This document discusses food poisoning, which can result from ingesting food containing bacteria, viruses, toxins, or chemicals. It defines food poisoning and outlines various causes like bacteria, toxins from plants/animals, and chemicals. Specific types of bacterial food poisoning from Salmonella, Staphylococcus, and Clostridium are explained. Treatment focuses on gastric lavage, fluids, antibiotics, and supportive care. Poisoning from botulinum toxin, Lathyrus sativus, mushrooms, and Argemone mexicana are also summarized.

1. Food Poisoning
By – Priyanka ( MBBS Student )

2. Definitions
• Food poisoning include all illnesses which result from ingestion of
food containing bacterial or non-bacterial products including viruses,
environmental toxins or toxins present within the food itself.
• The term is usually restricted to acute gastroenteritis due to the
bacterial infection of food or drink.

3. Defined by the following criteria:
i. Similar illness, often gastrointestinal, in a minimum
of 2 individuals
ii. Evidence of food as the source

4. Causes
i. Poisoning due to bacteria and toxins.
ii. Poisons of vegetable origin (natural food poisons):
• Lathyrus sativus,
• poisonous mushrooms
• Argemone mexicana.
iii. Poisons of animal origin: Poisonous fish and mussel.
iv. Chemical: Intentionally or accidentally added,
products of food processing and radio-nucleotides

5. Bacterial food poisoning
Infection type (Inflammatory diarrhea)
Organisms belong mainly to the Salmonella group and occasionally Proteus, E. coli,
Bacillus cereus, Streptococci, Shigella and paratyphoid bacilli are also involved.
Salmonella invade and destroy the mucosa of the small intestine.
Symptoms:
 Sudden onset of nausea/vomiting
 abdominal pain
 foul smelling watery diarrhea
 stained with blood and/or mucus occurs in 12 h to two days.
Diarrhea in several patients after 24-48 h of eating the same meal indicates ingestion of
salmonella.

6. Bacterial food poisoning
Toxin type (non-inflammatory diarrhea)
results from ingestion of preformed toxins (exotoxins) from
bacterial proliferation in (canned or preserved food)
e.g. enterotoxin of Staphylococci, Clostridium perfringens, Bacillus cereus and botulinum
toxin.
Symptoms:
 Salivation
 Diarrhea
 nausea vomiting
 Abdominal cramps
 occur for a short time
 patient recovers as soon as the enterotoxins have been neutralized and metabolized,
usually within 24 h of poisoning.

7.  Acute diarrhea in food poisoning usually lasts < 2 weeks.
 Diarrhea lasting 2-4 weeks is classified as persistent.
 Chronic diarrhea is defined by duration of > 4 weeks.

8. Treatment
i. Gastric lavage and purgatives are given.
ii. Glucose-saline infusion should be given to promote
elimination of the toxins from the system.
iii. Antibiotics are given depending upon the causative organism.

9. PMF
i. The mucosa of the GIT is swollen ,congested and there may be minute
ulcers.
ii. Microscopic examination shows fatty degeneration of the liver.
iii. The causative organism can be isolated from the blood and viscera.

10. Botulism (Allantiasis)
'botulism' is derived from 'botulismus' meaning sausage.
Botulism is an intoxication, not an infection.
Clostridium botulinum (gram-positive spore forming anaerobic bacilli) which
multiplies in the food, e.g. sausages, tinned meat, fish and fruits
produces a powerful exotoxin—a neurotoxin.
Seven distinct strains (type A to G) of C. botulinum have been identified.

11. Mechanism Of Action
The toxin inhibits acetylcholine and paralyzes the nerve endings by blocking the nerve impulses at
the myoneural junctions.
Its action is selective, being confined to the cholinergic fibres of the autonomic nervous system.
It affects the peripheral cholinergic nerve terminals including neuromuscular junctions, post-ganglionic
parasympathetic nerve endings and peripheral ganglia without affecting the CNS

12. Symptoms• The incubation period is 12-30 h.
• The GIT symptoms, like nausea, vomiting and abdominal pain are rare.
• Initial symptoms are
• dry/sore mouth or throat
• difficulty with visual accommodation
• diplopia,
• dysphonia,
• dysphagia
• descending bilaterally symmetrical motor
• paralysis initiated by—abducent (VI) or oculomotor (III) nerve palsy (strabismus, blepharospasms),
• constipation,
• hypothermia,
• respiratory insufficiency
• urinary retention.
• The patient is conscious till death preceded by delirium & coma

13. • Fatal dose: 0.01 mg or even less.
• Fatal period: 24-48 h, may extend to a week.

14. Treatment
Maintenance of ABC.
Decontamination—Gastric lavage, activated charcoal, purgatives and whole bowel irrigation.
Polyvalent botulinum antitoxin (types A, B and E)one vial by slow IV in normal saline and one
vial IM, repeated at 2-4 h intervals IV.8
Botulism immune globulin (BIG), 50 ml is given IV daily, till the patient recovers.
Frequent dose of brandy is beneficial as alcohol precipitates toxin.

