide and most injuries occur when they are trodden on or occasionally when they are picked up. Most spines are non-venomous and the type of spines range from chalk-like to strong thorn-like material. Crown-of-thorns sea stars in the Indo-Pacific region may cause similar injuries.

                Clinical effects

                Sea urchin spine injuries rarely cause severe pain. Multiple retained spines are the major problem. These can be difficult to remove and cause persistent pain.

                Treatment of penetrating marine injuries

                First aid

                The wound site should be washed and pressure applied if significant bleeding. Immerse the wound site in hot water (45º C) for up to 90 minutes if this improves the pain. Use an unaffected limb to check the temperature first, since excess heat can cause burns.


                Oral or parenteral analgesia can be given, e.g. a combination of ibuprofen (200–400 mg) and paracetamol (1 g) initially and oxycodone (5–10 mg) can be added. Treat severe pain with titrated intravenous opiates. Local or regional infiltration of anaesthetic may be useful, particularly for exploring and cleaning larger wound sites.

                Wound management

                Good wound management is essential in all cases, including generous irrigation and removing any foreign material. Radiography or ultrasound assists in identifying foreign bodies; essential with sea urchin injuries as multiple retained spines are common. Larger wounds are best left open for delayed primary closure. Stingray injuries may require surgical exploration and debridement. Treat rare thoracic or abdominal injuries with stingray initially as major trauma. Surgical involvement is essential for wounds into joints or sterile body cavities. Sea urchin spines are problematic, because they can be difficult to find and remove. Spines near the surface should be removed and the patient reviewed regularly until symptoms resolve, and if not have surgical review.

                Wound infection and antibiotics

                Although rare, an important complication of penetrating marine injuries is secondary infection. These include Vibrio spp. (marine environment) and Aeromonas spp. (fresh water) which can be associated with significant morbidity and mortality. All penetrating marine injuries should be followed up over the first week rather than using prophylactic antibiotics, particularly in uncomplicated wounds. Skin infections with normal flora can also occur and tetanus status should be reviewed and updated. Manage infections conventionally.

                The role of prophylactic antibiotics is controversial. Treatment should rather focus on good wound care and follow up so that infection can be treated early.


                An antivenom is available for stonefish stings. It should be used in cases not responsive to analgesia, or if there is evidence of systemic envenoming. Antivenom should be given intravenously as a 1:10 dilution over 15 minutes. The dose is one vial, in both children and adults.


                Of the thousands of sponge species only a few are medically important. Some produce toxic secretions, e.g. the fire sponges (Tedania spp.) and Neofibularia spp.

                Clinical effects

                Contact injuries with sponges are uncommon, often referred to as stinging sponge dermatitis. Most are minor injuries including local tingling, transient pain, itchiness, and numbness. Pain may develop in the hours after the sting and persist for a number of days. Fire sponges can cause delayed effects 2–3 weeks after contact, with painful swelling and erythema, followed by desquamation.


                First aid includes washing the sting site. Analgesia may be required and symptoms can be treated with antihistamines. Effects resolve over days to weeks irrespective of treatment.

                Blue-ringed octopus

                The Australian blue-ringed octopus (Hapalochlaena spp.) saliva contains tetrotodotoxin. Bites have caused deaths. The clinical effects are similar to tetrodotoxin (TTX) poisoning (see later in this section). Most cases cause bite marks and local pain and systemic TTX envenoming with paralysis is rare. Treatment is supportive and mechanical ventilation may be required. The recommended first aid is a pressure bandage with immobilization.

                Cone snails

                Cone snails are univalve creatures found in the Indo-Pacific region. They sting by projecting a harpoon-like apparatus and inject a neurotoxic venom. Stings are exceedingly rare, only if the snail is handled. There is usually local pain, followed by local numbness, rapidly spreading in severe envenoming. Partial and complete paralysis has been reported, including respiratory failure. Treatment is supportive; a pressure bandage can be used for first aid.

