Oxford Handbook of Expedition and Wilderness Medicine (2 edn)
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Dangers of living off the land
‘I wanted to eat of the fruit of all the trees in the garden of the world.’
(Oscar Wilde)
Please don’t do it!
The abundance of appetizing, fragrant, and diverse fruits, leaves, and fungi offered by the wilderness environment may tempt the expeditioner to ‘live off the land’. This ideal is enthusiastically encouraged in some military survival exercises and by certain heroic TV personalities! However, without expert guidance such attempts may prove lethal. In Europe, especially in France, Scandinavia, and Russia, enthusiastic amateur mushroom hunters seek novel gustatory experiences, but every year thousands are poisoned and hundreds die. Toxic plants and fungi are easily confused with edible ones and it is salutary that even expert botanists and mycologists are occasionally poisoned. You should not be reassured by seeing wild animals and birds feeding with apparent impunity. They have adapted to avoid poisoning in many clever and evolutionary ways. For example, Zanzibar’s red colobus monkeys (Piliocolobus kirkii) eat charcoal to prevent poisoning by phenolic compounds in the Indian almond (Terminalia catappa) and mango (Mangifera indica) leaves that are their staple diet. Sometimes poisoning results from rash experimentation in quest of psychedelic experiences, using fungal psilocybin or tropane-containing plants. In South India and Sri Lanka, toxic plants are commonly employed as a means of self-harm (e.g. yellow oleander—Cascabela thevetia and Kerala suicide nut—Cerbera manghas or C. odollam).
Since recognizing danger is the secret of survival, an essential adjunct to this chapter is a profusely illustrated guide, CDRom (e.g. 
http://www.kew.org/science-conservation/plants-fungi), or website covering the poisonous (and edible) plants and fungi of the expedition’s location.
Educate expedition members about the local toxic flora.
Rely on your own food supplies.
Confine collection of food from the environment to what you can identify with certainty as being safely edible or what is confidently recommended by local indigenous people.
Remember! Cooking does not destroy fungal toxins!
Experiment.
Eat ‘forbidden fruits’: those resembling familiar cultivated fruits may be highly poisonous. To a non-expert, the death cap toadstool looks very like an edible mushroom (see 
Fungal poisoning, p. 582).
Eat wild fungi and certainly none with white gills (see Fig. 18.1).
Accept invitations to inhale, ‘snort’, or ingest the local psychedelic brew: a splitting headache, nausea, vomiting, and terrifying hallucinations are more likely than any pleasurable trance or ‘out of body’ experience.
Distinguishing edible mushrooms from death cap.
Effects of contact with skin
Contact dermatitis is by far the commonest risk posed by plants. Examples include stinging nettles, euphorbias, and ‘dumb cane’ (Dieffenbachia).
Allergic dermatitis may be caused by a large variety of plants, notably poison ivy (Toxicodendron (Rhus) radicans) (see Plate 15) whose leaves have a trifoliate pattern (‘leaves of three, leave them be’), poison oak (Toxicodendron diversilobum), primula (Primula obconica), and citrous fruits. Some plant saps are photosensitizing, resulting in erythema, papules, vesicles, bullae, and persistent hyperpigmentation confined to exposed areas.
Poison ivy (Toxicodendron radicans) trifoliate leaves and berries
Treatment
Treatment is based on immediate decontamination by washing with water, followed by symptomatic use of systemic antihistamines and topical corticosteroids.
Prevention
To avoid further contact, try to identify the cause. Since photosensitization is a common sequel, try to reduce solar exposure. In general, avoid unnecessary contact of bare skin with plants, especially those that have stinging hairs or are exuding latex or sap. If your expedition is botanical, learn to recognize some of the most notoriously irritant plants in advance and wear gloves when necessary.
Effects of ingestion
Within minutes to hours (exceptionally 24 h) after ingesting any part of a wild fruit, plant, or fungus (mushroom or toadstool):
Nausea, vomiting, abdominal colic, diarrhoea.
Confusion, hallucinations, or convulsions.
Atropinic, nicotinic, or muscarinic symptoms.
Cardiac arrhythmias.
Flushing in response to alcohol ingestion.
Oliguria/anuria.
Effects on gut
Many of the plants that cause contact dermatitis also irritate the gut. Cuckoo pint/arum lily, dumb cane, and many other plants have an irritant sap containing oxalate crystals. Ingestion causes immediate soreness, reddening, and blistering of buccal mucosa, salivation, and dysphagia. Most poisonous plants cause rapidly evolving nausea, abdominal cramps, vomiting, and diarrhoea (e.g. laburnum, anemone, hellebore, horse chestnut, ivy, privet, pokeweed, and snowberry). Some even more toxic plants cause severe GI symptoms after a delay of several hours up to 2 days (e.g. autumn crocus (Colchicum autumnale), glory lily (Gloriosa superba), jequirity bean (Abrus precatorius), and castor oil bean (Ricinus communis).
Effects on cardiovascular system
Bradycardia, heart block, other arrhythmias, ECG changes (‘digoxin effect’), and GI irritation are caused by foxglove (Digitalis purpurea), white/pink oleander (Nerium oleander), yellow oleander (Cascabela thevetia, also known as Thevetia peruviana) (see Plate 19), monkshood (Aconitum napellus), yew (Taxus baccata), and death camas (Zigadenus).
