Food poisoning/ Food intoxication

Food intoxication is a health condition which caused by consuming contaminated food that contains certain toxins. It can be caused by

 - Due to naturally occurring toxins in some foods. Ex: Endemic ascitis (Pyrrolizidine alkaloids)

 - Due to toxins produced by certain bacteria. Ex: Botulism, Staphyloccal toxins

 - Due to toxins produced by some fungi. Ex: Aflatoxin, Fusarium toxins

 - Due to toxins produced by some algae like dinoflagellates, Diatoms, Cyanobacteria

-  Due to food-borne chemical poisoning

However, most common food intoxication is caused by the toxins produced by certain bacteria. It involves food poisoning in which the organism grows in food and releases a toxin from the cells. The presence of organism in the food is irrelevant to disease production. It is the toxin that gives rise to the disease. Bacterial toxins that produce intoxications are exotoxins of either enterotoxin (affecting the gut) or neurotoxin (affecting the nervous system).

Type of food poisoning	Causative agent	Type of toxin	Mode of transmission	Food commonly involve
Staphylococcus food poisoning	Staphylococcus aureus	Enterotoxin	Sources from where microorganisms enter food	Meat, fish, milk, poultry, custards, cream
Botulism	Clostridium botulinum	Neurotoxin	Spores are transferred from soil into food	Damaged leaky and rusty cans or cans with broken seals
Bacillus cereus food poisoning	Bacillus cereus	Enterotoxin	Spores from soil to food such as cereals and grains	Chinese fried rice spices, reheated boiled rice, corn flour sauce
Perfringes	Clostridium perfringens	Enterotoxin	From human feces to food via hand, flies	Meat dishes, reshuffled dishes, reheated dishes, pie salads

Staphylococcus food poisoning

The causative agent Staphylococcus aureus is gram positive coccus that occurs in singles, pairs, chains, tetrads and irregular shaped clusters. It is present in all places in the environment. Only those strains that produce enterotoxin can cause food poisoning. Food is usually contaminated from infected food handler with an active lesion or carriage can contaminate food.

Pathogenesis: When the food is stored at room temperature for a considerable time period the organism may multiply in the food and produce toxins. S.aureus produces six serologically different types of enterotoxins (A, B, C, C2, D and E). Most food poisoning is caused by enterotoxin A. Isolates commonly belong to phage type III. These enterotoxins are known to be heat stable. The type B is the most heat resistant. Enterotoxins that are inactivated in low temperatures can undergo reactivation in some food. Ingestion of as little as 23 µg of enterotoxin can induce vomiting and diarrhoea. Staphylococcal enterotoxins act as super antigens, binding to MHC II molecules and stimulating T cells to divide and produce lymphokines such as IL-2 and TNF-alpha, which induces diarrhea. The toxin acts on the receptors in the gut and sensory stimulus is carried to the vomiting center in the brain.

Incubation period: Usually 1-6 hours as it’s a preformed toxin.

Clinical features: The onset is sudden and is characterized by vomiting and diarrhea but no fever. The illness lasts less than 12 hours. There are no complications and treatment is usually not necessary.

Botulism

The causative agent is a gram positive anaerobic spore bearing bacillus that is widely distributed in soil, sediments of lakes and ponds, and decaying vegetation.

Pathogenesis: There are seven toxigenic types of the organism exist, each producing an immunologically distinct form of botulinum toxin. These neurotoxins are designated A, B, C1, D, E, F, and G. The spores may germinate and produce botulinum toxin when contaminated food has been inadequately sterilized or canned improperly. The toxin is released only after the death and lysis of cells. The toxin resists digestion and is absorbed by the upper part of the GI tract and then into the blood. It then reaches the peripheral neuromuscular synapses where the toxin binds to the presynaptic stimulatory terminals and blocks the release of the neurotransmitter acetylcholine. This results in flaccid paralysis. Even 1-2 µg of toxin can be lethal to humans.

Clinical features: Vomiting, thirst, dryness of mouth, constipation, blurred-vision, difficulty in speaking, breathing and swallowing. Coma or delirium may occur in some cases. Death may occur due to respiratory paralysis within 7 days.

Bacillus cereus food poisoning

The causative agent Bacillus cereus is a gram positive aerobic spore bearing bacillus. It is found abundantly in environment and vegetation.

Pathogenesis: Sporulation is associated with toxin production. This bacterium causes two types of food-borne intoxications; the ‘emetic-type’ or the short incubation type and ‘diarrheal form’ or the long-incubation type. The short-incubation form is caused by a preformed heat-stable enterotoxin. This is most often associated with fried rice that has been cooked and then held at warm temperatures for several hours. The toxin is heat-stable, and can easily withstand the brief high temperatures used to cook fried rice. The longincubation form of illness is mediated by a heat-labile enterotoxin which activates intestinal adenylate cyclase and causes intestinal fluid secretion. This is frequently associated with meat or vegetable-containing foods after cooking.

