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
– 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
A tin-like metal, cadmium accumulates in the body. Long-term exposure can lead to EMPHYSEMA, renal failure (see KIDNEYS, DISEASES OF) and urinary-tract CALCULI. Acute exposure causes GASTROENTERITIS and PNEUMONITIS. Cadmium contamination of food is the most likely source of poisoning. The EU Directive on the Quality of Water for Human Consumption lays down 5 milligrams per litre as the upper safe level.... cadmium poisoning
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
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
Treatment Administration of oxygen when available is the most important ?rst-aid management. Rescuers should be trained, must not put themselves at risk, and should use protective clothing and breathing apparatus. In unconscious victims, establish a clear airway and give 100 per cent oxygen. If breathing stops and oxygen is unavailable, initiate expired-air resuscitation. If cyanide salts were ingested, mouth-to-mouth contact must be avoided and a mask with a one-way valve employed instead. Some commercially available ?rst-aid kits contain AMYL NITRATE as an antidote which may be employed if oxygen is unavailable.
Once in hospital, or if a trained physician is on the scene, then antidotes may be administered. There are several di?erent intravenous antidotes that may be used either alone or in combination. In mild to moderate cases, sodium thiosulphate is usually given. In more severe cases either dicobalt edetate or sodium nitrite may be used, followed by sodium thio-sulphate. Some of these (e.g. dicobalt edetate) should be given only where diagnosis is certain, otherwise serious adverse reations or toxicity due to the antidotes may occur.... cyanide poisoning
Treatment This is urgent. If the skin has been contaminated with the lysol, it must be washed with water, and any lysol-contaminated clothing must be taken o?. Do not make the victim vomit if he or she has swallowed a corrosive substance such as lysol or phenol. Call an ambulance and say what the victim has taken. See APPENDIX 1: BASIC FIRST AID.... lysol poisoning
Drinking antifreeze initially produces effects similar to alcohol intoxication, but vomiting, stupor, seizures, and coma may follow; acute kidney failure may occur within 24–36 hours.
Antifreeze poisoning requires immediate medical attention.... antifreeze poisoning
The most common effects of opioid overdose are vomiting, drowsiness, pinpoint pupils, BRADYCARDIA, CONVULSIONS and COMA. Respiratory depression is common and may lead to CYANOSIS and respiratory arrest. HYPOTENSION occurs occasionally and in severe cases non-cardiogenic pulmonary oedema and cardiovascular collapse may occur. Cardiac ARRHYTHMIA may occur with some opioids. Some opioids have a HISTAMINE-releasing e?ect which may result in an urticarial rash (see URTICARIA), PRURITUS, ?ushing and hypotension. Activated CHARCOAL should be given following overdose and NALOXONE administered to reverse respiratory depression and deep coma.... opioid poisoning
An overdose of paracetamol is a common choice of those attempting to commit suicide. Since the government restricted the number of paracetamol tablets an individual may purchase over the counter, the incidence of people taking the drug in overdose with the intention of taking their lives has fallen sharply.... paracetamol poisoning
Defoliants are poisonous if swallowed.
Widely used defoliants include sodium chlorate, potassium chlorate, phenoxy herbicides, and paraquat.... defoliant poisoning
While an internal mechanism slows down the body, caffeine in tea, cola and coffee restores alertness. Caffeine acts by blocking the action of the compound, adenosine – one of the building blocks of DNA which promotes cell energy. Caffeine interferes with natural metabolic processes. In the aged, coffee increases production of uric acid, causing irritation of the kidneys, joint and muscle pains. vCaffeinism is responsible for a wide range of disorders. Increases the heart beat, promotes excessive stomach acid and increases flow of urine. It may give rise to birth defects and should be taken with caution in pregnancy.
Symptoms. Restlessness, nervous agitation, extreme sensitiveness. Intolerance of pain, nervous palpitation, all senses acute.
To antidote. Chamomile tea.
Practitioner. Tincture Nux vom BP: 10 drops to 100ml water. Dose: 1 teaspoon thrice daily. Inhalation: Strong spirits of Camphor.
Diet. Plenty asparagus. ... caffeine poisoning
Drug poisoning may cause drowsiness and breathing difficulty, irregular heartbeat, and, rarely, cardiac arrest, fits, and kidney and liver damage.
Antiarrhythmic drugs are given to treat heartbeat irregularity.
Fits are treated with anticonvulsants.
Blood tests to monitor liver function and careful monitoring of urine output are carried out if the drug is known to damage the liver or kidneys.... drug poisoning
Poisons may also originate in the body, as when bacteria produce endotoxins, or when metabolic disorders produce poisonous substances or allow them to build up.
Poisoning may be acute (a large amount of poison over a short time) or chronic (gradual accumulation of poison that is not eliminated quickly).
Unintentional poisoning occurs mainly in young children.
Adults may be poisoned by mistaking the dosage of a prescribed drug (see drug poisoning), by taking very high doses of vitamin or mineral supplements, by exposure to poisonous substances in industry, or by drug abuse.
Poisoning may also be a deliberate attempt to commit suicide.... poisoning
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.... strychnine poisoning