Strychnine is a poisonous chemical found in the seeds of Strychnos species (tropical trees and shrubs). Its main use is as an ingredient in some rodent poisons; most cases of strychnine poisoning occur in children who accidentally eat such poisons.
Symptoms begin soon after ingestion and include restlessness, stiffness of the face and neck, increased sensitivity of hearing, taste, and smell, and photosensitivity, followed by alternating episodes of seizures and floppiness. Death may occur from respiratory arrest.
The victim is given intravenous injections of a tranquillizer or a barbiturate, with a muscle-relaxant drug if needed.
Breathing may be maintained by a ventilator.
With prompt treatment, recovery usually occurs in about 24 hours.
This illness is characterised by vomiting, diarrhoea and abdominal pain, and results from eating food contaminated with metallic or chemical poisons, certain micro-organisms or microbial products. Alternatively, the foods – such as undercooked red kidney beans or ?sh of the scombroid family (mackerel and tuna) – may contain natural posions. Food poisoning caused by chemical or metallic substances usually occurs rapidly, within minutes or a few hours of eating. Among micro-organisms, bacteria are the leading cause of food poisoning, particularly Staphylococcus aureus, Clostridium perfringens (formerly Cl. welchii), Salmonella spp., Campylobacter jejuni, and Escherichia coli O157.
Staphylococcal food poisoning occurs after food such as meat products, cold meats, milk, custard and egg products becomes contaminated before or after cooking, usually through incorrect handling by humans who carry S. aureus. The bacteria produce an ENTEROTOXIN which causes the symptoms of food poisoning 1–8 hours after ingestion. The toxin can withstand heat; thus, subsequent cooking of contaminated food will not prevent illness.
Heat-resistant strains of Cl. perfringens cause food poisoning associated with meat dishes, soups or gravy when dishes cooked in bulk are left unrefrigerated for long periods before consumption. The bacteria are anaerobes (see ANAEROBE) and form spores; the anaerobic conditions in these cooked foods allow the germinated spores to multiply rapidly during cooling, resulting in heavy contamination. Once ingested the bacteria produce enterotoxin in the intestine, causing symptoms within 8–24 hours.
Many di?erent types of Salmonella (about 2,000) cause food poisoning or ENTERITIS, from eight hours to three days after ingestion of food in which they have multiplied. S. brendeny, S. enteritidis, S. heidelberg, S. newport and S. thompson are among those commonly causing enteritis. Salmonella infections are common in domesticated animals such as cows, pigs and poultry whose meat and milk may be infected, although the animals may show no symptoms. Duck eggs may harbour Salmonella (usually S. typhimurium), arising from surface contamination with the bird’s faeces, and foods containing uncooked or lightly cooked hen’s eggs, such as mayonnaise, have been associated with enteritis. The incidence of human S. enteritidis infection has been increasing, by more than 15-fold in England and Wales annually, from around 1,100 a year in the early 1980s to more than 32,000 at the end of the 1990s, but has since fallen to about 10,000. A serious source of infection seems to be poultry meat and hen’s eggs.
Although Salmonella are mostly killed by heating at 60 °C for 15 minutes, contaminated food requires considerably longer cooking and, if frozen, must be completely thawed beforehand, to allow even cooking at a su?cient temperature.
Enteritis caused by Campylobacter jejuni is usually self-limiting, lasting 1–3 days. Since reporting of the disease began in 1977, in England and Wales its incidence has increased from around 1,400 cases initially to nearly 13,000 in 1982 and to over 42,000 in 2004. Outbreaks have been associated with unpasteurised milk: the main source seems to be infected poultry.
ESCHERICHIA COLI O157 was ?rst identi?ed as a cause of food poisoning in the early 1980s, but its incidence has increased sharply since, with more than 1,000 cases annually in the United Kingdom in the late 1990s. The illness can be severe, with bloody diarrhoea and life-threatening renal complications. The reservoir for this pathogen is thought to be cattle, and transmission results from consumption of raw or undercooked meat products and raw dairy products. Cross-infection of cooked meat by raw meat is a common cause of outbreaks of Escherichia coli O157 food poisoning. Water and other foods can be contaminated by manure from cattle, and person-to-person spread can occur, especially in children.
