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WEL-COME

WEL-COME. DHANAJI NANA MAHAVIDYALAYA,FAIZPUR DEPARTMENT OF MICROBIOLOGY Mycotoxins Assi.Prof.Rupali B . Sali. 2. Characteristics of mycotoxin induced disease not transmitted among animals b. Pharmaceutical treatment does not alter the course of disease

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WEL-COME

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  1. WEL-COME

  2. DHANAJI NANA MAHAVIDYALAYA,FAIZPURDEPARTMENT OF MICROBIOLOGYMycotoxinsAssi.Prof.Rupali B . Sali

  3. 2. Characteristics of mycotoxin induced disease • not transmitted among animals b. Pharmaceutical treatment does not alter the course of disease c. Mycotoxicosis most often presents as a uncertain, sub-acute or chronic condition

  4. 3.Treatment of mycotoxin-induced disease a. For most mycotoxins, there is no specific treatment or antidote b. Supplement with vitamins & selenium may be helpful, and provision of adequate high-quality protein

  5. 4.Prevention of mycotoxin-induced disease a. Avoiding b. Diluting c. Cleaning d. Testing e. Drying f. Adding (organic acids will prevent mold growth)

  6. A- Aflatoxin • 1. Sources : Aspergillus flavus & A.paraciticus : Corn, peanuts • 2. Factor favoring production of aflatoxins a. Temperature : 25-30 ๐c b. Grain moisture

  7. 3. Chemical characteristics • Exhibit intense blue or green fluorescence under UV. • : aflatoxins B1, B2, G1 and G2 also : aflatoxin M1 is a metabolites of AFB1 found in animal urine, milk or tissues.

  8. 5.Mechanism of toxicologic damage Also called steatosis, fatty liver can be a temporary or long-term condition, which is not harmful itself, but may indicate some other type of problem. Left untreated, it can contribute to other illnesses. It is usually reversible once the cause of the problem is diagnosed and corrected. The liver is the organ responsible for changing fats eaten in the diet to types of fat that can be stored and used by the body. Triglycerides are one of the forms of fat stored by the body and used for energy and new cell formation. The break down of fats in the liver can be disrupted by alcoholism, malnutrition, pregnancy, or poisoning. In fatty liver, large droplets of fat, containing mostly triglycerides, collect within cells of the liver. The condition is generally not painful and may go unnoticed for a long period of time. In severe cases, the liver can increase to over three times its normal size and may be painful and tender

  9. a. Loss of enzyme • b. Lack of formation of lipid acceptor protein in liver • c. Decreased cellulose digestion, volatile fatty acid formation & proteolysis (breakdown of proteins ) • d. Necrosis

  10. 6.Toxicity • a. Young animals are more susceptible than adult. • b. Nutrition deficiency increase susceptibility

  11. 7. Diagnosis • Clinical sign : decreased growth rate, reduced feed efficiency,,, mild anemia, and increased susceptibility to infectious disease.

  12. 8.Treatment & Prevention • a. Detoxification : Hydrated sodium calcium aluminosilicate (HSCAS) can absorb aflatoxins • b. Supportive : Vitamin .E & selenium • c. Prevention - Mold inhibitor - Treatment of grain with anhydrous ammonia for 10-14 days.

  13. B- Zearalenone • 1. Sources : Fusarium roseum ( F.graminearum ): corn, wheat, barley, oats • 2. Factor favoring production a. High moisture 22% - 25% b. Alternating high and low temp. (7-21 ๐c)

  14. 3. Mechanism of toxicological damage a. initiating specific RNA synthesis b. Function as a weak estrogen. 4.Toxicity a. Swine are most susceptible b. low for all effects except reproductive function.

  15. C-Ergot 1.Source : Claviceps purpurea : barley, wheat & oats 2. Factor favoring : Warm & humid

  16. 3.Mechanism of toxic • a. potent initiators of contraction in smooth muscle • b. mimic the action of dopamine. 4.Clinical sign a. necrosis of the feet, ears and tail b. increased temperature., pulse & respiration rate c. lactation does not occur d. hyper-excitability & tremors e. heat intolerance in cattle

  17. E.Treatment a. animals should be provided with a warm, clean, stress-free environment b. Control secondary bacterial infection c. milk supplement

