Download - Food poisoning
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RAJALEKSHMY.P.RDEPT OF SWASTHAVRITTA
AMRITA SCHOOL OF AYURVEDA1
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FOOD POISONING
• Acute gastro-enteritis caused by the ingestion of the food or drink contaminated with either living bacteria or their toxins or inorganic chemical substances and poison delivered from plants and animals.
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CHARACTERISTICS
• There is history of the ingestion of a common food
• Attack of the many persons at the same time
• Similarity of the sign and symptoms in majority of the cases
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TYPESBACTERIAL NON-BACTERIAL
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BACTERIAL FOOD POISONING
• It is caused by the ingestion of the food contaminated by the living bacteria or their toxins.
Food infection
the presence of bacteria or other microbes which infect the body after
consumption.
Food intoxication
ingestion of toxins contained within the food, including
bacterially produced exotoxins .
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SALMONELLA FOOD POISONING
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SALMONELLA
• Common form of the food poisoning An increase in communal feeding An increase in international trade in human food A higher incidences of the salmonellosis in farm
animals Wide spread use of the household detergents
interfering with the sewage treatment Wide distribution of the prepared food
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AGENT
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Rod-shaped, flagellated, aerobic, Gram-negative bacteriumnegativ
Rod-shaped, flagellated, aerobic, Gram negative bacterium
Rod-shaped, flagellated, aerobic, Gram-negative bacteriumnegativ
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SOURCE
• Disease of the animals • Man get infection from the farm animal & poultry-
• Rat & mice are another source, they are often heavily infected and contaminate the foodstuffs by their urine & faeces.
Contaminated Meat Milk & Milk Products Sausages Custards Eggs & Eggs Products
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INCUBATION PERIOD
• 12 – 24 hours
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MECHANISM OF ACTION
• After ingestion the organisms multiply in the Intestine & give rise into acute enteritis & colitis.
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SIGNS & SYMPTOMS
• The onset is generally sudden with Chills Fever Nausea Vomiting Profuse Watery Diarrhea (Lasts 2 – 3 days)
• Convalescent carrier state may last for several weeks.
• The mortality rate is 1%.
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STAPHYLOCOCCALFOOD POISONING
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AGENT• Staphylococcus aureus• Gram positive anaerobic coccal bacteria that appears in
clusters.• Enterotoxins of the certain strain of the coagulase
positive staphylococcus aureus. • At least five different enterotoxins have been identified,• Toxins can be formed at optimum temperature of 35oC
to 37oC.• These toxins are relatively heat stable and resist a
boiling of 30 minutes or more.
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SOURCE• Staphylococci are ubiquitous in nature • Found on the
Skin Nose Throat
• They are common agents of the boil and pyogenic infection in man and animals.
• Cow suffering from the mastitis have been responsible for the outbreaks of the food poisoning involving the milk and milk products.
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INCUBATION PERIOD
• 1-6 hrs, short because of preformed toxin.
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MECHANISM OF ACTION
• Food poisoning resulting from the ingestion of the preformed toxins in the food.
• In food bacteria have grown (Intradietetic toxins).• Toxin remain in the food after the organism have
been died.• Action of The toxins:
The toxin act directly on the intestine and CNS.
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SIGNS & SYMPTOMS• Sudden onset of- vomiting
Diarrhoea Abdominal Cramps
• In severe cases blood & mucus may appear. • Unlike salmonella food poisoning the staphylococci
food poisoning rarely cause the fever. • Death is uncommon .
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DIAGNOSIS
Stool culture
•A stool culture is used to detect the presence of disease-causing bacteria (pathogenic) and help diagnose an infection of the digestive tract.• In the case of Staphylococcal enteritis it is conducted to see if the stool is +ve for a pathogenic bacterium.
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BOTULISM
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BOTULISM
• Botulism derived its name from Latin word (Sausage = Botulus).
• Most serious type but occurs rarely. • It kills about 2/3rd of the victims.
