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vendredi 2 décembre 2011

MYCOTOXINS AND MYCOTOXICOSES REVIEW

Mycotoxins and Mycotoxicoses Review

Mycotoxins, mycotoxicosis, review, aflatoxins, ochratoxins, trichothecene, T2 toxin, patulin,citrinin, Aspergillus, Fusarium, Penicillum, molds, foodstuff, livestock and poultry, carcinogenicity, toxicity

Mycotoxin contamination in foods is a common and is caused by molds of the type Aspergillus, Fusarium and Penicillum. Ingestion of mycotoxin foods leeds to losses in the poultry and livestock industry aswell as dairy and meat.

The mycotoxicoses are food very dangerous intoxications from the viewpoint of human health and animal.
unfortunately they remains been unaware of and especially not diagnosed

Table des matières



 LES AUTEURS


Salim Djelouat
Professor Medical Analyses and Medical bacteriology / Scientific Author / knolAuteur
Krishan Maggon
Krishan Maggon
Consultant Pharmaceutical Biotechnology R&D & Advisor, Geneva, Switzerland & New York, USA
 
 
 
 
Fluorescent Mycotoxin Detection under UV light





One calls mycotoxicoses the food toxic-infections generated by the moulds.


1 - Mycotoxins

    Mycotoxins are toxic metabolites produced by certain fungi mainly Aspergillus, Fusarium and Penicillium in/on foods and feeds . 
Aflatoxin B1     http://en.wikipedia.org/wiki/Aflatoxin
    Mycotoxins have been associated with various diseases , such as mycotoxicosis (aflatoxicosis) , in livestock , domestic animals and humans throughout the world .

    The occurence of mycotoxins is influenced by environmental factors like global warming, moisture, rains etc ; hence the extent of contamination changes  geographic location , agricultural and agronomic practices, and the susceptibility of commodities to fungal invasion during preharvest , storage, and/or processing periods . Many countries have limited exposure to mycotoxins by imposing regulatory limits on commodities intended for use as food and feed . Aspergillus flavus  pathport.vbi.vt.edu/pathinfo/pathogens/A-f.html


2 - Aflatoxins


    Aflatoxins (Aflatoxin B1 is the most potent hepatocarcinogen) are probably the best known and most intensively researched mycotoxins in the world.
    Humans are exposed to aflatoxins by consuming foods contaminated with products of fungal growth .
    Such exposure is difficult to avoid because fungal growth in foods is not easy to prevent .
    Even though heavily contaminated food supplies are not permitted in the market place in developed countries, concern still remains for the possible adverse effects resulting from long-term exposure to low levels of aflatoxins in the food supply .
    Evidence of acute aflatoxicosis in humans has been reported from many parts of the world , namely the countries, like Taiwan, Uganda, India, etc .
    The syndrome is characterized by vomiting, abdominal pain, pulmonary edema, convulsions, coma, and death with cerebral edema and fatty involvment of the liver , kidneys , and heart.
    Conditions increasing the likelihood of acute aflatoxicosis in humans include limited availability of food, environmental conditions that favor fungal development in crops and commodities, and lack of regulatory systems for aflatoxin monitoring and control.
    Because aflatoxins, especially aflatoxin B1, are potent carcinogens in some animals, there is interest in the effects of long-term exposure to low levels of these important mycotoxins on humans .
    In 1988, the IARC, Lyon placed aflatoxin B1 on the list of human carcinogens.
    This is supported by a number of epidemiological studies done in Asia and Africa that have demonstrated a positive association between dietary aflatoxins and Liver Cell Cancer (LCC) .
    Additionally , the expression of aflatoxin-related diseases in humans may be influenced by factors such as age, sex, nutritional status, and/or concurrent exposure to other causative agents such as viral hepatitis (HBV) or parasite infestation.
Since there is a delay between exposure and the development of the clinical disease, as well as difficulty in differentiating cancer origins between accidental and intentional exposure, even recognizing that a target population had been "attacked" would be laborious; this would be a case of a "stealth BW attack".
    The Iraqis reportedly produced ~600 gallons of concentrated aflatoxin which was loaded in 7 bombs and missiles. Recent reports that aflatoxins (of which aflatoxin B1 [AFB1] is a hepatoxic material and suspected carcinogen) were produced and deployed in Scud warheads were surprising because this family of toxins had not generally been considered to be militarily useful.
Image from fsrio.nal.usda.gov/document_fsheet.php?produc...

