Introduction

• Cause: ingestion of preformed toxin produced by Clostridium botulinum. Rarely seen and this topic is scarce in the literature for botulism in exotics species.
• Signs: symmetrical ascending weakness/paralysis. Death due to respiratory paralysis.
• Diagnosis: clinical signs, history, presence of toxin in ingested food or body fluids.
• Treatment: supportive therapy. Antitoxin not always available and off license for exotics species.
• Prognosis: depends on the amount of toxin ingested and the speed of treatment. Prognosis is fair to poor.

Pathogenesis

Etiology

• Ingestion of carrion or spoiled food containing the preformed Clostridium botulinum neurotoxin.
• Bacteria survive in aquatic environments and neutral or alkaline soil.

Predisposing factors

General

• Exposure of carcasses.

Specific

• Ingestion of spoiled foodstuff, eg carrion.

Pathophysiology

• Ingestion of carrion or spoiled food containing the neurotoxin.
• Toxin is absorbed from the stomach and upper small intestine into the lymphatic system.
• Acetylcholine release at neuromuscular junctions and autonomic cholinergic synapses is inhibited by the botulinal neurotoxin.
• Diffuse neuromuscular blockade and dysfunction of the autonomic nervous system, resulting in neuromuscular paralysis, generalized motor neuron disease and parasympathetic dysfunction.
• Sensory nerves are not affected.
• Contamination by Clostridium botulinum in wounds is possible.

Timecourse

• Onset of clinical signs is related to the dose of the toxin ingested.

Epidemiology

• Clostridium botulinum are present in aquatic environments and the soil.
• Spores may be present in the gastrointestinal tract and tissues of mammals and birds.
• Spores can germinate upon the death of the animal and generate a toxin. The carcass is then potentially ingested by another animal.
• Botulism can result from both spore ingestion and wound contamination of Clostridium botulinum.

Diagnosis

Treatment

Prevention

Outcomes