Mycotoxins

Mycotoxins are natural chemicals produced by certain fungi(molds) which occur as contaminants of some food crops, either in the field or during post-harvest storage. Cereals, nuts, fruits and foods derived from these crops are the most likely to contain mycotoxins. mycotoxins are toxic to humans and animals Three types of fungi are the major producers of mycotoxins – Fusarium, Pencillium, Aspergillus. Within each type of fungus, particular species may be mycotoxigenicor mycotoxin-producing

While hundreds of mycotoxins have been identified from a very large number of fungi, only 20-30 mycotoxins have been associated with potential toxicity to animals and humans Aspergillus penicillium fusarium

Types of mycotoxins There are over 300 mycotoxins but the commonly occurring ones in food and feed. about 20 mycotoxins occur in food at levels and frequency to be of food safety concern. Common Members of the Mycotoxin Family Aflatoxins, Fumonisin, Ochratoxins, Patulin, Zearalenone, Fumonisins Trichothecenes(Type A: DAS, T-2), Patulin, Moniliform, Sterigmatocystin Cyclopiazonic acid, Kojic acid, Maltoryzine, ß-nitropropionic acid Aspergillic acid, Penicillic acid, Roquefortine C

Common Members of the Mycotoxin Family

mycotoxin occurrence in foods Mycotoxin is produced by a fungus under special conditions of moisture and temperature in : 1- Mould damaged foodstuffs including agricultural products like cereals, oilseeds, fruits and consumer foods such as peanut butter 2-Residues in animal tissues and products e.g. milk, meat, dairy produce 3-Mould ripened foods e.g. cheeses, meats 4-Fermentation products e.g. microbial proteins and enzymes. Juices e.g. apple juice

Mycotoxin Chain of Events

Aflatoxins Toxins produced by the fungi Aspergillus flavus and Aspergillus parasiticus Four primary aflatoxins, named B1, B2, G1 and G2 plus two additional metabolic products, M1 and M2. Aflatoxins occur in nuts, cereals and rice under conditions of high humidity and temperature and present a risk to human and animal health  

Aflatoxins: Human, Animal, and Environmental Interactions Fungal growth / aflatoxin production Contamination of human & animal food Animal consumption Human consumption Environment: extreme drought, moisture, heat, compromised plants Breast milk In utero

Mechanism of toxicologic damage Because of aflatoxins’ common occurrence in feedstuffs, feeds and milk products. Although the oral route is the main contamination means, inhalation may also occur as a result of people or animals being exposed to the grains’ dust. After respiratory exposure, AfB1 may appear in the blood more quickly than after oral exposure. Nevertheless,. Following ingestion, aflatoxin B1 is efficiently absorbed in the intestinal tract, of which the duodenum appears to be the major site of absorption. Due to the particle’s low molecular weight, the main mechanism of absorption of mycotoxin, as suggested by several authors, is passive diffusion, in which no efflux pumps or transporters are involved.,The main metabolizing organ for aflatoxin is the live aflatoxins exert their toxic effects.

Mechanism of toxicologic damage At first stage, aflatoxin is oxidized into several hydroxylated metabolitesreduction to aflatoxicol and hydroxylation to epoxide (acutely toxic, mutagenic, and carcinogenic)   Aflatoxin binds to guanine in deoxyribonucleic acid (DNA), inhibiting the segnal for the formation of messenger ribonuceic acid (RNA), interruption of protein synthesis leads to deficies of structural protein, enzymes,lipid acceptor protein, the long term effects of impaired protein synthesis include hepatic steatosis and avariety of metabolic and fanction derangments

Effect of aflatoxin on health * Teratogenic * Immunosuppressive Many times enhanced in the presence of hepatitis B and C viruses. * Carcinogenic

Aflatoxin Symptoms 1- Onset of high fever 2- Progressive jaundice 3- Liver damage 4- Liver cancer 5- Abdominal Pain 6- Vomiting 7- Convulsions 8- Edema and Pulmonary Edema 9- Hemorrhaging 10- Disruption of food digestion, absorption or metabolism