                Sea snake envenoming

                Sea snakes are closely related to Australian elapids and occur in tropical parts of the Pacific and Indian Oceans. The most important species is the beaked sea snake (Enhydrina schistosa), which caused numerous fatalities in Southeast Asia when net fishing was common. The bite is generally painless, and it may initially go unnoticed. Systemic symptoms develop over 1–4 hours and depend on whether there is predominantly myotoxic or neurotoxic effects. There may be decreased mobility secondary to pain or paralysis. The creatine kinase will increase and may be diagnostic in some cases. Rhabdomyolysis will develop in severe cases and can be complicated by acute kidney injury. Some sea snake bites have been reported to cause predominantly neurotoxicity, with an ascending flaccid or spastic paralysis.

                First aid is the same as Australian elapids (see Common venomous snakes, pp. [link][link]).

                Marine poisoning

                Marine poisoning occurs when marine creatures that contain toxic substances are ingested. The most common and important marine poisoning is ciguatera resulting from eating some types of reef fish. Other marine poisoning includes TTX, shellfish poisoning, and scombroid.


                Ciguatera is the commonest marine poisoning and is endemic to regions of the Indo-Pacific and Caribbean. However, it can occur anywhere in the world with increased transport of fish. Ciguatera is due to accumulated toxins in tropical reef fish. Numerous fish have been implicated, such as moray eels, bass, Spanish mackerel, various cod species, emperors, and coral trout. Unfortunately there is no way to determine if a fish can cause ciguatera, including the appearance and taste of the fish.

                Clinical effects

                Ciguatera in the Indo-Pacific region is characterized by the combination of gastrointestinal and neurological effects, compared to the Caribbean where gastrointestinal effects predominate. Gastrointestinal effects (vomiting, diarrhoea, and abdominal cramping) usually occur first within hours of ingestion and last about 12–24 hours. Neurological effects are the characteristic features of ciguatera and are delayed, developing during the initial 24 hours. The predominant neurological effect is a sensory polyneuropathy:

                • cold allodynia: often referred to as a heat reversal and is an unpleasant sensation when touching cold objects

                • distal and perioral paraesthesia

                • numbness.

                Other effects are pruritis, arthralgia, and myalgia. Subacute and chronic forms are poorly defined with numerous non-specific symptoms. The diagnosis is made if there is both a history of eating fish known to cause ciguatera and gastrointestinal and neurological effects.


                There is no specific treatment for ciguatera. Management consists of supportive care and symptomatic relief. There is no evidence to support the use of mannitol and intravenous fluids should be administered for dehydration. Numerous medications have been suggested for acute and chronic symptoms with only anecdotal evidence to support their use. Non-steroidal anti-inflammatories appear to be beneficial for acute symptoms. Tricyclic antidepressants, gabapentin, and calcium antagonists, have been used for chronic symptoms with variable success.

                Tetrodotoxin poisoning

                TTX poisoning is rare and potentially lethal, and occurs most commonly from ingestion of puffer fish (e.g. fugu poisoning in Japan) and related fish. TTX is a sodium channel blocker that causes nerve conduction failure which manifests as paralysis.

                Clinical effects

                TTX poisoning manifests as a sensorimotor neuropathy which may be associated with mild gastrointestinal effects. Poisoning develops over hours and more rapidly with severe cases. Neurological effects include:

                • perioral paraesthesia and numbness

                • ataxia

                • progressive distal to proximal muscle weakness.

                Severe poisoning is characterized by respiratory muscle paralysis and rarely cardiovascular toxicity (bradycardia, arrhythmias and hypotension).


                No antidote exists for TTX poisoning. Treatment consists of supportive care, including early and often prehospital institution of airway and breathing support in severe cases. Severe poisoning will usually require mechanical ventilation for 2–5 days.

                Shellfish poisoning

                Shellfish poisoning is due to toxins that accumulate, in contrast to the more common viral and bacterial illnesses resulting from shellfish ingestion. There are four types of shellfish poisoning:

                • Diarrhoetic shellfish poisoning: similar to infectious gastroenteritis and requires supportive and symptomatic treatment.

                • Paralytic shellfish poisoning: similar to TTX poisoning, but results from other potent sodium channel blockers such as saxitoxin.

                • Neurotoxic shellfish poisoning: causes neuroexcitatory effects, sometimes similar to ciguatera.

                • Encephalopathic shellfish poisoning: due to domoic acid and only ever reported once as an outbreak.


                Scombroid poisoning occurs from ingestion of fish containing high concentrations of histamine and is similar to an acute allergic reaction. It results from the spoilage of fish after it has been caught, during storage or transport. Commonly implicated fish are from the Scombridae family—tuna, kingfish, mackerel, and wahoo.

