FOOD INTOXICATION AND ITS TYPES

MICROBIAL ORIGIN
SYNOPSIS:
 Introduction
 Food Borne Diseases
 Classification of Food Borne Diseases
i. Food Borne Infection
ii. Food borne Intoxication
 TYPES OF FOOD BORNE INTOXICATION
a. Bacterial intoxications
b. Fungal intoxications
c. Chemical intoxication
d. Plant toxicants
e. Poisonous animals

INTRODUCTION:
Food is a major determinant of health, nutritional status and productivity of the population.
It is, therefore, essential that the food we consume is wholesome and safe. Unsafe food can lead
to a large number of food-borne diseases. According to WHO reports , each year worldwide,
unsafe food causes 600 million cases of foodborne diseases and 420 000 deaths. 30% of food-
borne deaths occur among children under 5 years of age. So globally food borne illness is a
major problem of public health concern.

oodborne diseases can be defined as the illness due to

the ingestion of spoiled or poisonous food,
contaminated by microorganisms or toxicants, which
may occur at any stage during food processing
from production to consumption.
FOOD BORNE DISEASES
Food borne diseases can be defined as the illness due to the ingestion of spoiled or poisonous
food, contaminated by microorganisms or toxicants, which may occur at any stage during food
processing from production to consumption.

CLASSIFICATION OF FOOD BORNE DISEASES

Food borne diseases are classified into:

 Food borne infections and

 Food borne intoxications

FOOD BORNE INTOXICATIONS

A toxin is a poisonous substance produced by living cells or organisms. Ludwig Brieger
(1849–1919), an organic chemist was the first to use the term 'toxin‘. Food intoxication is a
form of food-borne illness caused by ingesting exotoxins made by organisms such as bacteria,
fungi etc. or by consuming the foods that are naturally toxic to humans and animals. Onset of
illness is usually very rapid with food intoxication and people can become very sick. Treatment
varies, depending on the toxin involved, but can include administrating medications, providing
the patient with fluids, and offering other supportive care to help patients recover.
So these are diseases caused by consumption of food containing:

1. Biotoxicants which are found in tissues of certain plants and animals.

2. Metabolic products (toxins) formed and excreted by microorganisms (such as
bacteria, fungi and algae), while they multiply in food, or in gastrointestinal tract of
man.
3. Poisonous substances, which may be intentionally or unintentionally added to
food during production, processing, transportation or storage.

Food borne intoxications have short incubation periods (minutes to hours) and are
characterized by lack of fever. The different types of food borne intoxications are :
I.Bacterial intoxications

II.Fungal intoxications

III.Chemical intoxication

IV. Plant toxicants, and

V. Poisonous animals.

I.BACTERIAL FOOD BORNE INTOXICATIONS :

1. Staphylococcus aureus intoxication
 2. Bacillus cereus food borne intoxication
3. Clostridium perfringens food borne intoxication
4. Clostridium botulinum food borne intoxication

1.STAPHYLOCOCCUS AUREUS FOOD BORNE INTOXICATION:

This is a type of food borne intoxication that is caused by consumption of food

contaminated with staphylococcal enterotoxins produced by certain strains of
Staphylococcus aureus while growing in food.
The organism produces the following five serologically different enterotoxins that
are involved in food borne intoxication.
The five enterotoxins are:

 Staphylococcal enterotoxin A(SEA),

 Staphylococcal enterotoxin B (SEB),
 Staphylococcal enterotoxin C (SEC),
 Staphylococcal enterotoxin D (SED),
 Staphylococcal enterotoxin E (SEE)

Individual strains of S. aureus may produce one or more of

enterotoxin types while growing in food.
GROWTH CONDITIONS
 Staphylococcus aureus is a facultative anaerobe, non-spore forming gram positive
coccids.
 It grows at a range temperature between 12-44°C (optimum 37°C) and pH range 4.0-
9.83 (optimum 7.4-7.6).
 Growth occurs in an environment containing up to 18% sodium chloride and
water activity of 0.86 - 0.88 when growing aerobically and 0.9 under anaerobic
conditions.

