Food poisoning caused by botulin exotoxins (Neurotoxins A, B, C, D, E, F, G) produced by Clostridium botulinum.
Characteristics: Gram-positive, spore-forming bacteria; grows in sausages, canned, and tinned food under unsterile conditions.
Cl. botulinum proliferates in contaminated food and releases exotoxins in anaerobic environments.
Toxins block the release of acetylcholine at synaptic vesicles, leading to flaccid muscular paralysis.
Impacts the myoneural junctions, inhibiting nerve impulses.
Fatal Dose: 0.005 mg
Fatal Period: 24-48 hours, potentially extending to a week.
Initial Symptoms: Dry mouth, difficulty swallowing, retching, vomiting, constipation.
Nervous Symptoms: Drooping eyelids, dilated pupils, diplopia, impaired vision.
Progressive Symptoms: Descending paralysis affecting muscles, including respiratory muscles, leading to respiratory failure.
Other Symptoms: Aphonia, sense of suffocation, muscular weakness, weak pulse, cyanosis of the face, dysphagia, dysarthria
Fluctuating body temperature (may rise to 103°F then fall before death).
Consciousness: Maintained until death, which is preceded by delirium and coma.
Myasthenia gravis, poliomyelitis, multiple sclerosis, Guillain-Barre syndrome, encephalitis, tetanus, CO poisoning, organophosphate poisoning, elapid snake bite.
Artificial respiration.
Anti-toxin: 50,000 units of Trivalent Anti-botulinum toxin (against serotypes A, B, and E).
Symptomatic management: Correct electrolyte imbalances.
Congestion of all internal organs, particularly the lungs (may appear edematous).
Isolation of Cl. botulinum from stomach contents and feces.
Accidental poisoning is common; spores found in honey can cause infant botulism (floppy baby syndrome).
Associated with Sudden Infant Death Syndrome (SIDS).
Suspected use of botulin toxin for homicide by intelligence agencies.
Uses:
Treats strabismus
Manages blepharospasm
Addresses risus sardonicus
Alleviates facial muscle pain disorders
Used for cervical dystonia
Risks:
Wound botulism can occur due to contamination or intravenous drug use.
Some mushrooms are edible, while others are toxic.
Common Toxic Varieties:
Amanita phalloides (Death Cap)
Amanita muscaria (Fly Agaric)
Characteristics:
White in color, cup-shaped base
Often mistaken for edible mushrooms (like Agaricus)
Contains white gills
Unpleasant taste, offensive odor as it ages
Grows in wooded areas
Amotoxins
Phallotoxins
Phallolysin
Antamonide
Amotoxins:
Inhibit DNA-dependent RNA polymerase.
Cause deficient protein synthesis leading to cell necrosis.
Phallotoxins:
Act on cell membranes and cellular metabolism.
Lead to liver and some renal cell necrosis.
Fatal Dose: 2 to 3 mushrooms
Fatal Period: 6 to 24 hours
Symptoms:
Abdominal pain, nausea, and vomiting
Burning throat pain and diarrhea
Possible sweating, cyanosis, circulatory collapse, death
Potential hepato-renal failure if the patient survives.
Stomach wash
Glucose saline and electrolytes
Activated charcoal
Symptomatic management
Dialysis (in case of renal failure)
Antiphalloidin serum
Silibin (hepatoprotective from Silybum marianum)
Inflammation of the GIT
Fatty liver changes and cloudy swelling of kidneys
Congestion in other internal organs, including the brain.
Characteristics:
Orange cap with white flecks, color may vary from yellow, orange, to red
White stem and gills
Known for attracting and killing flies.
Toxic Principles
Muscarin
Muscimol
Ibotenic Acid
Actions
Muscarine: Stimulates post-ganglionic cholinergic fibers, mimicking parasympathetic stimulation.
Effects include liver necrosis and renal damage.
Muscimol & Ibotenic Acid: Stimulate the GABA neurotransmitter system, inhibiting neuronal activity in the brain; exhibit psychoactive and hallucinogenic properties.
Fatal Dose: 2 to 3 mushrooms
Fatal Period: 6 to 24 hours
Symptoms typically appear 30 to 60 minutes post-ingestion:
Early signs: euphoria, hallucinations, muscle jerks, pupil dilation, and sweating.
Possible rise in body temperature.
Gastrointestinal symptoms: nausea, vomiting, diarrhea.
Severe outcomes: circulatory collapse, coma, convulsions, and potential death.
Stomach wash
Activated charcoal
Glucose saline and electrolytes
Atropine
Symptomatic management
Brain may appear congested and edematous.
Congestion of internal organs.
Liver exhibits fatty changes.
Clostridium perfringens
Staphylococci
Streptococci
Shigella
Vibrio parahaemolyticus
Definition: Produced by bacterial decomposition of proteins; not classified as bacterial poisons.
Types of Ptomaines:
Cadaveric Alkaloids: Produced in dead tissues.
Leucoamines: Produced during metabolism in living tissues.
Forms of Ptomaines:
Gaseous: Methylamine
Liquid: Ethylamine
Solid: Neurine, poisonous and causes symptoms akin to atropine and muscarine poisoning.
Common Names: Mexican poppy, Prickly poppy.
Grows widely in India, characterized by yellow flowers and spiny thistle-like leaves.
Seeds: Dark brown, resemble mustard seeds.
Oil is used for adulteration with edible oils
Oil causes epidemic dropsy.