                Clinical effects

                The clinical effects differ from an acute allergic reaction because they result from direct release of histamine. Scombroid develops in the first few hours of ingestion and lasts up to 6 hours. The major effects are:

                • skin effects: diffuse erythema, urticaria, flushing and itch.

                • gastrointestinal effects: nausea, vomiting, diarrhoea and abdominal cramps

                • hypotension

                • respiratory effects: wheeze, bronchospasm are rare.

                The diagnosis is clinical although it can be confirmed by the detection of high concentrations of histamine in the fish.


                Treatment includes intravenous fluids for hypotension or dehydration, and antihistamines (H1- and H2-receptor antagonists). Epinephrine is rarely used except in severe poisoning.

                Further reading

                Isbister GK (2001). Venomous fish stings in tropical northern Australia. Am J Emerg Med, 19:561–5.Find this resource:

                Isbister GK (2004). Marine envenomation and poisoning. In: Dart RC (ed), Medical Toxicology, 3rd edition, pp. 1621–44. Philadelphia, PA: Lippincott Williams & Wilkins.Find this resource:

                  Isbister GK, Hooper JN (2005). Clinical effects of stings by sponges of the genus Tedania and a review of sponge stings worldwide. Toxicon, 46:782–5.Find this resource:

                  Isbister GK, Kiernan MC (2005). Neurotoxic marine poisoning. Lancet Neurology, 4:219–28.Find this resource:

                  Isbister GK (2010). Trauma and envenomation from marine fauna. In: Tintinalli JE, Stapczynski JS, Cline DM, et al. (eds), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th edition, pp. 1358–1366. New York: McGraw-Hill.Find this resource:

                    Loten C, Stokes B, Worsley D, et al. (2006). A randomised controlled trial of hot water (45 degrees C) immersion versus ice packs for pain relief in bluebottle stings. Med J Aust, 18:329–33.Find this resource:

                    Williamson JA, Fenner PJ, Burnett JW, et al. (1996). Venomous and Poisonous Marine Animals. Sydney: University of New South Wales Press.Find this resource:

                      Common venomous snakes

                      Medically important snakes

                      Snakebite is an important cause of death in rural agricultural communities worldwide. In India alone, about 50,000 people die of snakebite each year. Most parts of the world, including the Indian and Pacific Oceans, have venomous snakes. The medically important groups are elapids, vipers, pit-vipers, burrowing asps, and some back-fanged colubrid snakes. In Europe, bites by captive exotic snakes may be more serious than those by indigenous species.


                      • Vipers only: in UK, Scandinavia, Benelux countries and Poland,the adder Vipera berus is the only venomous species.

                      Africa and the Middle East

                      • Elapids: cobras and spitting cobras (Naja), mambas (Dendroaspis)

                      • Vipers: saw-scaled vipers (Echis), puff adders (Bitis), desert horned-vipers (Cerastes)

                      • Burrowing asps: (Atractaspis)

                      • Back-fanged colubrid: boomslang (Dispholidus), twig snake (Thelotornis).


                      • Elapids: cobras (Naja) and kraits (Bungarus)

                      • Vipers: Russell’s vipers (Daboia), saw-scaled vipers (Echis)

                      • Pit-vipers: Malayan pit viper (Calloselasma rhodostoma), green tree vipers (Cryptelytrops), habus (Protobothrops), and mamushis (Gloydius)

                      • Back-fanged colubrids: red-necked keel back and yamakagashi (Rhabdophis).

                      Australia, New Guinea, Eastern Indonesian Islands

                      • Elapids only: taipans (Oxyuranus), black snakes (Pseudechis), brown snakes (Pseudonaja), tiger snakes (Notechis), death adders (Acanthophis).


                      • Elapids: coral snakes (Micrurus)

                      • Pit-vipers: lance-heads—Bothrops), moccasins (Agkistrodon), bushmasters—Lachesis), rattlesnakes (Crotalus and Sistrurus).

                      Indian and Pacific Oceans

                      • Elapids: sea snakes (Enhydrina, Hydrophis, Astrotia etc.).