TOXIN PRODUCTION
 Toxin production occurs at growth temperature of 12-44°C,at pH
of 4.2 and salt concentration of ≤10%.
  No toxin production occurs at temperatures below 12°C, pH < 4.2 and > 10 %
salt.
NATURE OF ENTEROTOXINS
 All the staphylococcal enterotoxins are heat stable(withstand heating at 100°C for
one hour) and ordinary cooking procedures, pasteurization and drying do not
inactivate these enterotoxins.
 They are insensitive to pH changes(pH stable) and resistant to most proteolysis
enzymes (trypsin, chymotrypsin, renin, and pepsin).
 The enterotoxins are also not affected by irradiation.

VEHICLE FOODS
Milk and milk products including pasteurized milk, yoghurt, chocolate milk, fermented
milk, cream filled pastries, poultry, fish, shellfish, meat and meat products, non meat salads,
egg and egg products, vegetables and cereal products have been involved.
DISEASE SYMPTOMS IN MAN:
Incubation period is 1-6 hrs after consumption of food contaminated with at least 1.0 µg of
•
enterotoxin.

• Clinical signs include salvation, nausea, vomiting, abdominal cramps,

sometimes diarrhea with prostration.
• It has an attack rate of 5-100%, but fatalities which occurs in children, the old and
debilitated victims are rare.

• Duration of illness is 24-72 hrs.

DIAGNOSIS
1. Use of clinical symptoms that include nausea, headache, vomiting and diarrhea.
2. Enumeration of organisms in food and stool (presence of ≥106 cfu/g of S. aureus in food in
indicative of involvement of the diseasae in an outbreak.
3. Enterotoxin detection in suspect food, stool and in vomitus of victims using various
methods which include:
a. Serological (e.g. ELISA, reverse passive latex agglutination, or
b. Biological e.g. monkey feeding tests

4. Use of molecular biology techniques, gene probing and polymerase chain reaction.
PREVENTIVE MEASURES
1. Good personal hygiene must be practiced including good personal conduct in food
establishment and when handling food.
2. Use of spoons when serving foods to prevent contamination of cooked foods.
3. Fast cooling of cooked food and keeping such foods at low temperatures.
4. Must discourage the consumption of left- overs .

2.BACILLUS CEREUS FOOD BORNE INTOXICATION

This is a food borne intoxication caused by consumption of enterotoxins

produced by some strains of Bacillus cereus.The organism produces the
following enterotoxins which are involved in a food borne intoxication .The two
diarrhoeal enterotoxins are:

 Hemolysin BL enterotoxin, non-hemolytic enterotoxin, and

 Emetic toxin
VEHICLE FOODS
Bacillus cereus is a common soil saprophyte and is easily spread to many types of
foods, especially of plant origin. It is frequently isolated from meat, eggs and dairy
products, cereal dishes e.g. rice, spice, mashed potatoes, herbs, vegetables, minced
meat, cream and milk pudding have been involved in B. cereus poisoning.

SYMPTOMS OF DISEASE IN MAN

1. Emetic syndrome
 The syndrome is characterized by nausea, vomiting, abdominal cramps and sometimes
diarrhea that occur 1-6 hrs after consumption of contaminated food. The syndrome
is associated with ingestion of rice and pasta based foods.
2. Diarrhoea syndrome
 In the diarrhea syndrome, patients experience profuse diarrhoea (watery stool),
abdominal cramps and tenesmus (rarely vomiting) beginning 8 to 16 hours after
ingestion of contaminated food.

 Fever is absent and symptoms resolve within approximately 12 hours.

DIAGNOSIS
1. Use of clinical signs
2. Enumeration of organism in food using selective media. B. cereus strains of same
serotype should be found present in significant number ≥ 105 cfu/g in incriminated
foods, in feces and vomitus of affected persons.
3. Detection of enterotoxins in foods. Enterotoxin detection has been done using
biological and immunological methods.
PREVENTION
1. Good hygiene should be observed in food establishments and by food handlers.
2. Proper cooking of foods to destroy spores

3. Keep food at low temperature and fast cooling of food.

3.CLOSTRIDIUM PERFRINGENS INTOXICATION

This is a food borne intoxication caused by Clostridium perfringens enterotoxin (CPE)

produced in the gastrointestinal tract by enterotoxigenic strains of C. perfringens. The
organism is found in the soil, dust, water, sewage marine sediments, decaying
materials, intestinal tracts of humans and other animals. This organism is a spore-
forming, anaerobic, gram positive bacillus.