Clinical features: The short incubation form has an incubation period of 1 to 6 hours. It is characterized by nausea, vomiting and abdominal cramps and resembles S. aureus food poisoning in its symptoms and incubation period. The second type is manifested primarily by abdominal cramps and diarrhea with an incubation period of 8 to 16 hours. Diarrhea may be a small volume or profuse and watery and it resembles food poisoning caused by Clostridium perfringens. In either type, the illness usually lasts less than 24 hours after onset.

Perfringes

The causative agent Clostridium perfringens is a gram positive anaerobic spore bearing bacilli that is present abundantly in the environment, vegetation, sewage and animal feces.

Pathogenesis: The bacterium is known to produce at least 12 different toxins. Food poisoning is mainly caused by Type A strains, which produces alpha and theta toxins. Spores in food may survive cooking and then germinate when they are improperly stored. When these vegetative cells form endospores in the intestine, they release enterotoxins. The toxins result in excessive fluid accumulation in the intestinal lumen.

Incubation period: 8-24 hours

Clinical features: Illness is characterized by acute abdominal pain, diarrhea, and vomiting. Illness is self-limiting and patient recovers in 18-24 hours.

Mushroom poisoning

Ingestion of potentially poisonous mushrooms leads to the harmful health effect of mushroom poisoning which is also known as Mycetism. Previous experience and observation make it possible to discriminate between poisonous and non-poisonous mushrooms. Depending on the type of mushroom, the adverse effects range from mild gastrointestinal (GI) symptoms to major cytotoxic effects resulting in organ failure and death. Toxicity may also vary depending on the amount and age of the mushroom, the season, the geographic location and the way in which the mushroom was prepared prior to ingestion. Consumption of poisonous mushrooms can cause various types of reactions, such as allergic gastroenteritis, psychological relaxation and fatal liver intoxication. Mushroom poisoning occurs among four main groups of individuals: young children who ingest mushrooms inadvertently, wild-mushroom foragers, individuals attempting suicide or homicide and individuals looking for a hallucinatory high. Mushroom poisoning cannot be made nontoxic by cooking, freezing or any other way other than avoiding the consumption of the poisonous species.

i.                    Protoplasmic poisoning

Poisoning by the poisonous mushrooms can severely affect the protoplasm of cell resulting disturbances in the essential life functions of a cell. Chemical toxins such as Amatoxins, Hydrazines and Orelanine in mushrooms cause the protoplasmic poisoning.

• Amatoxins

Amatoxins (cyclic octapeptides) represent 1 of the 3 major groups of cyclopeptides (in addition to phallotoxins and virotoxins); they are heat-stable, insoluble in water, and not destroyed by drying. The most significant of these are the alpha and beta subtypes of amanitin. Currently 10 types of amatoxins are recognized.

α-Amanitin                        Amanullin                               

Amanullinic acid               Proamanullin

Amaninamide                   Amanin

β-Amanitin                        γ-Amanitin                  ε-Amanitin     

Mushrooms that contain amatoxins;

-       Death cap: Amanita phalloides

Native to Europe. The smell has been described as initially faint and honey-sweet, but strengthening with time. Introduced to Africa, North America and Australia by importation of hardwoods and conifers especially Oak which the mushroom is associated with.

-        Destroying angel: Amanita bisporigera, A. ocreata, A. virosa

Amanita bisporigera and A. ocreata can be found in North America while A. virosa is native to Europe. Can be mistaken to button and horse mushrooms.

-        Fool’s mushroom: Amanita verna

Found in Europe.

-        Autumn skullcap: Galerina autumnalis

Found throughout the world but especially in America. Commonly grows on wood, and when on the ground when it has preference to mossy habbitats.

• Hydrazines

False morel mushrooms contains a carcinogenic hydrazine, gyromitrin. It is unstable and is easily hydrolyzed to the toxic compound monomethylhydrazine. Consuming a large amount of gyromitrin can in worst case cause liver damage leading to death. Most of this toxin is removed when the mushroom is double boiled and rinsed, rendering it relatively safe for consumption. Main species of false morel is Gyromitra esculenta which is widely distributed in Europe in North America.

• Orellalnine

A mycotoxin which is a pyridine N-oxide. An intense, burning thirst (polydipsia) and excessive urination (polyuria) are the first symptoms. This may be followed by nausea, headache, muscular pains, chills, spasms, and loss of consciousness. In severe cases, severe renal tubular necrosis and kidney failure may result in death (15%) several weeks after the poisoning. Caused by the Sorrel Webcap mushroom (Cortinarius orellanus) and some of its relatives.

ii.                  Neurotoxins

Poisonings by mushrooms that cause neurological problems are divided into three groups, based on the type of symptoms produced, and named for the substances responsible for these symptoms.

