Fixed Pupils in Infant Botulism

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A previously healthy 7-month-old child was admitted to our emergency room with a 24-hour history of poor feeding, sleepiness, and hypotonia. Main clinical signs were apyrexia, weak crying, poor head control, constipation, and a symmetrical flaccid paralysis affecting head, trunk, and limbs with normoevocable lower tendon reflexes. Patient was unable to avoid light due to ophthalmoplegia ([Video 1]). Blood and cerebrospinal fluid tests, electroencephalogram, and central nervous system (CNS) magnetic resonance imaging were unremarkable, excluding sepsis, encephalitis, inborn errors of metabolism, spinal muscular atrophy, and inflammatory diseases of the CNS.[1] The patient developed progressive respiratory failure within hours and required mechanical ventilation. The suspicion of botulism was confirmed by stool detection of Clostridium botulinum toxin subtype A. Parents denied the administration of honey; the father is a construction worker, so we believe the spores were brought home by the construction site dust.

Video 1 The video shows ophthalmoplegia with inability to avoid light and fixed mydriasis suggesting brain stem involvement.

Infant botulism is a life-threatening condition caused by botulinum toxin which affects infants younger than 12 months. Main findings are symmetrical cranial nerve palsy, followed by descending, flaccid paralysis, leading to respiratory failure and death. The sensorium remains intact because the toxin does not cross the blood–brain barrier.

Clinical diagnosis remains the cornerstone for detecting botulism and maintaining high clinical suspicion is the key to prompt clinical management; therefore, early recognition and scrupulous supportive care are required for complete recovery.[2] [3]

Publication History

Received: 25 January 2022

Accepted: 05 May 2022

Article published online:
28 August 2022

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