Etiology and transmission routes
The causative agents of the disease are ergot fungi — primarily Claviceps purpurea and Claviceps paspalum. Cereal plants (most commonly rye) serve as the primary substrate for their development.
During growth, the fungus forms specific structures called sclerotia. Commonly known as "ergot sclerotia" or "spurs," morphologically they are large, curved, dark-colored formations that develop directly in the ear of the grain, completely replacing healthy kernels.
Human infection occurs via two main routes:
- Alimentary (primary): through the consumption of the contaminated cereals themselves or products made from contaminated flour.
- Indirect: via the milk of farm animals if ergot-contaminated feed was previously included in their diet.
Toxins and pathogenesis
The development of ergotism is based on the action of specific toxins that accumulate in the fungal sclerotia. These include lysergic acid alkaloids and clavine alkaloids.
Upon entering the body, these substances exert a pronounced neurotoxic effect, which causes severe neurological disorders and determines the severity of the clinical course.
Clinical course of the disease
Ergotism can manifest in two main variants:
- Acute form. Characterized by rapid onset and high mortality. The clinical picture consists of symptoms of acute gastroenteritis, which are quickly joined by signs of severe central nervous system damage — pronounced paresthesias and convulsions.
- Chronic form. Proceeds with gastrointestinal disorders and intermittent vomiting. A specific neurological symptom is a persistent sensation of "creeping ants" (formication), localized predominantly in the extremities. Prolonged toxic exposure may lead to infertility.
Clinical Forms
Depending on the predominant symptoms, three main clinical forms of ergotism are distinguished:
- Convulsive form. Manifests as toxic tonic spasms affecting primarily the flexor muscles. This condition has a prolonged course — the convulsive syndrome can persist for about one month.
- Gangrenous form. Its development is usually delayed — occurring 10–20 days after the onset of intoxication. Characterized by necrosis of the peripheral parts of the extremities. The tissue death process is accompanied by severe, agonizing pain.
- Mixed form. Combines both convulsive manifestations and signs of tissue necrosis.
Briefly: answers to topical questions
Which specific ergot alkaloids cause ergotism?
Ergotism is caused by lysergic acid alkaloids and clavine alkaloids. The most common and toxic alkaloids produced by the fungus Claviceps purpurea include:
- Ergotoxin — a toxic ergot alkaloid.
- Ergotamine — an alkaloid affecting the vascular system.
- Ergometrine — an alkaloid used in obstetric practice.
Dihydrogenated derivatives of ergot alkaloids, such as dihydroergotamine, dihydroergotoxin, and dihydroergocryptine, are also distinguished.
What is the receptor mechanism of action of ergot alkaloids?
The receptor mechanism of action of ergot alkaloids involves affecting serotonin and adrenergic receptors.
- Stimulation of serotonin receptors — activation of 5-HT receptors occurs (particularly the $5-HT_{1D}$ subtype).
- Blockade of adrenoceptors — these compounds belong to the group of non-selective $\alpha_1, \alpha_2$-adrenoceptor blockers. Natural alkaloids possess $\alpha$-adrenoceptor blocking activity, and their dihydrogenated derivatives (e.g., dihydroergotamine) exhibit even greater $\alpha$-adrenoceptor blocking activity.
Through what pathogenetic mechanism does extremity necrosis develop in the gangrenous form of ergotism?
Extremity necrosis in the gangrenous form of ergotism develops as a result of persistent vasospasm of the limbs and endothelial damage. Involvement and thrombosis of blood vessels lead to necrosis of the peripheral parts of the extremities. The process is accompanied by severe pain and develops within 10–20 days.
To memorize the clinical forms, use the association: ergot toxins "flex" (flexor spasms) and "dry out" (peripheral extremity necrosis).
Class and exam questions
What are sclerotia and what do they look like?
Sclerotia (ergot bodies) are dark, curved, large formations produced by the fungus Claviceps purpurea in place of healthy grains in the ears of affected cereals.
Is ergotism infection possible without direct consumption of cereals?
Yes, ergot toxins can be transmitted through animal milk if the animals fed on contaminated feed.
Which muscles are primarily affected in the convulsive form?
In the convulsive form of ergotism, tonic spasms primarily affect the flexor muscles.
When do symptoms of the gangrenous form appear?
Necrosis of the peripheral parts of the extremities in the gangrenous form does not develop immediately, but 10–20 days after the onset of the disease.
What else to study on this topic
- Structure and life cycle of fungi of the genus Claviceps
- Properties of clavine alkaloids and lysergic acid alkaloids
- Pathogenesis of tissue necrosis in the gangrenous form of ergotism
- Differential diagnosis of acute gastroenteritis in ergotism
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