3 - the mycotoxicoses

    The toxic effects due to the development of the moulds in certain food, animals or human are known since the 19th century. Their interest in human medicine remained secondary to see unknown until the contribution of experimental proofs of their implication in some illnesses as:
 
  • The toxic aleucie
  • The disease of mildewed rice
  • And certain animal epizooties
 
    It is for this reason which we will open a debate around this subject of which the essential goal is to make become aware of this d' type; food intoxinations.
    One counts currently more than 200 species different from moulds toxinogenes being able to multiply in food and this under favorable conditions.
     Abut twenty mycotoxins are regarded as potentially dangerous for the man and the animal, because of their production and concentration in the food products.
 
     The greatest studies concerning the moulds were carried out on the kinds:
 
  • aspergillus flavus and aspergillus parasiticus
  • Penicillium verrucosum
  • fusarium
 

4 – General physiopathology of the mycotoxicoses


    The mycotoxicoses are intoxications resulting from the ingestion of food containing of the mycotoxins.
    They are thus by consequence, nor infectious, nor contagious
    The action of the mycotoxins is polymorphic and the same mycotoxin gives effects varied according to:
  • The concentration
  • The exposure time
  • The influence of infections viral, parasitic or bacterial simultaneous
  • The food state of deficiency
  • Of stress
  • Of individual genetic susceptibility…
 
    The ingestion of a food containing of the mycotoxins can be responsible for serious effects, to see mortals so much; man that at animal.
    The principal toxic effects (given for information only), are:

  • of the carcinogen preferentially hepatic
  • of the tremors
  • of the especially intestinal hemorrhages
  • of the néphrotoxicités
  • of the hépatotoxicités
  • of the dermatitis
  • an anorexia to see lethargy
  • a cytotoxicity
  • of the convulsions
  • of oedemas mesenteric
  • systemic toxicity
  • neurotoxicity
  • an attack of the bodies hematopoietic
 
    The clinical signs calculated in this chapter, risk to carry to confusion with the same signs of other pathologies and it is for this reason can be, that the mycotoxicoses remains unknown and their non calm diagnosis.
     A lot of studies in the world are about the mycotoxicoses throughout the world.

5 – Study of the principal mycotoxins


    This study relates to the principal ones and the most met as well at the man as in the animal.
    A - Aspergillus flavus and aspergillus parasiticus produce the B1 aflatoxins, G1 and M.
    Its aflatoxins have a very large distribution practically in all substrata that these last can colonize as in milk.          
     The aflatoxins are thermostable; the B1 aflatoxin is the most toxic of the three.

    B - Penicillium verrucosum produces the ochratoxin has, which is most dangerous.
     It is recovered in the corn, the barley, milk.            
     This toxin is not recovered among the herbivorous animals, of which their bacterial flora damages it in a non toxic métabolie.                      
     In normal conditions of cooking, the ochratoxine A, is destroyed partially.
Ochratoxin A Ochratoxin A.svg
http://en.wikipedia.org/wiki/Ochratoxin_A

    C - The fusarium kind produced of very many toxins and especially the T2 toxin and trichothecene.

    D - Many of other toxins are met such as:
  • The désoxynivalénol, the nivalénol and the fumonisines B1, B 2, that   meeting has in the but, wheat and the barley.

  • The zéaralénone, the patuline, the citrinine, the neurotoxic tremorgenes, are produced especially in the animals, but can be also present in the agricultural produce such as the sound and corn.

Tricothecene Structure    http://en.wikipedia.org/wiki/Trichothecene
 


6 – Preventive of measures


    In a general way, in professional environment, the preventive measures are developed little, contrary to the provisions taken with respect to food.
    It would be therefore prudent to apply measures of efficient prevention in order to limit, to prevent or to reduce the development of mildews in the sensitive products and in particular in:
  • the cereals
  • flours and bread
  • the oleaginous seeds
  • the fruits and the juices of fruits
  • the marmalades
  • the spices
  • dehydrated soups      

    The preventive measures will have to concern; the raw materials destined for the manufacture of the products for the human and animal consumption and will start:
  • of the culture
  • of the harvest
  • of all the stages of storage
  • of transport
  • and especially of their transformation

     The objective searched for of the prevention measures concerning food for animals, is not only to avoid the apparition of mycotoxicoses at these last but, especially to suppress the presence of residues of the mycotoxins in milk, the meats and eggs.   
     The mycotoxins are thermo resistant and it is therefore impossible to apply thermal treatments to destroy or to reduce the concentration of the mycotoxins in a food, whatsoever.
     Other important element to underline, the scraping of the parts gone moldy from some food cannot ELIMINATE the mycotoxins completely, because their toxin diffuses in all the food and this from colonies of mildews.
    It has been given to us to note that of the moldy bread (often becoming blue) is given to animals, particularly cows.
    I'll leave it to you to guess the dangers that the consumers can risk while drinking cow's milk and which costs currently very expensive.
    The moldy cheeses and this same after a mechanical cleaning should never be used like raw materials for the manufacture of cheese spread.
 

