Ergot

Characteristics:

Description: physical properties, appearance, physiological properties (neurotoxin, hemotoxin,

nephrotoxin)

Ergot alkaloids are derivatives of ergotine. Ergot alkaloids are compounds derived from the parasitic
fungus Claviceps purpurea, which grows on rye as well as other grains. Ergot alkaloids are often divided
into amine alkaloids and amino acid alkaloids and have a wide range of physiological effects. These
effects are largely due to their agonist, partial agonist, and/or antagonistic effects at biogenic amine
receptor sites.

The so-called ergot that replaces the grain of the rye is a dark, purplish sclerotium. Ergot is a neurotoxin

Signs and symptoms

Acute poisoning: nausea and vomiting, irritation in the throat, pain abdomen, diarrhea
Chronic poisoning: Ergotism
 Convulsive type: initially manifest as heaviness in the limbs and head associated with diarrhea.
As the illness progress, complaints ranged from the pins and needles feeling of paresthesias to
facial fasciculations. If the disease worsened, the patient could experience tonic-clonic spasms
and status epilepticus.
 Gangrenous type: The gangrenous syndrome often began with several weeks of intense burning
pain (St. Anthony’s fire), usually in the extremities, the sites most often affected. As the patient
continue to consume ergot, ischemia of the affected extremities lead to gangrene, most often
dry gangrene and subsequent auto-amputation of the limbs.

Mechanism of toxicity
Ergot derivatives directly stimulate vasoconstriction and uterine contraction, antagonize alpha-
adrenergic and serotonin receptors, and may also dilate some blood vessels via a CNS sympatholytic
action. Sustained vasoconstriction causes most of the serious toxicity. Reduced blood flow causes local
tissue hypoxia and ischemic injury, resulting in tissue edema and local thrombosis. At a certain point,
reversible vasospasm progresses to irreversible vascular insufficiency and limb gangrene.

Treatment
Emergency and supportive measures
Maintain an open airway and assist ventilation if necessary
Treat coma and convulsions if they occur

Decontamination
Administer activated charcoal if available.
Laxatives, gastric lavage, and enemas are given to remove the poison from the stomach and intestine.

Enhanced Elimination
Dialysis and hemoperfusion may also help.

Tolazoline has moderate alpha-adrenergic blocking activity and has histamine agonist activity. Tolazoline
usually reduces pulmonary arterial pressure and vascular resistance.
Sodium nitroprusside is further broken down in the circulation to release nitric oxide, which activates
guanylate cyclase in the vascular smooth muscle. This leads to increased production of intracellular
cGMP, which stimulates calcium ion movement reducing the level of available calcium ions that can bind
to calmodulin. This ultimately results in vascular smooth muscle relaxation and vessel dilation.

Pfaller et al. (2009). Clinical Mycology (2nd Ed.). Section 4: Mycotoxins and their effects on humans p.
651. Churchill livingstone.

Stanley et al. (2014). Current Therapy in Vascular and Endovascular Surgery. Ergotism p. 197. Saunders.

Karmakar, R.N. (2007).Forensic Medicine and Toxicology. Bimal Khumar.

Olson, K.R. (2004). Poisoning and Drug Overdose. Specific Poisons and Drugs pp 189-190. McGraw-Hill
Companies.