T-2 mycotoxin T-2 mycotoxins belong to the ‘trichothecene' group, and are mainly produced by Fusarium type moulds. These moulds develop on cereals in the fields, especially when the weather is wet and relatively cold during flowering. Although it can occur naturally from moldy, improperly stored gains. It cause 1- Hematopoietic effects, 2- Immunosuppression, 3- Gastro-intestinal effects, 4- Neurotoxic effects (restlessness; lack of reflexes; nervous syndrome), 5- Dermotoxicity(necrosis),

Absorption and Mechanism of action In general, absorption of T2 occurs very rapidly within the digestive tract and is widely distributed in many tissues and organs. Currently, there is no evidence for accumulation in tissues or transmission to milk or eggs. T2 toxin are inhibition of protein synthesis, thought to be the most important effect, inhibition of DNA synthesis, impairment of ribosome function, T2 bind to active polysomes and ribosomes inhibition of mitochondrial protein synthesis, immunosuppression, allowing secondary and opportunistic bacterial infections and possibly delayed hypersensitivity

Breathing T2 mycotoxin in an aerosol form * Ingestion possible methods of exposure * Inhalation Breathing T2 mycotoxin in an aerosol form * Ingestion Eating or drinking food or water contaminated with T2 mycotoxin * Contact Absorption through the skin possible symptoms Inhalation:  Nose/throat pain  Nasal discharge  Itching  Sneezing  Coughing up blood  Chest pain Ingestion:  Stomach pain  Diarrhea  Vomiting  Flu-like symptoms

Contact:  Skin pain  Itching  Redness  Blisters

Ochratoxin Ochratoxins are metabolites of Aspergillus ochraceus and Penicillium verrucosum in temperate regions and are present in a large variety of feeds and foods. There are four ochratoxins (A, B, C, and D) and the major mycotoxin among this group is ochratoxin A (OTA). This toxin is a contaminant of cereals, beans and other plant products. The most significant effect of ochratoxins in farm animals is nephrotoxicity. It is also immunosuppressive, teratogenic and carcinogenic. Ochratoxin is found in a large variety of foods including wheat, corn, soybeans, oats, barley, coffee beans, meats and cheese. Barley is thought to be the predominant source

Absorption and Mechanism of action ochratoxin is absorbed from the gastrointestinal tract depending on the different species. The small intestine has been shown to be the major site of absorption and maximal absorption occurrs in the jejunum. Ochratoxins bind rapidly to serum albumin and are distributed in the blood mainly in bound form, Generally, the toxin has a long biological half life due to its high rate of binding to serum protein but there are differences between species It primarily accumulates in the kidneys followed by the liver, muscle and fat. Due to this accumulation there has been a concern over the potential carryover into meat.

Effects and signes of ochratoxin in the body 1- Hematopoietic effects (hematological disorders, blood in urine and faeces) 2- Increased water consumption; kidney and bladder dysfunction 3- Immunosuppression 4- Gastro-intestinal effects (diarrhea : vomiting, dehydration & depression  

Viral hepatitis B

Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) which affects the liver It was originally known as "serum hepatitis Many people have no symptoms during the initial infection Some develop a rapid onset of sickness with vomiting ,yellow skin, dark urine and abdominal pain. Often these symptoms last a few weeks] and rarely result in death. It may take 30 to 180 days for symptoms to begin .Less than 10% of those infected develop chronic hepatitis B. In those with chronic disease cirrhosis and liver cancer may eventually develop. The virus is transmitted by exposure to infectious blood or body fluids. Infection around the time of birth is the most frequent way hepatitis B is acquired in areas of the world where the disease are the most frequent routes of infection  Other risk factors include working in a healthcare setting, blood transfusions , dialysis, sharing razors or toothbrushes with an infected person, travel in countries where the infection rate is high, and living in an institution Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterility. The hepatitis B viruses cannot be spread by holding hands, sharing eating utensils or drinking glasses, kissing, hugging, coughing, sneezing, or breastfeeding. It is 50 to 100 times more infectious than HIV

