Ergotism

Claviceps purpurea / Claviceps paspali

For medical students2 min readUpdated 2026-10-10

Ergotism is a severe medical condition resulting from the ingestion of grains contaminated with ergot fungi. The pathology is driven by the accumulation of plant toxins that exert potent neurotoxic and vasospastic effects on the human body.

Causative agentsFungi *Claviceps purpurea* and *Claviceps paspali*

Main substrateContaminated cereal crops, most commonly rye

ToxinsLysergic acid derivatives and clavine alkaloids

MechanismPronounced neurotoxic and vasospastic effects on the nervous and vascular systems

Etiology and Transmission

The causative agents of the disease are ergot fungi—primarily Claviceps purpurea and Claviceps paspali. The primary substrates for their growth are cereal crops (most frequently rye).

During its growth cycle, the fungus forms specialized structures known as sclerotia (commonly referred to as ergot bodies). Morphologically, these are large, curved, dark, elongated structures that develop directly within the ear of grain, completely replacing healthy kernels.

Human infection occurs via two main routes:

Alimentary (primary): Through the consumption of contaminated grains or products made from infected flour.
Indirect: Through the milk of farm animals if their feed previously contained ergot-contaminated forage.

Toxins and Pathogenesis

The pathophysiology of ergotism is driven by specific toxins accumulating within the fungal sclerotia. These include lysergic acid alkaloids and clavine alkaloids.

Upon entering the body, these compounds exert pronounced neurotoxic and vasoconstrictive effects, triggering severe neurological impairments and determining the overall clinical severity of the disease.

Clinical Course

Ergotism can manifest in two primary clinical courses:

Acute form. Characterized by a rapid onset and high mortality rate. The clinical presentation includes symptoms of acute gastroenteritis, quickly followed by signs of severe central nervous system involvement—marked paresthesias and seizures.
Chronic form. Features gastrointestinal disturbances and recurrent vomiting. A specific neurological symptom is a persistent sensation of "crawling ants" (formication), localized predominantly in the extremities. Prolonged toxic exposure can lead to reproductive failure.

Clinical Presentations

Depending on the predominant symptoms, ergotism is classified into three main clinical forms:

Convulsive form: Manifests as toxic tonic spasms affecting predominantly flexor muscles. This condition has a protracted course; the seizure syndrome can persist for about a month.
Gangrenous form: Typically develops with a delay of 10–20 days following the onset of intoxication. It is characterized by necrosis of the peripheral parts of the extremities. The tissue death process is accompanied by intense, agonizing pain.
Mixed form: Combines both convulsive manifestations and signs of tissue necrosis.

Mnemonic

To remember the clinical forms, use the association: ergot toxins "bend" (flexor muscle spasms) and "dry out" (peripheral extremity necrosis).

Frequently asked questions

Which specific ergot alkaloids cause ergotism?

Ergotism is caused by lysergic acid alkaloids and clavine alkaloids. The most common and toxic representatives produced by Claviceps purpurea include:

Ergotoxin — a toxic ergot alkaloid blend.
Ergotamine — an alkaloid affecting the vascular system.
Ergometrine — an alkaloid used in obstetric practice.

Additionally, there are hydrogenated derivatives of ergot alkaloids, such as dihydroergotamine, dihydroergotoxin, and dihydroergocryptine.

What is the receptor mechanism of action of ergot alkaloids?

The receptor mechanism involves interactions with serotonin and adrenergic receptors:

Serotonin receptor stimulation: Activation of 5-HT receptors (particularly the $5-HT_{1D}$ subtype).
Adrenoceptor blockade: These compounds act as non-selective $\alpha_1, \alpha_2$-adrenoceptor blockers. Natural alkaloids possess $\alpha$-blocking activity, and their hydrogenated derivatives (e.g., dihydroergotamine) exhibit even stronger $\alpha$-blocking potency.

Through what pathogenetic mechanism does extremity necrosis develop in the gangrenous form of ergotism?

Extremity necrosis develops due to persistent vascular spasm in the limbs and endothelial damage. Vessel involvement and thrombosis lead to ischemia and necrosis of the peripheral tissues. The process is accompanied by severe pain and manifests 10–20 days post-exposure.

What are sclerotia and what do they look like?

Sclerotia (ergot bodies) are dark, curved, and large structures formed by Claviceps fungi in place of healthy grains within the ears of infected crops.

Is ergotism transmission possible without directly eating contaminated grains?

Yes, ergot toxins can be transmitted through animal milk if the livestock consumed contaminated feed.

Which muscles are primarily affected in the convulsive form?

In the convulsive form of ergotism, tonic spasms predominantly affect the flexor muscles.

When do symptoms of the gangrenous form appear?

Necrosis of the peripheral extremities in the gangrenous form does not develop immediately, but rather 10–20 days after the onset of the disease.

Go deeper

Structure and life cycle of fungi of the genus Claviceps
Properties of clavine alkaloids and lysergic acid derivatives
Pathogenesis of tissue necrosis in the gangrenous form of ergotism
Differential diagnosis of acute gastroenteritis in ergotism