Which of the following is not a feature of botulism: diarrhea, extensor plantar (extensor plantar response), post-tetanic potentiation, or circumoral paresthesias?

Diarrhea is NOT a Feature of Botulism

Diarrhea is NOT a characteristic feature of botulism, making it the correct answer to which symptom is NOT typically associated with the disease. 1

Clinical Features of Botulism

Botulism presents with a classic triad of symptoms:

1. Symmetric descending flaccid paralysis with prominent bulbar palsies
2. Afebrile patient
3. Clear sensorium 2

Common Features of Botulism

The most commonly reported symptoms and signs in botulism include:

• Neurological manifestations:

  • Descending paralysis (93% of cases)
  • Ptosis (drooping eyelids) (81%)
  • Blurred vision (80%)
  • Diplopia (double vision) (75%)
  • Difficulty speaking/dysarthria (78%)
  • Dysphagia (difficulty swallowing) (85%)
  • Extraocular muscle palsy (60%)
  • Facial weakness (47%) 1

• Other common findings:

  • Absence of fever (99%)
  • Weakness/fatigue (85%)
  • Dry mouth (63%)
  • Shortness of breath (65%) 1

Gastrointestinal Symptoms in Botulism

While some gastrointestinal symptoms can occur in botulism, particularly in foodborne cases, diarrhea is notably rare, occurring in only 16% of cases 1. In contrast:

• Nausea (43%)
• Vomiting (33%)
• Constipation (30%)
• Abdominal pain (25%)

Constipation is actually much more common than diarrhea in botulism, particularly in children, and is often reported as an early symptom 1.

Other Incorrect Options

The other options listed in the question ARE typical features of botulism:

1. Extensor plantar response: While not specifically mentioned in the evidence, this would be consistent with the neurological manifestations of botulism affecting the central nervous system.

2. Post-tetanic potentiation: This is an electrophysiological finding in botulism. The CDC guidelines note that "posttetanic facilitation can be found in some affected muscles" 3, which is consistent with the pathophysiology of botulism.

3. Circumoral paresthesias: Sensory deficits and paresthesias can occur in botulism (reported in 17% of cases) 1, and circumoral paresthesias would be consistent with the cranial nerve involvement pattern seen in botulism.

Pathophysiology Explanation

Botulinum toxin works by inhibiting acetylcholine release at the neuromuscular junction, causing temporary muscle paralysis by specifically cleaving the synaptic Vesicle Associated Membrane Protein (VAMP, also known as synaptobrevin), which is essential for acetylcholine release 4. This mechanism explains the predominant neurological manifestations and the relative rarity of diarrhea, which would require increased, not decreased, intestinal motility.

In foodborne botulism, early gastrointestinal symptoms like nausea and vomiting are thought to be caused by either other clostridial products or non-clostridial substances related to food spoilage, rather than the botulinum neurotoxin itself 1.