• Food poisoning strains have a variety of origins including human and animal
feces, abattoirs, sewage and flies.
• Spores produced by these organisms can resist boiling for 4 or more hours.
• If the spores are present as contaminants on raw meat they may resist boiling or
steaming, and on slow cooling the spores will germinate into rapidly multiplying
bacterial cells, which produce large amounts of toxin.
CAUSE OF INTOXICATION

• Clostridium food borne intoxication is caused by the ingestion of food containing

large numbers of vegetative cells of enterotoxigenic C. perfringens type A and
some type C and D strains.
• These cells multiply in the intestine and sporulate releasing Clostridium perfringens
enterotoxin (CPE).
• Sometimes CPE may be pre-formed in food, and once the food is consumed,
symptoms may occur within 1-2 hours.

CHARACTERISTICS
Clostridium perfringens enterotoxin (CPE) is synthesized during sporulation.
 o
• CPE is heat labile (destroyed at 60 C for 10 min) and its activity is enhanced by
trypsin.
The food poisoning strains are heat resistant and survive heating at
o
100 C for 1hr
VEHICLE FOODS

 The food involved are those that are prepared one day and served the next day.
 Foods that have been involved include red meats, chickens, fish, pork, fruits,
vegetables, spices etc.
 The heating of such foods is inadequate to destroy heat resistant endospores,
 Upon cooling and warming the endospores germinate and grow.

 Cooking kills the vegetables cells of Cl. perfringens but activates surviving
spores, which will germinate and multiply.
7 8
 Foods poisoning occurs when the level reaches 10 -10 cells/g of
food
 Growth is enhanced by anaerobic conditions achieved after removal of oxygen by
cooking.

MODE OF TRANSMISSION TO FOODS

1. Directly from slaughter animals

2. Contamination of slaughter meat from containers, handlers, dust, and water.

3. Cross -contamination in the kitchen environment.

SYMPTOMS OF DISEASE IN MAN

 Symptoms appear 6-24 hours after ingestion of a large number of viable vegetative
8
cells up to 5x10 /g food, but not after ingestion of spores.
 Symptoms include nausea, intestinal cramps, pronounced diarrhea,
 Vomiting is rare and the illness takes a duration of 1-2 days.
DIAGNOSIS
 Use of clinical signs. Typical symptoms (abdominal pain and profuse diarrhea), 12-
24 hrs following consumption of food.
 Enumeration of C. perfringens in foods and stool (counts of ≥105 cfu/g of food)
 Detection of enterotoxin in food and patient stool using serological methods .e.g.
ELISA, RPLA etc.
PREVENTION

1. Proper cooking of food and eating freshly prepared foods.

2. Thorough washing and sanitation of containers
3. Hygiene handling of cooked food
4. Fast cooling of cooked food. Storing food in small quantities will enhance
cooling.
5. Proper reheating of cold cooked food before consumption
6. Storage of leftovers or unused foods in freezers

4.CLOSTRIDIUM BOTULINUM FOODBORNE NTOXICATION

Clostridium botulinum food borne intoxication (botulism) is a type of food
poisoning caused by consumption of enterotoxins produced by strains of
Clostridium botulinum.
 C. botulinum is an obligate, spore-forming anaerobe, and Gram positive
bacilli
 The strains are divided into proteolytic and non-proteolytic types according to
whether they hydrolyze proteins or not.

 The intoxication is caused by botulinal toxins A, B, E, F and G, produced by C.

botulinum type A, B, E, F and G, while the organism grows in food. C. botulinum
types C and D produce toxins C and D that cause disease in animals
 Type E strains are non-proteolytic while the rest are proteolytic.
o
 Spores of C. botulinum type A can survive temperatures of 120 C.

GROWTH CHARACTERISTICS
o
 Proteolytic strains grow at temperature range between 10-50 C, while non-
o o
proteolytic grow at 3.3-45 C (optimum 35-37 C).
o
 Toxin production occurs at temperature range between 25-30 C.
 Both strains grow at minimum pH of 4.5.