Yellow oleander (Cascabela thevetia also known as Thevetia peruviana).
Effects on nervous system
Hallucinogenic: e.g. cannabis (Cannabis sativa), khat (Catha edulis), morning glory (Ipomoea), and peyote (Lophophora williamsii).
Convulsant: e.g. cowbane (Cicuta virosa), ackee (Blighia sapida), and nux vomica (Strychnos nux-vomica). Cowbane poisoning causes gastroenteritis, increased secretions, and long-lasting intense episodes of generalized tonic–clonic convulsions, resulting in severe metabolic acidosis and multiple organ failure. Consumption of unripe ackee fruit is responsible for ‘Jamaican vomiting sickness’ associated with hypoglycaemia and fatal encephalopathy.
Atropine-like: e.g. deadly nightshade (Atropa belladonna) (see Plate 16), angels’ trumpets (Brugmansia suaveolens) (see Plate 18), and thorn apple or Jimson weed (USA) (Datura stramonium) and related species such as devil’s trumpet (D. metel). Clinical effects are: ‘red as a beet, dry as a bone’ (flushed, hot, red, dry face), tachycardia, and dilated pupils (mydriasis), and, in serious poisoning, arrhythmias, urinary retention, psychosis, convulsions, coma, and fatal respiratory failure. Some of these plants are hallucinogenic and therefore desirable to some people.
Nicotine-like: e.g. spotted hemlock (Conium maculatum), responsible for killing Soctrates and Hamlet’s father, first stimulates and then paralyses autonomic ganglia, and can cause convulsions and respiratory arrest.
Deadly nightshade (Atropa belladonna) flowers and berries.
Angel’s trumpet (Brugmansia suaveolans).
Effects on liver
Pyrrolizidine alkaloid-containing plants such as comfrey (Symphytum officinale) can cause hepatic veno-occlusive disease, which has occurred mainly in Jamaica, India, and Afghanistan. Nausea, abdominal pain and distension, hepatomegaly, and sometimes fever and vomiting develop a few days after ingestion.
Effects on kidneys
Oxalate-rich plants such as rhubarb (Rheum rhabarbarum), dock, and sorrel (Rumex), and plants containing other nephrotoxins may damage the kidneys.
Poisonous food plants
Staple food plants in many tropical countries can be poisonous if inadequately soaked, dried, fermented, or cooked:
Cassava (Manihot esculenta), sweet potato, yam, some fruit kernels, pips, and cherry laurel (Prunus laurocerasus) can cause acute or chronic cyanide poisoning.
In Africa, tropical ataxic neuropathy and spastic paraparesis (‘konzo’) are attributed to cassava poisoning.
Inadequately cooked beans and pulses (Leguminosae) can cause diarrhoea, while long-term exposure can lead to retarded growth and may even be fatal:
Lathyrism is an epidemic paralytic disease (e.g. in the Denbia depression of Ethiopia) caused by a neurotoxic amino acid in chick peas (Lathyrus sativus).
Favism occurs in some Mediterranean and Middle Eastern countries. Those with congenital glucose-6-phosphate dehydrogenase deficiency may develop intravascular haemolysis after eating broad (fava) beans (Vicia faba).
Fungal poisoning
Fungal poisoning is usually sporadic and accidental but occasionally may be homicidal, suicidal, or epidemic. In Europe (especially France, Scandinavia, and Russia), where there are many enthusiastic collectors and connoisseurs of wild mushrooms, poisoning is more common than elsewhere in the world. In 1999, 357 people were poisoned and 39 died from death cap mushroom (Amanita phalloides) poisoning in Voronezh in central Russia. Toxicity of fungi varies with location and season, from year to year, and with individual susceptibility.
The death cap, the world’s deadliest mushroom or toadstool (see Plate 17), looks superficially like an edible mushroom (Agaricus) but it has white gills (radiating linear structures under the mushroom’s cap) and a sac or volva at its base, whereas the edible mushroom has dark brown or black gills and no volva at the base of its stem (Fig. 18.1).
Deathcap mushroom (Amanita phalloides). Note white gills and sac at base of stem
Poisoning with early symptoms (within a few hours)
GI symptoms: vomiting, diarrhoea, and abdominal pain are usually transient but sometimes more intense, resulting in fluid and electrolyte disturbances. They may be caused by many species of common fungi, including honey agaric (Armillaria mellea) and Boletus luridus.
Cholinergic effects (muscarinic poisoning): abdominal pain and diarrhoea, sweating, lacrimation, salivation, miosis, bronchorrhoea, and sometimes bronchospasm, bradycardia, and hypotension may develop 5–120 min after ingesting Inocybe and Clitocybe spp.
Confusion (ibotenic poisoning): nausea, vomiting, confusion, disorientation, anxiety, euphoria, hallucinations, visual disturbances, ataxia, muscle cramps, and coma may develop 20–120 min after ingestion of panther cap (Amanita pantherina), fly agaric (Amanita muscaria), and Amanita strobiliformis.