                      Clinical features

                      Snakebite envenoming usually causes local pain and swelling, regional tender lymphadenopathy, malaise, nausea, vomiting, and other gastrointestinal symptoms. The following are the main clinical syndromes of envenoming:

                      Adder —(Vipera berus) and other European Vipera species

                      • Local pain and paraesthesiae, swelling, bruising, inflammation, lymphangitic lines and tender regional lymphadenopathy

                      • Hypotension (early, late, transient, recurrent or sustained with or without shock)

                      • Other anaphylactic features—urticaria, angio-oedema, bronchospasm, gastrointestinal symptoms

                      • Myocardial abnormalities (ECG arrhythmias, T wave/ST segment changes)

                      • Spontaneous systemic gastrointestinal bleeding and consumption coagulopathy.


                      • Descending paralysis, starting with ptosis and external ophthalmoplegia

                      • Local swelling and regional tender lymphadenopathy

                      • Asian cobras and African spitting cobras: local swelling, blistering, and necrosis

                      • Asian kraits: painless bites inflicted on sleepers, minimal local swelling, delayed descending paralysis

                      • Australasian elapids: descending paralysis, spontaneous systemic bleeding and consumption coagulopathy (sometimes shock (hypotension), rhabdomyolysis, microangiopathic haemolysis (MAH), acute kidney injury (AKI))

                      • sea snakes: minimal local swelling and pain, descending paralysis, rhabdomyolysis.

                      Vipers and pit vipers

                      • Local swelling, bruising, blistering, necrosis, regional tender lymphadenopathy

                      • Shock (hypotension)

                      • Spontaneous systemic bleeding and consumption coagulopathy

                      • AKI

                      • With some species: descending paralysis, rhabdomyolysis, MAH.

                      Burrowing asps

                      • Local swelling, blistering, necrosis

                      • Middle Eastern species (e.g. Atractaspis engaddensis in Israel): shock, cardiac conduction abnormalities, angina pectoris.

                      Back-fanged colubrids

                      • Minimal local swelling

                      • Delayed spontaneous systemic bleeding and consumption coagulopathy

                      • MAH, AKI.


                      Useful investigations include:

                      • Blood count—neutrophil leucocytosis, (initial) haemoconcentration from increased permeability, (later) anaemia from bleeding

                      • Blood film – schistocytes (MAH)

                      • Blood coagulation—20-minute whole blood clotting test (20 WBCT), prothrombin time (or INR), activated Partial thromboplastin time, fibrinogen concentration (consumption coagulopathy), fibrin degradation products or D-dimer (increased fibrinolysis), thrombocytopenia (DIC or MAH)

                      • Blood biochemistry—creatine kinase and transaminases (muscle/tissue damage), potassium, urea, and creatinine (AKI)

                      • Urine ‘sticks’ testing: blood/haemoglobin/myoglobin; microscopy—erythrocytes, casts.

                      Management of snake bite

                      First-aid treatment

                      Reassure the terrified victim. Do not interfere with the bite site in any way. Remove rings, bracelets, and tight clothing from the bitten limb.

                      In bites from non-European snakes immobilize the body, especially the bitten part. Consider using pressure immobilization or pressure pad (see later in section). Then:

                      • arrange transport to medical care as quickly, safely, passively, and comfortably as possible

                      • treat pain with paracetamol or codeine tablets (avoid aspirin and NSAIDs)

                      • do not attempt to catch or kill the snake. If already dead, bring it safely—do not touch.

                      • avoid useless and potentially harmful traditional remedies (incisions, ligatures, ice packs, instillation of chemicals or herbs, ‘snake stones’, etc.).

                      Pressure immobilization and pressure pad: these methods delay systemic absorption of lethal venom toxins by compressing lymphatics and veins draining the bite site, using pressures of 50–70 mmHg to avoid the unacceptable dangers of arterial occlusion. They are not necessary for UK bites from Vipera berus.

                      Pressure immobilization: elasticated bandages (10–15 cm wide, 4.5 metres long) are bound firmly around the entire bitten limb (but not so tightly as to occlude peripheral pulses), starting around the fingers or toes and continuing proximally up to the axilla or groin.

                      Pressure pad: a pad of rubber or folded fabric (5 cm square and 2–3 cm thick) is bound directly over the bite site using a non-elastic bandage.