 Proteolytic strains produce an active botulinal toxin, while non-proteolyic

 strains produce inactive pro-toxin that require activation by trypsin.
 Botulinus toxin is one of the most lethal poisons known. The calculated lethal dose
for an adult person is 10 µg.
TYPES OF FOOD IMPLICATED
 Foods associated with anaerobic conditions such as spoiled canned meat, or hams
and bacon stacked without air access, are particularly liable to be infective.
 Home - made fermented foods have been incriminated, together with smoked,
pickled and canned foods that are allowed to stand and then eaten without
adequate cooking.
 Uncooked fresh foods are safe because they are eaten before the toxin has had
time to develop, while, if foods are cooked, the toxin is destroyed.
MODE OF TRANSMISSION
1. Contamination of food due to improper handling.
2. Insufficient heating of food to destroy spores.
3. Spores present in animal tissues e.g. meat and fish.

SYMPTOMS OF THE DISEASE IN MAN

Adult botulism:
• The period of incubation in man is usually 12-72 hrs.
• Symptoms include nausea, vomiting, fatigue, dizziness, headache, dryness of skin,
mouth and throat, constipation, lack of fever, nerve paralysis and great muscular
weakness, double vision, respiratory failure and death.
• Duration of illness 1-10 days and mortality is high up to 60-100% of affected persons.
The earlier the appearance of symptoms, the higher the mortality rate.
Infant botulism:
• Occurs in infants less than 1 year of age following ingestion of spores in
honey and syrup.
• The spores germinate in the gastrointestinal tract with toxin production.
• A high number of spores are found in feces of infants during acute phase of the
disease. The number reduces as recovery progress.

• Symptoms are similar to adult botulism

DIAGNOSIS
1. Use of clinical symptoms
2. Isolation of C. botulinium strain from food.
3. Demonstration of botulinal toxins in suspected food, patient serum, vomit
and stool using the following methods:
i)Biological methods e.g. mouse challenge and protection test
ii)Serological methods e.g. diffusion, electrophoresis, ELISA etc

PREVENTIVE MEASURES
 Ensuring proper manufacturing practices e.g. ensure proper sterilization and preservation
of canned meat
 Preserved foods possessing rancid or other odors should be rejected
 Proper heating of food before consumption to destroy heat labile neurotoxins.Food
o
should be heated to 80 C and temperature maintained for at least 10 min before
eating.
 Picked foods are rendered safe if the brine used contain not less than 10 % common
salt, in weaker brines , microorganisms can continue to multiply.
 Ensuring fast cooling of food. This will ensure that spores that may be remaining do
not germinate in food.
 Utmost care should be taken in the manufacture of cans, their transport, handling,
storage and subsequent use during packaging of product.
II.FUNGAL INTOXICATIONS
These are caused by consumption of metabolites produced by fungi, when growing
in food.These metabolites are called mycotoxins. Grains, oilseeds, fruits and
vegetables are mostly involved if they are stored at high humidity (≥ 0.75) or if they
are not properly dried before storage. Poor dry storage practices of grains and other
foods leads to mould growth and production of mycotoxins. Of significance to
public health is aflatoxicosis .
1.AFLATOXICOSIS
 Aflatoxicosis is caused by aflatoxins produced by the fungi, e.g. Aspergillus
flavus.

 Four types of aflatoxins have been described i.e. aflatoxin B , B , G and G .

1 2 1 2
 Animals consuming feeds contaminated with aflatoxin B leads to secretion in the milk
of aflatoxin M and M 1
1 2.

EFFECTS OF AFLATOXINS

• When consumed in large doses, they are lethal in causing acute hemorrhagic
syndromes
• Sub-lethal doses cause histotoxic changes
• Long term consumption of small doses cause liver tumors as these are potent
carcinogens.

PREVENTION OF AFLATOXICOSIS
 • Proper drying and storage of grains and other affected foods
• Quality control of potentially hazardous foods to ensure that they do not contain above
the allowable limits of 20 ppb before consumption by use of appropriate analytical tests.
• Use of fungicides as seed dressings to protect stored cereals and other foods like
pulses and potatoes against fungal invasion.
2.PATULIN
 Patulin is a toxin produced by the P. expansum.
 P. expansum is especially associated with a range of moldy fruits and vegetables, in
particular rotting apples and figs.
 The presence of patulin has been detected in apple cider and apple juice.
 It also exhibits strong fungistatic activity and is toxic to seeds and seedlings of higher
plants including sugar beets, corn, wheat, peas, tomato, cucumber, and flax.