7 – Particular cases


     It is advisable to reconsider and this for ethics the case relating to certain food the development of the moulds is beneficial if non necessary.
     Concerning this particular case, the development of the moulds this fact from meaningful quantities but especially controlled.
     With regard to cheeses fermented by moulds such as:
    Camembert cheese, Roquefort and certain goat's milk cheeses, l' assumption was advanced according to which the stocks used for their manufacture could produce mycotoxicoses.
     The realized studies demonstrated that the original "chokes", do not produce an aflatoxin, or other mycotoxins.
     However the possibility for some stumps of mildews to produce some mycotoxins under manufacture of the traditional cheeses is not to exclude.
     The stumps used for the manufacture of cheeses as:  camembert and Roquefort, belong to stumps for:

  • camembert:  pénicillium camemberti
  • roquefort:  pénicillium roqueforti

    These two stumps of moulds can be responsible for toxic effects, of or the interest of the very serious microbiological control, at the time of the manufacture of the two cheeses.
     A last aspect deserves to be underlined concerning the use of the spices and this for the preparation of some food, it would be prudent to supervise the stumps used to be able to discover the possible production of mycotoxins in time.
     In conclusion, one will be able to say that the systematic prevention of the mycotoxins consists in preventing the growth of mildews in food and their raw materials.
Two processes will be able to be used:
 
1 - The dehydration
2 - The addition of antifungal suitable.

8 - Weaponization
    Aflatoxins do not appear to have attracted much of the military interest in toxins
    It was thus surprising when, after the War, Iraq informed the UN that it had produced aflatoxins and several trichothecene toxins.
    Aflatoxins have, however, been mentioned as possibly enhancing the toxicity of trichothecene mycotoxins after the latter were recognized as military agents. 
    Still, Iraq’s placing aflatoxins in long-range missiles has surprised and puzzled analysts. Zilinskas (1997) offers three hypotheses:
    1. The Iraqis discovered that aflatoxin possessed previously unknown propertiesuseful in biological warfare.
    2. The long-term potential for carcinogenesis was used to terrorize civilian populations.
    3. Because aflatoxin is easy to produce, it was produced and deployed to meet toxin production quotas set by higher authorities.
    Although concerns about human exposure have focused on carcinogenic risks, acute aflatoxin toxicity has been recognized, primarily from oral exposure but also via the respiratory route  Animal studies suggest that respiratory exposure is more toxic than oral exposure..T
    here is uncertainty about human clinical manifestations of low-dose respiratory exposure to aflatoxin, although both acute and chronic illnesses are expected.
    The symptom onset is delayed, and there is evidence of cumulative effects.
    Although many humans are exposed to aflatoxin in food, gastrointestinal symptoms predominate; neuropathy, rashes, memory problems, and joint pain are not commonly reported.
    GAO (1997) suggested that aflatoxin exposure arising from U.S. attacks on chemical storage sites might have contributed to illnesses in Gulf War veterans but did not provide evidence to support the hypotheses.

