Ashes to ashes, Dust to dust,

Rot and rust will harm all of us

DANGERS OF

MYCOTOXIN A very Brief Introduction

HADI AKBAR BIN DAHLAN VISUAL INTERPRETER Hadiakbar1591@rocketmail.com

http://easysciencenote.blogspot.com

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INTRODUCTION

Toxin that originate from fungi are termed Mycotoxin. Most of the fungi that produce these

were filamentous fungi; where the intoxication is by digestion. Some of the effects are:

Decreased Growth rate

Abnormal reproduction

Diseases

Early death (for animal)

A bread covered by mold. (left)

The structure of the filamentous mold on the bread (down)

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Ergotism

The case of ergotism toxication is due to

contamination of Claviceps Purpurea on

grain. The fungus proliferates throughout

the grain untill a “tumorous mass” called

sclerotium forms. The mass withholds the

resting stage of the fungus that dormant in

dry condition and germinate when

moistened.

There are 2 symptoms of ergotism:

Gangrenous ergot poisoning

Characterized by severe pain,

inflammation, and a burned appearance

of the extremities, which may become

blackened. In severe cases, loss of

fingers, toes, and even hands and feet can

occur.

Gangrenous ergot poisoning cause

constriction of blood vessels. This is due

to vasoconstriction in peripheral veins

and arteries. The fungus contains

ergotamine; an alkaloid compound

whose structure is almost similar to

neurotransmitter. This meant that

ergotamine can bind to cell receptor and

affect signal transduction in the cell.

Convulsive ergot poisoning

The symptoms are primarily neurological

in nature and include writhing, tremors,

numbness, blindness, convulsions, and

hallucinations. No physical features such

as inflammation appear.

Convulsive ergot poisoning was less

understood, and it is said to be caused by

psychoactive alkaloids. It is said that it

have the same effect as Lysergic acied

Diethyl (LSD).

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Alimentary Toxic Aleukia (ATA)

This mycotoxicoses is also knows as septic angina. The fungi most associated with ATA is genus

Fusarium. Most of the ATA outbreaks are due to population consumption of overwintered harvest of grain. Therefore, this outbreaks occurs in Russia and europe back in the spring of early half of the 20

th

Century.. This because cryophilic fungi because have a peculiar capability of producing toxic substances

in increased amounts when grown under conditions that include a period of growth at temperatures near 0’C. Investigators found that field conditions that included relatively high winter temperatures, deep snow

cover, frequent freezing and thawing were conductive for fungal growth as well as toxin production in

crops.

There are 4 stages of ATA:

Stage 1: Shortly after exposure to the toxins,

victims experience:

burning sensations in the mouth, throat,

esophagus, and stomach.

Diarrhea

abdominal pain due to inflammation of the

gastric and intestinal mucosa.

Reduce Leukocyte count

tachycardia

Stage 2: This stage start with reduction in intensity

of the symptoms. Although the victim may begin to

feel well and capable of normal activity, but:

The destruction of the bone marrow continues

with a further reduction of leukocyte

The body’s resistance to infection is reduced.

If the consumption of the contaminated food is discontinued at this time and the victim obtains

medical care, the chances of recovery are good.

Stage 3: This stage is signaled by the appearance of:

hemorrhages on the skin and on the

mucous membranes of the mouth and

tongue

necrotic lesions proliferate along with an

increased tendency for infection.

Esophageal lesions often occur and the

involvement of the epiglottis may cause

laryngeal edema leading in many cases to strangulation.

Stage 4: If the Stage 3 patient receives acute

medical treatment including blood transfusions and

heavy dose antibiotic treatment, he may survive the ordeal and thus enter Stage 4, the period of

convalescence. This period requires several months

of treatment for the nearly full recovery of the

hematopoietic system.

The toxin of genus Fusarium is called T-2 Toxin. These toxin inhibit protein synthesis by binding to

ribosomes; which activates stress kinase, inhibit DNA synthesis and mitochondrial function. T-2 toxin most strongly affects actively dividing cells such as those lining the gastrointestinal tract, skin, lymphoid,

and erythroid cells. Immunosuppression is a further major effect of inhibition of protein synthesis that is

caused by a decrease in antibody levels, in immunoglobulins, and in certain other humoral factors such as cytokines.

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Kashin-Beck Disease

This diseases is a disorder of the bones and joints of the hands and fingers, elbows, knees, and ankles of children and adolescents who

slowly develop stiff deformed joints, shortened limb length, and short

stature due to necrosis of the growth plates of bones and of joint

cartilage.

This disease is a multifactorial disease; Selenium deficiency with

consumption of fungal contamination of barley grains by Alternaria sp., Trichotecium sp., Cladosporium sp., Fusarium sp. and

Drechslera sp. Studies indicated that the metabolite vomitoxin

secreted by the fungal is the causative agent for this disease.

Patulin

Patulin is a fungal metabolite that is secreted by many Penicillium species. Exposure generally results from consumption of moldy fruits

and fruit products. Although patulin has been reported to produce

toxic effects in cattle and poultry and has been shown to be a mutagen, a weak carcinogen, and a teratogen in experimental systems,

a negative impact on human health has not been established.

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Zearalenone

a potent estrogenic substance that is produced by the fungus

Fusarium roseum and its sexual stage, Gibberella zeae, and

some related fungi. Consumption of corn infected with these

fungi can cause a loss of reproductive capacity and other

estrogenic effects in pigs and other domestic animals.

Symptoms of zearalenone poisoning in young pigs include

swelling and eversion of the vagina until, in some cases, the

cervix is visible. Recent studies have implicated this toxin in

the cause of precocious puberty in a group of girls.

Amanita Phalloides

Also known as Death cap mushroom, is mushroom that contains 2 types of substances;

phalloidins and amanitins. Of the 2, amanitin is much more toxic

in which it exhibit LD50 in rodents in range of only 0.1mg/kg,

regardless or intravenous or oral route. Amanitins target RNA

polymerase II; which can inhibit ribosome production, making

protein synthesis impossible.

The effects of A. phalloides poisoning may occur many hours

following consumption of the mushroom. The initial signs of

toxicity are:

Abdominal pain, diarrhea, and vomiting.

Within three to five days following exposure to the toxins,

failure of liver and kidneys occur

The chemical structures of the amanitins and the

phalloidins are complexes of cyclic peptides that contain

seven or eight amino acids. Although these cyclic

peptides are responsible for the toxic effects of the

mushroom, they exist in combination with polysaccharide

components as large molecular weight complexes called

myriamanins.

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REFERENCE

Takayuki Shibamoto and Leonard F. Bjeldanes, 2009, Introduction to Food toxicology (2nd

Edition), Chp. 7: Toxins from fungi, pg. 159 – 180, Academic Press, London.

Katherine Scurrah, 2010, Make it safe: A guide to food safety, Chp. 2 Food Safety Hazards pg

21-30, CSIRO Publishing, Collingwood.