Wound Botulism is due to a bacterial toxin that disturbs the transmission of acetylcholine to bind to nicotinic/muscarinic receptors.
Majority of patients get botulism primary from foodborne illnesses, only a small percentage get botulism from wounds.
Wound botulism can also be commonly seen in patients who use black tar heroin (skin poppers). Injection of material into subcutaneous and/or muscle tissue provides the ideal environment for anaerobic bacteria – Clostridium botulinum.
Clostridium botulinim can produce 8 different strains of toxin – A – H
Patients present initially with bulbar symptoms and occasionally ocular abnormalities (diplopia, disconjugate eye movement, pupillary defects)
Also present as a symmetric descending paralysis complicated respiratory drive
Check history for evidence of skin popping
Wound botulism is more likely to cause fever and leukocytosis compared to other forms of botulism.
Patients with foodborne botulism typically present first with GI symptoms prior to onset of neurologic abnormalities
Important to suspect this in a patient with evolving neurologic deficits
Important to obtain wound culture for those who perform skin popping.
Diagnosis made by injecting mice and observing clinical manifestation. Then you reinject a second mouse with patient’s serum and antitoxin. If second mouse lives, that’s the diagnosis.
Supportive care including close airway monitoring (intubation if needed)
Botulinum heptavalent antitoxin
Monitor clinical status – typically a prolonged course of recovery as new axons grow from neurons to develop new neuromuscular junctions for function.
fluctuating weakness worse with repetition/activity
Initially involves the bulbar muscles, ptosis
Classically associated with thymomas (~80%)
Lambert Eaton Syndrome
No bulbar involvement. Proximal muscle involvement, ptosis.
Improves with repetition
Classically associated with small cell lung CA
Guillan Barre Syndrome
ascending paralysis, sensation intact although patients complain of vague symptoms.
Preceding viral URI or GI symptoms
Presence of autonomic symptoms such as hyper/hypotension, fluctuating temperatures, urinary incontinence/retention, brady/tachycardia, etc
Very similar presentation to GBS except no autonomic symptoms
Often times a tick can be found on the patient’s skin.