Botulism
Basic Information 
Clinical Presentation
Physical Exam Findings
• The time to onset of clinical signs after exposure to toxin varies from 12 hours to several days. Sudden, unexplained death of one or more horses may be the initial signal of the onset of an outbreak.
• Decreased eyelid, tongue, and tail tone may be observed early in disease. Horses that walk may have a stilted, short-strided gait without ataxia. Muscle trembling and weakness may be apparent, particularly in foals.
• Pupillary dilation with sluggish pupillary light reflexes is common.
• There is normal cutaneous sensation with depressed spinal reflexes.
• Pharyngeal paralysis is frequently observed in adult horses with botulism and may be confirmed by endoscopic examination of the upper airway.
• Clinical signs may rapidly progress to recumbency.
• Tachycardia may occur, particularly in foals. Foals may appear or become constipated and dysuric.
• Signs of colic may be associated with diminished gastrointestinal (GI) motility.
• Dyspnea and cyanosis may be present initially or terminally.
• Death is generally attributed to respiratory failure secondary to respiratory muscle paralysis.
Etiology and Pathophysiology
• Three methods of toxin exposure in horses:
• Botulism intoxication occurs by a multistep process: binding to the target cell and internalization, translocation, and inhibition of neurotransmitter release.
• Botulinum neurotoxin (BoNT) prevents exocytosis of acetylcholine at the neuromuscular synapse by the cleavage of soluble N-ethylmaleimide sensitive factor attachment receptor proteins involved in the fusion of synaptic vesicles with the plasma membrane.
• The clinical effect is flaccid paralysis of large motor neuron units with lower motor neuron disease of the limbs, respiratory intercostal muscles, and pharyngeal muscles.
• Without intervention and supportive care, respiratory paralysis and death occur.
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