3.OCHRATOXIN A
 Ochratoxin A (OTA) is a naturally occurring foodborne mycotoxin found in a wide
variety of agricultural commodities worldwide, ranging from cereal grains to dried fruits
to wine and coffee.
 It is produced by several fungal species including Aspergillus ochraceus, A.
carbonarius, A. niger and Penicillium verrucosum.
 They are toxic to some animals and some are very heat resistant, e.g., prolonged
autoclaving does not destroy ochratoxin A when heated in oatmeal.
4. ALIMENTARY TOXIC ALEUKIA (ATA):
 The molds causing this toxins are species of cladosporium, Penicillium,
Fusarium and Alternaria .
5.MUSHROOM POISONING
 Mushroom poisoning (also known as mycetism) refers to harmful effects from ingestion
of toxic substances present in a mushroom.
 These symptoms can vary from slight gastrointestinal discomfort to death.
 Mushroom poisoning is usually the result of ingestion of wild mushrooms after
misidentification of a toxic mushroom as an edible species. The most common reason for
this misidentification is close resemblance in terms of colour and general morphology of
the toxic mushrooms species with edible species.
  A. phalloides is one of the most poisonous of all known toadstools. It has been involved
in the majority of human deaths from mushroom poisoning
III.CHEMICAL FOODBORNE INTOXICATION
This is a type of food borne intoxication arising from consumption of food containing
poisonous chemicals.These may be intentionally or unintentionally added to foods as a
result of producing, processing, transporting or storage.A number of substances can enter
the food chain from the environment and through their use as growth promoters or
veterinary therapeutics giving rise to chemical residues.

CHEMICAL SUBSTANCES INVOLVED

Chemical food borne intoxication involve the following substances:
• Heavy metals e.g. antimony, mercury, arsenic, flouride, lead, cadmium,
cyanide etc.
• Pesticides and insecticides e.g. DDT, BHC Organochlorines and
organophosphates.
• Herbicides
• Fungicides e.g. organomercurials
• Preservatives e.g. nitrites, nicotinate, etc
• Antibiotics e.g.pencillin, tetracyclines, chloramphenicol etc.
• Radionuclides e.g. cesium, strontium, radium, molybdenum, barium,
ruthenium, lanthanum, iodine isotopes etc.

HOW CHEMICALS ENTER FOODS

• Accidental contamination by Heavy metals, Pesticides, and
radionuclides.
• Intentional addition e.g preservatives such as nitrite and sodium nicotinate for color
preservation and fungicides used as dressing during storage.
• Leaching from containers e.g zinc galvanized containers by acid foods, copper
surfaces, lead pipes, asbestos roofs.
• Usage: Presence of such chemicals in food as a result of use of their use in animal and
crop husbandry

• Maliciously added to cause harm (is rare).

CLINICAL SIGNS AND SYMPTOMS
• Chemical food borne intoxication exhibit a very short incubation period, usually a
few minutes to a few hours, with an average of one hour.
• Symptoms are mainly due to effect on gastrointestinal tract and central nervous
system and include nausea, headache, convulsions, gastrointestinal irritation,
abdominal cramps, vomiting and diarrhea, pallor, cyanosis, blurred vision,
sweating, and collapse.
 • Other signs may be due to effects on circulatory system.
• Symptoms of radionuclide toxicity depend on dose, time and organ affected.

PREVENTIVE MEASURES

• Do not use utensils or containers that are able to leach chemicals such as antimony,
cadmium, zinc, copper, etc.
• Use of coloured pesticides and proper storage of the same.
• Prevent contamination of foods when using insecticides.
• Prevent acid foods or carbonated liquids from contact with exposed copper.
• Prevent misuse or avoid use of dangerous additive.e.g. sodium nicotinate.
• Education of persons preparing food (e.g. possibility of Zn poisoning).
• Ensure that withdrawal periods are observed after use of pesticides and antibiotics
in animal and crop husbandry.