Food poisoning associated with fried or boiled rice is caused by Bacillus cereus, whose heat-resistant spores survive cooking. An enterotoxin is responsible for the symptoms, which occur 2–8 hours after ingestion and resolve after 8–24 hours.
Viruses are emerging as an increasing cause of some outbreaks of food poisoning from shell?sh (cockles, mussels and oysters).
The incidence of food poisoning in the UK rose from under 60,000 cases in 1991 to nearly 79,000 in 2004. Public health measures to control this rise include agricultural aspects of food production, implementing standards of hygiene in abattoirs, and regulating the environment and process of industrial food production, handling, transportation and storage.... food poisoning
Lead and lead compounds are used in a variety of products including petrol additives (in the UK, lead-free petrol is now mandatory), piping (lead water pipes were once a common source of poisoning), weights, professional paints, dyes, ceramics, ammunition, homeopathic remedies, and ethnic cosmetic preparations. Lead compounds are toxic by ingestion, by inhalation and, rarely, by skin exposures. Metallic lead, if ingested, is absorbed if it remains in the gut. The absorption is greater in children, who may ingest lead from the paint on old cots
– although lead-containing paints are no longer used for items that children may be in contact with.
Acute poisonings are rare. Clinical features include metallic taste, abdominal pain, vomiting, diarrhoea, ANOREXIA, fatigue, muscle weakness and SHOCK. Neurological effects may include headache, drowsiness, CONVULSIONS and COMA. Inhalation results in severe respiratory-tract irritation and systemic symptoms as above.
Chronic poisonings cause gastrointestinal disturbances and constipation. Other effects are ANAEMIA, weakness, pallor, anorexia, insomnia, renal HYPERTENSION and mental fatigue. There may be a bluish ‘lead line’ on the gums, although this is rarely seen. Neuromuscular dysfunction may result in motor weakness and paralysis of the extensor muscles of the wrist and ankles. ENCEPHALOPATHY and nephropathy are severe effects. Chronic low-level exposures in children are linked with reduced intelligence and behavioural and learning disorders.
Treatment Management of patients who have been poisoned is supportive, with removal from source, gastric decontamination if required, and X-RAYS to monitor the passage of metallic lead through the gut if ingested. It is essential to ensure adequate hydration and renal function. Concentrations of lead in the blood should be monitored; where these are found to be toxic, chelation therapy should be started. Several CHELATING AGENTS are now available, such as DMSA (Meso-2,3dimercaptosuccinic acid), sodium calcium edetate (see EDTA) and PENICILLAMINE. (See also POISONS.)... lead poisoning
Around 2,000 mushrooms (toadstools) grow in England, of which 200 are edible and a dozen are classi?ed as poisonous. Not all the poisonous ones are dangerous. It is obviously better to prevent mushroom poisoning by ensuring correct identi?cation of those that are edible; books and charts are available. If in doubt, do not eat a fungus.
Severe poisoning from ingestion of fungi is very rare, since relatively few species are highly toxic and most species do not contain toxic compounds. The most toxic species are those containing amatoxins such as death cap (Amanita phalloides); this species alone is responsible for about 90 per cent of all mushroom-related deaths. There is a latent period of six hours or more between ingestion and the onset of clinical effects with these more toxic species. The small intestine, LIVER and KIDNEYS may be damaged – therefore, any patient with gastrointestinal effects thought to be due to ingestion of a mushroom should be referred immediately to hospital where GASTRIC LAVAGE and treatment with activated charcoal can be carried out, along with parenteral ?uids and haemodialysis if the victim is severely ill. In most cases where effects occur, these are early-onset gastrointestinal effects due to ingestion of mushrooms containing gastrointestinal irritants.