15. PMF
i. Kidneys, liver and meninges are congested.
ii. Histological examination of the organs may show thrombosis.

16. Lathyrus Sativus ('Kesari Dhal')
The staple food for the low income groups
Consumption of L. sativus seeds in quantities >30% of total diet > 6
months has been known to cause
paralysis.
Men are more susceptible than women.

17. Active Principles
 Beta-N-oxalyl amino-alanine (BOAA), a neurotoxic
amino acid present in the seed cotyledons

18. Clinical Features
The continued use of L. sativus produces neurolathyrism
Characterized by progressive spastic paraplegia with preservation of sphincters, sensation and mental
activity.
There may be pain in the back or weakness of legs and difficulty in sitting down and getting up.
The patient is unable to walk without the aid of a stick, the legs tremble and are dragged along with
difficulty.
A spastic gait develops characterized by 'walking on tiptoes' with the legs crossing scissor-wise.
Later, complete paraplegia occurs.
There is no atrophy or loss of the tone of muscles and no reaction of degeneration.
The knee jerks are increased, ankle clonus is marked and Babinski's sign is present

19. Walking on tiptoes

20. Treatment
Rich diet with exclusion of the pulse
massage and application of electricity are useful.
Steeping the pulse in hot water and parboiling remove 90% of toxic amino acid.
Death is very rare.
At autopsy, lateral columns of the spinal cord may show sclerosis.

21. Mushrooms
Common poisonous fungi are Amanita phalloides and
Amanita muscaria (deadly agaric/death cap).

22. Active Principles
Amanita muscaria contains an alkaloid muscarine which
stimulates postganglionic cholinergic fibres.
Amanita phalloides contains phalloidin, phallon, alpha-amanatin which are
cyclopeptides and virotoxins.
They are powerful inhibitors of cellular protein synthesis.

23. Clinical Features
Irritant symptoms are delayed by 6-24 h and include constriction of the throat, burning
pain in the stomach, nausea, vomiting and diarrhea followed by cyanosis, slow pulse,
labored respiration, convulsions, sweating, collapse and death.
Neurotic symptoms are giddiness, headache, delirium, diplopia, constriction of the
pupils, cramps, twitching of the limbs, convulsions, salivation, bradycardia and coma.
Icterus, hepatic and renal failure occurs in 3-6 days.

24. • Fatal dose: 2-3 mushrooms.
• Fatal period: Usually 24 h.
• Diagnosis: Meixner test (Wieland test) for detection of toxins (alpha-
amanitin) in stools and vomitus.

25. Treatment
i. Supportive: It comprises of aggressive correction of
fluid and electrolyte losses, and in the advanced stages, attention to liver and renal failure.
ii. Specific: Decontamination is required to remove the toxin rapidly. Oral activated charcoal
and lactulose are ideal.
iii. In amatoxin type of poisoning, penicillin, silybin, thioctic acid and corticosteroids have been
tried for their synergistic effect in inhibiting the binding of both toxins and interrupting
enterohepatic recirculation of toxins.
iv. In muscarine poisoning, the specific antidote is atropine sulphate, 0.01-0.02 mg/kg/dose IV
repeated every 30 min until atropinization.13 v. For convulsions, diazepam may be given.
vi. Hemodialysis may be done.
vii. Symptomatic treatment.

26. PMF
 Inflammation of the mucous membrane of the GIT, and fatty degeneration of
the liver, kidneys and heart may be found.
 In case of neurotic symptoms, congestion of the brain
and petechial hemorrhages in serous membranes are seen.

27. Argemone Mexicana (Prickly Poppy)
• All parts of the plant are poisonous.
• The argemone or katkar oil causes epidemic dropsy.
• The flowers are yellow
• seeds are dark-brown in color, smaller than mustard
seeds and covered with minute, regularly arranged
projections and depressions.

28. Active Principles
 The plant contains two alkaloids—berberine and protopine.
 The oil contains two alkaloids, sanguinarine and dihydrosanguinarine .They
cause abnormal permeability of blood vessels.

29. Clinical Features
• Symptoms appear slowly with loss of appetite, diarrhea, marked edema of the legs, and
sometimes generalized anasarca.
System Signs and symptoms
• Heart -Myocardial damage and dilatation of the heart.
• CVS- Hypotension, breathlessness and feeble pulse.
• Hepatic- Enlarged and tender liver.
• PNS -Tingling and hyperaesthesia of skin and tenderness of the calf muscles. The jerks are
feeble or absent.
• Ocular- Dimness of vision (in about 10% of cases) due to increased intraocular pressure.
• Skin- Bluish mottling of the skin due to dilation of the peripheral vessels.
• Death occurs from severe damage to the heart.

30. Treatment
Treatment: Good diet, decontamination, withdrawal of oil, diuretics,
corticosteroids and supportive treatment.
Medico-legal aspects: The oil from the seeds is sometimes used as
an adulterant of mustard oil or other edible oil.

31. Food Allergy
Some persons are hypersensitive to certain types of protein, e.g. meat,
fish, eggs or milk which are ordinarily quite harmless, and suffer from
gastroenteritis, local urticarial rashes joint pains or asthmatic attack.
Antihistaminics and steroids may be given.