Principal alkaloids:
Sanguinarine
Dihydrosanguinarine
Berberine
Protopine
Initial symptoms:
Loss of appetite
Diarrhea
Physical signs:
Edema in lower limbs
Enlarged and tender liver
Severe cases may present myocardial damage and cardiac dilatation
Tingling and hyperesthesia of skin
Tenderness in calf muscles
Other symptoms:
Breathlessness
Dimness of vision
Glaucoma
Possible development of subcutaneous telangiectasias
Possible cause of death:
Heart failure
Cease oil intake
Provide nutritious food
Implement supportive measures
Type: Pulse belonging to family Leguminosae
Usage: Common dietary item in North India
Disease caused by continuous use:
Lathyrism (characterized by spastic paraplegia)
Toxic Principle:
B-(N) Oxalyl amino-L-alanine (BOAA)
Its neurotoxic effects lead to paralysis of gluteal and lower limb muscles
Start with agonizing calf muscle pain
Spasmodic contractions in thigh
Progression of symptoms:
Weakness in legs
Difficulty sitting/standing from squatting ("no stick stage")
Progression to needing one stick, then two sticks for walking
Eventually, inability to stand, leading to crawling
Muscle pain without sensory loss
Increased knee jerks, marked ankle clonus, positive Babinski's sign
No loss of consciousness or bladder/rectal involvement
Later stages may affect lumbar segments
Risk of aortic aneurysm from toxin
Preventative measure: Parboil the pulse
Recommended dietary limit: Not more than 25% of total diet
Main types:
Ergotamine
Ergometrine
Ergonovine
Ergobasine
Source: Dried sclerotium of fungus Claviceps purpurea
Results from long-term consumption of flour contaminated with ergot:
Tingling, numbness, and burning sensation in lower limbs
Intense heat feeling
Development of red patches and blisters
Possible delirium and convulsions
Known as St. Anthony's fire
Food Poisoning: Poisoning due to consumption of fish and marine creatures is known as Icthyosarcotoxicosis.
General Information:
Puffer fish (fugu) is the second most poisonous vertebrate in the world.
They possess the ability to inflate their bodies as a defense mechanism, signaling that they are poisonous.
Toxicity:
Contains Tetradotoxin (TTX), a neurotoxin that is 1200 times more toxic than cyanide.
TTX blocks sodium channels in excitable tissues, leading to severe health effects.
Location of Toxin:
Present in the skin, ovaries, gonads, and liver of the fish.
Consumption Risks:
Despite known toxicity, puffer fish are in high demand, requiring trained chefs to prepare them safely.
Approximately 100 cases of poisoning and 3 deaths occur per 1,00,000 puffer fish servings annually.
Signs and Symptoms:
Immediate symptoms include tingling and numbness of lips and fingers, followed by muscular weakness, vomiting, and diarrhea.
Severe cases can lead to respiratory paralysis, convulsions, and coma, ultimately resulting in death.
Treatment:
Symptomatic management.
Electrolytes and glucose saline.
Mannitol to alleviate neurological symptoms.
A rare variety found in India, known as Carinotetraodon travancoricus.
Habitat: Found in the Pamba river in Kerala.
Size: World's smallest puffer fish; maximum length is around one inch.
Cause: Caused by Ciguatoxin (CTN) produced by certain algae (dinoflagellates and protozoa).
Mechanism: Algae proliferate during 'red tide' and accumulate toxins which are then ingested by herbivorous fish.
Bioaccumulation: Larger fish (e.g., sea bass, grouper, red snapper) accumulate these toxins by eating herbivorous fish.
Resistance to Cooking: Ciguatoxin is not destroyed by heating or boiling.
Timing: Symptoms may start 2-3 hours after ingestion of cooked fish.
Common Symptoms:
Abdominal pain
Vomiting and diarrhea
Tingling and numbness of the tongue and lips
Myalgia (muscle pain), muscular weakness, and arthralgia (joint pain)
Sensation of hot substances feeling cold and cold substances feeling hot
Feeling that teeth are loose
Metallic taste in the mouth
Headache
Low blood pressure and heart rate
Possible death due to respiratory paralysis
Treatment:
Symptomatic treatment
Mannitol may be given to reduce cerebral edema and neurological symptoms
Species Involved: Tuna, mahimahi, amberjack, bonito, etc.
Process: Increased histidine concentration converts to histamine during preservation.
Symptoms: Allergic reactions such as itching, urticaria, and breathlessness occurring 30-90 minutes after ingestion.
Affected Species: Clams, oysters, mussels, scallops (exoskeleton-bearing aquatic invertebrates).
Toxin: Saxitoxin (STX), a potent neurotoxin, accumulates from feeding on marine algae.
Onset: Symptoms start within 30 minutes post-ingestion.
Effects: Poison acts on the peripheral and autonomic nervous system, blocking depolarization at the neuromuscular junction.
Examples: Catfish, dragon fish, lion fish.
Details:
Catfish (Heteropneustes) have spines with venom produced by glandular cells in the epidermal layer.
Some catfish can deliver electric shocks upon contact.
Dragon fish are found in deep sea and may possess photophores (light-producing organs).
One of the most venomous animals in the world.
Box-shaped cap with four eyes on each side.
Tentacles contain potent poison.
Cardiotoxic
Causes sudden cardiac arrest; over 100 fatalities annually from poisoning.
Tentacles have biological booby traps known as cnidocysts.
When tentacles wrap around a prey, venom is injected.
Highly poisonous frogs found in subtropical and tropical regions (e.g., Bolivia, Brazil, Colombia, Venezuela).
Small in size (1-2 inches) and brightly colored.
Secrete poisonous alkaloids from skin glands.
One drop of poison can kill a human within 3 minutes.