Probable case of botulism: treating with a grain of salt

Objective: Foodborne botulism is caused by ingestion of neurotoxins of Clostridium botulinum. Confirmed diagnosis is based on isolation of toxin in patient and/or food samples, but there are also cases with suggestive clinical symptoms associated with negative laboratory testing and responsive to specific antitoxin therapy. Case report: On December 2016, a 39-year-old woman was admitted in a clinical department of Policlinico Umberto I for diarrhea and dysarthria. Antibiotic and antiviral therapy was prescribed. Neurological exam was normal, and computerised tomography (CT) scan, magnetic resonance imaging (MRI), and cerebrospinal fluid analysis were negative. Three days later, symptoms progressed with the onset of ptosis, mydriasis, ophthalmoplegia, diplopia, xerostomia, dysphagia, and constipation, and the Poison Control Center was alerted. Foodborne botulism was suspected based on the anamnestic data, symptom onset and exclusion of other possible conditions. Rectal swabs were taken and Trivalent-Equine-Antitoxin (TEqA, 750 IU-anti-A, 500 IU-anti-B, 50 IU-anti-E per mL) was requested. Food samples consisting of inoil industrial preparations of meat and vegetables in spreadable paste (patè) consumed regularly by the patient were collected and sent for laboratory analysis. Antitoxin was then administered with a slow and progressive clinical amelioration over 48 hours. Culture of food samples revealed the presence of toxin producing Clostridium, while patient samples were negative. In the following days, ocular symptoms continued to improve, although a nasogastric tube was positioned for nutrition as liquid and solid dysphagia persisted. Fourteen days later, dysphagia for liquids and constipation resolved. Gradual improvement of symptoms continued over one month and she was discharged with a persistent diplopia. Two outpatient ophthalmological examinations at two and three months showed a gradual resolution of diplopia. On telephone follow-up, the patient reported facial muscles weakness four months after recovery. Conclusion: This case allows the following considerations: (i) given that bacterial isolation in food does not constitute a valid laboratory diagnostic criterion, presence of clinical and epidemiological criteria may define a probable botulism case [1]; (ii) neuromuscular sequelae several years after the critical phase have been reported [2], and may escape recognition if long-term follow-up sessions are not scheduled.