BIOTOXICATIONS
These are disorders resulting from ingestion of a poisonous substance (a biotoxin) present in
the body of a plant or animal. Such substances are derived from plants or animals
presumably as a result of metabolic activities. Only a small proportion of the species of fish
and shellfish taken for human consumption throughout the world contain biotoxins.

IV.PLANT INTOXICANTS
1.SOLANINE:
It is a steroid and found in potatoes and other members of solanaceae family (e.g.,aubergine).
Normally it contains 2–15 mg/100 g (fresh weight). When potatoes are exposed to light and
turn green, the level of solanine is high in amount as 100 mg per 100 g.It is heat stable and
insoluble in water and not lost in normal cooking.

Symptoms:
– Solanine is an inhibitor of acetyl choline esterase enzyme, which is a key component
of nervous system and leads to neurological damage .

2.HYDROGEN CYANIDE:
Releases from glycosides in food. When there is tissue damage of tapioca during harvest or
preparing for cooking, cyanogenic glucosides formed from amygdalin, a glucoside in tapioca

Symptoms: Neurological damage occurs

3.LECTINS OR HAEMAGLUTININS:
Present in kidney beans, cereal grains, seeds, nuts, and potatoes It is harmful if consumed
in excess amounts as uncooked or improperly cooked form. Consumption of high lectin content
may lead to diarrhea, nausea, bloating and vomiting. Heat processing can reduce the toxicity but
some plant lectins are resistant to heat.

4.GRAYANOTOXIN

It is found in the leaves, flowers, and necter of some Rhododendron species and from
other members of the Ericaceae botanical family . Also known to be present in honey produced
from the pollen and nectar of certain plants in this family . Toxic compound are diterpenes and
polyhydrocarbons that do not contain nitrogen. The symptoms are nausea, vomiting, dizziness,
mental confusion, or impaired consciousness .

5.FAVISM:
It is a severe reaction occurring on ingestion of foodstuffs consisting of or containing
the beans of the leguminous plant Vicia faba (fava bean, broad bean). Within 6–24 h of the fava
bean meal, the reaction manifests itself with prostration, pallor, jaundice, and dark urine.

OTHER FOODS:
 Apple and pear seeds and the inner stony pit (kernel) of apricots and peaches contain a
naturally occurring substance called amygdalin. Amygdalin can release hydrogen
cyanide in the gut causing discomfort or illness. It can be fatal if too much is consumed
in a short period of time.
 All potatoes contain natural toxins called glycoalkaloids. The levels are usually low but
higher levels are found in potato sprouts, and the peel of potatoes that taste bitter and
causes stomach aches.
 Oxalic acid poisoning can cause muscle twitching, cramps, decreased breathing and heart
action, vomiting, pain, headache, convulsions and coma.
 Zucchini may occasionally contain a group of natural toxins known as cucurbitacins.

V.ANIMALS INTOXICANTS
• This type of intoxication occurs as a result of consumption of poisonous animals.
• Animal tissues may be rendered poisonous by bacterial and enzymatic decomposition,
but some are naturally toxic.
• Primary toxicity occurs due to inherent toxicants that arise due to normal
metabolic processes,
• Secondary toxicity arises due to external toxicants contaminating animal tissues such as
pesticides, heavy metals and drug residues.
• Inherent animal toxins are water soluble and heat labile.
• High concentrations of these toxins are usually found in viscera and dark meats.
• Most human poisoning involves secondarily transvectered toxins.
1.TOXIC FISHES
 They include puffers, triggerfish and parrot fish. The fish toxin affects the peripheral
nervous systems. The fishes may become poisonous by feeding on poisonous marine
organisms. A mortality rate of 50% may occur in humans. Types of biotoxications
associated with fish include ciguatera poisoning, tetraodon poisoning and scombroid
toxicity.

a.CIGUATERA POISONING (CIGUATOXICITY )

