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Aflatoxicosis

Aflatoxicosis

For medical students2 min readUpdated 2026-10-10

Aflatoxicosis is a group of severe foodborne illnesses caused by the ingestion of specific toxic mold metabolites. The disease is characterized by rapid symptom onset, high mortality, and primary damage to liver tissue.

Causative agentsFungi *Aspergillus flavus* and *Aspergillus parasiticus*
PropertiesAbsolute thermostability during cooking and food processing
Target organLiver (risk of necrosis, cirrhosis, and primary hepatocellular carcinoma)
Clinical courseAcute presentation with a high probability of a fatal outcome

Etiology and History

The disease is caused by microscopic mold fungi—specifically Aspergillus flavus and Aspergillus parasiticus. The name of the toxin group is an acronym derived from the Latin name of the primary producer: Aspergillus flavus toxins.

These dangerous metabolites were first discovered in 1960. The discovery was prompted by a sudden outbreak of a previously unknown disease in Great Britain, which drew researchers' attention to Aspergillus toxins.

Toxin Characteristics and Sources of Contamination

Aflatoxins are a complex group of chemical compounds. Several main fractions of these metabolites are identified: $B_1$, $B_2$, $B_{2a}$, $G_1$, $G_2$, $G_{2a}$, $M_1$, and $M_2$. The primary epidemiological danger of aflatoxins lies in their high toxicity and thermostability. They are not destroyed even by thorough thermal processing of food products.

The problem is geographically widespread. Human contamination occurs via the alimentary route through contaminated food:

Clinical Presentation of Acute Poisoning

Acute aflatoxicosis is characterized by an extremely rapid onset of symptoms and high lethality. The pathological process affects multiple body systems simultaneously:

  1. Internal organ damage: Pronounced gastrointestinal dysfunctions are observed. However, the key link in pathogenesis is severe hepatotoxicity. The toxins induce hepatic tissue necrosis, which can subsequently progress to cirrhosis. Furthermore, there is a high risk of developing primary liver cancer.
  2. Neurological symptoms: Patients suffer from generalized motor sluggishness, convulsive syndrome, and paresis.
  3. Vascular and tissue disorders: Toxic effects on the vascular wall lead to hemorrhages (multiple bleedings) and extensive edema.

Spectrum of Other Aspergillus Mycotoxins

In addition to classical aflatoxins, various species of the genus Aspergillus are capable of producing a range of other dangerous toxic substances.

MycotoxinProducing Species (Aspergillus)
Ochratoxins A, B, CA. ochraceus
PatulinA. terreus, A. niveus, A. candidum
GliotoxinA. giganteus, A. fumigatus
SterigmatocystinA. versicolor, A. nidulans
TremorgensA. clavatus, A. flavus, A. candidum
CytochalasinsA. clavatus
CitrininA. terreus, A. niveus, A. candidum

Mnemonic

The name "Aflatoxin" is easily remembered via the acronym: A-fla-toxin = Aspergillus flavus toxins. This immediately reveals the primary causative agent and the nature of the poison.

Frequently asked questions

What is the molecular mechanism of the hepatotoxic and carcinogenic action of aflatoxin B1?

The molecular mechanism of aflatoxin B1 action involves its biotransformation in the liver into an active alkylating metabolite. Microsomal oxidation of the toxin is mediated by the cytochrome P450 system.

  • Aflatoxin B1-8,9-epoxide is a potent alkylating agent that covalently binds to DNA nitrogenous bases (primarily guanine).

This interaction induces mutations in tumor suppressor genes (such as p53). Consequently, malignant transformation of hepatocytes is initiated, leading to primary hepatocellular carcinoma.

What pathomorphological and histological changes develop in liver tissue during aflatoxicosis?

Pathomorphological changes in the liver during aflatoxicosis are characterized by severe toxic tissue injury with a high risk of malignant transformation. The following processes develop in the tissues:

  • Necrosis — death of hepatocytes, serving as the core link of hepatotoxicity.
  • Cirrhosis — the outcome of progressive liver injury.
  • Vascular and tissue disorders — emergence of hemorrhages (bleedings) and edema.
  • Carcinogenesis — development of primary liver cancer.

These changes are accompanied by rapid symptom progression and high lethality.

What methods are used for the laboratory identification of aflatoxins in food products and biological material?

Laboratory detection of aflatoxins involves extracting the mycotoxin from a sample using an organic solvent followed by its identification. The following methods are used for testing crops, food products, feed, and animal-derived raw materials:

  • Physicochemical methods — chromatography and spectrophotometry.
  • Immunological methods — enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA).
  • Biological assays (bioassays) — utilizing chicken embryos, cell cultures, sensitive microorganisms, laboratory animals (rats, mice, guinea pigs), and birds (ducklings, pigeons).
Can foods containing aflatoxins be detoxified by boiling or frying?

No, aflatoxins exhibit pronounced thermostability. They are not destroyed by thermal processing, meaning contaminated food products remain toxic.

What effect do aflatoxins have on the liver?

Hepatotoxicity is the core mechanism of poisoning. The metabolites cause hepatic necrosis, which can progress to cirrhosis, and they drastically increase the risk of primary liver cancer.

Are animal-derived products dangerous in aflatoxicosis?

Yes. Aflatoxins can accumulate in the tissues of animals that consumed contaminated feed. Therefore, meat, milk, and cheese can also serve as fully active sources of human poisoning.

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