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AGENT
• Botulinum toxin is broken into 8 neurotoxins A, B, C, D, E, F, G which are antigenically and serologically distinct but structurally similar.
• Discovery of H toxin- Oct 2013• Exotoxin of the clostridium
botulinum generally type A, B or E cause toxicity in man.
• Cl. Botulinum C and D cause toxicity in animals.
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SOURCE
• The bacteria is widely distributed in soil, dust and intestinal tract of the animals.The organism enters into the food as spores.
• Food Responsible For The Botulism: These are preserved home food such as Home – canned vegetables Smoked or pickled fish Home made cheese Other low – acid foods
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INCUBATION PERIOD
• 12 – 36 hours
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MECHANISM OF ACTION
• Under suitable anaerobic condition the toxins will be preformed into the foods.
• It act on the parasympathetic nervous system.• Its action on the GI – Tract is very slight.• Botulinum toxin is one of the most powerful known
toxins: about one microgram is lethal to humans when inhaled.
• It acts by blocking nerve function through inhibition of the excitatory neurotransmitter acetylcholine's release from the presynaptic membrane of neuromuscular junctions in the SNS.
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SIGNS & SYMPTOMS• Dysphagia • Diplopia • Ptosis• Dysarthria • Blurring of the vision • Muscle weakness & even
quadriplegia • Fever is generally absent. • Consciousness is generally
retained. • The condition is generally fatal. • Death occurs 4 – 8 days later due
to respiratory or cardiac failure.
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CHARACTERISICS OF BOTULISM TOXINS
• Botulism toxin is thermolabile.• Foods contaminated with the botulism toxins heated
for 100oC for a few minutes are safe for consumption.
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INFANT BOTULISM• The botulism occurring in the infants less
than 6 months of age.• It is due to the infection of the gut by the
Cl.botulinum, with subsequent in vivo production of the toxins.
• Toxins are then absorbed into the bloodstream and taken throughout the body causing paralysis by blocking the release of acetylcholine at the neuromuscular junction.
• Constipation, lethargy, weakness, difficulty feeding and an altered cry, often progressing to a complete descending flaccid paralysis.
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WOUND BOTULISM• Wound botulism results from the
contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream.
• This has become more common in intravenous drug users since the 1990s, especially people using black tar heroin and those injecting heroin into the skin rather than the veins.
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BOTULISM ANTITOXINS• When a case of the botulism have occurred, antitoxins should be
given to all individuals partaking of the food.
• The dose varies from the 50,000 – 100,000 unit IV.
• The antitoxin is of no value if the toxin is already fixed to the nervous tissues.
• Guanidine hydrochloride given orally in doses of the 15 – 40 mg/kg of the body weight have been shown to reverse the neuromuscular block of the botulism.
• Active immunization with botulism toxoid is available.
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PREVENTION
•A recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. •In older children and adults the normal intestinal bacteria suppress development of C. botulinum.
•Commercially canned goods are required to undergo a "botulinum cook" in a pressure cooker at 121 °C (250 °F) for 3 minutes.
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Cl. PERFRINGENS FOOD POISONING
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AGENT
• Cl. perfringens (Welchii)
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SOURCE
• The organism have been found in the faeces of the human and animals, soil, water and air.
• The majority of the outbreak have been associated with the ingestion of the meat, meal dishes and poultry.
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INCUBATION PERIOD
• 6-24 hrs with peak from 10 to 14 hrs.
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MECHANISM OF ACTION
• The spores are able to survive the cooking.• If the cooked meat and poultry are not cooled
enough, they will germinate. • The organism multiply between the 30o C – 50oC
and produce a variety of the toxins such as alpha – toxin, theta – toxins etc.
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SIGNS & SYMPTOMS
• Diarrhoea• Abdominal Cramps • Little or no fever
• Nausea & vomiting are rare. • Illness is usually of the short duration (1 day or
less). • Recovery is rapid and no death have been reported.
Occurs 8-24hrs after food consumption
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DIAGNOSIS• C. perfringens can be diagnosed
by Nagler's reaction where the suspect organism is cultured on an egg yolk media plate.
