Mycotoxicosis is food intoxication (less often respiratory and dermal lesions) caused by mycotoxins of mold fungi. The symptoms depend on the type of mycotoxin and the way it enters the body. There may be signs of gastroenteritis, headaches, mental disorders, leukopenia, sore throat, convulsions, gangrene of the extremities, etc. anamnesis, cultural isolation of the fungus from food and biomaterial, and the results of bioassays are of crucial diagnostic importance. In acute poisoning, gastric and intestinal lavage is performed, enterosorbents, forced diuresis, hemosorption, symptomatic therapy are prescribed.
ICD 10
T64 Toxic effect of aflatoxin and other mycotoxins polluting food products
General information
Mycotoxicoses are acute or chronic pathological conditions caused by the ingestion of toxic fungal metabolites. Contamination of food and animal feed with mycotoxins reaches 30%, which causes significant economic damage to agriculture and poses a serious danger to the health of consumers of agricultural products. Mycotoxins have carcinogenic, mutagenic, embryotoxic, allergic, immunosuppressive effects – all this makes the problem of mycotoxicosis interdisciplinary and extremely relevant in modern conditions.
Causes
Ways and sources of infection
Diseases are caused by exometabolites – the waste products of microscopic fungi that accumulate in plant or animal products and have various toxigenic properties. The main way of infection with mycotoxicosis is alimentary (when eating contaminated food), much less often – respiratory (when inhaled) or transdermal (with direct contact).
The sources of mycotoxins are more often cereals (wheat, rice, barley, corn), legumes (peas, beans, chickpeas), oilseeds (sunflower, sesame), nuts (forest, walnut, peanuts). They are affected by fungi with insufficient agrotechnical and chemical treatment of soils, violation of harvesting technology and storage rules (high humidity, lack of aeration). In addition, mycotoxins can also enter the human body with animal products: poultry meat, eggs, milk.
If infected plant products change their appearance, and fungi on them can be detected visually, then there is often no visible mold growth in mycotoxin-contaminated animal products. The emergence of mycotoxicosis is also facilitated by the resistance of fungal metabolites to the effects of chemical and physical factors: they are only partially destroyed by boiling, freezing, drying, and the use of preservatives. The optimal conditions for the growth of fungi and toxin formation are the absence of sunlight, humid conditions, cool or warm air temperature.
Types of fungi and toxins
Mycotoxicoses caused by pathogenic fungi are dangerous for humans:
- the genus Fusarium (F. sporotrichioides, F. graminearum) – produce over 40 trichothecene toxins, of which the main food contaminants are T-2 toxin, vomitoxin.
- genera Aspergillus (A. flavus, A. parasiticus) – produce about 20 aflatoxins, the most dangerous of which are B1 and M1.
- genus Penicillium – produce ochratoxins, the most toxic of which is ochratoxin A.
- genus Claviceps (C. purpurea, C. paspalum) – ergot sclerotia contain toxic alkaloids of the clavine group (agroclavin, setoclavin, elimoclavin) and lysergic acid (ergoalkaloids: ergosine, ergotamine, ergosecalin, ergocristine).
Pathogenesis
The absorption of mycotoxins mainly occurs in the gastrointestinal tract (mainly in the small intestine), to a lesser extent the metabolites are absorbed by the alveoli of the lungs, absorbed through the epithelium of the skin, eyes. With the flow of blood and lymph, they spread throughout the body, exerting local and systemic toxic effects. Various mycotoxins have their own target organs. Almost all metabolites have neurotropicity, which is associated with the development of symptoms of central nervous system damage in most mycotoxicoses.
Aflatoxins have a pronounced hepatotoxic effect, causing fatty and protein liver dystrophy, and in severe cases ‒ necrosis of hepatocytes, proliferation of bile ducts. Currently, they are classified as the strongest hepatotropic poisons with a carcinogenic effect. In addition, aflatoxins cause a decrease in prothrombin synthesis, a violation of vitamin D metabolism and mineral metabolism, suppression of the immune system, gonadotoxic, embryotoxic effects.
Trichotecenes provoke the development of ulcerative-necrotic processes of the skin and mucous membranes of the oral cavity, nose, gastrointestinal tract. They cause inhibition of hematopoiesis (anemia, leukopenia, thrombocytopenia), immunosuppression. They have teratogenic and mutagenic effects.
Ochratoxins primarily affect the kidneys. The nephrotoxic effect is manifested by atrophy of the renal tubules, glomerular fibrosis, and the development of toxic nephropathy. Possible hemorrhages in the gastrointestinal tract. They have a teratogenic, embryotoxic, carcinogenic effect.
The main effect of ergotoxins of ergot is neurotoxic. They cause hallucinations, spasm of smooth muscles, narrowing of blood vessels, trophic disorders.
Classification
Taking into account the ways of penetration of mycotoxins, food mycotoxicoses, respiratory (pneumomycotoxicoses), skin (dermatomycotoxicoses) are isolated. Depending on the type of fungal pathogen, the following groups of human mycotoxicoses are distinguished:
- Fusariotoxicoses (fusarioses). They are caused by fungi of the genus Fusarium. They include alimentary-toxic aleikia, poisoning with “drunk bread”, acacabitoxicosis.
- Aflatoxicoses. They are caused by fungi of the genus Aspergillus and Penicillium. They are represented by acute poisoning and chronic intoxication.
- Ergotism (clavicepsotoxicosis). It is caused by microscopic fungi of the genus Claviceps. It can occur in three forms: gangrenous, convulsive and mixed.