Numerous species of fish have been implicated in ciguatera poisoning; however, the
fish do not produce the poison but acquire it as a consequence of feeding on smaller fish which
may have been fed on toxic plankton, plants, or algae. Isolated incidences of fish poisonous to
humans have been shown to be a result of the fish feeding on the toxic alga Lyngbya
majuscula.Over 400 species of fishes are involved including sharks, eels, jacks and groupers.
The illness is caused by a heat stable ciguatoxin. Symptoms include mild paralysis and
gastrointestinal disturbances.
b.TETRAODON POISONING
This type of poisoning is associated with puffer fish mainly of the genus
fugu from the Pacific, Atlantic and Indian oceans.Puffers contain tetraodotoxin, the
most lethal poison from fish that can kill 60-70 % of human victims. The toxin is heat
stable, concentrates in liver and gonads of puffer fish. One must ensure that the toxic
organs are removed before the fish is eaten.

c.SCOMBROID TOXICITY
This poisoning is caused by the ingestion of histamine, formed in the fish product
as a result of bacterial degradation. The name comes from a certain group of fish, i.e., the
scombroid fishes (tuna, mackerel, skipjack, and bonito). Symptoms include nausea, facial
flushing, vomiting, labial edema, oral burning sensation, and itching of the skin. Bacteria such
as Proteus morganii and Klebsiella pneumoniae are involved. Treatment involves use of anti-
histamines which give effective relief. Control of illness is through hygienic handling of fish to
prevent bacterial decomposition.
2.MOLLUSCA
Mollusca may either be inherently or secondarily toxic. Poisoning is mainly due to
the transvection of dinoflagellate protozoa toxins by the mollusca.Mollusca are however not
harmed by ingestion of dinoflagellates. Involved toxins are stored in the digestive glands,
gills and siphore from where they poison vertebrates.Mollusca involved are oysters, mussels
and clams, which feed on dinoflagellates and planktons containing alkaloids making them
toxic.
3.PARALYTIC SHELLFISH POISONING
Many shellfish become toxic to humans as a result of feeding on toxic algae,
particularly the dinoflagellates, including Gonyaulax catenella and G. tamareusis. Symptoms
include numbness of lips, fingertips, and tongue shortly after consumption of the shellfish.
Death can result within 2 to 12 hr as a result of eventual respiratory paralysis.
PREVENTION
 1. Avoiding sea foods from waters laden with toxic dinoflagellates.
2. Reduce toxin activity by heating above 100°C. Thorough cooking may
reduce 70 % of the toxin activity in muscles.
4.POISONOUS MAMMALS
Mammals are not commonly inherently poisonous, but secondary toxicity may affect
many of them. The toxin may be of various types e.g. heavy metals, pesticides, toxic
plants, therapeutics, fungal or bacterial toxins.

PREVENTION OF ANIMAL BIOTOXICATIONS

• Eating of unknown meats from vertebrates or invertebrates sources is always a threat
to the consumer.
• Local eating customs should be followed and local quarantine regulations strictly
adhered to in order to reduce the risk.
o
• Avoid sea foods and always heat foods to above 100 C to denature the inherent
heat labile toxins that may be present in animal tissues.
CONCLUSION:
Food borne intoxications are the most wide spread global public health problem in
present scenario. From every bite one is potentially exposed to illness from either
microbiological or chemical contamination. They are an important cause of mortality and
morbidity and an significant impediment to socioeconomic development worldwide.
Nationwide policy development and establishment of regulatory frameworks and its
implementation are the essential and foremost steps in food safety system. Proper education and
training are needed among food producers, suppliers, handlers, and the general public,
including women and school children. All food operators and consumers should understand the
roles that they must play to protect their health and for the wider community.

REFERENCE:
Websites:
1.https://www.researchgate.net/publication/324930927_Food_Poisoning_and_Intoxication_A_
Global_Leading_Concern_for_Human_Health
2. https://study.com/academy/lesson/what-is-a-foodborne-illness-definition-and-common-
types.html

3. http://www.uop.edu.pk/ocontents/Lecture%20no%201.pdf

Books:
1. Potter, M. E. (2013),  Foodborne Infections and Intoxications, Elsevier Science, Second
Edition, Pp.371 to 380 , 420-425.
2. William.C.Frazier and Dennis.C.Westhoff (2013), Food microbiology, Mc Graw Hill
Education, Fifth Edition, Pp.417-421, 427-428.

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Journal :
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2.Ogori, A.F. and Ogori, J.J.(2014), Review on Mechanism of Food Poisoning by

Microorganisms, International Journal of Advanced Research in Biological Sciences, Vol.1(5),
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