  18. D- Ochratoxin & Citrinin • 1.Sources : Aspergillus orchraceus & • Penicillium viridicatum • 2. Mechanism of toxic : target the renal proximal tubule • - Disrupt protein synthesis • -Bind strongly to protein (albumin) • -Interfere with synthesis of tRNA & mRNA • -Disrupt carbohydrate metabolism • -Increase the generation of free radical

  19. 4.Clinical sign • a. Acute : vomiting, diarrhea, dehydration & depression • b. Subacute to chronic : weight loss, feed efficiency, & dehydration. Immunosupression, teratogenicity, carcinogenesis & hemorrhage

  20. Mycotoxin Mycotoxin is a convenient generic term describing the toxic secondary metabolites produced by fungi. “Myco” means fungal (mold) and “toxin” represents poison. They encompass a considerable variety of low molecularweight compounds with diverse chemical structures and biological activities. Some mycotoxins could also be toxic to plants or other microorganisms; but these compounds are not classified as antibiotics of fungal origin. Like most microbial secondary metabolites, the benefit of mycotoxins for the fungi themselves is still not clearly defined.

  21. In considering the effects of mycotoxins on animals, it is important to distinguish between “mycotoxicosis” and “mycosis.”: • Mycotoxicosis is used to describe the action of mycotoxin(s) and is frequently mediated through a number of organs, notably the liver, kidney, lungs, and the nervous, endocrine, and immune systems. • Mycosis” refers to a generalized invasion of living tissue(s) by growing fungi.

  22. Due to their diverse chemical structures, mycotoxins may exhibit a number of biological effects, including both acute and chronic toxic effects as well as carcinogenic, mutagenic, genotoxic, and immunotoxic effects. • The interaction of mycotoxins with cellular macromolecules plays a dominant role in their toxic actions. Recent studies on the effect of mycotoxins on apoptosis have further revealed their mode of action at the cellular level.

  23. Historical • Modern mycotoxicology was not developed until the discovery of aflatoxins in the early 1960s as the causative agent in the • peanut meal causing the “Turkey X” disease that killed more than 10,000 turkeys fed with the contaminated meal. • Because aflatoxins are a series of highly potent carcinogens produced by commonly occurring Aspergillus flavus and A. parasiticus, research has focused new attention on mycotoxins. • In the last 40 years, many new mycotoxins have been identified and characterized, and their biosynthetic origin in various fungi elucidated. It has been estimated that at least 25% of the world’s agricultural product is contaminated with mycotoxins and certain diseases have been linked to ingestion of food and feed contaminated with mycotoxins.

  24. Economic Impact of Mycotoxin Contamination • The most obvious negative economic impact of mycotoxins is an outright loss of crops and affected animals. • Also, humans may encounter severe health hazard or high mortality rates in countries with less regulation or monitoring programs. • Thus, the negative economic impact resulting from mycotoxin contamination is certainly very significant and estimated to be $932 million annually.

  25. PRODUCTION OF MYCOTOXINS BY TOXICOGENIC FUNGI Invasion by fungi and production of mycotoxins in commodities can occur under favorable conditions in the field, at harvest, and during processing, transportation and storage Fungi that are frequently found in the field include: A. flavus, Alternaria longipes, A. alternata, Claviceps purpura, Fusarium verticillioides (previously called moniliforme), F. graminearum, and a number of other Fusarium spp. Species most likely introduced at harvest include: F. sporotrichioides, Stachybotrys atra, Cladosporium sp., Myrothecium verrucaria, Trichothecium roseum, as well as A. alternata. Most penicillia are storage fungi. These include:Penicillium citrinum, P. cyclopium, P. citreoviride, P. islandicum, P. rubrum, P. viridicatum, P. urticae, P. verruculosum, P. palitans, P. puberulum, P. expansum, and P. roqueforti. All of which are capable of producing mycotoxins in grains and foods.

  26. Other toxicogenic storage fungi are: Aspergillus. parasiticus, A. flavus, A. versicolor, A. ochraceus, A. clavatus, A. fumigatus, A. rubrum, A. chevallieri, Fusarium verticillioides, F. tricinctum, F. nivale, and several other Fusarium spp. • It is apparent, most of the mycotoxin producing fungi belong to three genera: Aspergillus, Fusarium, and Penicillium. However, not all species in these genera are toxicogenic

  27. Factors Affecting Mycotoxin Production • Genetics and environmental and nutritional factors greatly affect the formation of mycotoxins. • Depending on the susceptibility of the crop, geographic and seasonal factors, as well as cultivation, harvesting, storage, and transportation practices, mycotoxins are found worldwide. • In the field, weather conditions, plant stress, invertebrate vectors, species and spore load of infective fungi, variations within plant and fungal species, and microbial competition all significantly affect mycotoxin production.