9 - Conclusions, and Recommendations


    Why Iraq developed weapon systems for aflatoxin remains speculative; respiratory toxicity at low levels and immunosuppression at low doses may provide hints, although there is little information about primate respiratory toxicity.
    Oral exposure in Malaysia led to deaths; if exposure at similar levels could be achieved through inhalation, pulmonary and systemic effects would be delayed, and there would have been no detection means (and no effective therapy).
    The agent, if spread in the vicinity of U.S. troops, would be stable enough to provide recurrent exposures. Although the estimated lethal dose of 2 to 4 mg/kg is not as toxic as some substances, it would be possible to create an aerosol that would deliver the 140 mg of toxin sufficient to kill a 150-pound person (if the
    Malay experience with children can be generalized). Of course, a full-blown outbreak of this nature would have been noted during the Gulf War.
    Lower levels of exposure might resemble acute oral exposure in animals, with vomiting, malaise, and nonspecific signs and symptoms.
    Several steps might still be taken to assess the possibility of aflatoxin exposure in the Gulf. These include following up on a report that aflatoxin antibodies could be detected in exposed persons by measuring antibody levels in Gulf personnel and controls.
    The antibody level in the Danish controls was low compared to that in Kenyans with high dietary intake, so finding antibodies in Gulf war veterans would not be conclusive proof of exposure to military toxin, since food exposure alone could promote antibody formation.
     Harrison and Garner (1991) detected aflatoxin and adducts in formalin-fixed pathology specimens a long time after the event in Malaysia. AFIP could consider analyzing some of its preserved tissues from Gulf cases for aflatoxins and adducts.
    Also, an analysis could be made of whether material from other Gulf War veterans shows adducts from aflatoxin. Adducts in Gulf War tissue material higher than those in controls would not prove a particular source of aflatoxin exposure but, if found, would require more research on this toxin.
     Aflatoxin is sufficiently stable that it might still be detectable in clothing, equipment, filters, and mask canisters from the Gulf War, if they can be located.
    It would be useful to ask Malaysian health officials about any long-term effects in the less severe cases from the 1988 outbreak.
    Such a follow-up period would be about two years longer than the current Gulf War period of observation.
    The aflatoxins are potent and poorly understood.
    They do not seem a likely explanation for the pattern of illnesses in Gulf War veterans, but it does at least appear possible to detect exposure of U.S. personnel to low levels of aflatoxins.
    Aflatoxins are a poorly understood agent, so further research on their possible military threats should be considered.
     The respiratory toxicity of aflatoxins in primates and other species should beevaluated seriously, with some selective evaluation of combined toxicities (e.g.,with trichothecenes or infectious agents).
    A better understanding of the mechanisms of central nervous system toxicity and immune suppression would be helpful (e.g., do aflatoxins alter responses to leishmaniasis, malaria, sand flyfever?).
     Aflatoxins are known carcinogens. The induction of cancer has generally been seen in populations with sustained exposures to fairly high dietary levels of the toxin after many years (and in some situations in populations with a high prevalence of chronic hepatitis B infections).
    A short (few weeks), low-level exposure to aflatoxins should have little risk of increased cancer because the incremental additional amount compared to the background level in Western diets would be small.

 

10 - bibliography

 



Update of survey, regulation and toxic effects of mycotoxins in EuropeToxicology Letters, Volume 127, Issues 1-3, 28 February 2002, Pages 19-28
Edmond E. Creppy
 
Selected Mycotoxins Affecting Animal and Human HealthHandbook of Toxicologic Pathology (Second Edition), 2002, Pages 645-699
Wanda M. Haschek, Kenneth A. Voss, Val R. Beasley
 
An historical overview of field disease outbreaks known or suspected to be caused by consumption of feeds contaminated with Fusarium toxinsAnimal Feed Science and Technology, Volume 137, Issues 3-4, 1 October 2007, Pages 201-212
D.P. Morgavi, R.T. Riley
 
Mycotoxins contaminating cereal grain crops: Their occurrence and toxicityApplied Mycology and Biotechnology, Volume 2, 2002, Pages 171-196
Deepak Bhatnagar, Robert Brown, Kenneth Ehrlich, Thomas E. Cleveland
 
Fungi and fungal toxins as weaponsMycological Research, Volume 110, Issue 9, September 2006, Pages 1003-1010
R. Russell M. PATERSON
 
Trichothecene MycotoxinsHandbook of Toxicology of Chemical Warfare Agents, 2009, Pages 353-369
Wanda M. Haschek, Val R. Beasley
 
Mycotoxins, general view, chemistry and structureToxicology Letters, Volumes 82-83, December 1995, Pages 843-851
Pieter S. Steyn
Veterinary Toxicology
Basic and Clinical Principles
Copyright © 2007 Elsevier Ltd. All rights reserved

Edited by: Ramesh C. Gupta, DVM, MVSC, PHD, DABT, FACT
ISBN: 978-0-12-370467-2
 

 
 
Chapter 75 - Aflatoxins, Pages 939-950, Robert W. Coppock, Ralph G. Christian
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Chapter 76 - Trichothecenes, Pages 951-976, Michelle S. Mostrom, Merl F. Raisbeck
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Chapter 80 - Tremorgenic mycotoxins, Pages 1004-1010, Tim J. Evans, Ramesh C. Gupta
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Chapter 82 - Ergot, Pages 1015-1018, Steven S. Nicholson
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