Muscarine is the poisonous constituent of some species. Within two hours of ingestion, the victim starts salivating and sweating, has visual disturbances, vomiting, stomach cramps, diarrhoea, vertigo, confusion, hallucinations and coma, the severity of symptoms depending on the amount eaten and type of mushroom. Most people recover in 24 hours, with treatment.
‘Magic’ mushrooms are a variety that contains psilocybin, a hallucinogenic substance. Children who take such mushrooms may develop a high fever and need medical care. In adults the symptoms usually disappear within six hours.
Treatment If possible, early gastric lavage should be carried out in all cases of suspected poisoning. Identi?cation of the mushroom species is a valuable guide to treatment. For muscarine poisoning, ATROPINE is a speci?c antidote. As stated above, hospital referral is advisable for people who have ingested poisonous fungi.... fungus poisoning
The toxic effect of mercury has been known since days of the medieval alchemists. Charles II presented all the symptoms we now recognise as mercurial poisoning, presumably the result of medication received over many years. Its symptoms simulate multiple sclerosis, when chronic. They are: constant fatigue, pins and needles in the limbs, resting tremor, nausea, dizziness, ataxia, pains in the bones and joints, drooling (excessive salivation), blue line along the gums. In children they may include all kinds of vague aches and pains, chorea, hyperthyroidism and facial neuralgia. Weakness, walking difficulties, metallic taste in the mouth, thirst, mental deterioration. It is now known to cause a number of serious nerve dystrophies.
Mercury has an affinity for the central nervous system. Soon it concentrates in the kidney causing tubular damage. A common cause is the mercurial content (50 per cent) in the amalgam fillings in teeth which, under certain conditions, release a vapour. Fortunately, its use in dentistry is being superceded by an alternative composite filling.
A common cause of poisoning was demonstrated in 1972 when 6,000 people became seriously ill (600 died) from eating bread made from grain treated with a fungicide containing methylmercury. For every fungus in grain there is a mercuric compound to destroy it. The seed of all cereal grain is thus treated to protect its power of germination.
Those who are hypersensitive to the metal should as far as possible avoid button cells used in tape recorders, cassette players, watch and camera mechanisms. As the mercury cells corrode, the metal enters the environment and an unknown fraction is converted by micro organisms to alkylmercury compounds which seep into ground waters and eventually are borne to the sea. When cells are incinerated, the mercury volatilises and enters the atmosphere. (Pharmaceutical Journal, July 28/1984)
Mercury poisoning from inhalation of mercury fumes goes directly to the brain and pituitary gland. Autopsies carried out on dentists reveal high concentrations of mercury in the pituitary gland. (The Lancet, 5-27-89,1207 (letter))
Treatment. For years the common antidote was sulphur, and maybe not without reason. When brought into contact sulphur and mercury form an insoluble compound enabling the mercury to be more easily eliminated from the body. Sulphur can be provided by eggs or Garlic.
Old-time backwoods physicians of the North American Medical School used Asafoetida, Guaiacum and Echinacea. German pharmacists once used Bugleweed and Yellow Dock. Dr J. Clarke, USA physician recommends Sarsaparilla to facilitate breakdown and expulsion from the body.
Reconstructed formula. Echinacea 2; Sarsaparilla 1; Guaiacum quarter; Asafoetida quarter; Liquorice quarter. Dose: Liquid Extracts: 1 teaspoon. Tinctures: 2 teaspoons. Powders: 500mg (two 00 capsules or one-third teaspoon). Thrice daily.
Chelation therapy.