                      Hospital treatment

                      Specific treatment with antivenom: antivenoms (hyperimmune animal serum immunoglobulins) are the only specific antidotes. Monovalent antivenoms neutralize the venom of only one species. Polyvalent antivenoms neutralize venoms of selected important venomous species of a particular region.

                      Indications for antivenom treatment worldwide are any of the following:

                      • spontaneous systemic bleeding (see earlier in section)

                      • consumption coagulopathy

                      • shock: low or falling blood pressure or cardiac arrhythmia

                      • descending paralysis

                      • black or dark brown urine (haemoglobinuria from haemolysis or myoglobinuria from rhabdomyolysis)

                      • local swelling involving more than half the bitten limb.

                      Mild local swelling alone is not an indication for antivenom.

                      Antivenom is administered by slow IV injection (2 mL per minute) or IV infusion diluted in about 5 mL/kg body weight over about 30–60 minutes. Initial dosage depends on the type of antivenom, species of snake, and severity of symptoms. A second dose is justified if, after 1–2 hours, life-threatening bleeding or shock have not resolved or paralysis has intensified, or if, after 6 hours, the blood remains incoagulable.

                      Early anaphylactic and pyrogenic antivenom reactions occur within 2 hours of starting treatment. They can be prevented with SC epinephrine (0.25 mL of 0.1% solution). Treatment is with IM epinephrine (adult dose 0.5 mL of 0.1% solution) given into the lateral thigh, followed by IV hydrocortisone and a histamine H1 blocker (e.g. chlorphenamine). Asthmatic reactions require an inhaled bronchodilator.

                      Late serum sickness reactions (urticaria, arthralgia and joint swellings, fever, lymphadenopathy, etc.) occur after 5–14 days. Treatment is with a 5-day course of oral prednisolone and/or histamine H1 blocker.

                      Supportive treatment

                      Hypovolaemic shock

                      Massive external bleeding or leakage of blood and tissue fluid into a swollen limb may leave the patient with an inadequate circulating volume so that the blood pressure falls. Plasma expanders such as 0.9% saline may be needed.

                      Respiratory failure from bulbar and respiratory muscle paralysis

                      This requires endotracheal intubation and assisted ventilation. Neuromuscular block from elapid postsynaptic toxins (cobras and Australasian death adders) may respond to the ‘Tensilon test’ (atropine and edrophonium). Anticholinesterase treatment can be continued with atropine and neostigmine.

                      Acute kidney injury

                      Clinical and biochemical evidence of AKI indicates the need for dialysis.

                      Wound infection

                      Wound infection introduced by the snake’s fangs or by ill-advised tampering with the bite site presents as local inflammation or abscess treated by aspiration and antibiotics such as co-amoxiclav or chloramphenicol. A tetanus toxoid booster is indicated.

                      Surgical complications

                      Necrotic tissue should be debrided and the area grafted. Fasciotomy to relieve suspected compartmental syndrome is commonly practised but rarely indicated. It can be considered after normal haemostasis has been restored with antivenom and raised intracompartmental pressure has been confirmed by direct measurement with a pressure transducer.

                      Spitting cobra eye injuries

                      Spitting elapids (cobras and ringkals) can spray venom from the tips of their fangs into an aggressor’s eyes, causing painful conjunctivitis and risking corneal ulceration and blindness.

                      First aid

                      First aid is urgent irrigation with generous volumes of water under a tap. Topical 1% epinephrine or local anaesthetic eye drops (caution!) relieve the pain. Exclude corneal abrasion (slit lamp) or give prophylactic antibiotic eye ointment. Topical antivenom or corticosteroid should not be used.

                      Further reading

                      Australia Toxinology. <>.

                      Mackessy SP (ed) (2010). Handbook of Venoms and Toxins of Reptiles. Boca Raton, FL: CRC Press.Find this resource:

                        Meier J, White J (eds) (1995). Handbook of Clinical Toxicology of Animal Venoms and Poisons. Boca Raton, FL: CRC Press.Find this resource:

                          Munich AntiVenom INdex (MAVIN) Poison Centre Munich: antivenoms holdings in Europe <>.

                          Sutherland SK, Tibballs J (2001). Australian Animal Toxins. The Creatures, their Toxins and Care of the Poisoned Patient, 2nd edition. Melbourne: Oxford University Press.Find this resource:

                            Vapaguide <>.

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