Sings and symptoms Signs and symptoms of hepatitis B, ranging from mild to severe, usually appear about one to four months after you've been infected. Signs and symptoms of hepatitis B may include: 1- Abdominal pain 2- Dark urine 3- Fever 4- Joint pain 5- Loss of appetite 6- Nausea and vomiting 7- Weakness and fatigue 8- Yellowing of your skin and the whites of your eyes (jaundice)

mechanism Hepatitis B virus primarily interferes with the functions of the liver by replicating in liver cells, known as  hepatocytes .   The virions bind to the host cell via the preS domain of the viral surface antigen and are subsequently internalized by endocytosis. HBV-preS-specific receptors are expressed primarily on hepatocytes; however, viral DNA and proteins have also been detected in extrahepatic sites, suggesting that cellular receptors for HBV may also exist on extrahepatic cells During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. Although the innate immune response does not play a significant role in these processes, the adaptive immune response, in particular virus-specific cytotoxic T lymphocytes(CTLs), contributes to most of the liver injury associated with HBV infection. CTLs eliminate HBV infection by killing infected cells and producing antiviral cytokines, which are then used to purge HBV from viable hepatocytes.] Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection may facilitate the accumulation of CTLs in the liver.

transmission 1- sexual contact 2- Blood transfusions 3-re-use of contaminated needles and syringes 4- vertical transmition

prevention A- Prevention of transmission of the virus: 1-Practise safe sex 2- Clear up blood or body fluids, using warm water and detergent 3-Ensure surgical instruments are disposable or adequately sterilised 4-Handle 'sharps' safely 5-Do not permit healthcare workers (who are positive for hepatitis B e antigen (HBeAg)) to work in areas where they could be a risk to others. 6-Wear goggles if there is risk of infected material splashing into the eye. B- Immunisation

Noro virus))Norwalk virus Introduction Noro virus is an RNA virus(taxonomic family calciviridae)that causes approximately %90 of epidemic non-bacterial outbreaks of gastroenteritis around the world. The virus: Formerly called (norwalk like virus) Highly contagious stable in the enviroment Resistant to routine disinfection methods Carriers may not be symptomatic

Route of transmission Fecally contaminated food and water. Person-to-person contact. Contaminated surfaces. Aerosols of the virus.

Symptoms Symptoms usually start within 24-48 hours after exposure. Vomiting Watery diarrhea Abdominal cramps Headache,muscle aches Fever(minority) Dehydration Up to %30 may be asymptomatic

Diagnosis specific diagnosis of the virus is routinely Polymerase chain reaction (PCR) assays or real-time PCR assays which give results in few hours.these assays are very sensitive and can detect concentrations as low as 10 particles

prevention The best way to prevent the spread of Norwalk viruses is by thorough handwashing after toilet use and before preparing or serving foods for at least 15 seconds. In addition, have plenty of rest and stay home until your Norwalk virus symptoms are gone. Other preventive measures are: 1. People who already have a Norwalk virus infection should never prepare food for others. 2. Those who are sick with diarrhea or vomiting should not work in daycare centers or health care facilities until these symptoms have stopped. .

3. Dispose or clean and disinfect infected materials or contaminated surfaces immediately after an incident of Norwalk virus infection in your home. 4. Eat only thoroughly cooked shellfish. Avoid food or water that might be prepared in an unsanitary way such as party foods and raw or uncooked foods. 5. Immediately wash clothing that may be contaminated with Norwalk virus after an illness incident. 6. Avoid handshaking when it's not necessary.

References 1- N. Magan and M.Olsen. (2004). Mycotoxins in food Detection and control (1st ed ). New York. 2- Lucic, A., Pavlovic, M., Peraica, M., & Radic, B. (1999). Toxic effects of mycotoxins in humans, 77(7). 3- Series, F. (2009). Mycotoxins in Food, (1), 1–13 4- Lucic, A., Pavlovic, M., Peraica, M., & Radic, B. (1999). Toxic effects of mycotoxins in humans, 77(7). 5- Dienstag, J. L. (2008). Hepatitis B Virus Infection. The new England Journal of Medicine.