Formula. Tinctures. Skullcap 2-15 drops; Pleurisy root 20-45 drops; Horehound 5-40 drops. Mercurial salivation. Thrice daily. (Indian Herbology of North America, by Alma Hutchens) Dental fillings: replace amalgam with safe alternative – ceramic, etc. Evidence of a link between tooth fillings containing mercury and ME has caused the use of dental amalgam to be banned in Sweden. ... mercury poisoning
Strychnos nux-vomicaLoganiaceaeSan: Karaskara;Hin: Kajra, Kuchila;Mal: Kanjiram; ;Tam: Itti, Kagodi, Kanjirai Mar:Jharkhatchura;Kan: Hemmushti, Ittangi;Tel: Mushti, Mushidi; Ori: Kora, KachilaImportance: It is a large deciduous tree, with simple leaves and white fragrant flowers.Strychnos is highly toxic to man and animals producing stiffness of muscles and convulsions, ultimately leading to death. However, in small doses it can also serve as efficacious cure forms of paralysis and other nervous disorders. The seeds are used as a remedy in intermittent fever, dyspepsia, chronic dysentery, paralytic and neuralgic affections, worms, epilepsy, chronic rheumatism, insomnia and colic. It is also useful in impotence, neuralgia of face, heart disease, spermatorrhoea, skin diseases, toxins, wounds, emaciation, cough and cholera. Leaves are applied as poultice in the treatment of chronic wounds and ulcers and the leaf decoction is useful in paralytic complaints. Root and root bark used in fever and dysentery (Nadkarni, 1982; Kurup et al, 1979).Distribution: The plant is distributed throughout India in deciduous forests up to 1200m. It is also found in Sri Lanka, Siam, Indochina and Malaysia.Botany: Strychnos nux-vomica Linn. is a large tree belonging to the family Loganiaceae. Leaves are simple, opposite, orbicular to ovate, 6-11.5x6-9.5cm, coriaceous, glabrous, 5 nerved, apex obtuse, acute or apiculate, transverse nerves irregular and inconspicuous. Inflorescence is many flowered terminal cymes, 2.5-5cm across. Bracts (5mm) and bracteoles (1.5mm) small. Flowers are white or greenish white and fragrant. Calyx 5 lobed, pubescent and small (2mm). Corolla salver shaped, tube cylindrical slightly hairy near the base within and greenish white, tube much elongate than the lobes. Tube 7mm and lobes 2.5mm long. Lobes 5 and valvate. Stamens 5, filaments short, 0.1mm long. Anthers 1.5mm subexerted, linear oblong. Ovary 1.5 mm, pubescent, 2 celled, ovules one to many. Style 9mm, stigma capitate. Fruit is a berry, 5-6cm diameter, globose, indehiscent, thick shelled, orange red when ripe with fleshy pulp enclosing the seeds. Seeds 1-many, discoid, compressed, coin like, concave on one side and convex on the other, covered with fine grey silky hairs.The leaf fall is during December (do not shed all the leaves at a time) and new foliage appears in February. Flowering is during March - April and fruiting during May - December. Fruits take about 8-9 months to mature.Properties and activity: Strychnine and brucine are the most important and toxic alkaloids present in the plant. They occur not only in the seeds but also in roots, wood, bark, fruit pulp and hard fruit shells. The minor alkaloids present in the plant are vomicine, -colubrine, -colubrine, pseudostrychnine and N-methyl-sec-pseudobrucine (novacine). Loganin a glycoside is also present (Warnat, 1932; Martin et al, 1953; Guggisberg et al, 1966; Bisset and Chaudhary, 1974). Chatterji and Basa (1967) reported vomicine as the major constituent alkaloid along with unidentified alkaloid in leaves and identified another alkaloid kajine (N-methyl pseudostrychnine) from the leaves of very young plants.Root bark of S. nux-vomica yeilded 4-hydroxy-3-methoxy strychnine, 4 hydroxy strychine, nor-macusine, a new alkaloid 12 , 13 dihydro-12 -hydroxy isostrychnine named protostrychnine (Baser et al, 1979) methoxy strychnine, and mavacurine (Guggisberg et al, 1966). Leaves and root bark also yeilded 11 new alkaloids. 