• One side of the plate contains anti-alpha-toxin, while the other side does not. A streak of suspect organism is placed through both sides.
• An area of turbidity will form around the side that does not have the anti-alpha-toxin, indicating uninhibited lecithinase activity.
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PREVENTION
• Cooking food just prior to its consumption or if it has to be stored, by rapid and adequate cooling.
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B. CEREUS FOOD POISONING
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AGENT• Bacillus – cereus is an aerobic, spore – bearing,
motile gram positive rod.• It is ubiquitous in soil and in raw, dried and
processed foods.• The spore can survive cooking and germinate and
multiply rapidly when the food is held at favorable temperature.
• B – cereus has been recognized as a cause of the food poisoning with increasing in frequency in recent years .
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ENTEROTOXINS
• B – cereus produce at least two distinct enterotoxins causing two distinct form of the food poisoning
• 1) Emetic form of food poisoning • 2) Diarrheal form Of food Poisoning
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EMETIC FORM• Short incubation period in between 1 – 6 hours • It is characterized pre-dominantly by the upper gastro –
intestinal tract symptoms.• The 'emetic' form is commonly caused by rice cooked for a
time and temperature insufficient to kill any spores present, then improperly refrigerated. It can produce a toxin cereulide, which is not inactivated by later reheating.
• This form leads to nausea and vomiting one to five hours after consumption.
• Emetic toxin can withstand 121 °C (250 °F) for 90 minutes.
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DIARRHOEAL FORM• longer incubation period of about 12 – 24 hours • It is characterized predominantly by the
Diarrhoea Abdominal pain
Nausea with little or no vomiting and no fever• The recovery within the 24 – hours is usual • The toxins are preformed and stable.• Enterotoxin can be inactivated after heating at
56 °C (133 °F) for 5 minutes.
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DIAGNOSIS
• Diagnosis can be confirmed by the isolation of the organism of 105 or more B – cereus organism per gram of the epidemiologically incriminated food.
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PROGNOSIS
• Most emetic patients recover within six to 24 hours,
but in some cases, the toxin can be fatal.• In 2014, 23 neonates receiving total parenteral
nutrition contaminated with B. cereus developed septicaemia, with three of the infants later dying as a result of infection.
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DIFFERENTIAL DIAGNOSIS
• Cholera • Acute bacillary dysentery • Arsenic poisoning
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CHOLERA & FOOD POISONING
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Cholera Food poisoningEpidemology Occur often in
epidemic form associated with other
cases in the neighbourhood
Often a single group of persons who shared a
common meal
Incubation From a few hours upto 5 days
1 to 24 hrs
Onset With purging With vomitingNausea & retching None Present
Vomiting Projectile, effortless, watery and continuous
Often single, severe vomit, mucuous and
blood streaked
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Cholera Food poisoningStools Copious, rice watery,
inoffensivefrequent, may contain
mucus and blood, offensive
Tenesmus None Yes
Abdominal tenderness None Yes
Dehydration Very marked Distinct
Muscular cramps Constant and severe Less constant
Surface temp Subnormal Often upto 100-102 deg F
Headache None Often
Urine Suppressed Seldom suppressed
Blood Leucocytosis Normal
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INVESTIGATION OF FOOD POISONING
1) Secure complete list of the people involved and their history 2) Laboratory Investigation 3) Animal Experiments 4) Blood for the antibodies 5) Environmental Study 6) Analysis of the data according to descriptive method of time, place and person 7) A case control study may be undertaken to establish the epidemiologic association between illness and the intake of the particular foods. 53
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PREVENTION & CONTROL
Food sanitation
•Meat inspection•Personal hygiene
•Excluding diseased foodhandlers
•Food handling techiques•Sanitary improvements
•Health education
Refrigeration
•‘Cook and eat the food same day immediately’
•Food held between 10oC and 49oC are in danger zone for
bacterial growth.
Surveillance
To avoid outbreaks of foodborne illness54
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