  28. Factors Affecting……. • Physical factors such as time of exposure, temperature during exposure, humidity, and extent of insect or other damage to the commodity prior to exposure determine mycotoxin contamination in the field or during storage. • Chemical factors including the nutritional status of the crops or chemicals (such as fungicides) used in crop management could affect fungal populations, and consequently toxin production

  29. In general, mycotoxins are optimally produced at 24–28C, but some toxins such as T-2 toxin is maximally produced at 15C. • Contamination during crop storage may be affected by changes in temperature and water activity, that allow ecological succession of different fungi as water activity and temperature of stored grain changes. Water activity = It is defined as the vapor pressure of water above a sample divided by that of pure water at the same temperature;

  30. During storage and transportation, water activity (aw), temperature, crop damage, and a number of physical and chemical factors, such as aeration (O2, CO2 levels), types of grains, pH, and presence or absence of specificnutrients and inhibitors are important.

  31. B A R3 R1 R1 R4 R2 C D R1 R1 Aflatoxins Chemical structure of flatoxins • The B-type aflatoxins are characterized by a cyclopentane E-ring. These compounds have a blue fluorescence under long-wavelength ultraviolet light. • (B) The G-type aflatoxins, with a green fluorescence, have a xanthone ring in place of the cyclopentane. • (C) Aflatoxins of the B2 and G2 type have a saturated bis-furanyl ring. Only the bis-furan is shown. • (D) Aflatoxin of the B1a and G1a type have a hydrated bis-furanyl structure.

  32. At least 16 structurally related toxins in this group are produced by Asparagillus flavus and A. parasiticusand infrequently by A. pseudotamariiandA. nominus • A. ochraceoroseus has also been found to produce aflatoxins • The optimal temperatures and water activity (aw) for the growth of A. flavus and A. parasiticus are around 35–37C (range from 6–54C) and 0.95 (range from 0.78–1.0), respectively; whereas for aflatoxin production, they are 28–33C and 0.90–0.95 (range from 0.83–0.97), respectively.

  33. Aflatoxin B1 is most toxic in this group and is one of the most potent naturally occurring carcinogens). • Other significant members of the aflatoxin family, such as M1 and M2, are metabolites of AFB1 and AFB2, respectively, and originally isolated from bovine milk.

  34. Toxic Effects • Aflatoxins are mutagenic, teratogenic, and hepatocarcinogenic. • Aflatoxin B1 is one of the most potent naturally occurring carcinogen, extensive research was primarily done on this toxin. The main target organ of AF is the liver. • AFB1 also affects other organs and tissues including the lungs and the entire respiratory system. • For the carcinogenic effects, rats, rainbowtrout, monkeys, and ducks are most susceptible and mice are relatively resistant. • Consumption of AFB1-contaminated feed by dairy cows results in the excretion of AFM1 in milk. AFM1, a hydroxylated metabolite of AFB1, is about 10 times less toxic than AFB1; but its presence in milk is of concern for human health.

  35. Impact on Human Health • Whereas AFB1 has been found to be a potent carcinogen in many animal species, the role of AF in carcinogenesis in humans is complicated by hepatitis B virus (HBV) infections in humans). • Epidemiological studies have shown a strong positive correlation between AF levels in the diet and primary hepatocellular carcinoma. • Since multiple factors are important in carcinogenesis and environmental contaminants such as AFs and other mycotoxins may, either in combination with HBV or independently.

  36. Although most OA producers can grow in a range from 48C to 37C and at aw as low as 0.78, optimal conditions for toxin production are narrower with temperature at 24–25C and aw values .0.97. • Ochratoxins are produced primarily in cereal grains (barley, oats, corn, wheat) and mixed feed during storage in temperate climatic conditions, with levels higher than 1 ppm being reported. • OA has been found in other commodities, including beans, coffee, nuts, olives, raisin, cheese, fish, pork, milk powder, fruit juices wine beer, peppers. • OA can be carried through the food chain because of the presence of OA residues in animal products as result of its binding with serum albumin. Natural occurrence of OA in kidneys, blood serum, blood sausage.

  37. THANK YOU….

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