Hallucinations (psilocybin poisoning): LSD-like, mainly visual hallucinations are induced by eating ‘magic mushrooms’ (Psilocybe, Conocybe, Gymnopilus, Panaeolina, Panaeolus, Pluteus, and Stropharia spp.). Within 30 min, there is mydriasis, tachycardia, euphoria, confusion, dizziness, and vomiting.
Antabuse-like reactions (Coprine poisoning): eating ink cap (Coprinus atramentarius) or club foot (Clitocybe clavipes) may produce a reaction similar to that induced by disulfiram (Antabuse®). If alcohol is drunk within 72 h of eating the fungi, there is flushing of the skin, metallic taste, sweating, mydriasis, nausea, vomiting, anxiety, confusion, dyspnoea, severe headache, tachycardia, chest pain, and hypotension.
Poisoning with delayed symptoms (6 h to several days)
Gastroenteritis with hepatotoxicity and nephrotoxicity (Amatoxin poisoning): may result from eating the death cap (Amanita phalloides; Fig. 18.1), destroying angel (Amanita virosa), fool’s mushroom (Amanita verna), Conocybe filaris, and some Galerina and Lepiota spp. Abdominal pain and vomiting, but in particularly severe cases, watery or bloody diarrhoea, starts 6–24 h (usually 12 h) after ingestion, leading to dehydration. After a period of apparent recovery, lasting up to 72 h, fatal hepatorenal failure may supervene.
Gastroenteritis with neurological symptoms (gyromitrin poisoning): there is gastroenteritis with a feeling of bloating, severe headache, vertigo, pyrexia, sweating, diplopia, nystagmus, ataxia, cramps, delirium, and sometimes coma, lethargy, hypoglycaemia, hepatic damage, haemolysis, and renal damage starting 2–24 h after ingesting false Morel (Gyromitra esculenta) or inhaling fumes while it is being cooked.
Renal damage (orellanine poisoning) may develop 2–17 days after eating Cortinarius species. There is fatigue, intense thirst, headache, chills, paraesthesiae, tinnitus, and abdominal, lumbar, and flank pain. After a transient polyuric phase, oliguria and anuria may ensue.
Ergotism (‘St Anthony’s fire’) results from eating cereal crops whose seed heads are infected with the hard, purplish-black fruiting bodies of Claviceps purpurea. Symptoms include vasoconstriction, leading to peripheral gangrene and muscular tremors, convulsions, and hallucinations.
Treating plant and fungal ingestion
First aid
Gastric lavage is potentially dangerous and is discouraged because of the risks of aspiration and trauma to pharynx and oesophagus.
Give the patient a glass of milk to drink provided they are fully conscious and not vomiting.
Give oral activated charcoal 50 g immediately, followed by 25 g every 2 h for at least 48 h (this is not evidence based but is very unlikely to be harmful).
At the base hospital
Severe cases will require supportive treatments for organ failure such as mechanical ventilation and renal dialysis, with therapy for hypovolaemia, acid–base disturbances, hypoglycaemia, cardiac arrhythmias, and convulsions.
For cholinergic (muscarinic) symptoms—atropine (adult 0.6–1.8 mg IV).
For central and peripheral anticholinergic (atropine-like) effects— physostigmine (adult 1–2 mg IV) to control hallucinations, delirium, and psychotic behaviour.
For confusion or hallucinations—tranquillizers such as diazepam (adults 5–10 mg).
For psychotic behaviour—chlorpromazine or haloperidol may be required.
Specific antidotes:
For poisoning by yellow oleander, other Apocynaceae, and any plant containing cardiac glycosides: digoxin-specific antibodies (ovine Fab fragments such as DigibindTM or DigiTabTM).
For severe autumn crocus (Colchicum autumnale) poisoning: colchicine-specific Fab antibodies.
For amatoxic fungal poisoning: infuse silibinin (silybin, silymarin) 5 mg/kg IV over 1 h, followed by 20 mg/kg/24 h (available in Germany but not in the UK or USA) or large doses (300,000–1,000,000 U/kg/day by continuous IV infusion) of benzylpenicillin. N-acetyl cysteine might reduce liver damage. In severe cases, liver transplantation is life-saving.
For gyromitrin fungal poisoning: pyridoxine 25 mg/kg over 30 min, glucose IV, and promote diuresis.
Resource
Poisonous Plants and Fungi in Britain and Ireland. ISBN 1 900347 92 X. Interactive CDRom from Publications Sales, Royal Botanic Gardens, Kew, Richmond, Surrey TW9 3AE, UK. http://www.kew.org/science-conservation/plants-fungi
Advice about plant and fungal poisoning
United Kingdom
TOXBASE® Administered by National Poisons Information Service (Edinburgh) website (registered users): http://www.toxbase.org
24/7 poisons information in the UK: 0844 892 0111.
Phone: +44 (0)131 242 1383 (office). FAX: +44 (0)131 242 1387. Email: [email protected]
Plants and fungi identification: telephone advice service for urgent poisoning case enquiries—Kew Gardens. Phone: +44(0)020 8332 5000.