Symptoms
Fusariotoxicoses
Alimentary toxic aleikia in a mild variant proceeds with the phenomena of stomatitis, gingivitis, glossitis. Sometimes the clinical picture of acute gastroenteritis develops. Recovery occurs within 3-5 days. With a significant intake of trichothecenes into the body, leukopenia occurs, turning into aleikia, hemorrhagic diathesis, coagulopathy (gingival, nasal, intestinal, uterine bleeding), necrotic angina.
Symptoms of poisoning with “drunk bread” develop 30-60 minutes after ingestion of contaminated grain products. They include abdominal pain, vomiting, diarrheal syndrome. Patients are concerned about extreme weakness, uncertainty of gait, heaviness in the legs. The next day comes a stage resembling a severe hangover: dizziness, pronounced cephalgia. Chronic mycotoxicosis caused by trichothecenes is accompanied by exhaustion, decreased vision, and mental disorders.
Cases of acacabitoxicosis are sporadically reported in Korea and Japan, where rice is the main food. Clinically resembles food poisoning with vomiting, diarrhea, abdominal pain, chills, headache. Sometimes there is a strong sore throat.
Aflatoxicoses
Acute mycotoxicosis develops within 30 minutes after eating food contaminated with aflatoxins. There is weakness, headache, soreness in the right hypochondrium, gastrointestinal disorders. Neurotoxic syndrome is manifested by impaired coordination of movements, paresis, convulsions. Hemorrhagic syndrome, edema, jaundice are characteristic. Chronic aflatoxicosis is manifested by enteritis, slowing of growth and development in children, weight loss in adults, the development of cirrhosis of the liver.
Ergotism
The convulsive form of ergot poisoning (“evil writhing”) is characterized by body aches, paresthesia, tonic convulsions and epileptiform seizures. Often in the clinical picture there are phenomena of gastroenteritis. Sometimes affective disorders, hallucinations develop.
In the gangrenous form of mycotoxicosis (“St. Anthony’s fire”) there are burning pains in the extremities, against which dry gangrene develops. With prolonged treatment of migraine with ergotamine preparations, gangrenous processes can occur in the gastrointestinal tract.
Complications
Most mycotoxins are capable of causing mutations in the genetic apparatus, embryo death in the early stages of gestation, organogenesis disorders in the fetus. All acute mycotoxicoses can end fatally.
Chronic intoxication with aflatoxins is dangerous for the development of liver cancer. Hepatocellular carcinoma associated with aflatoxicosis is 30 times more likely to develop in people suffering from viral hepatitis B and C. It is possible that aflatoxins play a role in the development of Reye’s syndrome and kwashiorkor in children. In acute poisoning, the risk of acute liver failure is extremely high.
With ergotism, rejection of necrotized soft tissues and entire limb segments along the border of articular joints (mutation) may occur. The most dangerous complications of alimentary toxic aleikia are sepsis and DIC syndrome.
Diagnostics
Patients with suspected mycotoxicosis are treated by toxicologists or infectious disease specialists. The identification of the source of mycotoxins, the establishment of the culture of the producing fungus plays a primary role for the etiological diagnosis. For this purpose, clinical and epidemiological, laboratory and instrumental studies are used:
- Clinical and epidemiological data. The patient’s food history, professional, household contact with fungi are found out. Clinical manifestations are evaluated: complaints, symptoms, results of physical examination, neuropsychiatric status.
- Laboratory methods. The laboratory analyzes urine, feces, vomit for toxin metabolites, microbiological isolation of fungus from food and biomaterial. Enzyme immunoassay and radioimmunological analysis are also used to identify the toxic agent. To assess the patient’s condition, blood test and urine are performed, liver samples and coagulogram are examined. If necessary, they resort to conducting bioassays with mycotoxins on laboratory animals.
- Other research. The diagnosis of various etiological forms of mycotoxicosis is supplemented with instrumental studies: pharyngoscopy, neuromyography, EEG, ultrasound of internal organs, radiography of limbs, etc.
Differential diagnosis
If mycotoxicosis is suspected, pathological conditions occurring with signs of gastrointestinal and nervous system damage should be excluded:
- poisoning with bacterial toxins (staphylococcal toxicoinfection, botulism);
- tetanus;
- viral gastroenteritis;
- poisoning by poisonous plants;
- heavy metal poisoning.
Treatment
If there are signs of acute poisoning, the patient is hospitalized in the department of toxicology. There is no specific treatment for mycotoxicosis. As an emergency measure, a probe gastric lavage is performed, saline laxatives are given. In the future, enterosorbents are prescribed, infusion therapy is carried out, forced diuresis, and hemosorption is performed with severe intoxication.
Symptomatic therapy of mycotoxicoses is aimed at preventing infectious complications (antibiotic therapy), supporting liver function (hepatoprotectors), stimulating hematopoiesis (folic acid, vitamin B12, leukopoiesis stimulants), increasing blood clotting (vitamin K, calcium preparations). According to the indications, an anti-gangrenous serum is administered.
Prognosis and prevention
With the timely withdrawal of contaminated products from the diet and the beginning of treatment, pathological symptoms are reversible. Factors of unfavorable prognosis are a high dose of mycotoxins, the addition of septic and hemorrhagic complications, multiple organ failure. Measures for the prevention of mycotoxicosis include compliance with harvesting technology and storage conditions of grain crops, careful monitoring of the condition of food and the content of mycotoxins in them. Products with visible traces of mold should absolutely not be eaten.