10-hydroxy strychnine, 3-12-dihydroxystrychnine, 12-hydroxy–11- methoxy strychnine, 3-12-dihydroxy- 11-methoxy strychnine,12-hydroxy strychnine-N- oxide 12-hydroxy-11-methoxy strychnine- N-oxide-19,20–dihydro isostrychnine, 16 , 17 dihydro-17 -hydroxy isostrychnine, O- methyl-macusine B, 16-epi-o-methyl–macusine B and normelinone B (Baser and Bisset, 1982).De and Datta (1988) isolated 5 tertiary indole alkaloids viz. strychnine, brucine, vomicine, icajine and novacine from S.nux-vomica flowers. Bisset et al (1989) isolated and identified two phenolic glycosides salidroside and cuchiloside – a compound consisting of salidroside and an attached xylose unit, from the fruit of S.nux-vomica.Rodriguez et al (1979) isolated an indole alkaloid from the seeds of S. nux- vomica and identified as a 3-methoxy icajine. A new alkaloid 15-hydroxy strychnine has been isolated from the seeds and the structure of the alkaloid established by spectroscopic data (Galeffi et al, 1979). Cai et al (1990a) isolated 4 new alkaloids isobrucine, isobrucine N-oxide, isostrychnine N-oxide and 2 hydroxy–3-methoxy strychnine from the heat treated seeds of S. nuxvomica and the structure of the alkaloids were determined by 13 CNMR (Cai et al, 1994). Cai et al (1990 b) studied the changes in the alkaloid composition of the seeds during drug processing. Saily et al (1994) determined the mineral elements in Strychnos nux-vomica. Corsaro et al (1995) reported polysaccharides from the seeds of Strychnos species.Seeger and Neumann (1986) reviewed the physico-chemical characteristics, occurrence, identification, utilisation, poisoning, toxicity, kinetics, differential diagnosis and therapeutic uses of strychnine and brucine. Aspergillus niger, A. flavus and Pencillium citrinum showed regular association with Strychnos seeds and effectively deteriorated the alkaloid content of the seeds (Dutta, 1988; Dutta and Roy, 1992). Nicholson (1993) described the history, structure and synthesis of strychnine which occur in the seeds of S. nux-vomica. Rawal and Michoud (1991) developed a general solution for the synthesis of 2- azabicyclo (3.3.1) nonane substructure of Strychnos alkaloids.Villar et al (1984) and Hayakawa et al (1984) developed HPLC method for the analysis of strychnine and brucine. Graf and Wittliner (1985), Kostennikova (1986) and Gaitonde and Joshi (1986) suggested different methods for the assay of strychnine and brucine. Biala et al, (1996) developed new method for the assay of alkaloids in S. nux- vomica.The seeds are bitter, acrid, alexeteric, aphrodisiac, appetiser, antiperiodic, anthelmintic, digestive, febrifuge, emmenagogue, purgative, spinal, respiratory and cardiac stimulant and stomachic. The bark is bitter, and tonic and febrifuge (Nadkarni, 1954; Kurup et al, 1979; Warrier et al, 1996).The quarternery alkaloid from the root bark of the Sri Lankan plant exhibited muscle-relaxant activity (Baser and Bisset, 1982). Antimicrobial activity of indole alkaloid isolated from the Strychnos nux-vomica was studied by Verpoorte et al, 1983. Shukla et al (1985) evaluated the efficacy of Rasnadigugglu compound consisting of S. nux-vomica, on rheumatoid arthritis and found to be effective in reducing inflammatory oedoma and rheumatoid arthritis. It also exhibited analgesic activity. A compound Unani formulation containing S. nux-vomica significantly attenuated withdrawal intensity in morphine dependent rats (Zatar et al, 1991). Shahana et al (1994) studied the effect of Unani drug combination (UDC) having Strychnos nux-vomica on the abstinence syndrome in moderately and severely morphine dependent rats. The UDC strikingly suppressed the abstinence syndrome was seen to possess central depressant and analgesic action.Melone et al (1992) reported brucine-lethality in mice. Panda and Panda (1993) and Satyanarayanan et al (1994) reported antigastric ulcer activity of nux vomica in Shay rats. Banerjee and Pal (1994) reported the medicinal plants used by the tribals of plain land in India for hair and scalp preparation and S. nux-vomica being used to cure alopecia (baldness) by the tribals. Tripathi and Chaurasia (1996) studied the effect of S. nux-vomica alcohol extract on lipid peroxidation in rat liver.... strychnine tree
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