• Muscarine Poisoning

This is due to the substance Muscarine which is particularly found in Inocybe and Clitocybe mushroom species. It is a highly toxic alkaloid related to the cholines and nonselective agonist of the muscarinic acetylcholine receptor. Within 15 to 30 minutes after ingestion of the mushroom increased salivation, perspiration, and lacrimation occur. Abdominal pain, severe nausea, diarrhea, blurred vision and breathing difficulties occur with large doses.

• Ibotenic acid/Muscimol Poisoning

Ibotenic acid is a powerful neurotoxic isoxazole substance and Muscimol is a psychoactive alkaloid. Both substances cause the same effects, but muscimol is approximately 5 times more effective than ibotenic acid. Naturally occurring in Fly Agaric (Amanita muscaria) and Panthercap (Amanita pantherina) mushrooms Drowsiness and dizziness are the main symptoms of this type of poisoning.

• Psilocybin Poisoning

Psilocybin is a tryptamine compound with a chemical structure containing an indole ring linked to an ethylamine substituent. It is structurally similar to the neurotransmitter serotonin. This is a naturally occurring toxin in mushrooms known as Psilocybin mushrooms. When consumed this cause a syndrome similar to alcohol intoxication.

iii.                Gastro-Intestinal irritants

The gastrointestinal irritants are the least defined and most widespread of the mushroom toxins.  Symptoms are mild, short-lived stomach discomfort to vomiting and diarrhea. The specific responsible toxins are generally unknown, but can be due to mushrooms of unusual sugars, amino acids, peptides, resins, and other compounds. Ex: Green Gill (Chlorophyllum molybdites), Tigertop (Tricholoma pardinum), Jack O'Lantern (Omphalotus illudens), Naked Brimcap (Paxillus involutus), Sickener (Russula emetica)

iv.                Disulfiram-like poisoning

The disulfiram-like compound coprine, an amino acid produced by mushrooms of the genus Coprinus, notably C. atramenarius, the Alcohol Inky causes this type of poisoning. Coprine is converted to cyclopropanone hydrate in the human body. This compound interferes with the breakdown of alcohol. The symptoms are generally mild, consisting of flushing of the head and neck, tingling of the extremities, heart palpitations, headache and nausea.  It is regarded as edible, with caution as  it has no adverse side effects if alcohol is not consumed for about three days.

v.                  Miscellaneous poisoning

Young fruiting bodies of the sulfur shelf fungus Laetiporus sulphureus are regarded as edible but ingestion of it has caused digestive problems and allergies in some people. It is recommended not to it in raw form. 

Aflatoxins

Aflatoxin belongs to a group of fungal toxins known as mycotoxins, and is widespread in agricultural products and food.

Toxin producing agent:  Produced primarily by the fungi Aspergillus;

·         Aspegillus flavus

·         parasiticus

·         nomius and A. niger

Associated food: Corn, figs, nuts, cereals, milk and milk products, peanuts, cottonseed, spices.

Characteristics and chemical mechanism of the toxin:

·        
Classified into a number of subtypes. The most important ones are B1, B2, G1 and G2, distinguished by their fluorescent colour under ultraviolet light. In addition, aflatoxin M1 and M2 are hydroxylated metabolites of aflatoxin B1 and B2.

·         Odourless, tasteless and colourless.

·         Chemically stable in foods and resistant to degradation under normal cooking procedures.

·         Accumulation is dependent upon weather conditions. Before harvest, the risk for the development of aflatoxin is greatest during major droughts as the number of Aspergillus spores in the air increases. These spores infect crops through areas of damage caused by insects, and inclement weather. Once infected, plant stress occurs; the production of aflatoxin is favoured. During post-harvest stage, production of aflatoxin can be worsened under storage conditions such as hot and humid storage atmosphere.

Natural occurrence:

·         Aspergillus sp infect agricultural supplies either before harvest or at post-harvest stages under favourable conditions of temperature and humidity.

·         The aflatoxigenic moulds are mainly found in soils and decaying vegetation.

·         Occur in warmer parts of the world such as tropical/sub-tropical regions where temperature and moisture are high.

·         Milk, eggs, and meat products can be contaminated because of the animal consumption of aflatoxin-contaminated feed.

Impact:

·         Associated with both acute and chronic toxicity in animals and humans.

·         Include acute liver damage, liver cirrhosis, and liver cancers. Symptoms may include fever, vomiting and jaundice.

·         Chronic toxicity associated with consumption of low dose aflatoxin mainly in peanuts and grains.

·         Epidemiologically implicated as a carcinogen in humans and an environmental contaminant which is widespread in nature.

·         Recent medical research indicates that a regular diet including apiaceous vegetables such as carrots, parsnips and parsley, may reduce the carcinogenic effects of aflatoxin.

·         Aflatoxin B1 can permeate through the skin. Dermal exposure to these aflatoxin in particular environmental conditions can lead to serious health risks.

·         As aflatoxin B1 can cause immune suppression, exposure is associated with an increased viral load in HIV positive individuals.